Acne vulgaris, psoriasis and atopic dermatitis handout_2.pdf

vulgaris psoriasis

1. Acne vulgaris
By:
Mohammed Gebre (BPharm, MSc in clinical Pharmacy)
Department of Pharmacy
1

2. Introduction
Inflammatory skin disorder of the pilosebaceous
units of the skin
Sebaceous glands, predominant on the face, chest, and
upper back, respond to androgen stimulation.
These glands provide sebum to the follicular canal and
eventually to the skin surface through the follicular
opening (the pore).
Follicular canal contents include keratinocytes,
Propionibacterium acnes, and free fatty acids.

2

3. Introduction…
Generally a self-limiting condition

Long-term physical complications of acne may
include extensive scarring and psychological
distress

Acne can also be associated with anxiety,
depression, and higher-than-average
unemployment rates

3

4. EPIDEMIOLOGY
In the United States affecting up to 50 million people
Acne vulgaris affects approximately 80% of the
population between the ages of 11 and 30 years,
More often in males during adolescence and
females during adulthood
4

5. ETIOLOGY AND PATHOPHYSIOLOGY
Genetic, racial, hormonal, dietary, and environmental
factors have been implicated in its development.
Four major etiologic factors are involved in the
development of acne:
increased sebum production, due to hormonal influences;
alteration in the keratinization process and
hyperproliferation of ductal epidermis;
bacterial colonization of the duct with Propionibacterium
acnes; and
production of inflammation with release of inflammatory
mediators in acne sites.
5

6. INCREASED SEBUM PRODUCTION
Androgen stimulation is enhanced at puberty and
sebaceous glands actively produce sebum.
Conversion of androgens to dihydrotestosterone in
acne anatomic site.
Androgenic activity drives sebum production in the
sebaceous glands; however, most acne patients do not
have an endocrine abnormality.
Increased sebum production is not necessarily
responsible for acne
6

7. SLOUGHING OF KERATINOCYTES
A primary factor in the development of acne
Follicular keratinization cause plugging of the hair follicle
pore
Increased sloughing of keratinocytes correlates with
comedo formation and can be related to influences such as:
Local cytokine modulation
Decrease in sebaceous linoleic acid and
Androgen stimulation
Abnormal follicular keratinization can be a primary event,
or can be a secondary response to irritation or other
factors.
7

8. BACTERIAL GROWTH AND COLONIZATION
Propionibacterium acnes flourish
It triggers immune responses such that titers of
antibodies to P. acnes are higher in patients with severe
acne than in non-acne control subjects.
8

9. INFLAMMATION AND IMMUNE RESPONSE
Inflammation can be a consequence of
increased:
Sebum production,
Keratinocyte sloughing, and
Bacterial growth.
9

10. Principal influence in the formation of acne lesions.
10

11. Types of Acne
1. Non-inflammatory acne
Whitehead
When the trapped sebum and bacteria stay below the skin
surface, a whitehead is formed.
Whiteheads may show up as tiny white spots, or they may
be so small that they are invisible to the naked eye.


11

12. Types of acne
blackhead occurs
when the pore opens to the surface, and the sebum, which
contains the skin pigment melanin, oxidizes and turns a
brown/black color.
Blackheads can last for a long time because the contents
very slowly drain to the surface
12

13. Types of acne
2. Inflammatory acne

Papule
occurs when there is a break in the follicular wall.
White blood cells rush in and the pore becomes inflamed.

13

14. Types of acne

Pustule

forms several days later when white blood cells make their
way to the surface of the skin.
Pustule= "zit" or a "pimple".
14

15. Types of acne
Nodules

elevated, firm, distinct, palpable, round or oval that occurs in
the dermis and/ or hypodermis.

Cysts

Severe inflammatory reaction with a very large pus
filled lesions.
15

16. Clinical presentation
occur on the face, back, upper chest, and shoulder
area
described as mild, moderate, or severe
many practitioners consider the presence of 5 to 10
comedones to be diagnostic
16

17. Predominance of Acne Lesion Type by Acne Severity
17

18. TREATMENT
Most therapeutic interventions function primarily to
prevent the formation of new acne lesions and have
minimal impact on existing lesions.

