Psoriasis 2018
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Mar 02, 2018
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About This Presentation
Introduction
Classification of the disease
History of disease
Epidemiology of disease
Clinical signs and symptoms
Genetic,
immunology and Pathogenesis
Diagnosis
Treatment
Vaccination
Prevention
Slide Content
PSORIASIS
0
0
PSORIASIS
1
Content:
Introduction…………………… ………….…. 2
Classification of the disease ……………….…2
History of disease ……………………… ….. 12
Epidemiology of disease …..………………. 1 2
Clinical signs and symptoms …………….…13
Genetic, immunology and Pathogenesis ……13
Diagnosis ………………………………….. 1 7
Treatment ……………………………… .…. 17
Vaccination …………………………… .….. 21
Prevention …………………………………. 2 2
Summary…………………………………… 2 2
References…………………………………. 2 3
1
Content:
Introduction…………………… ………….…. 2
Classification of the disease ……………….…2
History of disease ……………………… ….. 12
Epidemiology of disease …..………………. 1 2
Clinical signs and symptoms …………….…13
Genetic, immunology and Pathogenesis ……13
Diagnosis ………………………………….. 1 7
Treatment ……………………………… .…. 17
Vaccination …………………………… .….. 21
Prevention …………………………………. 2 2
Summary…………………………………… 2 2
References…………………………………. 2 3
PSORIASIS
2
Introduction:
Psoriasis is a complex, prevalent, chronic, multifactorial, inflammatory disease that involves
hyperproliferation of the keratinocytes in the epidermis, with an increase in the epidermal cell
turnover rate [1]. Environmental, genetic, and immunologic factors appear to play a role.
This chronic and so far incurable skin disorder is immune-mediated and most commonly manifests
on the skin of the elbows, knees, scalp, lumbosacral areas, intergluteal clefts, and glans penis. In
up to 30% of patients, the joints are also affected [1] [2].
Psoriasis may have significant systemic involvement, which is underscored by the coexistence
of various clinical disorders, including eye, cardiovascular, intestinal problems, metabolic
syndrome and joint inflammation. It has a very high negative impact on quality of life, requires
long-term treatment which usually has a high social and economic impact and is also associated
with a decreased life span [3] [4].
Classification of the disease:
The term psoriasis (from the Greek psora, to itch) encompasses a number of distinct clinical
phenotypes [5] , sometimes representing a dynamic, anatomical, or qualitative spectrum of the
same disease (e.g., large and small plaque psoriasis), whereas, in other cases, most likely
corresponds to a quite different entity (e.g., generalized pustular psoriasis [GPP]).
Historically, disease classification has been based on clinical appearance, mainly differentiating
according to localization and morphology. Here, we follow the recent classification proposed by
the International Psoriasis Council, which identifies the main forms of psoriasis and several further
subphenotypes according to distribution (localized vs. widespread), anatomical localization
(flexural, scalp, palms/soles/nail), size (large vs. small) and thickness (thick vs. thin) of plaques,
onset (early vs. late), and disease activity (active vs. stable) [6].
Psoriasis, a papulosquamous (i.e. being manifested by both scales and papules) skin disease, has
several different types, including: psoriasis vulgaris (common type), guttate psoriasis (small, drop
like spots), inverse psoriasis (in the folds like of the underarms, navel, and buttocks), and pustular
psoriasis (pus-filled, yellowish, small blisters). When the palms and the soles are involved, this
is known as palmoplantar psoriasis.
1. Psoriasis vulgaris (chronic stationary psoriasis, plaque-like psoriasis):
The commonest type of psoriasis, accounting for 90% of all cases [7-9] , (vulgar being Latin for
common), in which papulosquamous plaques are well-delineated from surrounding normal skin.
The plaques are red or salmon pink in color, covered by white or silvery scales and may be thick,
thin, large or small (Figure 1). So The size of a lesion may vary considerably from punctiform
papules to widespread plaques measuring over 30 cm in diameter.
They are most active at the edge: rapidly progressing lesions may be annular, with normal skin in
the centre, gyrate, and serpiginous psoriasis. Plaques are usually distributed symmetrically, and
occur most commonly on the extensor aspects of elbows and knees; scalp (Typically, the frontal
hair line and the temporal regions are involved and pruritus can be severe and recalcitrant) (Figure
2), lumbosacral region, and umbilicus. Active inflammatory psoriasis is characterized by the
Koebner phenomenon, in which new lesions develop at sites of trauma or pressure [10].
2
Introduction:
Psoriasis is a complex, prevalent, chronic, multifactorial, inflammatory disease that involves
hyperproliferation of the keratinocytes in the epidermis, with an increase in the epidermal cell
turnover rate [1]. Environmental, genetic, and immunologic factors appear to play a role.
This chronic and so far incurable skin disorder is immune-mediated and most commonly manifests
on the skin of the elbows, knees, scalp, lumbosacral areas, intergluteal clefts, and glans penis. In
up to 30% of patients, the joints are also affected [1] [2].
Psoriasis may have significant systemic involvement, which is underscored by the coexistence
of various clinical disorders, including eye, cardiovascular, intestinal problems, metabolic
syndrome and joint inflammation. It has a very high negative impact on quality of life, requires
long-term treatment which usually has a high social and economic impact and is also associated
with a decreased life span [3] [4].
Classification of the disease:
The term psoriasis (from the Greek psora, to itch) encompasses a number of distinct clinical
phenotypes [5] , sometimes representing a dynamic, anatomical, or qualitative spectrum of the
same disease (e.g., large and small plaque psoriasis), whereas, in other cases, most likely
corresponds to a quite different entity (e.g., generalized pustular psoriasis [GPP]).
Historically, disease classification has been based on clinical appearance, mainly differentiating
according to localization and morphology. Here, we follow the recent classification proposed by
the International Psoriasis Council, which identifies the main forms of psoriasis and several further
subphenotypes according to distribution (localized vs. widespread), anatomical localization
(flexural, scalp, palms/soles/nail), size (large vs. small) and thickness (thick vs. thin) of plaques,
onset (early vs. late), and disease activity (active vs. stable) [6].
Psoriasis, a papulosquamous (i.e. being manifested by both scales and papules) skin disease, has
several different types, including: psoriasis vulgaris (common type), guttate psoriasis (small, drop
like spots), inverse psoriasis (in the folds like of the underarms, navel, and buttocks), and pustular
psoriasis (pus-filled, yellowish, small blisters). When the palms and the soles are involved, this
is known as palmoplantar psoriasis.
1. Psoriasis vulgaris (chronic stationary psoriasis, plaque-like psoriasis):
The commonest type of psoriasis, accounting for 90% of all cases [7-9] , (vulgar being Latin for
common), in which papulosquamous plaques are well-delineated from surrounding normal skin.
The plaques are red or salmon pink in color, covered by white or silvery scales and may be thick,
thin, large or small (Figure 1). So The size of a lesion may vary considerably from punctiform
papules to widespread plaques measuring over 30 cm in diameter.
They are most active at the edge: rapidly progressing lesions may be annular, with normal skin in
the centre, gyrate, and serpiginous psoriasis. Plaques are usually distributed symmetrically, and
occur most commonly on the extensor aspects of elbows and knees; scalp (Typically, the frontal
hair line and the temporal regions are involved and pruritus can be severe and recalcitrant) (Figure
2), lumbosacral region, and umbilicus. Active inflammatory psoriasis is characterized by the
Koebner phenomenon, in which new lesions develop at sites of trauma or pressure [10].
PSORIASIS
3
A further distinction arises according to the age of onset of plaque psoriasis [11]. Henseler and
Christophers are credited with identifying two ages of onset: Early onset psoriasis (also referred
to as type I) has onset before the age of 40 years, with peak onset at 16–22 years of age, and
comprises 70% of all psoriatics. Late-onset psoriasis, also termed type II psoriasis, shows onset at
or after age 40 years, with a peak age of onset between 57 and 60 years [12].
Depending on the size of the affected area, the disease may be divided into three severity levels:
Mild (the rush affects up to 3 percent of the skin)
Moderate (up to 10 percent of patient’s body are covered with rush)
Severe (more than 10 percent of the skin is affected by the disease). [13]
Figure 1. Typical plaque of Psoriasis Vulgaris. (1)
Figure 2. Scalp psoriasis. (2)
3
A further distinction arises according to the age of onset of plaque psoriasis [11]. Henseler and
Christophers are credited with identifying two ages of onset: Early onset psoriasis (also referred
to as type I) has onset before the age of 40 years, with peak onset at 16–22 years of age, and
comprises 70% of all psoriatics. Late-onset psoriasis, also termed type II psoriasis, shows onset at
or after age 40 years, with a peak age of onset between 57 and 60 years [12].
Depending on the size of the affected area, the disease may be divided into three severity levels:
Mild (the rush affects up to 3 percent of the skin)
Moderate (up to 10 percent of patient’s body are covered with rush)
Severe (more than 10 percent of the skin is affected by the disease). [13]
Figure 1. Typical plaque of Psoriasis Vulgaris. (1)
Figure 2. Scalp psoriasis. (2)
PSORIASIS
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2. Guttate Psoriasis:
Guttate psoriasis, from the Latin “gutta” for tear drop, is characterized by multiple small scaly
plaques usually occurring around the trunk , upper arms and thighs. The rash has often sudden
onset, usually within 2–4 wk after a bacterial infection of the upper ways, notably streptococcal
pharyngitis in children and young adults, and is therefore associated with type I psoriasis [14].
Guttate psoriasis can either completely clear spontaneously or following topical treatment, become
chronic, or worsen into the plaque type.
The clinical picture is characterized by a sudden onset of diffuse red and scaling papules generally
measuring between 1 and 2 cm mostly affecting sun-protected areas (Figure 3). The
etiopathogenesis of the disease is still largely unknown but studies indicate that it is caused by an
interaction of multiple genetic components and environmental factors including β-hemolytic
streptococci[15].
It was first reported in 1916 that the onset of guttate psoriasis is often preceded by throat infections
with b-hemolytic streptococci. [16]
The paradoxical development of guttate psoriasis in the setting of Crohn,s disease patients treated
with infliximab has also been reported [17].
It is generally accepted that guttate psoriasis has a better prognosis than other types of psoriasis
because it may clear spontaneously after a period of months and usually has a longer remission
period. However, the eruption may progress into chronic plaque psoriasis or recur even after
spontaneous involution[18,19].
Figure 3. Detail of guttate lesions of psoriasis. (3)
4
2. Guttate Psoriasis:
Guttate psoriasis, from the Latin “gutta” for tear drop, is characterized by multiple small scaly
plaques usually occurring around the trunk , upper arms and thighs. The rash has often sudden
onset, usually within 2–4 wk after a bacterial infection of the upper ways, notably streptococcal
pharyngitis in children and young adults, and is therefore associated with type I psoriasis [14].
Guttate psoriasis can either completely clear spontaneously or following topical treatment, become
chronic, or worsen into the plaque type.
The clinical picture is characterized by a sudden onset of diffuse red and scaling papules generally
measuring between 1 and 2 cm mostly affecting sun-protected areas (Figure 3). The
etiopathogenesis of the disease is still largely unknown but studies indicate that it is caused by an
interaction of multiple genetic components and environmental factors including β-hemolytic
streptococci[15].
It was first reported in 1916 that the onset of guttate psoriasis is often preceded by throat infections
with b-hemolytic streptococci. [16]
The paradoxical development of guttate psoriasis in the setting of Crohn,s disease patients treated
with infliximab has also been reported [17].
It is generally accepted that guttate psoriasis has a better prognosis than other types of psoriasis
because it may clear spontaneously after a period of months and usually has a longer remission
period. However, the eruption may progress into chronic plaque psoriasis or recur even after
spontaneous involution[18,19].
Figure 3. Detail of guttate lesions of psoriasis. (3)
PSORIASIS
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3. Erythodermic Psoriasis:
Erythrodermic psoriasis represents one of the most severe and life-threatening variants of psoriasis.
This form affects greater than 90% of the body surface area and presents as large coherent sheets
of stratum corneum or fine scales over a predominant dusky red color reflecting the great degree
of cutaneous inflammation (Figure 4)
It is also one of the rarest forms of psoriasis, with an estimated prevalence of 1%–2.25% of patients
with psoriasis.[20,21]
This form of psoriasis can arise in patients with longstanding psoriasis vulgaris or it can occur de
novo as the initial presentation of psoriasis. It generally develops if there is poor control of a
patient, existing psoriasis; abrupt withdrawal of systemic medication, such as corticosteroids.
as a response to a drug reaction, such as lithium and beta-blockers; or due to an underlying systemic
infection[22].
There is a wide range of severity and acuity in patients with erythrodermic psoriasis. Some may
present with a rapid course that may require aggressive systemic therapy to achieve disease control,
whereas others may experience a more prolonged course of chronic erythroderma and experience
frequent relapses[23].
In rare instances, both the erythrodermic and the generalized pustular variants of psoriasis have
been associated with acute noncardiogenic pulmonary edema with hypoxemia attributed to
pulmonary capillary leak syndrome. Skin manifestations include diffuse edema, purpuric lesions,
livedo, and eruptions in sun-exposed areas. The condition is caused by increased capillary
permeability resulting in accumulation of fluids and proteins in the interstitial or extravascular
space with subsequent hypovolemic shock. It is a serious condition and can be potentially fatal if
not treated in a timely manner and with appropriate intensive therapy [24-26].
It is important to distinguish erythrodermic psoriasis from other inflammatory skin conditions that
can present with generalized erythroderma, such as pityriasis rubra pilaris, severe cases of atopic
dermatitis, generalized drug eruptions, and the erythrodermic stage of cutaneous lymphoma.
Overall, 25% of cases of erythroderma are caused by psoriasis. Although controversy exists, one
or more biopsies of representative areas can occasionally be useful in differentiating the underlying
cause of erythroderma[26].
5
3. Erythodermic Psoriasis:
Erythrodermic psoriasis represents one of the most severe and life-threatening variants of psoriasis.
This form affects greater than 90% of the body surface area and presents as large coherent sheets
of stratum corneum or fine scales over a predominant dusky red color reflecting the great degree
of cutaneous inflammation (Figure 4)
It is also one of the rarest forms of psoriasis, with an estimated prevalence of 1%–2.25% of patients
with psoriasis.[20,21]
This form of psoriasis can arise in patients with longstanding psoriasis vulgaris or it can occur de
novo as the initial presentation of psoriasis. It generally develops if there is poor control of a
patient, existing psoriasis; abrupt withdrawal of systemic medication, such as corticosteroids.
as a response to a drug reaction, such as lithium and beta-blockers; or due to an underlying systemic
infection[22].
There is a wide range of severity and acuity in patients with erythrodermic psoriasis. Some may
present with a rapid course that may require aggressive systemic therapy to achieve disease control,
whereas others may experience a more prolonged course of chronic erythroderma and experience
frequent relapses[23].
In rare instances, both the erythrodermic and the generalized pustular variants of psoriasis have
been associated with acute noncardiogenic pulmonary edema with hypoxemia attributed to
pulmonary capillary leak syndrome. Skin manifestations include diffuse edema, purpuric lesions,
livedo, and eruptions in sun-exposed areas. The condition is caused by increased capillary
permeability resulting in accumulation of fluids and proteins in the interstitial or extravascular
space with subsequent hypovolemic shock. It is a serious condition and can be potentially fatal if
not treated in a timely manner and with appropriate intensive therapy [24-26].
It is important to distinguish erythrodermic psoriasis from other inflammatory skin conditions that
can present with generalized erythroderma, such as pityriasis rubra pilaris, severe cases of atopic
dermatitis, generalized drug eruptions, and the erythrodermic stage of cutaneous lymphoma.
Overall, 25% of cases of erythroderma are caused by psoriasis. Although controversy exists, one
or more biopsies of representative areas can occasionally be useful in differentiating the underlying
cause of erythroderma[26].
PSORIASIS
6
Figure 4. Erythrodermic psoriasis. (4)
4. Pustular psoriasis:
In a population survey of psoriasis, pustular lesions were reported at any time during the course of
psoriasis by about 20% of patients [27]:
Pustular psoriasis is characterized by sterile pustules on an erythematous base. The Von Zumbusch
pattern is a rare and life-threatening subtype in which pustules erupt abruptly throughout the body,
coalescing into lakes of pus. The eruption may be triggered by withdrawal of systemic
corticosteroids. Systemic symptoms often occur, including fever, dehydration, hepatitis, and
pneumonitis [28]. Eruptive generalized pustular psoriasis rarely occurs in pregnancy, known as
impetigo herpetiformis. Less severe, localized pustular psoriasis subtypes also exist, including a
variant limited to the palms and soles (palmoplantar pustular psoriasis) and one limited to the distal
digits (acrodermatitis continua of Hallopeau).
