Prurigo.pdf

Prurigo is a chronic inflammatory disease characteristic by solid papule over shin of tibia

1. Prurigo
Dr Yugandar

2. •Group of skin diseases characterized by
intensely pruriticpapules or nodules.
•Some authors have stressed the intense
pruritus
•visible excoriations
•No identifiable local cause for the
scratched lesions.

3. •chronic inflammatory skin disorder
characterized by severe pruritusand
papules and nodules with excoriations and
ulcerations due to scratching.

4. •Prurigois derived from the Latin and
means “itch”, which simply refers to the
common feature shared by all pruriginous
diseases, a sometimes intractable pruritus.
•The term was originally introduced by
Hebra
•He denote papules induced by scratching.

5. Pruriginousdermatoses
•Nodular prurigo
•chronic prurigo
•prurigopigmentosa
•prurigoof pregnancy
•actinic prurigo.

6. •AcutePrurigo:Urticarialerythema or wheals
appear and become exudativepapules, usually
in small children k/a Strophulusinfantum
•Subacuteprurigo: urticarialpapule
accompanied by intense itching occurs on
extensor surface of the extremities or the
trunk.whenit is rubbed and scratched, erosion
or crust forms

7. •Chronicprurigo:prurigochronica
multiformis,withaggregatedindividual
papulesthattendtoformalichenoid
l e s i o n ;
•prurigonodularis,withlargenodular
papulesthatformsparselyand
i n d i v i d u a l l y .

8. Prurigochronicamultiformis:
•trunk and legs of the elderly
•Exudativeor solid papules aggregate to
form invasive plaques. The lesions are
rubbed as a result of intense itching, and
exudate and crusts form to present
intermingled pruriticpapules and lichenoid
lesions.
•often chronic, with recurrences and
remissions

9. Nodular prurigo
•Nodular prurigois characterized clinically
by chronic, intensely itchy nodules and
histologicallyby marked hyperkeratosis
and acanthosis, with downward
projections of the epidermis.

10. •history of atopic dermatitis
•Aetiology : unknown,Hyde is credited
with being the first describe
•Hyde’s prurigo,prurigo simplex chronica,
and lichen obtususcorneus

11. •Woman > man
•No genetic factos
•Some authors suggested with atopic
eczema
early-onset atopic Late-onset atopic
•Close a/watopic D
•Initial manifeatationat
19
•a/w environmental
allergens
•Initial manifestation at 48
years
•No h/o atopicD
•No a/w allergens

12. Etiopathogenesis
•severe chronic pruritusleads to repetitive
mechanical trauma as a result of scratching, and
•chronic skin irritation then leads to a characteristic
tissue reaction
•marked by recruitment of a lymphocyte-rich
inflammatory infiltrate,
•activation of epidermal keratinocytes,
•a circumscribed increase in collagen tissue, and
•activation & proliferation of peripheral sensory
nerves.

15. •Leukocyte recruitment and activation :after
mechanical trauma primary pro-inflammatory
cytokines such as interleukin(IL)-1 and tumor
necrosis factor alpha (TNF-α) induce chemokine
cascades in keratinocytes
•Recruitment of Lymphocytes,eosinophils, and
mast cells

16. •Keratinocyte and fibroblast activation:
acanthosis, parakeratosis,and
hyperkeratosis of the epidermis
•Theschanges are due to the chronic
stimulation of keratinocytesby scratching

17. •Activation of sensory neurons:marked
hyperplasia of peripheral cutaneous nerves
•peripheral nerves in prurigonodularislesions
have increased amounts of nerve growth factor
(NGF)-receptor p75.
•produce high levels of NGF,calcitoningene
related peptide and substance P

18. •A further study has shown that the
vanilloidreceptor, subtype 1
(VR1/TRPV1), an ion channel, binds to
capsaicin,
•found in much higher levels on cutaneous
nerves in lesionalskin in prurigonodularis
patients

19. •These results show that activation and
proliferation of cutaneous nerves in patients
with prurigonodularisare associated with
increased production of
•the neuropeptides
•CGRP and
•substance P possibly intensifying the pruritus
via neurogenicinflammatory pathways.

21. CLINICAL FEATURES
•massive, and sometimes excruciating pruritus
•extensor aspects of the extremities, the
shoulders,andthe chest and sacral regions
•The face, palms of the hands, and plantar
surfaces of the feet are usually not affected
•No involvement of the mucous membranes

23. •sharply demarcated,tough, mildly
erythematousnodule
•patients often scratch intensely leading to
gray or purple and sometimes verruciform
keratoticareas, excoriations, crater-like
ulcerations, and
hemorrhagic crusts

24. •After the lesions heal, residual lesions are left
behind with
•post-inflammation hyperpigmentationor
•areas of hypopigmentationor
•Scarring
•The skin between individual lesions is
generally normal,butthere is sometimes
xerosiscutis