Among the factors that can affect acne are genetics,
climate, diet, environment, stress, and physical activity.
18

19. Nonpharmacologic Therapy
Non-comedogenic facial soap used twice daily
Avoid oily skin products
Avoid manipulating or squeezing lesions
19

20. Pharmacologic Therapy
Topical Agents
Benzoyl Peroxide
Superficial inflammatory acne is typically treated with
benzoyl peroxide (BPO), antibacterial agent that is
rapidly bacteriostatic and possibly bactericidal against P.
acnes.
has a comedolytic effect
Propionibacterium acnes resistance is not known to develop
Available in concentrations ranging from 1% to 10% in
various formulations including creams, lotions, gels, and
facial washes.
20

21. Adverse effects:
Dryness, irritation, redness, and stinging of the skin.
Bleaching effect that tends to discolor hair and
fabrics.
Fair or moist skin usually is more sensitive to irritation
from BPO
To minimize irritation potential, BPO should be
applied to cool, clean, dry skin, no more frequently
than twice daily
21

22. Retinoids
Tretinoin, adapalene, and tazarotene
Highly effective in the treatment of acne
Comedolytic and antiinflammatory effects, topical
retinoids are recommended as first-line treatment for
mild to moderate comedonal and inflammatory acne.
While success is seen with monotherapy, using a
retinoid in combination with benzoyl peroxide or
topical antibacterials is also an appropriate and
effective therapeutic treatment option.
22

23. Retinoids (2)
Adverse effects
Erythema, irritation, dryness, and peeling at the site of
application
Photosensitivity
Use at bedtime
Lesion improvement occurring in 3 to 4 months.
Topical retinoids should be avoided in children less
than 12 years old and in pregnant women
23

24. Antibacterials
Topical antibacterials
First-line agents used in the treatment of mild to moderate
inflammatory acne
Clindamycin 1% and erythromycin 2% preparations [bid]
Sodium sulfacetamide
Adverse effects
Mild and include dryness, erythema, and itching.
Pseudomembranous colitis can occur with the use of topical
clindamycin.
Co-administration of erythromycin and benzoyl
peroxide has been shown to decrease the incidence of
resistance
24

25. Azelaic Acid
Antibacterial, anti-inflammatory properties and
comedolytic activity
stabilize keratinization
alternative in the treatment of mild to moderate acne in
patients who cannot tolerate benzoyl peroxide or topical
retinoids
has a hypopigmentation effect that may prove effective in
patients who are prone to post-inflammatory
hyperpigmentation
Adverse effects
minimal and transient with erythema and skin irritation
Azelaic acid 20% cream bid over 1 to 2 months
25

26. Keratolytics
Sulfur, resorcinol, and salicylic acid are not as effective as
other topical agents, but can be used as second-line
therapies

Less skin irritation than benzoyl peroxide or the topical
retinoids

Sulfur preparations produce an unpleasant odor when
applied to the skin, while resorcinol may cause brown
scaling.

The possibility of salicylism exists with continual salicylic
acid use
26

27. Oral Agents Used in the Treatment of Moderate to Severe
Acne

27

28. Isotretinoin
Isotretinoin is effective in up to 80% of patients with
severe nodulocystic acne
Isotretinoin works on the four pathogenic factors that
contribute to acne development and can produce acne
remission for several years.
used in patients who have failed conventional
treatment, those who have scarring acne, those who
have chronic relapsing acne, and those who have acne
with severe psychological distress
28

29. Drying of the mucosa of the mouth, nose, and eyes is
the most common problem
Cheilitis and skin desquamation
Disturbances in lipid metabolism
increased creatine phosphokinase and blood glucose,
as well as photosensitivity
hepatomegaly with abnormal liver function tests, bone
abnormalities, arthralgias, muscle stiffness, and
headaches
29

30. Isotretinoin’s Adverse Effects and Management Strategies
30

31. Oral Contraceptives
Valuable second-line treatment option for moderate
to severe acne in female patients
Oral contraceptives decrease the production of
androgens by the ovaries, which in turn leads to a
decrease in sebum production
Adverse effects:
Nausea, weight gain, breast tenderness, and breakthrough
bleeding.
Increased incidence of thromboembolic disease, particularly
in women who use tobacco products or have other risk
factors for thromboembolism.
31

32. Other Agents
Although use is infrequent, several other agents are
available as second or third-line treatment options for
acne when first-line therapies fail and include the
following:
Corticosteroids
Chemical peels
Antiandrogens
Estrogens
Gonadotropin-releasing hormone agonists
32

33. 33

34. OUTCOME EVALUATION
Depending on severity, complete resolution of acne
may take weeks to months.
Monitor patients after 6 weeks of pharmacologic
therapy for any improvement of signs and symptoms:
Decreased number of lesions
Decreased severity of lesions
Relief of pain/irritation
34

35. Psoriasis
35

36. Introduction
Psoriasis is a common chronic inflammatory skin
disorder characterized by recurrent exacerbations
and remissions of thickened, erythematous, and
scaling plaques.