There are 2 types of Pustular psoriasis:
Generalized Pustular Psoriasis:
In its typical form, GPP is a severe cutaneous and multisystemic inflammatory disease with life-
threatening potential characterized by sudden, repeated episodes of a generalized eruption of
disseminated aseptic pustules, associated with high fever, and general symptoms such as asthenia
and polymyalgia. Characteristic histopathological findings consist of a dense, pleomorphic dermal
6
Figure 4. Erythrodermic psoriasis. (4)
4. Pustular psoriasis:
In a population survey of psoriasis, pustular lesions were reported at any time during the course of
psoriasis by about 20% of patients [27]:
Pustular psoriasis is characterized by sterile pustules on an erythematous base. The Von Zumbusch
pattern is a rare and life-threatening subtype in which pustules erupt abruptly throughout the body,
coalescing into lakes of pus. The eruption may be triggered by withdrawal of systemic
corticosteroids. Systemic symptoms often occur, including fever, dehydration, hepatitis, and
pneumonitis [28]. Eruptive generalized pustular psoriasis rarely occurs in pregnancy, known as
impetigo herpetiformis. Less severe, localized pustular psoriasis subtypes also exist, including a
variant limited to the palms and soles (palmoplantar pustular psoriasis) and one limited to the distal
digits (acrodermatitis continua of Hallopeau).
There are 2 types of Pustular psoriasis:
Generalized Pustular Psoriasis:
In its typical form, GPP is a severe cutaneous and multisystemic inflammatory disease with life-
threatening potential characterized by sudden, repeated episodes of a generalized eruption of
disseminated aseptic pustules, associated with high fever, and general symptoms such as asthenia
and polymyalgia. Characteristic histopathological findings consist of a dense, pleomorphic dermal
PSORIASIS
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infiltrate of innate immune cells, where neutrophils and monocytes predominate, along with a
significant T lymphocytic component [29].
Patients with generalized pustular psoriasis (GPP) may have preexisting plaque psoriasis or
develop it after pustular episodes. Acute episodes may be triggered in patients with plaque
psoriasis by irritating topical therapy or abrupt corticosteroid withdrawal [30]. At the onset of an
attack of acute GPP (von Zumbusch type) the skin becomes very red and tender. There may be
fever and systemic symptoms such as anorexia and nausea. Within hours, myriads of pinhead-
sized pustules appear, studding the erythematous background. Pustules may become confluent,
producing lakes of pus. Subsequently, the pustules dry out, and the skin peels off, leaving a glazed,
smooth erythematous surface on which new crops of pustules may appear [31]. GPP should be
distinguished from acute generalized exanthematic pustulosis, a self-limiting febrile drug reaction
usually resolving in 2 weeks after withdrawal of the suspected agent, characterized by pinpoint
nonfollicular pustules on erythematous patches mainly involving folds. Single necrotic cells in
the epidermis, eosinophils, and vasculitic changes in the dermis are peculiar pathologic features
[32,33].
Localized pustular psoriasis:
Besides so-called psoriasis with pustules (sometimes referred to by the misleading term
“localized form of generalized pustular psoriasis”), 2 main clinical varieties are reported as
localized pustular psoriasis: acrodermatitis continua of Hallopeau and palmoplantar pustulosis.
- Acrodermatitis continua, also known as dermatitis repens, is a rare, chronic, pustular
eruption of the fingers and toes (Figure 5). Often, it begins after a localized trauma starting at the
tip of a single digit [34].
- Palmoplantar psoriasis: appears between the ages of 20 and 60. PPP causes large pustules
to form at the base of the thumb or on the sides of the heel. Classification of palmoplantar
pustulosis within the spectrum of psoriasis is controversial. The disease predominates in women
(more than 70% of patients are women) and is much more strongly associated with smoking than
plaque psoriasis[35]. Generally In time, the pustules turn brown and peel. The disease usually
becomes much less active for a while after peeling (Figure 6).
7
infiltrate of innate immune cells, where neutrophils and monocytes predominate, along with a
significant T lymphocytic component [29].
Patients with generalized pustular psoriasis (GPP) may have preexisting plaque psoriasis or
develop it after pustular episodes. Acute episodes may be triggered in patients with plaque
psoriasis by irritating topical therapy or abrupt corticosteroid withdrawal [30]. At the onset of an
attack of acute GPP (von Zumbusch type) the skin becomes very red and tender. There may be
fever and systemic symptoms such as anorexia and nausea. Within hours, myriads of pinhead-
sized pustules appear, studding the erythematous background. Pustules may become confluent,
producing lakes of pus. Subsequently, the pustules dry out, and the skin peels off, leaving a glazed,
smooth erythematous surface on which new crops of pustules may appear [31]. GPP should be
distinguished from acute generalized exanthematic pustulosis, a self-limiting febrile drug reaction
usually resolving in 2 weeks after withdrawal of the suspected agent, characterized by pinpoint
nonfollicular pustules on erythematous patches mainly involving folds. Single necrotic cells in
the epidermis, eosinophils, and vasculitic changes in the dermis are peculiar pathologic features
[32,33].
Localized pustular psoriasis:
Besides so-called psoriasis with pustules (sometimes referred to by the misleading term
“localized form of generalized pustular psoriasis”), 2 main clinical varieties are reported as
localized pustular psoriasis: acrodermatitis continua of Hallopeau and palmoplantar pustulosis.
- Acrodermatitis continua, also known as dermatitis repens, is a rare, chronic, pustular
eruption of the fingers and toes (Figure 5). Often, it begins after a localized trauma starting at the
tip of a single digit [34].
- Palmoplantar psoriasis: appears between the ages of 20 and 60. PPP causes large pustules
to form at the base of the thumb or on the sides of the heel. Classification of palmoplantar
pustulosis within the spectrum of psoriasis is controversial. The disease predominates in women
(more than 70% of patients are women) and is much more strongly associated with smoking than
plaque psoriasis[35]. Generally In time, the pustules turn brown and peel. The disease usually
becomes much less active for a while after peeling (Figure 6).
PSORIASIS
8
Figure 5. Acrodermatitis continua showing crops of pustular lesions at the tips of the fingers. (5)
Figure 6. Palmoplantar pustulosis.(6)
8
Figure 5. Acrodermatitis continua showing crops of pustular lesions at the tips of the fingers. (5)
Figure 6. Palmoplantar pustulosis.(6)
PSORIASIS
9
5. Inverse Psoriasis:
Unlike plaque psoriasis that commonly affects the extensor surfaces, inverse psoriasis may
manifest over any area of skin where two surface areas meet. It most commonly affects the inguinal
folds, armpits, under the breasts, skin folds around the groin and between the buttocks. and the
external genitalia [36]. It is particularly subject to irritation from rubbing and sweating because of
its location in skin folds and tender areas (Figure 7). This type of psoriasis is red, and often shiny
and smooth.
The lesions are smooth, well demarcated, and are typically less scaly and more erythematous than
the lesions of classic plaque psoriasis [37,38].
Inverse psoriasis affecting the genital skin folds is seen in up to 79% of patients with inverse
psoriasis [39] and is one of the most commonly seen dermatoses of this region in both females
and males [40]. Typically, genital psoriasis accompanies psoriasis lesions on other parts of the
body, but may also be isolated to the genital skin. Approximately two-thirds of patients with
psoriasis of all types will experience genital involvement at some point in their disease course [41].
Psoriasis of all forms can have a negative impact on social functioning, relationships, and sexual
health,[42] but psoriasis involving the genital region has been shown to be the most stigmatizing
area of involvement independent of overall disease severity [43].
Symptoms associated with genital psoriasis include itch, pain, dyspareunia, a worsening of their
genital psoriasis after intercourse, and a decreased frequency of sexual intercourse. Irritation and
trauma caused by intercourse, urine, feces, underwear, clothes, and local infections can worsen
genital involvement and perpetuate the process through the Köebner phenomenon [38].
Genital psoriasis usually does not produce scarring but one case report of two patients has
described atrophic scarring of the labia minora, mimicking the scarring caused by genital lichen
sclerosus [44]. A study characterizing factors associated with the development of genital psoriasis
showed associations with a younger age of onset of psoriasis, male sex, more severe disease, and
involvement of the scalp, flexures, or nails[41]
Figure 7. Flexural psoriasis, notes the relative lack of scale.(7)
9
5. Inverse Psoriasis:
Unlike plaque psoriasis that commonly affects the extensor surfaces, inverse psoriasis may
manifest over any area of skin where two surface areas meet. It most commonly affects the inguinal
folds, armpits, under the breasts, skin folds around the groin and between the buttocks. and the
external genitalia [36]. It is particularly subject to irritation from rubbing and sweating because of
its location in skin folds and tender areas (Figure 7). This type of psoriasis is red, and often shiny
and smooth.
The lesions are smooth, well demarcated, and are typically less scaly and more erythematous than
the lesions of classic plaque psoriasis [37,38].
Inverse psoriasis affecting the genital skin folds is seen in up to 79% of patients with inverse
psoriasis [39] and is one of the most commonly seen dermatoses of this region in both females
and males [40]. Typically, genital psoriasis accompanies psoriasis lesions on other parts of the
body, but may also be isolated to the genital skin. Approximately two-thirds of patients with
psoriasis of all types will experience genital involvement at some point in their disease course [41].
Psoriasis of all forms can have a negative impact on social functioning, relationships, and sexual
health,[42] but psoriasis involving the genital region has been shown to be the most stigmatizing
area of involvement independent of overall disease severity [43].
Symptoms associated with genital psoriasis include itch, pain, dyspareunia, a worsening of their
genital psoriasis after intercourse, and a decreased frequency of sexual intercourse. Irritation and
trauma caused by intercourse, urine, feces, underwear, clothes, and local infections can worsen
genital involvement and perpetuate the process through the Köebner phenomenon [38].
Genital psoriasis usually does not produce scarring but one case report of two patients has
described atrophic scarring of the labia minora, mimicking the scarring caused by genital lichen
sclerosus [44]. A study characterizing factors associated with the development of genital psoriasis
showed associations with a younger age of onset of psoriasis, male sex, more severe disease, and
involvement of the scalp, flexures, or nails[41]
Figure 7. Flexural psoriasis, notes the relative lack of scale.(7)
PSORIASIS
10
6. Nail Psoriasis:
Nail psoriasis occurs in up to 80% of patients with plaque psoriasis and is more prevalent in
patients with psoriatic arthritis. Nail psoriasis is far more than just a cosmetic problem. Psoriasis
of the fingernails is psychologically distressing and can cause pain, functional deficits in fine motor
manipulation of small objects, and when toenails are involved, it can cause difficulty with
ambulation. Although nail psoriasis can be extensively destructive to the nail plate, it is a
nonscarring process. If treated effectively, nails with psoriasis can return to a normal or close to
normal condition. Nail psoriasis takes a vast toll on patients, but with treatment and hopefully
clearing of nail psoriasis the quality of life can greatly increase [45].
Nearly 80% of patients with plaque psoriasis and 90% of patients with psoriatic arthritis have nail
involvement at some time during their life [46-48].
Nail psoriasis is more common in adults than in pediatric populations. In pediatric populations,
nail psoriasis is relatively uncommon with a prevalence of 7%–13% [49-51].
Psoriasis of highly visible areas of the body (including face, hands, scalp, and nails) affects
patients’ quality of life sometimes more compared with other chronic diseases [47, 52-54].
The most frequent signs of nail psoriasis are pitting and distal onycholysis [55].
Clinical manifestations range from pitting, yellowish discoloration, and paronychia, to subungual
hyperkeratosis, onycholysis, and severe onychodystrophy (Figure 8) [56].
Nail psoriasis can cause:
Nail pitting
Grooves
Discoloration
Loosening or crumbling of the nail
Thickened skin under the nail
Colored patches or spots under the nail
Sometimes, the nail can even crumble and fall off. There is no cure for psoriatic nails, but some
treatments may improve the health and appearance of nails [57].
Figure 8. Yellowish discoloration of fingernails.(8)
10
6. Nail Psoriasis:
Nail psoriasis occurs in up to 80% of patients with plaque psoriasis and is more prevalent in
patients with psoriatic arthritis. Nail psoriasis is far more than just a cosmetic problem. Psoriasis
of the fingernails is psychologically distressing and can cause pain, functional deficits in fine motor
manipulation of small objects, and when toenails are involved, it can cause difficulty with
ambulation. Although nail psoriasis can be extensively destructive to the nail plate, it is a
nonscarring process. If treated effectively, nails with psoriasis can return to a normal or close to
normal condition. Nail psoriasis takes a vast toll on patients, but with treatment and hopefully
clearing of nail psoriasis the quality of life can greatly increase [45].
Nearly 80% of patients with plaque psoriasis and 90% of patients with psoriatic arthritis have nail
involvement at some time during their life [46-48].
Nail psoriasis is more common in adults than in pediatric populations. In pediatric populations,
nail psoriasis is relatively uncommon with a prevalence of 7%–13% [49-51].
Psoriasis of highly visible areas of the body (including face, hands, scalp, and nails) affects
patients’ quality of life sometimes more compared with other chronic diseases [47, 52-54].
The most frequent signs of nail psoriasis are pitting and distal onycholysis [55].
Clinical manifestations range from pitting, yellowish discoloration, and paronychia, to subungual
hyperkeratosis, onycholysis, and severe onychodystrophy (Figure 8) [56].
Nail psoriasis can cause:
Nail pitting
Grooves
Discoloration
Loosening or crumbling of the nail
Thickened skin under the nail
Colored patches or spots under the nail
Sometimes, the nail can even crumble and fall off. There is no cure for psoriatic nails, but some
treatments may improve the health and appearance of nails [57].
Figure 8. Yellowish discoloration of fingernails.(8)
PSORIASIS
11
7. Psoriatic arthritis (PsA):
is a chronic systemic inflammatory disease that affects approximately 0.3% of the general
population and up to 20%–30% of patients with skin psoriasis [58].
The typical primary presentation is an asymmetric mono- or oligoarticular arthritis. The affected
joints are painful and may appear red, warm, and swollen. Common sites of involvement include
the hands, feet, and spine. Distal joint involvement is frequent and often occurs in a ‘ray’ pattern,
affecting all of the joints in a single digit rather than the same individual joints bilaterally, as seen
in rheumatoid arthritis (RA) [59]. 80% of patients with psoriatic arthritis have nail psoriasis
(Figure 9) [60].
Recognition of bone as an active organ that interacts with its environment is a relatively new
development. In the pathogenesis of bone destruction associated with rheumatoid arthritis, the
synovium is a site of active interplay between immune and bone cells. The interaction between T
cells and osteoclasts is a critical issue in the field of osteoimmunology [61]. Further differentiate
mechanisms of bone resorption and repair in PsA and RA and likely will uncover additional
therapeutic targets [62].
Figure 9. Psoriatic arthritis hand changes over time. (9)
11
7. Psoriatic arthritis (PsA):
is a chronic systemic inflammatory disease that affects approximately 0.3% of the general
population and up to 20%–30% of patients with skin psoriasis [58].
The typical primary presentation is an asymmetric mono- or oligoarticular arthritis. The affected
joints are painful and may appear red, warm, and swollen. Common sites of involvement include
the hands, feet, and spine. Distal joint involvement is frequent and often occurs in a ‘ray’ pattern,
affecting all of the joints in a single digit rather than the same individual joints bilaterally, as seen
in rheumatoid arthritis (RA) [59]. 80% of patients with psoriatic arthritis have nail psoriasis
(Figure 9) [60].
Recognition of bone as an active organ that interacts with its environment is a relatively new
development. In the pathogenesis of bone destruction associated with rheumatoid arthritis, the
synovium is a site of active interplay between immune and bone cells. The interaction between T
cells and osteoclasts is a critical issue in the field of osteoimmunology [61]. Further differentiate
mechanisms of bone resorption and repair in PsA and RA and likely will uncover additional
therapeutic targets [62].
