Prurigo: Types & management

1. Prurigo
Dr Yugandar

2. • Group of skin diseases characterized by
intensely pruritic papules 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 pruritus and
papules and nodules with excoriations and
ulcerations due to scratching.

4. • Prurigo is 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. Pruriginous dermatoses
• Nodular prurigo
• chronic prurigo
• prurigo pigmentosa
• prurigo of pregnancy
• actinic prurigo.

6. • Acute Prurigo:Urticarial erythema or wheals
appear and become exudative papules, usually
in small children k/a Strophulus infantum
• Subacute prurigo: urticarial papule
accompanied by intense itching occurs on
extensor surface of the extremities or the
trunk.when it is rubbed and scratched, erosion
or crust forms

7. • Chronic prurigo: prurigo chronica
multiformis,with aggregated individual
papules that tend to form a lichenoid
l e s i o n ;
• prurigo nodularis, with large nodular
p a pu les tha t f orm s pars ely a n d

8. Prurigo chronica multiformis:
• trunk and legs of the elderly
• Exudative or 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 pruritic papules and lichenoid
lesions.
• often chronic, with recurrences and

9. Nodular prurigo
• Nodular prurigo is characterized clinically
by chronic, intensely itchy nodules and
histologically by 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 obtusus corneus

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

12. Etiopathogenesis
• severe chronic pruritus leads 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

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
• Thes changes are due to the chronic
stimulation of keratinocytes by scratching

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

18. • A further study has shown that the
vanilloid receptor, subtype 1
(VR1/TRPV1), an ion channel, binds to
capsaicin,
• found in much higher levels on cutaneous
nerves in lesional skin in prurigo nodularis
patients

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

21. CLINICAL FEATURES
• massive, and sometimes excruciating pruritus
• extensor aspects of the extremities, the
shoulders,and the 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
erythematous nodule
• patients often scratch intensely leading to
gray or purple and sometimes verruciform
keratotic areas, excoriations, crater-like
ulcerations, and
hemorrhagic crusts

24. • After the lesions heal, residual lesions are left
behind with
• post-inflammation hyperpigmentation or
• areas of hypopigmentation or
• Scarring
• The skin between individual lesions is
generally normal,but there is sometimes
xerosis cutis

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
nodularis is referred to as the “butterfly
sign”
• significance of the mechanical trauma for
the development of lesions

27. • The development of areas of
keratosis, excoriation,and ulceration 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”which causes the nodules to persist
and leads to secondary lesions

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

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

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

31. • More no of Eosinophilic granulocytes with
degranulation in 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
lichenifi cation.
• The epidermal
downgrowth is
pseudoepitheliomatou
s in extent.
• mixed inflammatory
cell infi ltrate in the
dermis
• sclerosis of the
dermal collagen

35. Differential Diagnosis

36. • antipruritic measures 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
• mometasone furoate or
methylprednisolone aceponate
• application of topical corticosteroids
should be under occlusion
• Intralesional application of corticosteroids :
triamcinolone acetonide suspension 10-40
mg/ml

38. • Calcineurin inhibitors :
• topical tacrolimus
• antipruritic effect of calcineurin inhibitors
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 fibers and
interrupting transmission of cutaneous
pruritus
• gradually increasing doses (0.025% -
0.05% - 0.075% - 0.1%).
• In prurigo nodularis, concentrations of up
to 0.3% may be necessary

42. • Cannabinoid agonists:
• Topical use of the cannabinoid agonists N-
palmitoylethanolamine (PEA)

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

44. Systemic antipruritic therapies
• Antihistamines
• Cyclosporine : inhibits the function of
lymphocytes as well as mast cells
• Anticonvulsant agents : gabapentin also
has an antipruritic effect
• Antidepressants :
mirtazapine, paroxetine, ondansetron,
• Opioid receptor antagonist: Naltrexone

45. • Thalidomide:dosage between 100 mg/day
and a maximum of 400 mg/day
• Roxithromycin with 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, intralesional triamcinolone
acetonide 40 mg/ml

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

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