The clinical appearance of psoriasis can be
cosmetically disfiguring, and the disease can be
physically and emotionally debilitating, especially
for patients with severe disease.
36

37. ▫Prevalence among blacks (0.45% to 0.7%) is lower
than in the remainder of the United States population
(1.4% to 4.6%).
▫It is equally common in males and females.
•Between 10% and 30% of patients develop psoriatic
arthritis.
▫In 10% to 15% joint symptoms appear prior to skin
involvement.
•Cause Clinical depression
▫8% to 10% of psoriatic patients aged 18 to 54 years old
actively contemplated suicide because of their psoriasis.
37

38. ETIOLOGY
•Psoriasis is a T-lymphocyte–mediated inflammatory
disease that results from
▫a complex interplay between multiple genetic
factors and environmental factors
38

39. Genetic factors
MZ twins (73 %) show higher disease concordance
than DZ twins (20 %)
When both parents are affected the rate in siblings is
as high as 50%,
 When one parent is affected, the rate is 16.4%
When neither parent has psoriasis, only 7.8%


39

40. Environmental Factors
•Local
▫Trauma: e g, physical, chemical, electrical, surgical, infective, and
inflammatory types of injury or even excessive scratching can
aggravate or precipitate localized psoriasis
▫strong sunlight
•Systemic
▫ Infection:
Pharyngeal streptococcal infections (guttate psoriasis)
streptococcal colonization or overgrowth (refractory plaque
psoriasis).
HIV

40

41. Drugs: Lithium, withdrawal from systemic
corticosteroids, Beta-blockers, some antimalarials,
NSAIDs and tetracyclines.
psychological stress
Smoking
Alcohol
Warm seasons and sunlight improve psoriasis in 80%
of patients, whereas 90% of patients worsen in cold
weather

41

42. PATHOPHYSIOLOGY
Cell-mediated immune mechanisms play a
central role
Cutaneous inflammatory T-cell–mediated
immune activation requires two T-cell signals
that are mediated via cell–cell interactions by
surface proteins and by antigen-presenting cells
(APCs) such as dendritic cells or macrophages
T cells migrate into the epidermis, whereas T cells
are not normally located in the epidermis of
normal skin
42

43. Once in the skin, activated T cells secrete various
cytokines (IL-2, IFN-γ) that induce the pathologic
changes of psoriasis
Defects in the epidermal cell cycle
Psoriatic epidermal cells proliferate at a rate
sevenfold faster than normal epidermal cells
43

44. CLINICAL PRESENTATION OF PSORIASIS
psoriasis is a nonmalignant, hyperproliferative
epidermal cell disorder,
it results in accumulated, immature, excessively
thickened skin that is manifested as plaques.
lesions are relatively asymptomatic
pruritus is a complaint in about 25% of patients
Severe, widespread psoriasis can have fever and
chills
44

45. Distal interphalangeal joints and adjacent nails are
most commonly involved

45

46. 46
Auspitz sign- the appearance of wet surface with pin-
point bleeding after scratching of the scale

47. Psoriatic arthritis-both psoriatic lesions and
inflammatory arthritis-like symptoms occur
Scalp psoriasis-vary from diffuse scaling on an
erythematous scalp to thickened plaques with
exudation, microabcess and fissures
Generalized or erythrodermic psoriasis-the whole
body is affected
Pustular psoriasis-Pus-like blisters, noninfectious,
fluid contains white blood cells

47

48. Guttate psoriasis(small drop like plaques)- acute
onset, occur in children, is often associated with
infections of group A beta- hemolytic
streptococci

Elbows, scalp, lower part of buttock, palms, soles,
face, and genitalia can be commonly involved.
48

49. Psoriatic Plaque
49

50. Chronic Plaque Psoriasis
50

51. Erythrodermic Psoriasis
51

52. Pustular psoriasis
52

53. Napkin psoriasis
Napkin psoriasis: begins between the ages of 3 and 6
months

53

54. Guttate psoriasis
54

55. Diagnosis
Based on physical examination findings of the
characteristic lesions of psoriasis
Patient medical history
family history of psoriasis,
onset and duration of lesions
presence of exacerbating factors,
previous history of antipsoriatic treatment
exposure to chemicals and toxins, and allergies (food,
drugs, and environmental)
Skin biopsy confirming the diagnosis