Figure 9. Psoriatic arthritis hand changes over time. (9)
PSORIASIS
12
History of psoriasis:
The roots of the identification of psoriasis lie in Ancient Greece. The Greeks, who pioneered the
field of medicine, divided skin disease into the categories of psora, lepra and leichen [64]. Psora
referred to itch, while lepra was derived from the Greek words lopos (the epidermis) and lepo (to
scale) [65]. Hippocrates (460–377 BC) was one of the first authors to write descriptions of skin
disorders. He utilized the word lopoi to describe the dry, scaly, disfiguring eruptions of psoriasis,
leprosy, and other inflammatory skin disorders [66]. Similar to Hippocrates’ works, the Old
Testament also lumped together many cutaneous disorders. The biblical term tsaraat, or zaraath,
described a range of skin conditions including leprosy and psoriasis. Lepers were often ostracized
because they were considered divinely punished, and cruelty was imposed upon those who
suffered from psoriasis and leprosy alike [67, 68]. Many historians credit the Roman thinker Celsus
(ca. 25 BC–45 AD) with the first clinical description of papulosquamous diseases [63, 64, 67].
Celsus described impetigines and specified that the second species of impetigo was characterized
by red skin covered with scales. This description suggested a type of papulosquamous disease,
such as psoriasis [69]. Galen (133–200 AD) first utilized the term psoriasis, but his description
was not consistent with the disorder that we now call psoriasis. He described psoriasis as a pruritic,
scaly skin disease of the eyelids and scrotum. Although he used the term psoriasis, his description
is now believed to most likely represent seborrheic dermatitis [65, 67, 70]. Indiscriminate grouping
together of all inflammatory skin diseases led to stigmatization of patients with psoriasis. For
centuries, patients with psoriasis received the same cruel handling as lepers. They were required
to carry a bell or clapper to announce their approach, and had to wear a special dress. In addition,
they could only touch or dine with others considered lepers. In 1313, Phillip the Fair of France
ordered that they be burned at the stake [63].
Epidemiology of psoriasis:
Psoriasis affects 2 to 3 percent of the world population[71] and 2 to 4 percent of the population in
Western countries, with prevalence rates influenced by age, geographic location, and genetic
background [72].
A recent systematic review of psoriasis epidemiology confirms that psoriasis is a common disease,
based on 46 studies reporting on prevalence of psoriasis and seven studies related to the incidence
of disease in the general population [73].
Prevalence is higher in adults (from 0.91% to 8.5%) as compared with children (from 0% to 2.1%)
with a dual peak of incidence: ∼30–39 years and ∼60 years of age. Disease prevalence is different
across countries, with a geographical pattern suggesting less prevalence in those closer to the
equator as compared with the more distant ones, in line with the beneficial effects of UV radiation
exposure and clinical amelioration of psoriasis [74]. Prevalence in Europe varies from 0.73% to
2.9%, similar to the Unites States (0.7%–2.6%) and higher than Latin America, Africa, and Asia
(from 0 to <0.5%). Psoriasis has traditionally been considered to affect both genders equally
[75][76].
12
History of psoriasis:
The roots of the identification of psoriasis lie in Ancient Greece. The Greeks, who pioneered the
field of medicine, divided skin disease into the categories of psora, lepra and leichen [64]. Psora
referred to itch, while lepra was derived from the Greek words lopos (the epidermis) and lepo (to
scale) [65]. Hippocrates (460–377 BC) was one of the first authors to write descriptions of skin
disorders. He utilized the word lopoi to describe the dry, scaly, disfiguring eruptions of psoriasis,
leprosy, and other inflammatory skin disorders [66]. Similar to Hippocrates’ works, the Old
Testament also lumped together many cutaneous disorders. The biblical term tsaraat, or zaraath,
described a range of skin conditions including leprosy and psoriasis. Lepers were often ostracized
because they were considered divinely punished, and cruelty was imposed upon those who
suffered from psoriasis and leprosy alike [67, 68]. Many historians credit the Roman thinker Celsus
(ca. 25 BC–45 AD) with the first clinical description of papulosquamous diseases [63, 64, 67].
Celsus described impetigines and specified that the second species of impetigo was characterized
by red skin covered with scales. This description suggested a type of papulosquamous disease,
such as psoriasis [69]. Galen (133–200 AD) first utilized the term psoriasis, but his description
was not consistent with the disorder that we now call psoriasis. He described psoriasis as a pruritic,
scaly skin disease of the eyelids and scrotum. Although he used the term psoriasis, his description
is now believed to most likely represent seborrheic dermatitis [65, 67, 70]. Indiscriminate grouping
together of all inflammatory skin diseases led to stigmatization of patients with psoriasis. For
centuries, patients with psoriasis received the same cruel handling as lepers. They were required
to carry a bell or clapper to announce their approach, and had to wear a special dress. In addition,
they could only touch or dine with others considered lepers. In 1313, Phillip the Fair of France
ordered that they be burned at the stake [63].
Epidemiology of psoriasis:
Psoriasis affects 2 to 3 percent of the world population[71] and 2 to 4 percent of the population in
Western countries, with prevalence rates influenced by age, geographic location, and genetic
background [72].
A recent systematic review of psoriasis epidemiology confirms that psoriasis is a common disease,
based on 46 studies reporting on prevalence of psoriasis and seven studies related to the incidence
of disease in the general population [73].
Prevalence is higher in adults (from 0.91% to 8.5%) as compared with children (from 0% to 2.1%)
with a dual peak of incidence: ∼30–39 years and ∼60 years of age. Disease prevalence is different
across countries, with a geographical pattern suggesting less prevalence in those closer to the
equator as compared with the more distant ones, in line with the beneficial effects of UV radiation
exposure and clinical amelioration of psoriasis [74]. Prevalence in Europe varies from 0.73% to
2.9%, similar to the Unites States (0.7%–2.6%) and higher than Latin America, Africa, and Asia
(from 0 to <0.5%). Psoriasis has traditionally been considered to affect both genders equally
[75][76].
PSORIASIS
13
Signs and symptoms:
Psoriasis signs and symptoms are different for everyone. Common signs and symptoms
include:
Red patches of skin covered with thick, silvery scales.
Small scaling spots (commonly seen in children).
Dry, cracked skin that may bleed.
Itching, burning or soreness.
Thickened, pitted or ridged nails.
Swollen and stiff joints.
Psoriasis patches can range from a few spots of dandruff-like scaling to major eruptions
that cover large areas.
Most types of psoriasis go through cycles, flaring for a few weeks or months, then
subsiding for a time or even going into complete remission.[77]
Genetics, immunology, and pathogenesis:
Genetic susceptibility:
Many lines of evidence, including familial aggregation, disease concordance in twins, and
genome-wide association studies (GWAS), suggest a strong genetic component in PsA. The high
occurrence of PsA and psoriasis within families indicates a significant genetic predisposition to
developing these diseases, with first-degree relatives having a 30-fold increased risk of developing
PsA compared with the general population [78]. Twin studies in psoriasis patients reveal an
increased rate of concordance in monozygotic versus dizygotic twins (72% versus 15%–23%,
respectively) [79]. In contrast, no large twin cohort studies have been conducted to date in PsA.
One twin study in PsA did not demonstrate a significant genetic effect, with almost identical
concordance rates observed in monozygotic and dizygotic twins [80]. Difficulty in differentiating
PsA from other forms of inflammatory arthritis and inclusion of psoriasis patients without true
inflammatory articular and periarticular disease in PsA cohorts has likely complicated the study of
PsA, as their inclusion introduces a lack of uniformity. The Classification of Psoriatic Arthritis
(CASPAR) criteria should help create a more uniform patient population for future studies[81].
Genome-wide scans have identified the contribution of several susceptibility genes, indicating that
psoriasis and PsA are polygenic disorders. Of the many genes proposed, the most relevant appear
to be certain class I human leukocyte antigen (HLA) genes occurring within the major
histocompatibility complex (MHC) region on chromosome 6p, which account for roughly 30% of
genetic susceptibility[82]. Polymorphisms of class I HLA alleles that are associated with PsA
include HLA-B7, HLA-B27, HLA-B38, and HLA-B39[83]. Although HLA-B alleles seem to
confer increased risk for articular manifestations, HLA-C alleles confer greater susceptibility to
cutaneous manifestations: HLA-Cw6 is associated with early-onset skin psoriasis, with a more
13
Signs and symptoms:
Psoriasis signs and symptoms are different for everyone. Common signs and symptoms
include:
Red patches of skin covered with thick, silvery scales.
Small scaling spots (commonly seen in children).
Dry, cracked skin that may bleed.
Itching, burning or soreness.
Thickened, pitted or ridged nails.
Swollen and stiff joints.
Psoriasis patches can range from a few spots of dandruff-like scaling to major eruptions
that cover large areas.
Most types of psoriasis go through cycles, flaring for a few weeks or months, then
subsiding for a time or even going into complete remission.[77]
Genetics, immunology, and pathogenesis:
Genetic susceptibility:
Many lines of evidence, including familial aggregation, disease concordance in twins, and
genome-wide association studies (GWAS), suggest a strong genetic component in PsA. The high
occurrence of PsA and psoriasis within families indicates a significant genetic predisposition to
developing these diseases, with first-degree relatives having a 30-fold increased risk of developing
PsA compared with the general population [78]. Twin studies in psoriasis patients reveal an
increased rate of concordance in monozygotic versus dizygotic twins (72% versus 15%–23%,
respectively) [79]. In contrast, no large twin cohort studies have been conducted to date in PsA.
One twin study in PsA did not demonstrate a significant genetic effect, with almost identical
concordance rates observed in monozygotic and dizygotic twins [80]. Difficulty in differentiating
PsA from other forms of inflammatory arthritis and inclusion of psoriasis patients without true
inflammatory articular and periarticular disease in PsA cohorts has likely complicated the study of
PsA, as their inclusion introduces a lack of uniformity. The Classification of Psoriatic Arthritis
(CASPAR) criteria should help create a more uniform patient population for future studies[81].
Genome-wide scans have identified the contribution of several susceptibility genes, indicating that
psoriasis and PsA are polygenic disorders. Of the many genes proposed, the most relevant appear
to be certain class I human leukocyte antigen (HLA) genes occurring within the major
histocompatibility complex (MHC) region on chromosome 6p, which account for roughly 30% of
genetic susceptibility[82]. Polymorphisms of class I HLA alleles that are associated with PsA
include HLA-B7, HLA-B27, HLA-B38, and HLA-B39[83]. Although HLA-B alleles seem to
confer increased risk for articular manifestations, HLA-C alleles confer greater susceptibility to
cutaneous manifestations: HLA-Cw6 is associated with early-onset skin psoriasis, with a more
PSORIASIS
14
severe and extensive presentation, but appears to have less of an association with articular
symptoms[84]. In addition to influencing disease phenotype, certain HLA antigens confer
increased risk for disease progression (e.g., HLA-B39 alone and HLA-B27 in the presence of
HLA-DR7), whereas others may reduce the risk of disease progression (e.g., HLA-B22 may
be protective)[85]. Other genes, such as the shared epitope HLADRB1, when found in linkage
disequilibrium with the aforementioned alleles, confer a worse radiological outcome (i.e., more
erosive disease in peripheral joints) in PsA[86]. Other susceptibility genes identified by genome-
wide scans that are associated with an increased risk of psoriasis and PsA includes polymorphisms
of the tumor necrosis factor-alpha (TNF-α) promoter region (TNFA) and the MHC class I chain–
related A gene (MICA-A9)[87,88]. NonMHC susceptibility regions conferring increased risk for
psoriasis have also been identified (e.g., the PSORS1 [psoriasis susceptibility 1]-9 loci); however,
relevant candidate genes have not yet been identified[89]. Thus, although high rates of familial
aggregation occur in PsA and psoriasis, the disease phenotype can vary widely depending on the
presence or absence of various susceptibility genes.
Environmental factors:
Environmental factors appear to play a role in the development of PsA among some individuals.
Evidence for the role of environmental factors in the pathogenesis of psoriasis and PsA comes
largely from observational studies. The two most commonly reported associations are infection
and trauma; however, the mechanism underlying how these processes contribute to disease
pathogenesis remains poorly understood. There is a strong association of streptococcal pharyngitis
preceding an acute form of guttate psoriasis in children[90]. Similarly, human immunodeficiency
virus (HIV) infection, particularly before the introduction of antiretroviral therapy, has been
associated with a more aggressive form of psoriasis and PsA[91]. Thus, certain prior infections
may confer an increased risk of developing PsA[92]. Of note, this is not the case for most patients,
as antecedent infections typically do not seem to initiate PsA. There is some evidence for the role
of trauma in skin psoriasis and possibly PsA. The Koebner phenomenon is an uncommon but well-
described occurrence in psoriasis wherein skin plaques develop at sites of trauma to nonlesional
skin. Trauma or biomechanical stress has been proposed as a potential cause of enthesitis and joint
inflammation in PsA, sometimes referred to as “deep Koebner phenomenon.”[93]. Interestingly,
a history of trauma preceding the onset of peripheral arthritis was reported in 8%–9% of patients
with newly diagnosed PsA[94,95]. Case–control studies have suggested several other potential
causative factors, including joint injury, vaccination, recurrent oral ulceration, repetitive heavy
lifting, and infections requiring treatment with antibiotics[93,96]. In patients with nail dystrophy,
repetitive microtrauma has been hypothesized to play a role in the pathogenesis of distal
interphalangeal (DIP) joint involvement by eliciting an aberrant immune response that results in
persistent inflammation of the adjacent enthesis and synovium[97].
14
severe and extensive presentation, but appears to have less of an association with articular
symptoms[84]. In addition to influencing disease phenotype, certain HLA antigens confer
increased risk for disease progression (e.g., HLA-B39 alone and HLA-B27 in the presence of
HLA-DR7), whereas others may reduce the risk of disease progression (e.g., HLA-B22 may
be protective)[85]. Other genes, such as the shared epitope HLADRB1, when found in linkage
disequilibrium with the aforementioned alleles, confer a worse radiological outcome (i.e., more
erosive disease in peripheral joints) in PsA[86]. Other susceptibility genes identified by genome-
wide scans that are associated with an increased risk of psoriasis and PsA includes polymorphisms
of the tumor necrosis factor-alpha (TNF-α) promoter region (TNFA) and the MHC class I chain–
related A gene (MICA-A9)[87,88]. NonMHC susceptibility regions conferring increased risk for
psoriasis have also been identified (e.g., the PSORS1 [psoriasis susceptibility 1]-9 loci); however,
relevant candidate genes have not yet been identified[89]. Thus, although high rates of familial
aggregation occur in PsA and psoriasis, the disease phenotype can vary widely depending on the
presence or absence of various susceptibility genes.
Environmental factors:
Environmental factors appear to play a role in the development of PsA among some individuals.
Evidence for the role of environmental factors in the pathogenesis of psoriasis and PsA comes
largely from observational studies. The two most commonly reported associations are infection
and trauma; however, the mechanism underlying how these processes contribute to disease
pathogenesis remains poorly understood. There is a strong association of streptococcal pharyngitis
preceding an acute form of guttate psoriasis in children[90]. Similarly, human immunodeficiency
virus (HIV) infection, particularly before the introduction of antiretroviral therapy, has been
associated with a more aggressive form of psoriasis and PsA[91]. Thus, certain prior infections
may confer an increased risk of developing PsA[92]. Of note, this is not the case for most patients,
as antecedent infections typically do not seem to initiate PsA. There is some evidence for the role
of trauma in skin psoriasis and possibly PsA. The Koebner phenomenon is an uncommon but well-
described occurrence in psoriasis wherein skin plaques develop at sites of trauma to nonlesional
skin. Trauma or biomechanical stress has been proposed as a potential cause of enthesitis and joint
inflammation in PsA, sometimes referred to as “deep Koebner phenomenon.”[93]. Interestingly,
a history of trauma preceding the onset of peripheral arthritis was reported in 8%–9% of patients
with newly diagnosed PsA[94,95]. Case–control studies have suggested several other potential
causative factors, including joint injury, vaccination, recurrent oral ulceration, repetitive heavy
lifting, and infections requiring treatment with antibiotics[93,96]. In patients with nail dystrophy,
repetitive microtrauma has been hypothesized to play a role in the pathogenesis of distal
interphalangeal (DIP) joint involvement by eliciting an aberrant immune response that results in
persistent inflammation of the adjacent enthesis and synovium[97].
PSORIASIS
15
Immunology:
Aberrations in both innate and adaptive immunity occur in PsA, resulting in a chronic systemic
inflammatory process[98]. The disease is characterized by cellular infiltration, with substantial
accumulation of T lymphocytes and macrophages among other cells in the synovial tissue along
with prominent new vessel formation[99]. A complex interaction between T cells, dendritic cells,
keratinocytes, and synoviocytes results in a self-perpetuating loop of sustained inflammation in
the skin and synovium[100].