25. •The development of nodules first occurs
as a result of intense scratching.
•Typically there is an area of skin that is
unaffected which the patient cannot
reach, such as the middle of the back.
•This characteristic feature of prurigo
nodularisis referred to as the “butterfly
sign”
•significance of the mechanical trauma for
the development of lesions

27. •The development of areas of
keratosis, excoriation,andulceration on
primary lesions is attributed to the constant
irritation caused by scratching
•“scratching” of a lesion produces only
temporary relief from pruritus, which quickly
starts again, leading to an “itch-scratch-
cycle”whichcauses the nodules to persist
and leads to secondary lesions

28. •Due to the simultaneous appearance of
recent and older lesions,patientsusually
present with a
•Polymorphous appearance consisting of
recent
•nodules, excoriations
•crater-like ulcerations
•residual lesions such as hypopigmentation
or hyperpigmentationas well as scarring.

29. Histopathology
•Marked hyperkeratosis
•focal parakeratosis
•irregular acanthosis
•appearance of pseudocarcinomatous
or pseudoepitheliomatoushyperplasia
•arises from papillomatosis and an irregular,
•downward proliferation of epidermis and
epithelia of adnexalstructures

30. •In the papillary dermis
•increased amounts of multinucleated fibroblasts as
well as thick collagen fiberbundles arranged
perpendicularly to the surface.
•Proliferation of nerve fibersand Schwann cells may be
observed.
•dilated, vertically-oriented capillaries.
•At the surface, around vessels and in interstitial
spaces dense infiltrate of lymphocytes, isolated
eosinophilicgranulocytes,mastcells, macrophages,

31. •More no of Eosinophilicgranulocytes with
degranulationin atopic diathesis.
•If there are erosions or
excoriations, crusting around the margin
with exudation
•It shows parakeratosis, plasma cells and
neutrophils

32. •gross accentuation of
the changes of
lichenification.
•The epidermal
downgrowthis
pseudoepitheliomatou
sin extent.
•mixed inflammatory
cell infiltratein the
dermis
•sclerosis of the
dermal collagen

35. Differential Diagnosis

36. •antipruriticmeasures should be
undertaken to eliminate pruritus
•cutting the fingernails and
•wearing cotton gloves
•instruments such as brushes are used to
combat the itching.

37. •Topical corticosteroids
•mometasonefuroateor
methylprednisoloneaceponate
•application of topical corticosteroids
should be under occlusion
•Intralesionalapplication of corticosteroids :
triamcinoloneacetonidesuspension 10-40
mg/ml

38. •Calcineurininhibitors :
•topical tacrolimus
•antipruriticeffect of calcineurininhibitors
can possibly be explained by their anti-
inflammatory effect and direct effect on
nerve fibers

39. •Vitamin D3 analogues : topical therapy
calcipotriol, tacalcitol

40. •Menthol and polidocanol:
•menthol (0.5-2%)
•urea (2-10%)
•polidocanol(3-5%)

41. •Capsaicin : Topical capsaicin acts by
desensitizing sensory nerve fibersand
interrupting transmission of cutaneous
pruritus
•gradually increasing doses (0.025% -
0.05% -0.075% -0.1%).
•In prurigonodularis, concentrations of up
to 0.3% may be necessary

42. •Cannabinoidagonists:
•Topical use of the cannabinoidagonists N-
palmitoylethanolamine(PEA)

43. •Phototherapy : broadband UVB, narrow
band UVB, narrow band UVB in
combination with thalidomide,UVA-1
phototherapy,bathPUVA
•induction of anti-inflammatory and
immunosuppressive factors as well as
antiproliferativeeffects
•UVB-induced apoptosis of mast cells

44. Systemic antipruritictherapies
•Antihistamines
•Cyclosporine : inhibits the function of
lymphocytes as well as mast cells
•Anticonvulsant agents : gabapentinalso
has an antipruriticeffect
•Antidepressants :
mirtazapine,paroxetine,ondansetron,
•Opioidreceptor antagonist: Naltrexone

45. •Thalidomide:dosagebetween 100 mg/day
and a maximum of 400 mg/day
•Roxithromycinwith tranilast: roxithromycin
at a dosage of 300 mg/day with tranilast
(N-(3,4-dimethoxycinnamoyl)) in a dosage
of
200 mg/day in patients with prurigo
nodularis

46. •Cryosurgery: use of liquid
nitrogen, depending on their size, vary from
10-30 seconds with two to four “freeze-thaw
cycles.”
•It can take up to four weeks until the treated
nodules heal.
•Residual scarring can occur.
•After cryosurgery, patients can be pruritus-
free for up to three months,
•Combination therapy with
cryosurgery, intralesionaltriamcinolone
acetonide40 mg/ml

48. Partheniumdermatitis manifesting clinically
as polymorphic light eruption and prurigo
nodularis-

49. LATE ONSET NODULAR
PRURIGO –THE SOLE AND INITIAL
MANIFESTATION OF OCCULT
HODGKIN’S DISEASE