55

56. TREATMENT
Desired Outcome
•chronic illness with no known cure, the goals focus on
controlling the signs and symptoms of disease:
▫Minimizing or eliminating the signs of psoriasis
▫Alleviating pruritus and minimizing excoriations
▫Reducing the frequency of flare-ups.
▫Ensuring appropriate treatment of associated conditions such
as psoriatic arthritis.
▫Maintaining or improving the patient’s quality of life.
56

57. NONPHARMACOLOGIC THERAPY
Emollients (moisturizers)
hydrate the stratum corneum and minimize water
evaporation
lotions, creams, or ointments, emollients often need to be
applied several times per day (about four times per day)
to achieve a beneficial response.
Balneotherapy (and climatotherapy)
bathing in waters containing certain salts, often combined
with natural sun exposure
• reduce activated T cells in skin

57

58. PHARMACOLOGIC THERAPY
Topical treatments for mild to moderate psoriasis
include corticosteroids, vitamin D analogues,
tazarotene, and others.

The systemic treatments for moderate to severe
psoriasis include biologic agents, cyclosporine,
acitretin, and others
58

59. Topical Therapy: First-Line Agents
Keratolytics
Salicylic acid’s cause disruption in corneocyte-to-
corneocyte cohesion in the abnormal horny layer of
psoriatic skin
used to remove scale, smooth the skin, and decrease
hyperkeratosis.
enhances penetration and efficacy of some other
topical agents such as corticosteroids
Adverse effect - salicylism, with symptoms of nausea,
vomiting, tinnitus, and hyperventilation
a gel or lotion, is usually applied two to three times a
day in concentrations of 2% to 10%.
59

60. Corticosteroids
used to decrease erythema, scaling, and pruritus.
Topical vasoconstricting potencies of corticosteroids
are ranked by the Stoughton-Cornell classification in
seven classes
Class I corticosteroids-clobetasol propionate,
halobetasol propionate, and betamethasone
dipropionate (optimized vehicle)
Class VII corticosteroids -hydrocortisone 1%

60

61. Topical corticosteroids are usually applied 2 to 4
times daily during long-term therapy
ADR- Local tissue atrophy, epidermal and dermal
degeneration, and striae
Acneiform eruptions and masking of symptoms of
bacterial or fungal skin infections
suppression of the hypothalamic-pituitary-adrenal
axis, hyperglycemia, and development of
cushingoid features
Tachyphylaxis and rebound flare of psoriasis
after abrupt cessation of topical corticosteroid
therapy can also occur

61

64. Vitamin D Analogues

inhibits keratinocyte differentiation and
proliferation, suggesting a role in the treatment
of hyperkeratotic skin disease
use of vitamin D has been limited by its
propensity to cause hypercalcemia
64

65. Calcipotriene

binds to vitamin D receptors as does vitamin D,
but it is 100 times less active on systemic calcium
metabolism because of its rapid local metabolism
improvement is seen within 2 weeks of treatment
with calcipotriene, with approximately 70% of
patients demonstrating marked improvement
after 8 weeks of therapy.
Irritation consisting of mild burning and stinging
65

66. Available in a 0.005% concentration as a cream,
ointment, and solution, is generally applied one to
two times per day (no more than 100 g/wk).

Tazarotene

a synthetic retinoid, is a prodrug that exerts its
pharmacologic activity when hydrolyzed to its active
metabolite, tazarotenic acid
pruritus, burning, stinging, or erythema
available as a 0.05 or 0.1% gel and cream, and is
applied once a day, usually in the evening

66

67. Topical Therapy: Second-Line Agents
Coal Tar
stimulates transient epidermal hyperplasia followed
by a cytostatic effect with epidermal thinning
preparations of 2% to 5% tar are available in lotions,
creams, shampoos, ointments, gels, and solutions
applied in the evening
local irritation, unpleasant odor, staining of skin and
clothing, and increased sensitivity to ultraviolet (UV)
light, including the sun
67

68. Anthralin

possesses antiproliferative activity on human
keratinocytes, inhibiting DNA synthesis by
intercalation between DNA strands
Apply only to affected areas of skin  excessive
and unwanted irritation and staining
68

69. Systemic Therapy
Biologic Therapy
infliximab, etanercept, alefacept, efalizumab and
adalimumab

Acitretin
an oral retinoid indicated for the treatment of
severe psoriasis, including erythrodermic and
generalized pustular types but is more useful as
an adjunct in the treatment of plaque psoriasis
69