Pathogenesis:
The precise immunopathogenic mechanisms in PsA remain incompletely understood, but they
are thought to share some of the same disease mechanisms seen in psoriasis. As mentioned, a
genetically susceptible individual exposed to some environmental or other stimulus may develop
an aberrant immune response of both innate and adaptive immunity that leads ultimately to a
chronic systemic inflammatory process that causes the clinical manifestations of PsA. On a
histopathologic level, the sequence may occur as follows ( Figure 10) [101]:
(1) A genetically susceptible host is exposed to an environmental stimulus (e.g., trauma or
infection). (2) Damage to keratinocyte results in release of antigenic material (e.g., antimicrobial
peptides) that activates the innate immune response, possibly via binding to Toll-like receptors.
(3) Plasmacytoid dendritic cells and other innate cells located in the epidermis are activated and
produce proinflammatory cytokines (e.g., IFN-α, TNF-α). (4) These cytokines stimulate myeloid
dendritic cells (CD83+) located in the dermis, which subsequently migrate to lymph nodes
and present antigen to T cells. (5) T cells are activated by antigen presentation and subsequently
proliferate (adaptive immunity). The cytokine milieu favors increased production of Th17 and Th1
cells resulting in an inflammatory response. (6) T cells migrate to the tissues (e.g., skin and
synovium) where they perpetuate a chronic inflammatory immune response (e.g., keratinocyte
hyperproliferation and synovitis). (7) The overexpression of proinflammatory cytokines results in
activation of transcription factors and upregulation of proinflammatory genes. (8) A self-
sustaining loop results in a chronic systemic inflammatory process.
15
Immunology:
Aberrations in both innate and adaptive immunity occur in PsA, resulting in a chronic systemic
inflammatory process[98]. The disease is characterized by cellular infiltration, with substantial
accumulation of T lymphocytes and macrophages among other cells in the synovial tissue along
with prominent new vessel formation[99]. A complex interaction between T cells, dendritic cells,
keratinocytes, and synoviocytes results in a self-perpetuating loop of sustained inflammation in
the skin and synovium[100].
Pathogenesis:
The precise immunopathogenic mechanisms in PsA remain incompletely understood, but they
are thought to share some of the same disease mechanisms seen in psoriasis. As mentioned, a
genetically susceptible individual exposed to some environmental or other stimulus may develop
an aberrant immune response of both innate and adaptive immunity that leads ultimately to a
chronic systemic inflammatory process that causes the clinical manifestations of PsA. On a
histopathologic level, the sequence may occur as follows ( Figure 10) [101]:
(1) A genetically susceptible host is exposed to an environmental stimulus (e.g., trauma or
infection). (2) Damage to keratinocyte results in release of antigenic material (e.g., antimicrobial
peptides) that activates the innate immune response, possibly via binding to Toll-like receptors.
(3) Plasmacytoid dendritic cells and other innate cells located in the epidermis are activated and
produce proinflammatory cytokines (e.g., IFN-α, TNF-α). (4) These cytokines stimulate myeloid
dendritic cells (CD83+) located in the dermis, which subsequently migrate to lymph nodes
and present antigen to T cells. (5) T cells are activated by antigen presentation and subsequently
proliferate (adaptive immunity). The cytokine milieu favors increased production of Th17 and Th1
cells resulting in an inflammatory response. (6) T cells migrate to the tissues (e.g., skin and
synovium) where they perpetuate a chronic inflammatory immune response (e.g., keratinocyte
hyperproliferation and synovitis). (7) The overexpression of proinflammatory cytokines results in
activation of transcription factors and upregulation of proinflammatory genes. (8) A self-
sustaining loop results in a chronic systemic inflammatory process.
PSORIASIS
16
Figure 10. Hypothetical model of the pathogenesis of psoriatic arthritis. An
environmental stimulus (e.g., trauma or infection) causes damage to keratinocytes in
a genetically susceptible host. Antigenic peptides released from the damaged area
activate the innate immune system, resulting in the release of proinflammatory cytokines.
Myeloid dendritic cells subsequently migrate to skin draining lymph nodes, where they
cause T-cell activation and proliferation. These activated T cells migrate to the tissues
(e.g., skin, synovium, or entheses) and mediate a chronic inflammatory process.[159]
16
Figure 10. Hypothetical model of the pathogenesis of psoriatic arthritis. An
environmental stimulus (e.g., trauma or infection) causes damage to keratinocytes in
a genetically susceptible host. Antigenic peptides released from the damaged area
activate the innate immune system, resulting in the release of proinflammatory cytokines.
Myeloid dendritic cells subsequently migrate to skin draining lymph nodes, where they
cause T-cell activation and proliferation. These activated T cells migrate to the tissues
(e.g., skin, synovium, or entheses) and mediate a chronic inflammatory process.[159]
PSORIASIS
17
Diagnosis of psoriasis:
In most cases diagnosis of psoriasis is fairly straightforward:
Physical exam and medical history: by taking the medical history and examining of the
skin, scalp and nails.
Skin biopsy: by taking a small sample of the skin. This acquires a local anesthetic. The
sample is examined under microscope to determine the exact type of psoriasis and to rule out other
disorders.[102]
Treatment of psoriasis:
Treatment of psoriasis depends on the type and severity of the disease. Typically, topical therapies
are used to treat mild and localized psoriasis. Topical treatments are the foundation for mild to
moderate psoriasis. However, this approach can decrease the number and thickness of the plaque
lesions, and reduce the percentage of body surface involved. In general, pharmacological
treatment should start with the use of topical corticosteroids [103]. The complete clearance of
lesions is often not a realistic goal with topical therapy but eventually remission can be reached.
Frustration related to medication efficacy expectations, poor cosmetic characteristics of topical
preparations, time consumption, fear of side effects, and inconvenience were found to be the most
important reasons patients chose to deviate from provider recommendations of topical therapy
[104]. Studies suggest that adherence with topical treatment in psoriasis is poor. Research has
shown that only 50% of topical agent applications prescribed by physicians are actually used [105].
Patients with chronic psoriasis may be candidates for topical therapy depending on their baseline
severity. Topical treatments include creams, ointments, and lotions. The choice of formulation
depends on the area affected. Physicians should also select formulations that will be acceptable to
the patient [106]. There is a consensus that topical emollients and salicylic acid are effective as
initial and adjunctive therapy for people with chronic plaque psoriasis, but it is unclear whether
tars are effective [107].
Various topical agents exist for the treatment of psoriasis and include topical corticosteroids,
vitamin D analogs, tazarotene, calcineurin inhibitors, anthralin, coal tar, and combination
therapies. Just as the topical treatment options are numerous, so too are the choices of vehicle. The
choice of the vehicle often impacts efficacy, penetration, and adherence to the treatment regimen.
Multiple new topical options are also on the horizon.
17
Diagnosis of psoriasis:
In most cases diagnosis of psoriasis is fairly straightforward:
Physical exam and medical history: by taking the medical history and examining of the
skin, scalp and nails.
Skin biopsy: by taking a small sample of the skin. This acquires a local anesthetic. The
sample is examined under microscope to determine the exact type of psoriasis and to rule out other
disorders.[102]
Treatment of psoriasis:
Treatment of psoriasis depends on the type and severity of the disease. Typically, topical therapies
are used to treat mild and localized psoriasis. Topical treatments are the foundation for mild to
moderate psoriasis. However, this approach can decrease the number and thickness of the plaque
lesions, and reduce the percentage of body surface involved. In general, pharmacological
treatment should start with the use of topical corticosteroids [103]. The complete clearance of
lesions is often not a realistic goal with topical therapy but eventually remission can be reached.
Frustration related to medication efficacy expectations, poor cosmetic characteristics of topical
preparations, time consumption, fear of side effects, and inconvenience were found to be the most
important reasons patients chose to deviate from provider recommendations of topical therapy
[104]. Studies suggest that adherence with topical treatment in psoriasis is poor. Research has
shown that only 50% of topical agent applications prescribed by physicians are actually used [105].
Patients with chronic psoriasis may be candidates for topical therapy depending on their baseline
severity. Topical treatments include creams, ointments, and lotions. The choice of formulation
depends on the area affected. Physicians should also select formulations that will be acceptable to
the patient [106]. There is a consensus that topical emollients and salicylic acid are effective as
initial and adjunctive therapy for people with chronic plaque psoriasis, but it is unclear whether
tars are effective [107].
Various topical agents exist for the treatment of psoriasis and include topical corticosteroids,
vitamin D analogs, tazarotene, calcineurin inhibitors, anthralin, coal tar, and combination
therapies. Just as the topical treatment options are numerous, so too are the choices of vehicle. The
choice of the vehicle often impacts efficacy, penetration, and adherence to the treatment regimen.
Multiple new topical options are also on the horizon.
PSORIASIS
18
Topical corticosteroids:
Corticosteroids remain the most commonly used topical medications in the treatment of psoriasis
[108]. By regulating the gene transcription of proinflammatory cytokines, topical corticosteroids
exert anti-inflammatory, antiproliferative, and immunosuppressive effects on target tissues [109].
topical steroids should be used judiciously in the longterm treatment of chronic conditions such as
psoriasis due to their cutaneous and systemic side effect profiles. Cutaneous side effects including
atrophy, purpura, striae distensiae, periorificial dermatitis, and acne may limit treatment duration,
especially in the treatment of steroid-sensitive anatomic sites such as the face, groin, or skin folds.
Although much less common, systemic steroid side effects can occur when potent or superpotent
topical steroids are used over large body surface areas for prolonged periods of time. Disturbance
of the hypothalamic–pituitary axis, Cushing’s syndrome, osteonecrosis of the femoral head,
cataracts, and glaucoma have all been reported [110-114]
Several innovative methods to reduce the potential for these serious adverse events have been
implemented. These include “weekend-only” steroid regimens and combination therapies with
noncorticosteroid topical formulations.
Vitamin D analogs:
At this time, three vitamin D analogs, calcipotriene (calcipitriol), calcitriol, and tacalcitol, exist for
the treatment of psoriasis. Vitamin D analogs result in keratinocyte differentiation and inhibition
of keratinocyte proliferation that is mediated by binding of intracellular vitamin D receptors and
subsequent gene regulation [115]. Calcipotriene is available as a cream, solution, foam, and
ointment. When used as monotherapy, calcipotriene ointment was found to result in greater than
75% improvement in patients with chronic plaque-type psoriasis compared with a 19%
improvement in patients treated with vehicle alone [116]. When compared with potent topical
corticosteroids such as betamethasone dipropionate, no significant differences in efficacy were
seen in the treatment of psoriatic plaques on the body [117]. However, studies have shown that
calcipotriene in solution is inferior in treatment of scalp psoriasis when compared with potent or
superpotent topical steroids [118]. Calcitriol is another synthetic vitamin D analog that is approved
for use in the United States and is available as an ointment. Calcitriol has been shown to be as
effective in the treatment of psoriasis as calcipotriene. However, calcitriol appears to be better
tolerated in sensitive areas such as the face or intertriginous folds [119]. Tacalcitol is available for
use outside of the United States but has not yet been approved for use in the United States. Unlike
calcipotriene, which is approved for once or twice daily dosing, and calcitriol, which is approved
for twice daily dosing, tacalcitol is designed to be used once daily. Although its efficacy for the
treatment of psoriasis has been established in vehicle-controlled studies [120], tacalcitol appears
to be less efficacious than potent topical corticosteroids in the treatment of scalp psoriasis [121].
As a class, vitamin D analogs are generally welltolerated. Local side effects, including burning,
pruritus, edema, peeling, and erythema, are among the most common to occur and can affect up to
25% of patients[122]. The risk of more serious systemic adverse events including hypercalcemia
and impaired parathyroid hormone regulation is rare and can be avoided if patients do not exceed
the maximum allotted doses of the vitamin D analogs. Patients with chronic kidney disease or on
medications that can concurrently result in hypercalcemia, such as thiazide diuretics, are at
increased risk of hypercalcemia [123].
In addition, vitamin D analogs can be combined with phototherapy. The use of twice daily
regimens of calcipotriene with twice weekly narrowband ultraviolet B (UVB) phototherapy
18
Topical corticosteroids:
Corticosteroids remain the most commonly used topical medications in the treatment of psoriasis
[108]. By regulating the gene transcription of proinflammatory cytokines, topical corticosteroids
exert anti-inflammatory, antiproliferative, and immunosuppressive effects on target tissues [109].
topical steroids should be used judiciously in the longterm treatment of chronic conditions such as
psoriasis due to their cutaneous and systemic side effect profiles. Cutaneous side effects including
atrophy, purpura, striae distensiae, periorificial dermatitis, and acne may limit treatment duration,
especially in the treatment of steroid-sensitive anatomic sites such as the face, groin, or skin folds.
Although much less common, systemic steroid side effects can occur when potent or superpotent
topical steroids are used over large body surface areas for prolonged periods of time. Disturbance
of the hypothalamic–pituitary axis, Cushing’s syndrome, osteonecrosis of the femoral head,
cataracts, and glaucoma have all been reported [110-114]
Several innovative methods to reduce the potential for these serious adverse events have been
implemented. These include “weekend-only” steroid regimens and combination therapies with
noncorticosteroid topical formulations.
Vitamin D analogs:
At this time, three vitamin D analogs, calcipotriene (calcipitriol), calcitriol, and tacalcitol, exist for
the treatment of psoriasis. Vitamin D analogs result in keratinocyte differentiation and inhibition
of keratinocyte proliferation that is mediated by binding of intracellular vitamin D receptors and
subsequent gene regulation [115]. Calcipotriene is available as a cream, solution, foam, and
ointment. When used as monotherapy, calcipotriene ointment was found to result in greater than
75% improvement in patients with chronic plaque-type psoriasis compared with a 19%
improvement in patients treated with vehicle alone [116]. When compared with potent topical
corticosteroids such as betamethasone dipropionate, no significant differences in efficacy were
seen in the treatment of psoriatic plaques on the body [117]. However, studies have shown that
calcipotriene in solution is inferior in treatment of scalp psoriasis when compared with potent or
superpotent topical steroids [118]. Calcitriol is another synthetic vitamin D analog that is approved
for use in the United States and is available as an ointment. Calcitriol has been shown to be as
effective in the treatment of psoriasis as calcipotriene. However, calcitriol appears to be better
tolerated in sensitive areas such as the face or intertriginous folds [119]. Tacalcitol is available for
use outside of the United States but has not yet been approved for use in the United States. Unlike
calcipotriene, which is approved for once or twice daily dosing, and calcitriol, which is approved
for twice daily dosing, tacalcitol is designed to be used once daily. Although its efficacy for the
treatment of psoriasis has been established in vehicle-controlled studies [120], tacalcitol appears
to be less efficacious than potent topical corticosteroids in the treatment of scalp psoriasis [121].
As a class, vitamin D analogs are generally welltolerated. Local side effects, including burning,
pruritus, edema, peeling, and erythema, are among the most common to occur and can affect up to
25% of patients[122]. The risk of more serious systemic adverse events including hypercalcemia
and impaired parathyroid hormone regulation is rare and can be avoided if patients do not exceed
the maximum allotted doses of the vitamin D analogs. Patients with chronic kidney disease or on
medications that can concurrently result in hypercalcemia, such as thiazide diuretics, are at
increased risk of hypercalcemia [123].
In addition, vitamin D analogs can be combined with phototherapy. The use of twice daily
regimens of calcipotriene with twice weekly narrowband ultraviolet B (UVB) phototherapy
PSORIASIS
19
resulted in greater reductions in Psoriasis Area and Severity Index (PASI) scores than with either
therapy alone [124].
Tazarotene:
Tazarotene is a synthetic retinoid that exerts its antiproliferative and anti-inflammatory effects
through the binding of nuclear retinoid acid receptors (RARs). It is the only topical retinoid
approved for use in psoriasis and is available at concentrations of either 0.05% or 0.1% in both
cream and gel preparations.
Unfortunately, use of tazarotene is often limited by local irritation, characterized by erythema,
burning, and stinging. Irritation can be mitigated by use of the cream formulation, use of the 0.05%
concentration, and short-contact (30–60 minutes) treatment [125]. The concomitant use of
tazorotene with a potent topical steroid not only improves tolerability but has also been shown to
result in efficacy rates as high as 95% [126]. In addition, although the combination of tazarotene
and phototherapy provides enhanced efficacy,[127] UV light doses should be decreased to avoid
burning[128].
