Prurigo is a group of skin diseases characterized by intensely itchy papules or nodules without an identifiable local cause. It is caused by severe chronic itching leading to repetitive scratching and skin irritation. This results in a lymphocyte-rich inflammatory infiltrate, activated keratinocytes and sensory nerves, and increased collagen tissue. Prurigo nodularis specifically presents as intensely itchy nodules on the extremities. Histology shows hyperkeratosis, acanthosis, and proliferation of cutaneous nerves and fibroblasts. Treatment focuses on eliminating pruritus through antipruritic medications and phototherapy to break the itch-scratch cycle and reduce inflammation.

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