70. shown good results when combined with other
psoriatic therapies(PUVA,UVB and topical
calcipotriol)
ADR-hypervitaminosis A (i.e., dry lips/cheilitis, dry
mouth, dry nose, dry eyes/conjunctivitis, dry skin,
pruritus, scaling, and hair loss), hepatotoxicity,
skeletal changes, hypercholesterolemia, and
hypertriglyceridemia
contraindicated in females who are pregnant or
who plan pregnancy within the 3 years following
drug discontinuation
70

71. Absorption is enhanced when taken with food.
Concurrent ingestion of alcohol converts acitretin
to etretinate, which has a longer half-life
25 to 50 mg once daily, with therapy continued
until lesions have resolved.
 A dosage of 50 mg/day is typically required for
plaque psoriasis
71

72. Cyclosporine

An effective immunosuppressive agent that
inhibits the first phase of T-cell activation.
Cyclosporine is used in the treatment of both
cutaneous and arthritic manifestations of severe
psoriasis
2.5 or 5 mg/kg per day
The major concerns with the use of cyclosporine
are nephrotoxicity, hypertension, and potential
risk of malignancy
72

73. To decrease the risk of nephrotoxicity, the dose of
cyclosporine should be kept below 5 mg/kg per
day, and if serum creatinine levels increase by
more than 30% the dose of cyclosporine should
be decreased or discontinued

hypomagnesemia, hyperkalemia, decreased liver
function, elevation of serum lipids,
gastrointestinal intolerance, paresthesias,
hypertrichosis, and gingival hyperplasia
73

74. Methotrexate

inhibits replication and function of T and B cells
and suppresses secretion of various cytokines
such as IL-1, INF-γ, and TNF-α.
also suppresses epidermal cell division.
is indicated in patients with moderate to severe
psoriasis, psoriatic arthritis and refractory to
topical or UV therapy
ADR- nausea and vomiting as well as mucosal
ulceration, stomatitis, malaise, headaches,
macrocytic anemia, and pulmonary toxicity
74

75. Bone marrow toxicity that leads to leukopenia,
anemia, and thrombocytopenia
Hepatotoxicity and malignant lymphomas
starting dose is 7.5 to 15 mg per week, and this is
increased incrementally by 2.5 mg every 2 to 4
weeks until a response is evident.
Maximal doses are typically approximately 25 mg
per week
75

76. Tacrolimus, pimecrolimus, mycophenolate
mofetil, sulfasalazine, 6-thioguanine and
hydroxyurea
76

77. Phototherapy
Ultraviolet B Light Therapy and PUVA Therapy
UVB light (290 to 320 nm) continues to be an
important phototherapeutic intervention for psoriasis
310 to 315 nm is the most effective wavelength of UVB
Emollients enhance efficacy of UVB
calcipotriene or topical retinoids application should
be after or at least 2 hours before UVB therapy
because phototherapy can inactivate the topical
product
77

78. PUVA is a photochemotherapeutic approach to
treatment of psoriasis.
moderate to severe, incapacitating psoriasis
unresponsive to conventional topical and
systemic therapies
Psoralen(methoxsalen)
mechanism of action of both UVB and PUVA in
treating psoriasis is thought to be
immunomodulatory (antiproliferative,
antiinflammatory, and immunosuppressive
effects)
78

79. Adverse effects from oral methoxsalen include
nausea, dizziness, and headache.
Long-term adverse effects from combined
psoralen (methoxsalen) and UV light include
actinic skin damage, solar elastosis, dry and
wrinkled skin, and hyperpigmentation or
hypopigmentation.
An increased risk of skin cancers
Oral methoxsalen is usually dosed with milk or
food to minimize risk of nausea and
gastrointestinal upset 79

80. COMBINATION, ROTATIONAL, AND
SEQUENTIAL THERAPY

Combination therapy of systemic agents with
other modalities can enhance therapeutic benefit
and reduce dose of each pharmacotherapeutic
agent
80

81. Combinations can include:
Acitretin + UVB light
Acitretin + PUVA (UVA combined with psoralen,
usually methoxsalen)
Methotrexate + UVB light
PUVA + UVB light
Methotrexate + cyclosporine
81

82. Rotational therapy with biologic and non biologic
agents
Reduce the cumulative drug toxicity

Sequential therapy-eg. Cyclosporin then acitretin
82

83. Atopic Dermatitis
83

84. Introduction
Atopic dermatitis (AD) is a common skin disease. It is
often referred to as eczema, which is a general term
for several types of skin inflammation.
AD is a common chronic inflammatory skin
condition, is notorious for creating a vicious cycle of
itching and scratching
Chronic, relapsing, itchy and inflamed skin is the
trademark symptom of atopic dermatitis (or atopic
eczema)
Associated with Bronchial asthma, allergic rhinitis,
family history of atopic dermatitis, and hay fever
84