Tazarotene is pregnancy Category X. Caution is advised in the use of this medication in women
of child-bearing age given the potential for systemic absorption and subsequent teratogenicity.
Calcineurin inhibitors:
Calcineurin inhibitors are not FDA approved for the treatment of psoriasis; however, they have
been used for this indication off-label. Topical calcineurin inhibitors include pimecrolimus 1%
cream and tacrolimus 0.1% ointment. By their inhibition of calcineurin, they prevent the
production of TH2 cytokines that play an essential role in the pathogenesis of psoriasis. Initial
studies revealed that topical calcineurin inhibitors were ineffective in the treatment of psoriasis
[129]. However, subsequent studies applied these preparations under occlusion to enhance
penetration and found a decrease in erythema and induration of psoriatic plaques on the body after
2 weeks of treatment [130].
The most common side effects reported with the use of the topical calcineurin inhibitors include
burning and itching at the sites of application. These local skin reactions resolve with time and can
be minimized by applying to dry skin [122]. In addition, all patients should be counseled on the
“black box” warning placed on these medications in 2005 by the FDA due to potential for
development of lymphoma and skin cancer seen in animal models. Fortunately, no studies to date
have been able to establish a causal relationship between the use of topical calcineurin inhibitors
and subsequent development of malignancies in humans [131,132].
The topical calcineurin inhibitors are pregnancy category C and should be used only when the
benefits of their use outweigh the risks. They are approved for use in children 2 years of age or
older for atopic dermatitis.
19
resulted in greater reductions in Psoriasis Area and Severity Index (PASI) scores than with either
therapy alone [124].
Tazarotene:
Tazarotene is a synthetic retinoid that exerts its antiproliferative and anti-inflammatory effects
through the binding of nuclear retinoid acid receptors (RARs). It is the only topical retinoid
approved for use in psoriasis and is available at concentrations of either 0.05% or 0.1% in both
cream and gel preparations.
Unfortunately, use of tazarotene is often limited by local irritation, characterized by erythema,
burning, and stinging. Irritation can be mitigated by use of the cream formulation, use of the 0.05%
concentration, and short-contact (30–60 minutes) treatment [125]. The concomitant use of
tazorotene with a potent topical steroid not only improves tolerability but has also been shown to
result in efficacy rates as high as 95% [126]. In addition, although the combination of tazarotene
and phototherapy provides enhanced efficacy,[127] UV light doses should be decreased to avoid
burning[128].
Tazarotene is pregnancy Category X. Caution is advised in the use of this medication in women
of child-bearing age given the potential for systemic absorption and subsequent teratogenicity.
Calcineurin inhibitors:
Calcineurin inhibitors are not FDA approved for the treatment of psoriasis; however, they have
been used for this indication off-label. Topical calcineurin inhibitors include pimecrolimus 1%
cream and tacrolimus 0.1% ointment. By their inhibition of calcineurin, they prevent the
production of TH2 cytokines that play an essential role in the pathogenesis of psoriasis. Initial
studies revealed that topical calcineurin inhibitors were ineffective in the treatment of psoriasis
[129]. However, subsequent studies applied these preparations under occlusion to enhance
penetration and found a decrease in erythema and induration of psoriatic plaques on the body after
2 weeks of treatment [130].
The most common side effects reported with the use of the topical calcineurin inhibitors include
burning and itching at the sites of application. These local skin reactions resolve with time and can
be minimized by applying to dry skin [122]. In addition, all patients should be counseled on the
“black box” warning placed on these medications in 2005 by the FDA due to potential for
development of lymphoma and skin cancer seen in animal models. Fortunately, no studies to date
have been able to establish a causal relationship between the use of topical calcineurin inhibitors
and subsequent development of malignancies in humans [131,132].
The topical calcineurin inhibitors are pregnancy category C and should be used only when the
benefits of their use outweigh the risks. They are approved for use in children 2 years of age or
older for atopic dermatitis.
PSORIASIS
20
Anthralin/ Dithranol:
Anthralin has been a principal treatment modality for psoriasis since the early 20th century. Due
to significant skin irritation as well as red-brown staining that occurs upon application, its use has
declined in recent years as numerous more acceptable alternatives have been developed.
Although its exact mechanism of action is not fully understood, anthralin has been shown to
normalizekeratinocyte differentiation and prevent T-cell activation [133].
Efficacy of anthralin in patients with moderate to severe psoriasis with inpatient regimens appears
to be higher when compared withoutpatient short-contact therapy alone[134]. However, when
compared with calcipotriol ointment applied twice daily for 8 weeks, short- contact anthralin 1%
cream therapy for 30 minutes daily for 8 weeks was less effective at reducing PASI scores [135].
The most common adverse effects of anthralin include skin irritation, which begins shortly after
initiation of treatment. Even at low concentrations of anthralin, irritation has been reported to occur
in as many as 85% of patients [136].
Anthralin is pregnancy category C and considered safe to use in children [137].
Coal tar:
Coal tar is available in various vehicles including shampoos, creams, lotions, ointments, oils,
solutions, and foams. Coal tar is a safe and cost-effective treatment for scalp psoriasis [138].
Combination therapies with coal tar have also been effective in the treatment of psoriasis. In
particular, the Goeckerman regimen, which involves the combined use of coal tar and
phototherapy, has been found to be effective in the treatment of even widespread psoriatic
lesions [139].
Furthermore, patients should be made aware of conf licting data linking the use of coal tar with
malignancy. It is thought that the potential for carcinogenicity associated with coal tar is due to
the presence of polyaromatic hydrocarbons [140] Studies assessing occupational exposure to coal
tar have shown an increased risk of developing nonmelanoma skin cancers [141] In addition,
animal studies have confirmed an increased risk of development of cutaneous malignancies with
the use of coal tar, especially in conjunction with UV radiation exposure [142]. However,
human studies on dermatologic use of coal tar have failed to verify these claims [140]. Studies on
the safety of coal tar preparations in pregnancy and in children have not been conducted and its
use in these populations should be undertaken with caution [143].
Salicylic acid:
Salicylic acid is a topical keratolytic agent that reduces scaling of psoriatic plaques by potentially
disrupting keratinocyte–keratinocyte binding and altering the pH of the stratum corneum [122].
Because of its ability to decrease scaling and enhance penetration, salicylic acid is often used in
combination with other topical psoriatic treatments. Treatment with combinations of salicylic acid
and topical steroid [144] and calcineurin inhibitors [145]. led to greater improvements when
compared with either component alone. These combination therapies are not FDA approved for
the treatment of psoriasis. Salicyclic acid should not be used in combination with oral salicylate
drugs due to risk of systemic salicylism. Salicylism is characterized by nausea, vomiting, tinnitus,
confusion, psychosis, coma, and even death [146]. Furthermore, because percutaneous absorption
of salicylic acid does occur, it should not be applied to over 20% body surface area[122]. This risk
is heightened with application to areas of skin breakdown [146].
20
Anthralin/ Dithranol:
Anthralin has been a principal treatment modality for psoriasis since the early 20th century. Due
to significant skin irritation as well as red-brown staining that occurs upon application, its use has
declined in recent years as numerous more acceptable alternatives have been developed.
Although its exact mechanism of action is not fully understood, anthralin has been shown to
normalizekeratinocyte differentiation and prevent T-cell activation [133].
Efficacy of anthralin in patients with moderate to severe psoriasis with inpatient regimens appears
to be higher when compared withoutpatient short-contact therapy alone[134]. However, when
compared with calcipotriol ointment applied twice daily for 8 weeks, short- contact anthralin 1%
cream therapy for 30 minutes daily for 8 weeks was less effective at reducing PASI scores [135].
The most common adverse effects of anthralin include skin irritation, which begins shortly after
initiation of treatment. Even at low concentrations of anthralin, irritation has been reported to occur
in as many as 85% of patients [136].
Anthralin is pregnancy category C and considered safe to use in children [137].
Coal tar:
Coal tar is available in various vehicles including shampoos, creams, lotions, ointments, oils,
solutions, and foams. Coal tar is a safe and cost-effective treatment for scalp psoriasis [138].
Combination therapies with coal tar have also been effective in the treatment of psoriasis. In
particular, the Goeckerman regimen, which involves the combined use of coal tar and
phototherapy, has been found to be effective in the treatment of even widespread psoriatic
lesions [139].
Furthermore, patients should be made aware of conf licting data linking the use of coal tar with
malignancy. It is thought that the potential for carcinogenicity associated with coal tar is due to
the presence of polyaromatic hydrocarbons [140] Studies assessing occupational exposure to coal
tar have shown an increased risk of developing nonmelanoma skin cancers [141] In addition,
animal studies have confirmed an increased risk of development of cutaneous malignancies with
the use of coal tar, especially in conjunction with UV radiation exposure [142]. However,
human studies on dermatologic use of coal tar have failed to verify these claims [140]. Studies on
the safety of coal tar preparations in pregnancy and in children have not been conducted and its
use in these populations should be undertaken with caution [143].
Salicylic acid:
Salicylic acid is a topical keratolytic agent that reduces scaling of psoriatic plaques by potentially
disrupting keratinocyte–keratinocyte binding and altering the pH of the stratum corneum [122].
Because of its ability to decrease scaling and enhance penetration, salicylic acid is often used in
combination with other topical psoriatic treatments. Treatment with combinations of salicylic acid
and topical steroid [144] and calcineurin inhibitors [145]. led to greater improvements when
compared with either component alone. These combination therapies are not FDA approved for
the treatment of psoriasis. Salicyclic acid should not be used in combination with oral salicylate
drugs due to risk of systemic salicylism. Salicylism is characterized by nausea, vomiting, tinnitus,
confusion, psychosis, coma, and even death [146]. Furthermore, because percutaneous absorption
of salicylic acid does occur, it should not be applied to over 20% body surface area[122]. This risk
is heightened with application to areas of skin breakdown [146].
PSORIASIS
21
Due to the risk of systemic absorption, salicylic acid should not be used in children. It is, however,
considered safe to use for localized psoriasis in pregnancy.
Light therapy (Phototherapy): [102]
Sunlight.
UVB photography.
Narrow band UVB phototherapy.
Goeckerman therapy.
Psoralen plus ultraviolet A (PUVA).
Excimer laser.
Vaccination:
Research from the Universities of Dundee and Oxford has shown how combining the tetanus
vaccine with a viral particle that normally affects cucumbers can be used to treat psoriasis and
allergies, and may even protect against Alzheimer’s disease. Scientists led by Dundee’s Dr John
Foerster and Oxford’s Professor Martin Bachmann, were able to take the protein coat of cucumber
mosaic virus and incorporate a tetanus vaccine-derived protein structure known to stimulate the
immune system in order to create vaccines to treat multiple chronic diseases. The vaccine showed
positive results in models of psoriasis and cat allergy and was shown to raise antibody levels
thought to be beneficial in Alzheimer’s disease. These vaccines can be either preventative, which
is the hope for Alzheimer’s but also therapeutic, meaning they can cure a disease like psoriasis
after it has already been established. More research is required to test the efficacy of the therapeutic
in a clinical setting, but the Dundee-Oxford study raises the possibility of hundreds of thousands
of people being spared the ravages of chronic diseases. Dr Foerster said, “As an academic
dermatologist with special interest in the immune system, my specific attention is on vaccines to
be developed against chronic skin diseases. The idea is pretty simple – for diseases such as
psoriasis or eczema, the newest and most effective medicines on the market are so-called
‘antibodies’, which are what you and I produce against bugs in a common cold. “For chronic
diseases, these antibodies are specially made against one of the body’s own proteins. By blocking
that single protein, the disease gets better. To use the example of psoriasis, a protein called
Interleukin 17 needs to be active for the disease to progress. By creating a vaccine that stimulates
the body to make antibodies against Interleukin 17 itself we can replace the need for frequent and
expensive injections and make this type of treatment much more affordable and accessible to
patients who could otherwise not afford specially made antibodies. “Our research shows that this
technique works in mice and, importantly, our new vaccine technology shows that it is likely to be
a more effective type of vaccine than existing ones in older people. Since many patients with
chronic conditions like psoriasis are elderly this technology may work much better to obtain
effective vaccines”. The paper is published today in the journal Nature Vaccines. The researchers
are now looking to begin clinical testing of the vaccine and have already received regulatory
approval to initiate testing in humans. Present antibodies for psoriasis treatment typically need to
be injected at least once a month to keep working, and cost around £10,000 per patient annually.
A vaccine would offer much more affordable treatment [147].
21
Due to the risk of systemic absorption, salicylic acid should not be used in children. It is, however,
considered safe to use for localized psoriasis in pregnancy.
Light therapy (Phototherapy): [102]
Sunlight.
UVB photography.
Narrow band UVB phototherapy.
Goeckerman therapy.
Psoralen plus ultraviolet A (PUVA).
Excimer laser.
Vaccination:
Research from the Universities of Dundee and Oxford has shown how combining the tetanus
vaccine with a viral particle that normally affects cucumbers can be used to treat psoriasis and
allergies, and may even protect against Alzheimer’s disease. Scientists led by Dundee’s Dr John
Foerster and Oxford’s Professor Martin Bachmann, were able to take the protein coat of cucumber
mosaic virus and incorporate a tetanus vaccine-derived protein structure known to stimulate the
immune system in order to create vaccines to treat multiple chronic diseases. The vaccine showed
positive results in models of psoriasis and cat allergy and was shown to raise antibody levels
thought to be beneficial in Alzheimer’s disease. These vaccines can be either preventative, which
is the hope for Alzheimer’s but also therapeutic, meaning they can cure a disease like psoriasis
after it has already been established. More research is required to test the efficacy of the therapeutic
in a clinical setting, but the Dundee-Oxford study raises the possibility of hundreds of thousands
of people being spared the ravages of chronic diseases. Dr Foerster said, “As an academic
dermatologist with special interest in the immune system, my specific attention is on vaccines to
be developed against chronic skin diseases. The idea is pretty simple – for diseases such as
psoriasis or eczema, the newest and most effective medicines on the market are so-called
‘antibodies’, which are what you and I produce against bugs in a common cold. “For chronic
diseases, these antibodies are specially made against one of the body’s own proteins. By blocking
that single protein, the disease gets better. To use the example of psoriasis, a protein called
Interleukin 17 needs to be active for the disease to progress. By creating a vaccine that stimulates
the body to make antibodies against Interleukin 17 itself we can replace the need for frequent and
expensive injections and make this type of treatment much more affordable and accessible to
patients who could otherwise not afford specially made antibodies. “Our research shows that this
technique works in mice and, importantly, our new vaccine technology shows that it is likely to be
a more effective type of vaccine than existing ones in older people. Since many patients with
chronic conditions like psoriasis are elderly this technology may work much better to obtain
effective vaccines”. The paper is published today in the journal Nature Vaccines. The researchers
are now looking to begin clinical testing of the vaccine and have already received regulatory
approval to initiate testing in humans. Present antibodies for psoriasis treatment typically need to
be injected at least once a month to keep working, and cost around £10,000 per patient annually.
A vaccine would offer much more affordable treatment [147].
PSORIASIS
22
Psoriasis prevention: [148],[149]
1. Use moisturising lotions: Psoriasis symptoms get worse when the skin is dry, so the skin
should be moistened with cream and lotions.
2. Take care about skin, nails and scalp.
3. Avoid dry and cold weather: For a lot of people, cold and dry weather can make the
symptoms of psoriasis worse. In general, hot weather is better for people with psoriasis, although
some have worsening symptoms when the heat and humidity rise.
4. Use humidifier
5. Avoid medications that may cause flare-ups
6. Avoid scraps, cuts, bumps and infection.
7. Get some sun, but not too much: Because ultraviolet rays in sunlight slow the growth of
skin cells, but sunburn can make the psoriasis worse and too much sun increases the risk of having
skin cancer.
8. Decrease stress:
Psoriasis tends to flare up during stressful times.
9. Eliminate alcohol: The connection between alcohol and psoriasis is not clear, but alcohol
can worsen psoriasis, at least in men. Alcohol can also be a risk if you're using certain systemic
medications to treat psoriasis.
10. Exercise, good diet, and maintain a healthy weight: Although no studies have shown a
connection between diet and psoriasis, experts recommend that people with the condition eat a
well-balanced diet, high in fruits and vegetables. Exercise also helps, In some cases, excess weight
can worsen psoriasis symptoms, so maintaining a healthy weight may help prevent flare-ups.
Summary:
Psoriasis is a Multifactorial disease caused by combination of genetic and environmental factors.
It is a chronic, inflammatory skin disease. Plaque psoriasis is the most common form of Psoriasis.
Obesity, diabetes, and heart disease are more common in people with psoriasis. Psoriasis is
controllable with medication and is currently not curable. Psoriasis is not contagious. A
predisposition for psoriasis is inherited in genes. The gene locus PSORS-1 is the major determinant
of psoriasis, and identification of the specific gene is imminent. Psoriasis can be initiated by certain
environmental triggers. Signs and symptoms of psoriasis vary, they include red, scaling plaques
of itchy, elevated skin affecting the elbow, knees and scalp. Psoriasis gets better and worse
spontaneously and can have periodic remissions (clear skin). There are many promising new
therapies, including newer biologic drugs.
22
Psoriasis prevention: [148],[149]
1. Use moisturising lotions: Psoriasis symptoms get worse when the skin is dry, so the skin
should be moistened with cream and lotions.
2. Take care about skin, nails and scalp.
3. Avoid dry and cold weather: For a lot of people, cold and dry weather can make the
symptoms of psoriasis worse. In general, hot weather is better for people with psoriasis, although
some have worsening symptoms when the heat and humidity rise.
4. Use humidifier
5. Avoid medications that may cause flare-ups
6. Avoid scraps, cuts, bumps and infection.
7. Get some sun, but not too much: Because ultraviolet rays in sunlight slow the growth of
skin cells, but sunburn can make the psoriasis worse and too much sun increases the risk of having
skin cancer.
8. Decrease stress:
Psoriasis tends to flare up during stressful times.
9. Eliminate alcohol: The connection between alcohol and psoriasis is not clear, but alcohol
can worsen psoriasis, at least in men. Alcohol can also be a risk if you're using certain systemic
medications to treat psoriasis.
10. Exercise, good diet, and maintain a healthy weight: Although no studies have shown a
connection between diet and psoriasis, experts recommend that people with the condition eat a
well-balanced diet, high in fruits and vegetables. Exercise also helps, In some cases, excess weight
can worsen psoriasis symptoms, so maintaining a healthy weight may help prevent flare-ups.
Summary:
Psoriasis is a Multifactorial disease caused by combination of genetic and environmental factors.
It is a chronic, inflammatory skin disease. Plaque psoriasis is the most common form of Psoriasis.
Obesity, diabetes, and heart disease are more common in people with psoriasis. Psoriasis is
controllable with medication and is currently not curable. Psoriasis is not contagious. A
predisposition for psoriasis is inherited in genes. The gene locus PSORS-1 is the major determinant
of psoriasis, and identification of the specific gene is imminent. Psoriasis can be initiated by certain
environmental triggers. Signs and symptoms of psoriasis vary, they include red, scaling plaques
of itchy, elevated skin affecting the elbow, knees and scalp. Psoriasis gets better and worse
spontaneously and can have periodic remissions (clear skin). There are many promising new
therapies, including newer biologic drugs.
PSORIASIS
23
Report References:
[1] Jacquiline Habashy, Do, MSc, William D James, MD, Oct 10,2017.
[2] Natural dietary supplements and comics, all about psoriasis- causes, symptoms , treatment.
Available from: https://bodyempire.co.uk/health/everything-about-psoriasis [accessed February
25, 2018]
[3] Lebwohl M, Menter A, Koo J, Feldman S.Case studies in severe psoriasis: A clinical
strategy. J Dermatolog Treat. 2003; 14 Suppl 2: 26-46.
[4] Naldi L, Mercuri SR. Smoking and psoriasis: from epidemiology to pathomechanisms.
J Invest Dermatol. 2009; 129: 2741-3.
[5] van de Kerkhof PCM, Nestle FO 2012. Psoriasis. In Dermatology (ed. Bolognia JL, Jorizzo
JL, Schaffer JV). Elsevier, Amsterdam.
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Menter A, Ortonne JP, Fry L 2007. A classification of psoriasis vulgaris according to
phenotype. Br J Dermatol 156: 258
[7] Griffiths CE, Barker JN. Pathogenesis and clinical features of psoriasis. Lancet.
2007;370:263–271.
[8] Levine D, Gottlieb A. Evaluation and management of psoriasis: An internist,s guide. Med
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[9] Naldi L, Gambini D. The clinical spectrum of psoriasis. Clin Dermatol. 2007;25(6):510–
518.
[10] aGriffiths CE, Barker JN. Pathogenesis and clinical features of psoriasis. Lancet. 2007;
370 (9583): 263-71.
[11] bGriffiths CE, Christophers E, Barker JN, Chalmers RJ, Chimenti S, Krueger GG,
Leonardi C, Menter A, Ortonne JP, Fry L. A classification of psoriasis vulgaris according
to phenotype. Br J Dermatol. 2007; 156: 258-62.
[12] Henseler T, Christophers E. Psoriasis of early and late onset: characterization of two
types of psoriasis vulgaris. J Am Acad Dermatol 1985; 13:450–6.
[13] http://psoriasismedication.org/psoriasis-symptoms-and-signs/
[14] Griffiths CE, Christophers E, Barker JN, Chalmers RJ, Chimenti S, Krueger GG, Leonardi C,
Menter A, Ortonne JP, Fry L 2007. A classification of psoriasis vulgaris according to
phenotype. Br J Dermatol 156: 258–262
[15] Gudjonsson JE, Thorarinsson AM, Sigurgeirsson B, Kristinsson KG, Valdimarsson H.
Streptococcal throat infections and exacerbation of chronic plaque psoriasis: A prospective study.
Br J Dermatol. 2003;149:530–534.
[16] Winfield JM. Psoriasis as a sequel to acute inflammations of the tonsils: A clinical note. J
Cutan Dis. 1916;34:441–443.
[17] Costa-Romero M, Coto-Segura P, Suarez-Saavedra S, Ramos-Polo E, Santos-Juanes J.
Guttate psoriasis induced by infliximab in a child with Crohn’s disease. Inflamm Bowel Dis.
2008;14:1462–1463.
[18] Farber EM, Nall ML. The natural history of psoriasis in 5,600 patients. Dermatologica.
1974;148:1–18.
[19] Owen CM, Chalmers RJ, O’sullivan T, Griffiths CE. A systematic review of antistreptococcal
interventions for guttate and chronic plaque psoriasis. Br J Dermatol. 2001;145:886–890.
[20] Boyd AS, Menter A. Erythrodermic psoriasis: Precipitating factors, course, and prognosis
in 50 patients. J Am Acad Dermatol. 1989;21:985–991.
23
Report References:
[1] Jacquiline Habashy, Do, MSc, William D James, MD, Oct 10,2017.
[2] Natural dietary supplements and comics, all about psoriasis- causes, symptoms , treatment.
Available from: https://bodyempire.co.uk/health/everything-about-psoriasis [accessed February
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[39] Van de Kerkhof PCM, Murphy GM, Austad J, Ljungberg A, Cambazard F, Duvold LB.
Psoriasis of the face and flexures. J Dermatol Treat. 2007;18(6):351–360.
[40] Meeuwis KAP, de Hullu JA, Massuger LFAG, van de Kerkhof PCM, van Rossum MM.
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Venereol. 2011;91(1):5–11.
24
[21] Farber EM, Nall L. Erythrodermic (exfoliative) psoriasis. Cutis. 1993;51(2):79–82.
[22] Raychaudhuri SK, Maverakis E, Raychaudhuri SP. Diagnosis and classification of
psoriasis. Autoimmun Rev. 2014;13(4–5):490–495.
[23] Rosenbach M, Hsu S, Korman NJ, et al. Treatment of erythrodermic psoriasis: From the
medical board of the National Psoriasis Foundation. J Am Acad Dermatol. 2010;62(4):655–656.
[24] Sadeh JS, Rudikoff D, Gordon ML, Bowden J, Goldman BD, Lebwohl M. Pustular and
erythrodermic psoriasis complicated by acute respiratory distress syndrome. Arch Dermatol.
1997;133(6):747–750.
[25] O’Donnell PG, Hughes JR, Higgins EM, Groves RW, Pembroke AC. A fatal case of capillary
leak syndrome in erythrodermic psoriasis. Br J Dermatol. 1995;132(1):160–161.
[26] Bressan AL, Gripp A, Oliveira EF, Silva RS. Systemic capillary leak syndrome. An Bras
Dermatol. 2011;86(3):593–595.
[27] bNaldi L, Colombo P, Benedetti EP, Piccitto R, Chatenoud L, La Vecchia C. Study
design and preliminary results from the pilot phase of the PraKtis study: self-reported
diagnoses of selected skin diseases in a representative sample of the Italian population.
Dermatology. 2004; 208: 38–42.
[28] Varman KM, Namias N, Schulman CI, Pizano LR. Acute generalized pustular psoriasis, von
Zumbusch type, treated in the burn unit. A review of clinical features and new therapeutics.
Burns. 2014;40:35-39.
[29] Umezawa Y, Ozawa A, Kawasima T, et al. Therapeutic guidelines for the treatment of
generalized pustular psoriasis (GPP) based on a proposed classification of disease severity. Arch
Dermatol Res. 2003;295:S43–S54.
[30] Zelickson BD, Muller SA. Generalised pustular psoriasis. A review of 63 cases. Arch
Dermatol. 1991; 127: 1339–1345.
[31] Viguier M, Allez M, ZagdanskiAM High frequency of cholestasis in generalised pustular
psoriasis. Evidence for neutrophilic involvement of the biliary tract. Hepatology. 2004; 40:
452–458.
[32] Sidoroff A, Halevy S, Bavinck JN, Vaillant L, Roujeau JC. Acute generalized
exanthematous pustulosis (AGEP) a clinical reaction pattern. J Cutan Pathol. 2001; 28:
113–119.
[33] Saissi EH, Beau-Salinas F, Jonville-Bera AP, Lorette G, Autret-Leca E. Drugs associated
with acute generalized exanthematic pustulosis. Ann Dermatol Venereol. 2003; 130: 612–
618.
[34] Roelandts R. The history of phototherapy: something new under the sun? J Am Acad
Dermatol. 2002; 46: 926-30.
[35] O'Doherty CJ, MacIntyre C. Palmoplantar pustulosis and smoking. 1985; 291: 861864.
[36] Van de Kerkhof PCM, Murphy GM, Austad J, Ljungberg A, Cambazard F, Duvold LB.
Psoriasis of the face and flexures. J Dermatol Treat. 2007;18(6):351–360.
[37] Varghese M, Kindel S. Pigmentary disorders and inflammatory lesions of the external
genitalia. Urol Clin North Am. 1992;19(1):111–121.
[38] Farber EM, Nall L. Genital psoriasis. Cutis. 1992;50(4):263–266.
[39] Van de Kerkhof PCM, Murphy GM, Austad J, Ljungberg A, Cambazard F, Duvold LB.
Psoriasis of the face and flexures. J Dermatol Treat. 2007;18(6):351–360.
[40] Meeuwis KAP, de Hullu JA, Massuger LFAG, van de Kerkhof PCM, van Rossum MM.
Genital psoriasis: A systematic literature review on this hidden skin disease. Acta Derm-
Venereol. 2011;91(1):5–11.
PSORIASIS
25
[41] Ryan C, Sadlier M, de Vol E, et al. Genital psoriasis is associated with significant
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psoriasis: No evidence of candida. Acta Derm-Venereol. 2003;83(2):121–123.
[43] Schmid-Ott G, Kuensebeck HW, Jaeger B, et al. Validity study for the stigmatization
experience in atopic dermatitis and psoriatic patients. Acta DermVenereol. 1999;79(6):443–
447.
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Dermatol. 2004;29(4):354–356.
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Ryan, Psoriasis 11, second edition. 2017, p.79.
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Dermatol. 2007;57:1–27.
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Study Group on Seronegative Spondyloarthropathies. J Rheumatology. 1999;26:1752.
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Acad Med Singapore. 1988;17:482–485.
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Venereol Suppl (Stockh). 1994;186:113.
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and therapy. Hautarzt. 2012; 63: 184-91.
[56] Salomon J, Szepietowski JC, Proniewicz A. Psoriatic nails: a prospective clinical study.
J Cutan Med Surg. 2003; 7: 317–321.
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Symptoms, and Treatments. Available from: https://www.healthline.com/health/photos-types-
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clinical features, course, and outcome. Ann Rheum Dis. 2005;64:ii14–ii17.
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Rep. 2012; 14: 349-57.
[63] Bechet PE (1936) Psoriasis, a brief historical review. Arch Dermatol Syph 33: 327–334
25
[41] Ryan C, Sadlier M, de Vol E, et al. Genital psoriasis is associated with significant
[42] Flytström I, Bergbrant IM, Bråred J, Brandberg LL. Microorganisms in intertriginous
psoriasis: No evidence of candida. Acta Derm-Venereol. 2003;83(2):121–123.
[43] Schmid-Ott G, Kuensebeck HW, Jaeger B, et al. Validity study for the stigmatization
experience in atopic dermatitis and psoriatic patients. Acta DermVenereol. 1999;79(6):443–
447.
[44] Albert S, Neill S, Derrick EK, Calonje E. Psoriasis associated with vulval scarring. Clin Exp
Dermatol. 2004;29(4):354–356.
[45] PHOEBE RICH and RACHEAL MANHART, Nail Psoriasis, M. Alan Menter caitriona
Ryan, Psoriasis 11, second edition. 2017, p.79.
[46] Jiaravuthisan MM, Sasseville D, Vender RB, Urphy F, Muhn CY: Psoriasis of the nail:
Anatomy, pathology, clinical presentation, and a review of the literature on therapy. J Am Acad
Dermatol. 2007;57:1–27.
[47] Cohen MR, Reda DJ, Clegg DO. Baselne relationship between psoriasis and psoriatic
arthritis: Analysis of 221 patients with active psoriatic arthritis. Department of VA Cooperative
Study Group on Seronegative Spondyloarthropathies. J Rheumatology. 1999;26:1752.
[48] Samman PD. Samman’s the Nails in Disease, Fifth Edition. Boston: Butterworth Heinenman,
1994.
[49] Nestle FO, Kaplan DH, Barker J. Psoriasis. N Engl J Med. 2009;361:496–509.
[50] Tham SN, Lim JJ, Tay SH, et al. Clinical observations on nail changes in psoriasis. Ann
Acad Med Singapore. 1988;17:482–485.
[51] Lavaroni G, Kokelj F, Pauluzzi P, Trevisan G. The nails in psoriatic arthritis. Acta Derm
Venereol Suppl (Stockh). 1994;186:113.
[52] Klaassen KM, van de Kerkhof PC, Bastiaens MT, Plusjé LG, Baran RL Pasch MC. Scoring
nail psoriasis. Am Acad Dermatol. 2014;70(6):1061–1066.
[53] Zaias N. Psoriasis of the nail. A clinical-pathologic study. Arch Dermatol. 1969;99:567–
579.
[54] Zaias N. Embryology of the human nail. Arch Dermatol. 1963;87:37–53.
[55] Kahl C, Hansen B, Reich K. Nail psoriasis--an ignored disorder. Pathogenesis, diagnosis
and therapy. Hautarzt. 2012; 63: 184-91.
[56] Salomon J, Szepietowski JC, Proniewicz A. Psoriatic nails: a prospective clinical study.
J Cutan Med Surg. 2003; 7: 317–321.
[57] Debra Sullivan, Katie Brind’Amour and Rachel Nall. Types of psoriasis: Pictures,
Symptoms, and Treatments. Available from: https://www.healthline.com/health/photos-types-
psoriasis#nail [accessed February 24,2017]
[58] Gladman DD, Antoni C, Mease P, Clegg DO, Nash P. Psoriatic arthritis: Epidemiology,
clinical features, course, and outcome. Ann Rheum Dis. 2005;64(Suppl 2):ii14–7.
[59] Gladman DD, Antoni C, Mease P, Clegg DO, Nash P. Psoriatic arthritis: epidemiology,
clinical features, course, and outcome. Ann Rheum Dis. 2005;64:ii14–ii17.
[60] Baran R. The burden of nail psoriasis: an introduction. Dermatology. 2010; 221 Suppl
1:1-5.
[61] Takayanagi H. Osteoimmunology and the effects of the immune system on bone. Nat
Rev Rheumatol. 2009; 5: 667-76.