85. Levels of air pollution, industrialization and
urbanization, dietary modifications, and higher
socioeconomic class are some of the factors that have
been attributed to the increase in prevalence
a disease of complicated genetic, environmental, and
immunologic mechanisms
if one parent has an atopic condition, there is a 60%
likelihood that the child will be atopic. If both
parents are afflicted, it is possible that the child will
have an 80% chance of developing an atopic
condition
85

86. Pathophysiology
The initial mechanisms that trigger inflammatory
changes in the skin in patients with AD are unknown.
Neuropeptides, irritation, or pruritus-induced
scratching may be causing the release of
proinflammatory cytokines from keratinocytes.
Alternatively, allergens in the epidermal barrier or in
food may cause T-cell mediated but IgE-independent
reactions.
Allergen-specific IgE is not a prerequisite.
86

87. Characteristic features in pathophysiology are skin
barrier dysfunction, and immune deviation toward
TH2 with subsequent increased IgE.
The disease is further complicated by microbial
colonization with pathologic organisms resulting in
increased susceptibility for skin infections.

87

88. Clinical Presentation
Intense itching (pruritus) and skin reactivity are the
hallmarks
The clinical presentation of AD differs depending on
the age of the patient.
Infantile phase
The onset is in the third month of life
The child is fair, fat, anxious with shiny eyes and glassy
expression
The face particularly the checks are the usually affected
sites
It is erythematous and dry with few papulovesicles and
scant oozing
The course is marked by remissions and relapse

88

90. Childhood phase
It recurs between the ages of 4 and 10 years
It tend to localize in flexural areas, the
antecubital and popliteal fossa, neck, eye lid and
behind the ears.
Erythema, edema, vascularization and oozing

90

92. Adolescent and adult phase
The lesions are dry and lichenfied and hyper
pigmented plaques in flexural areas
92

94. DIAGNOSIS
Diagnostic criteria include the presence of
pruritus, with three (major criteria) of more of
the following
History of flexural dermatitis of the face in
children younger than 10 years of age
History of asthma or allergic rhinitis in the child or
first-degree relative
History of generalized xerosis (dry skin) within
past year
Visible flexural eczema
Onset of rash younger than 2 years of age
94

95. Minor features(must have 3 or more)
Cataract, cheilitis, conjuctivitis-recurrent, facial
erythema, eczema-perifollicular, food intolerance,
hand dermatitis, ichthyosis, infections, double
intraorbital fold(Morgan’s sign), itching when
sweating, nipple deramtitis, orbital darkening,
wool intolerance, xerosis and white dermography
95

96. Complications
predisposition for increased microbial organisms,
namely Staphylococcus aureus, which is found in
more than 90% of atopic dermatitis skin lesions

more prone to herpes simplex infections than in
the general population
96

97. TREATMENT
no 100% cure for atopic dermatitis
97

98. NONPHARMACOLOGIC
98

99. PHARMACOLOGIC
Topical Corticosteroids
the standard in treating the inflammation and
pruritus related to atopic dermatitis

Antihistamines used to attempt to break the
“scratch–itch cycle.”
hydroxyzine or diphenhydramine
99

100. 100

101. Topical Immunomodulators

Calcineurin inhibitors, such as tacrolimus and
pimecrolimus, offer a more long-term option, as
they can be used on all body locations for
prolonged periods without fear of corticosteroid
induced adverse effects.
101

102. 102

103. Coal tar
preparations demonstrated antipruritic and
antiinflammatory properties on the skin
used in combination with topical corticosteroids,
as an adjunct to reduce the strength of a
corticosteroid, and in conjunction with UV light
therapies
should not be used on acute oozing lesions
103

104. REFRACTORY THERAPIES
Wet Dressings and Occlusion
effective in relieving itch, particularly at night
Wet wraps used in conjunction with topical
corticosteroids can be used for acute flares, or
those with chronic, lichenified lesions
Tepid compresses applied to skin for 20 minutes
four to six times daily can aid in drying out the
oozing lesions

104

105. Ultraviolet Light
Systemic immunosuppressants
Systemic corticosteroids, cyclosporine,
azathioprine, mycophenolate mofetil,
methotrexate and interferon-γ
105