[62] Rahimi H, Ritchlin CT. Altered bone biology in psoriatic arthritis. Curr Rheumatol
Rep. 2012; 14: 349-57.
[63] Bechet PE (1936) Psoriasis, a brief historical review. Arch Dermatol Syph 33: 327–334
PSORIASIS
26
[64] Hebra F (1868) On disease of the skin. New Sydenham Society, London
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skin. The Lowell Press, Kansas City, MO
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Explores Molecular Phenotypes with Clinical Implications. Simon M, ed. PLoS ONE.
2015;10(7):e0132454.
[72] Chandran V, Raychaudhuri SP 2010. Geoepidemiology and environmental factors of psoriasis
and psoriatic arthritis. J Autoimmun 34: J314–J321
[73] Parisi R, Symmons DP, Griffiths CE, Ashcroft DM 2013. Global epidemiology of psoriasis:
A systematic review of incidence and prevalence. J Invest Dermatol 133: 377–385.
[74] Hart PH, Gorman S, Finlay-Jones JJ 2011. Modulation of the immune system by UV
radiation: More than just the effects of vitamin D? Nat Rev Immunol 11: 584–596
[75] Icen M, Crowson CS, McEvoy MT, Dann FJ, Gabriel SE, Maradit Kremers H 2009. Trends
in incidence of adult-onset psoriasis over three decades: A population-based study. J Am Acad
Dermatol 60: 394–401
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in children: A population-based study. J Am Acad Dermatol 62: 979–987
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Ann Rheum Dis. 2009;68:664–667.
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Rev Immunol. 2005;5:699–711.
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arthritis. Disease concordance among monozygotic and dizygotic twins. Ann Rheum Dis.
2008;67:1417–1421.
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Development of new criteria from a larger international study. Arthritis Rheum. 2006;54:2665–
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1994;8:263–276.
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heterogeneity in psoriatic arthritis and in the psoriasis phenotype. Arthritis Rheum.
2012;64:1134–1144.
[85] Gladman DD, Farewell VT, Kopciuk K, Cook RJ. HLA antigens and progression in psoriatic
arthritis. J Rheumatol. 1998;205:730–733.
[86] Korendowych E, Dixey J, Cox B, Jones S, McHugh N. T he influence of the HLA-DRB1
rheumatoid arthritis shared epitope on the clinical characteristics and radiological outcome of
psoriatic arthritis. J Rheumatol. 2003;30:96–101.
26
[64] Hebra F (1868) On disease of the skin. New Sydenham Society, London
[65] Fox H (1915) Dermatology of the ancients. JAMA 65: 469
[66] Sutton RL (1986) Sixteenth century physician and his methods mercurialis on diseases of the
skin. The Lowell Press, Kansas City, MO
[67] Pusey WA (1933) The history of dermatology. Charles C Thomas, Springfield, IL
[68] Glickman FS (1986) Lepra, psora, psoriasis. J Am Acad Dermatol 14(5 Pt 1): 863–866
[69] Celsus AC (1837) De re medica. East Portwine, London
[70] Willan, R (1809) On Cutaneous Diseases. Kimber and Conrad, Philadelphia
[71] Kim J, Nadella P, Kim DJ, et al. Histological Stratification of Thick and Thin Plaque Psoriasis
Explores Molecular Phenotypes with Clinical Implications. Simon M, ed. PLoS ONE.
2015;10(7):e0132454.
[72] Chandran V, Raychaudhuri SP 2010. Geoepidemiology and environmental factors of psoriasis
and psoriatic arthritis. J Autoimmun 34: J314–J321
[73] Parisi R, Symmons DP, Griffiths CE, Ashcroft DM 2013. Global epidemiology of psoriasis:
A systematic review of incidence and prevalence. J Invest Dermatol 133: 377–385.
[74] Hart PH, Gorman S, Finlay-Jones JJ 2011. Modulation of the immune system by UV
radiation: More than just the effects of vitamin D? Nat Rev Immunol 11: 584–596
[75] Icen M, Crowson CS, McEvoy MT, Dann FJ, Gabriel SE, Maradit Kremers H 2009. Trends
in incidence of adult-onset psoriasis over three decades: A population-based study. J Am Acad
Dermatol 60: 394–401
[76] Tollefson MM, Crowson CS, McEvoy MT, Maradit Kremers H 2010. Incidence of psoriasis
in children: A population-based study. J Am Acad Dermatol 62: 979–987
[77] Mayo Clinic staff, “Psoriasis Symptoms”, Mayo Clinic, June 17, 2015
[78] Chandran V, Schentag CT, Brockbank JE, et al. Familial aggregation of psoriatic arthritis.
Ann Rheum Dis. 2009;68:664–667.
[79] Bowcock AM, Krueger JG. Getting under the skin: T he immunogenetics of psoriasis. Nat
Rev Immunol. 2005;5:699–711.
[80] Pedersen OB, Svendsen AJ, Ejstrup L, Skytthe A, Junker P. On the heritability of psoriatic
arthritis. Disease concordance among monozygotic and dizygotic twins. Ann Rheum Dis.
2008;67:1417–1421.
[81] Taylor W, Gladman D, Helliwell P, et al. Classification criteria for psoriatic arthritis:
Development of new criteria from a larger international study. Arthritis Rheum. 2006;54:2665–
2673.
[82] Fitzgerald O, Winchester R. Psoriatic arthritis: From pathogenesis to therapy. Arthritis Res
Ther. 2009;11:214.
[83] Eastmond CJ. Psoriatic arthritis: Genetics and HLA antigens. Baillieres Clin Rheumatol.
1994;8:263–276.
[84] Winchester R, Minevich G, Steshenko V, et al. HLA associations reveal genetic
heterogeneity in psoriatic arthritis and in the psoriasis phenotype. Arthritis Rheum.
2012;64:1134–1144.
[85] Gladman DD, Farewell VT, Kopciuk K, Cook RJ. HLA antigens and progression in psoriatic
arthritis. J Rheumatol. 1998;205:730–733.
[86] Korendowych E, Dixey J, Cox B, Jones S, McHugh N. T he influence of the HLA-DRB1
rheumatoid arthritis shared epitope on the clinical characteristics and radiological outcome of
psoriatic arthritis. J Rheumatol. 2003;30:96–101.
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[95] Punzi L, Pianon M, Berazzolo N, et al. Clinical, laboratory and immunogenetic aspects of
post-traumatic psoriatic arthritis: A study of 25 patients. Clin Exp Rheumatol. 1998;16:277–281.
[96] Eder L, Law T, Chandran V, et al. Association between environmental factors and onset
of psoriatic arthritis in patients with psoriasis. Arthritis Care Res. 2011;63:1091–1097.
[97] McGonagle D. Enthesitis: An autoinflammatory lesion linking nail and joint involvement in
psoriatic disease. J Eur Acad Dermatol Venereol. 2009;23 (Suppl 1):9–13.
[98] Lories RJ, de Vlam K. Is psoriatic arthritis a result of abnormalities in acquired or innate
immunity? Curr Rheumatol Rep. 2012;14:375–382.
[99] Balding J, Kane D, Livingstone W, et al. Cytokine gene polymorphisms: Association with
psoriatic arthritis susceptibility and severity. Arthritis Rheum. 2003;48:1408–1413.
[100] Diani M, Altomare G, Reali E. T cell responses in psoriasis and psoriatic arthritis.
Autoimmun Rev. 2015;14:286–292.
[101] de Vlam K, Gottlieb AB, Mease PJ. Current concepts in psoriatic arthritis: Pathogenesis and
management. Acta Derm Venereol. 2014;94:627–634.
[102] Myo Clinic. Psoriasis diagnosis and treatment. Available from:
https://www.mayoclinic.org/diseases-conditions/psoriasis/diagnosis-treatment/drc-20355845
[103] Nast A, Boehncke WH, Mrowietz U, Ockenfels HM, Philipp S, Reich K, et al. S3
Guidelines on the treatment of psoriasis vulgaris (English version). Update. J Dtsch Dermatol
Ges. 2012 Mar;10 Suppl 2:S1-95.
[104] Laws PM, Young HS. Topical treatment of psoriasis. Expert Opin Pharmacother.
2010 Aug;11(12):1999-2009.
[105] Devaux S, Castela A, Archier E, Gallini A, Joly P, Misery L, et al. Adherence to
topical treatment in psoriasis: a systematic literature review. J Eur Acad Dermatol Venereol.
2012 May;26 Suppl 3:61-7.
[106] Hendriks AG, Keijsers RR, de Jong EM, Seyger MM, van de Kerkhof PC.
Combinations of classical time-honoured topicals in plaque psoriasis: a systematic review.
J Eur Acad Dermatol Venereol. 2012 Jul 11.
27
[87] Balding J, Kane D, Livingstone W, et al. Cytokine gene polymorphisms: Association with
psoriatic arthritis susceptibility and severity. Arthritis Rheum. 2003;48:1408–1413.
[88] Gonzalez S, Martinez-Borra J, Lopez-Vazquez A, García-Fernández S, Torre-Alonso JC,
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[91] Morar N, Willis-Owen SA, Maurer T, Bunker CB. HIV-associated psoriasis: Pathogenesis,
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[92] Luxembourg A, Cailla H, Roux H, Roudier J. Do viruses play an etiologic role in ankylosing
spondylitis or psoriatic arthritis? Clin Immunol Immunopathol. 1987;45:292–295.
[93] Pattison E, Harrison BJ, Griffiths CE, Silman AJ, Bruce IN. Environmental risk factors for
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2008;67:672–676.
[94] Scarpa R, Del Puente A, Di Girolamo C, della Valle G, Lubrano E, Oriente P. Interplay
between environmental factors, articular involvement, and HLA-B27 in patients with psoriatic
arthritis. Ann Rheum Dis. 1992;51:78–79.
[95] Punzi L, Pianon M, Berazzolo N, et al. Clinical, laboratory and immunogenetic aspects of
post-traumatic psoriatic arthritis: A study of 25 patients. Clin Exp Rheumatol. 1998;16:277–281.
[96] Eder L, Law T, Chandran V, et al. Association between environmental factors and onset
of psoriatic arthritis in patients with psoriasis. Arthritis Care Res. 2011;63:1091–1097.
[97] McGonagle D. Enthesitis: An autoinflammatory lesion linking nail and joint involvement in
psoriatic disease. J Eur Acad Dermatol Venereol. 2009;23 (Suppl 1):9–13.
[98] Lories RJ, de Vlam K. Is psoriatic arthritis a result of abnormalities in acquired or innate
immunity? Curr Rheumatol Rep. 2012;14:375–382.
[99] Balding J, Kane D, Livingstone W, et al. Cytokine gene polymorphisms: Association with
psoriatic arthritis susceptibility and severity. Arthritis Rheum. 2003;48:1408–1413.
[100] Diani M, Altomare G, Reali E. T cell responses in psoriasis and psoriatic arthritis.
Autoimmun Rev. 2015;14:286–292.
[101] de Vlam K, Gottlieb AB, Mease PJ. Current concepts in psoriatic arthritis: Pathogenesis and
management. Acta Derm Venereol. 2014;94:627–634.
[102] Myo Clinic. Psoriasis diagnosis and treatment. Available from:
https://www.mayoclinic.org/diseases-conditions/psoriasis/diagnosis-treatment/drc-20355845
[103] Nast A, Boehncke WH, Mrowietz U, Ockenfels HM, Philipp S, Reich K, et al. S3
Guidelines on the treatment of psoriasis vulgaris (English version). Update. J Dtsch Dermatol
Ges. 2012 Mar;10 Suppl 2:S1-95.
[104] Laws PM, Young HS. Topical treatment of psoriasis. Expert Opin Pharmacother.
2010 Aug;11(12):1999-2009.
[105] Devaux S, Castela A, Archier E, Gallini A, Joly P, Misery L, et al. Adherence to
topical treatment in psoriasis: a systematic literature review. J Eur Acad Dermatol Venereol.
2012 May;26 Suppl 3:61-7.
[106] Hendriks AG, Keijsers RR, de Jong EM, Seyger MM, van de Kerkhof PC.
Combinations of classical time-honoured topicals in plaque psoriasis: a systematic review.
J Eur Acad Dermatol Venereol. 2012 Jul 11.
PSORIASIS
28
[107] Albrecht L, Bourcier M, Ashkenas J, Papp K, Shear N, Toole J, et al. Topical
psoriasis therapy in the age of biologics: evidence-based treatment recommendations. J Cutan
Med Surg. 2011 Nov-Dec;15(6):309-21.
[108] Samarasekera EJ, Sawyer L, Wonderling D, Tucker R, Smith CH. Topical therapies for the
treatment of plaque psoriasis: Systematic review and network meta-analyses. Br J Dermatol.
2013;168:954–967.
[109] Van de Kerkhof PC, Vissers WH. The topical treatment of psoriasis. Skin Pharmacol Appl
Skin Physiol. 2003;16:69–83.
[110] Levin C, Maibach HI. Topical corticosteroid- induced adrenocortical insufficiency: Clinical
implications. Am J Clin Dermatol. 2002;3:141–147.
[111] Nathan AW, Rose GL. Fatal iatrogenic Cushing’s syndrome. Lancet. 1979;1:207.
[112] Kubo T, Kojima A, Yamazoe S, Ueshima K, Yamamoto T, Hirasawa Y. Osteonecrosis of
the femoral head that developed after long-term topical steroid application. J Orthop Sci.
2001;6:92–94.
[113] Katz HI, Hien NT, Prawer SE, Mastbaum LI, Mooney JR, Samson CR. Superpotent
topical steroid treatment of psoriasis vulgaris—Clinical efficacy and adrenal function. J Am Acad
Dermatol. 1987;16:804–811.
[114] Munro DD. The effect of percutaneously absorbed steroids on hypothalamic–pituitary–
adrenal function after intensive use in in-patients. Br J Dermatol. 1976;94:67–76.
[115] Hansen CM, Mathiasen IS, Binderup L. The antiproliferative and differentiation-induced
effects of vitamin D analogs are not determined by the binding affinity for the vitamin D receptor
alone. J Invest Dermatol Symp Proc. 1996;1:44–48.
[116] Highton A, Quell J. Calcipotriene ointment 0.005% for psoriasis: A safety and efficacy
study. Calcipotriene Study Group. J Am Acad Dermatol. 1995;32:67–72.
[117] Cunliffe WJ, Berth-Jones J, Caudy A, et al. Comparative study of calcipotriol (MC 903)
ointment and betamethasone 17-valerate ointment in patients with psoriasis vulgaris. J Am Acad
Dermatol. 1992;26:736–743.
[118] Mason A, Mason J, Cork M, Hancock H, Dooley G. Topical treatments for chronic plaque
psoriasis: An abridged Cochrane Systematic Review. J Am Acad Dermatol. 2013;69:799–807.
[119] Dubertret L, Wallach D, Souteyrand P, et al. Efficacy and safety of calcipotriol (MC 903)
ointment in psoriasis vulgaris. A randomized, double-blind, right/ left comparison, vehicle-
controlled study. J Am Acad Dermatol. 1992;27: 983–988.
[120] Scarpa C. Tacalcitol ointment is an efficacious and well tolerated treatment for psoriasis. J
Eur Acad Dermatol Venereol. 1996;6:142–146.
[121] Ruzicka T, Trompke C. Treatment of scalp psoriasis: An effective and safe tacalcitol
emulsion. Hautarzt. 2004;55:165–170.
[122] Menter A, Korman NJ, Elmets CA, et al. Guidelines of care for the management of psoriasis
and psoriatic arthritis. Section 3. Guidelines of care for the management and treatment of
psoriasis with topical therapies. J Am Acad Dermatol. 2009;60:643–659.
[123] Braun GS, Witt M, Mayer V, Schmid H. Hypercalcemia caused by vitamin D3 analogs in
psoriasis treatment. Int J Dermatol. 2007;46:1315–1317.
[124] Takahashi H, Tsuji H, Ishida-Yamamoto A, Iizuka H. Comparison of clinical effects of
psoriasis treatment regimens among calcipotriol alone, narrowband ultraviolet B phototherapy
alone, combination of calcipotriol and narrowband ultraviolet B phototherapy once a week,
and combination of calcipotriol and narrowband ultraviolet B phototherapy more than twice a
week. J Dermatol. 2013;40:424–427.
28
[107] Albrecht L, Bourcier M, Ashkenas J, Papp K, Shear N, Toole J, et al. Topical
psoriasis therapy in the age of biologics: evidence-based treatment recommendations. J Cutan
Med Surg. 2011 Nov-Dec;15(6):309-21.
[108] Samarasekera EJ, Sawyer L, Wonderling D, Tucker R, Smith CH. Topical therapies for the
treatment of plaque psoriasis: Systematic review and network meta-analyses. Br J Dermatol.
2013;168:954–967.
[109] Van de Kerkhof PC, Vissers WH. The topical treatment of psoriasis. Skin Pharmacol Appl
Skin Physiol. 2003;16:69–83.
[110] Levin C, Maibach HI. Topical corticosteroid- induced adrenocortical insufficiency: Clinical
implications. Am J Clin Dermatol. 2002;3:141–147.
[111] Nathan AW, Rose GL. Fatal iatrogenic Cushing’s syndrome. Lancet. 1979;1:207.
[112] Kubo T, Kojima A, Yamazoe S, Ueshima K, Yamamoto T, Hirasawa Y. Osteonecrosis of
the femoral head that developed after long-term topical steroid application. J Orthop Sci.
2001;6:92–94.
[113] Katz HI, Hien NT, Prawer SE, Mastbaum LI, Mooney JR, Samson CR. Superpotent
topical steroid treatment of psoriasis vulgaris—Clinical efficacy and adrenal function. J Am Acad
Dermatol. 1987;16:804–811.
[114] Munro DD. The effect of percutaneously absorbed steroids on hypothalamic–pituitary–
adrenal function after intensive use in in-patients. Br J Dermatol. 1976;94:67–76.
[115] Hansen CM, Mathiasen IS, Binderup L. The antiproliferative and differentiation-induced
effects of vitamin D analogs are not determined by the binding affinity for the vitamin D receptor
alone. J Invest Dermatol Symp Proc. 1996;1:44–48.
[116] Highton A, Quell J. Calcipotriene ointment 0.005% for psoriasis: A safety and efficacy
study. Calcipotriene Study Group. J Am Acad Dermatol. 1995;32:67–72.
[117] Cunliffe WJ, Berth-Jones J, Caudy A, et al. Comparative study of calcipotriol (MC 903)
ointment and betamethasone 17-valerate ointment in patients with psoriasis vulgaris. J Am Acad
Dermatol. 1992;26:736–743.
[118] Mason A, Mason J, Cork M, Hancock H, Dooley G. Topical treatments for chronic plaque
psoriasis: An abridged Cochrane Systematic Review. J Am Acad Dermatol. 2013;69:799–807.
[119] Dubertret L, Wallach D, Souteyrand P, et al. Efficacy and safety of calcipotriol (MC 903)
ointment in psoriasis vulgaris. A randomized, double-blind, right/ left comparison, vehicle-
controlled study. J Am Acad Dermatol. 1992;27: 983–988.
[120] Scarpa C. Tacalcitol ointment is an efficacious and well tolerated treatment for psoriasis. J
Eur Acad Dermatol Venereol. 1996;6:142–146.
[121] Ruzicka T, Trompke C. Treatment of scalp psoriasis: An effective and safe tacalcitol
emulsion. Hautarzt. 2004;55:165–170.
[122] Menter A, Korman NJ, Elmets CA, et al. Guidelines of care for the management of psoriasis
and psoriatic arthritis. Section 3. Guidelines of care for the management and treatment of
psoriasis with topical therapies. J Am Acad Dermatol. 2009;60:643–659.
[123] Braun GS, Witt M, Mayer V, Schmid H. Hypercalcemia caused by vitamin D3 analogs in
psoriasis treatment. Int J Dermatol. 2007;46:1315–1317.
[124] Takahashi H, Tsuji H, Ishida-Yamamoto A, Iizuka H. Comparison of clinical effects of
psoriasis treatment regimens among calcipotriol alone, narrowband ultraviolet B phototherapy
alone, combination of calcipotriol and narrowband ultraviolet B phototherapy once a week,
and combination of calcipotriol and narrowband ultraviolet B phototherapy more than twice a
week. J Dermatol. 2013;40:424–427.
PSORIASIS
29
[125] Veraldi S, Caputo R, Pacifico A, Peris K, Soda R, Chimenti S. Short contact therapy with
tazarotene in psoriasis vulgaris. Dermatology. 2006;212:235–237.
[126] Gollnick H, Menter A. Combination therapy with tazarotene plus a topical corticosteroid for
the treatment of plaque psoriasis. Br J Dermatol. 1999;140:18–23.
[127] Koo JY. Tazarotene in combination with phototherapy. J Am Acad Dermatol.
1998;39:S144–S148.
[128] Hecker D, Worsle J, Yueh G, Kuroda K, Lebwohl M. Interactions between tazarotene and
ultraviolet light. J Am Acad Dermatol. 1999;41:927–930.
[129] Gupta AK, Chow M. Pimecrolimus: A review. J Ear Acad Dermatol Venereol.
2003;17:493–503.
[130] Mrowietz U, Graeber M, Brautigam M, et al. The novel ascomycin derivative SDZ ASM
981 is effective for psoriasis when used topically under occlusion. Br J Dermatol.
1998;139:992–996.
[131] Siegfried EC, Jaworski JC, Hebert A. Topical calcineurin inhibitors and lymphoma risk:
Evidence update with implications for daily practice. Am J Clin Dermatol. 2013;14:163–178.
[132] Tennis P, Gelfand JM, Rothman KJ. Evaluation of cancer risk related to atopic dermatitis
and use of topical calcineurin inhibitors. Br J Dermatol. 2011;165:465–473.
[133] McGill A, Frank A, Emmett N, Turnbull DM, BirchMachin, MA, Reynolds NJ. The anti-
psoriatic drug anthralin accumulates in keratinocyte mitochondria, dissipates mitochondrial
membrane potential, and induces apoptosis through a pathway dependent on respiratory
competent mitochondria. FASEB J. 2005;19:1012–1014.
[134] Sminkels OQ, Prins M, Veeniiuis RT, et al. Effectiveness and side effects of UVB-
phototherapy, dithranol inpatient therapy and a care instruction programme of short contact
dithranol in moderate to severe psoriasis. Eur J Dermatol. 2004;14:159–165.
[135] Berth-Jones J, Chu AC, Dodd WA. A multicentre, parallel-group comparison of calcipotriol
ointment and short-contact dithranol therapy in chronic plaque psoriasis. Br J Dermatol.
1992;127:266–271.
[136] Kucharekova M, Lieffers L, van de Kerkhof PC, Van Der Valk PG. Dithranol irritation in
psoriasis treatment: A study of 68 inpatients. J Eur Acad Dermatol Venereol. 2005;19:176–179.
[137] de Jager ME, van de Kerkhof PC, de Jong EM, Seyger MM. Dithranol therapy in childhood
psoriasis: Unjustifiably on the verge of falling into oblivion. Dermatology. 2010;220: 329–332.
[138] Paghdal KV, Schwartz RA. Topical tar: Back to the future. J Am Acad Dermatol.
2009;61:294–302.
[139] Serrao R, Davis M. Goeckerman treatment for remission ofpsoriasis refractory to biologic
therapy. J Am Acad Dermatol. 2009;60:348–349.
[140] Pion IA, Koenig KL, Lim HW. Is dermatologic usage of coal tar carcinogenic? A review of
the literature. Dermatol Surg. 1995;21:227–231.
[141] Kubasiewicz M, Starzynski Z. Cancer of the skin in Poland related to occupational factors.
Med Pr. 1987;38:441–446.
[142] Mukhtar H, Link CM, Cherniack E, Kushner DM, Bickers DR. Effect of topical application
of defined constituents of coal tar on skin and liver aryl hydrocarbon hydrolase and 7-
ethoxycoumarin diethylase activities. Toxicol Appl Pharmacol. 1982;64: 541–549.
[143] Roelofzen J, Aben K, Khawar A, van de Kerkhof PC, Kiemeney LA, Van Der Valk PG.
Treatment policy for psoriasis and eczema: A survey among dermatologists in the Netherlands
and Belgian Flanders. Eur J Dermatol. 2007;17:416–421.
29
[125] Veraldi S, Caputo R, Pacifico A, Peris K, Soda R, Chimenti S. Short contact therapy with
tazarotene in psoriasis vulgaris. Dermatology. 2006;212:235–237.
[126] Gollnick H, Menter A. Combination therapy with tazarotene plus a topical corticosteroid for
the treatment of plaque psoriasis. Br J Dermatol. 1999;140:18–23.
[127] Koo JY. Tazarotene in combination with phototherapy. J Am Acad Dermatol.
1998;39:S144–S148.
[128] Hecker D, Worsle J, Yueh G, Kuroda K, Lebwohl M. Interactions between tazarotene and
ultraviolet light. J Am Acad Dermatol. 1999;41:927–930.
[129] Gupta AK, Chow M. Pimecrolimus: A review. J Ear Acad Dermatol Venereol.
2003;17:493–503.
[130] Mrowietz U, Graeber M, Brautigam M, et al. The novel ascomycin derivative SDZ ASM
981 is effective for psoriasis when used topically under occlusion. Br J Dermatol.
1998;139:992–996.
[131] Siegfried EC, Jaworski JC, Hebert A. Topical calcineurin inhibitors and lymphoma risk:
Evidence update with implications for daily practice. Am J Clin Dermatol. 2013;14:163–178.
[132] Tennis P, Gelfand JM, Rothman KJ. Evaluation of cancer risk related to atopic dermatitis
and use of topical calcineurin inhibitors. Br J Dermatol. 2011;165:465–473.
[133] McGill A, Frank A, Emmett N, Turnbull DM, BirchMachin, MA, Reynolds NJ. The anti-
psoriatic drug anthralin accumulates in keratinocyte mitochondria, dissipates mitochondrial
membrane potential, and induces apoptosis through a pathway dependent on respiratory
competent mitochondria. FASEB J. 2005;19:1012–1014.
[134] Sminkels OQ, Prins M, Veeniiuis RT, et al. Effectiveness and side effects of UVB-
phototherapy, dithranol inpatient therapy and a care instruction programme of short contact
dithranol in moderate to severe psoriasis. Eur J Dermatol. 2004;14:159–165.
[135] Berth-Jones J, Chu AC, Dodd WA. A multicentre, parallel-group comparison of calcipotriol
ointment and short-contact dithranol therapy in chronic plaque psoriasis. Br J Dermatol.
1992;127:266–271.
[136] Kucharekova M, Lieffers L, van de Kerkhof PC, Van Der Valk PG. Dithranol irritation in
psoriasis treatment: A study of 68 inpatients. J Eur Acad Dermatol Venereol. 2005;19:176–179.
[137] de Jager ME, van de Kerkhof PC, de Jong EM, Seyger MM. Dithranol therapy in childhood
psoriasis: Unjustifiably on the verge of falling into oblivion. Dermatology. 2010;220: 329–332.
[138] Paghdal KV, Schwartz RA. Topical tar: Back to the future. J Am Acad Dermatol.
2009;61:294–302.
[139] Serrao R, Davis M. Goeckerman treatment for remission ofpsoriasis refractory to biologic
therapy. J Am Acad Dermatol. 2009;60:348–349.
[140] Pion IA, Koenig KL, Lim HW. Is dermatologic usage of coal tar carcinogenic? A review of
the literature. Dermatol Surg. 1995;21:227–231.
[141] Kubasiewicz M, Starzynski Z. Cancer of the skin in Poland related to occupational factors.
Med Pr. 1987;38:441–446.
[142] Mukhtar H, Link CM, Cherniack E, Kushner DM, Bickers DR. Effect of topical application
of defined constituents of coal tar on skin and liver aryl hydrocarbon hydrolase and 7-
ethoxycoumarin diethylase activities. Toxicol Appl Pharmacol. 1982;64: 541–549.
[143] Roelofzen J, Aben K, Khawar A, van de Kerkhof PC, Kiemeney LA, Van Der Valk PG.
Treatment policy for psoriasis and eczema: A survey among dermatologists in the Netherlands
and Belgian Flanders. Eur J Dermatol. 2007;17:416–421.
PSORIASIS
30
[144] Katz HI, Tanner DJ, Cuffie CA. A comparison of the efficacy and safety of the combination
mometasone furoate 0.1%–salicylic acid 5% ointment with each of its components in psoriasis. J
Dermatolog Treat. 1998;9:151–156.
[145] Carroll CL, Clarke J, Camacho F, Balkrishnan R, Feldman SR. Topical tacrolimus
ointment combined with 6% salicylic acid gel for plaque psoriasis treatment. Arch Dermatol.
2005;141:43–46.
[146] Madan RK, Levitt J. A review of toxicity from topical salicylic acid preparation. J Am
Acad Dermatol. 2014;70:788–792.
[147] Grant Hill, University of Dundee. Vaccinating against psoriasis, allergies and Alzheimer’s.
Available from: https://www.dundee.ac.uk/news/2017/vaccinating-against-psoriasis-allergies-and-
alzheimers-a-possibility-research-shows.php [accessed Mon 23 Oct 2017]
[148] WebMD. 10 ways to prevent flare-ups of psoriasis. Available from:
https://www.webmd.boots.com/skin-problems-and-treatments/guide/prevent-psoriasis-flare-ups
[149] WebMD. 10 ways to prevent flare-ups of psoriasis.. Available from:
https://www.webmd.boots.com/skin-problems-and-treatments/guide/prevent-psoriasis-flare-
ups?page=2
Figure References:
(1) Lima H. (Ed.), Psoriasis: types, causes and medication, 2017, P.12
(2) Menter, Alan, Ryan, Caitriona, Psoriasis, second edition, CRC Press, 2017, P.95
(3) Menter, Alan, Ryan, Caitriona, Psoriasis, second edition, CRC Press, 2017, P.61
(4) Menter, Alan, Ryan, Caitriona, Psoriasis, second edition, CRC Press, 2017, P.62
(5) Lima H. (Ed.), Psoriasis: types, causes and medication, 2017, P.18
(6) Lima H. (Ed.), Psoriasis: types, causes and medication, 2017, P.13
(7) Lima H. (Ed.), Psoriasis: types, causes and medication, 2017, P.19
(8) Lima H. (Ed.), Psoriasis: types, causes and medication, 2017, P.20
(9) Menter, Alan, Ryan, Caitriona, Psoriasis, second edition, CRC Press, 2017, P.149
30
[144] Katz HI, Tanner DJ, Cuffie CA. A comparison of the efficacy and safety of the combination
mometasone furoate 0.1%–salicylic acid 5% ointment with each of its components in psoriasis. J
Dermatolog Treat. 1998;9:151–156.
[145] Carroll CL, Clarke J, Camacho F, Balkrishnan R, Feldman SR. Topical tacrolimus
ointment combined with 6% salicylic acid gel for plaque psoriasis treatment. Arch Dermatol.
2005;141:43–46.
[146] Madan RK, Levitt J. A review of toxicity from topical salicylic acid preparation. J Am
Acad Dermatol. 2014;70:788–792.
[147] Grant Hill, University of Dundee. Vaccinating against psoriasis, allergies and Alzheimer’s.
Available from: https://www.dundee.ac.uk/news/2017/vaccinating-against-psoriasis-allergies-and-
alzheimers-a-possibility-research-shows.php [accessed Mon 23 Oct 2017]
[148] WebMD. 10 ways to prevent flare-ups of psoriasis. Available from:
https://www.webmd.boots.com/skin-problems-and-treatments/guide/prevent-psoriasis-flare-ups
[149] WebMD. 10 ways to prevent flare-ups of psoriasis.. Available from:
https://www.webmd.boots.com/skin-problems-and-treatments/guide/prevent-psoriasis-flare-
ups?page=2
Figure References:
(1) Lima H. (Ed.), Psoriasis: types, causes and medication, 2017, P.12
(2) Menter, Alan, Ryan, Caitriona, Psoriasis, second edition, CRC Press, 2017, P.95
(3) Menter, Alan, Ryan, Caitriona, Psoriasis, second edition, CRC Press, 2017, P.61
(4) Menter, Alan, Ryan, Caitriona, Psoriasis, second edition, CRC Press, 2017, P.62
(5) Lima H. (Ed.), Psoriasis: types, causes and medication, 2017, P.18
(6) Lima H. (Ed.), Psoriasis: types, causes and medication, 2017, P.13
(7) Lima H. (Ed.), Psoriasis: types, causes and medication, 2017, P.19
(8) Lima H. (Ed.), Psoriasis: types, causes and medication, 2017, P.20
(9) Menter, Alan, Ryan, Caitriona, Psoriasis, second edition, CRC Press, 2017, P.149
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