Prurigo

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Prurigo: Types & management

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Prurigo

  1. 1. Prurigo Dr Yugandar
  2. 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. 3. • chronic inflammatory skin disorder characterized by severe pruritus and papules and nodules with excoriations and ulcerations due to scratching.
  4. 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. 5. Pruriginous dermatoses • Nodular prurigo • chronic prurigo • prurigo pigmentosa • prurigo of pregnancy • actinic prurigo.
  6. 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. 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. 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. 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. 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. 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. 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
  13. 13. • 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
  14. 14. • Keratinocyte and fibroblast activation: acanthosis, parakeratosis,and hyperkeratosis of the epidermis • Thes changes are due to the chronic stimulation of keratinocytes by scratching
  15. 15. • 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
  16. 16. • 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
  17. 17. • 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.
  18. 18. 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
  19. 19. • 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
  20. 20. • 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
  21. 21. • 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
  22. 22. • 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
  23. 23. • 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.
  24. 24. 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
  25. 25. • 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,
  26. 26. • 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
  27. 27. • 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
  28. 28. Differential Diagnosis
  29. 29. • 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.
  30. 30. • 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
  31. 31. • Calcineurin inhibitors : • topical tacrolimus • antipruritic effect of calcineurin inhibitors can possibly be explained by their anti- inflammatory effect and direct effect on nerve fibers
  32. 32. • Vitamin D3 analogues : topical therapy calcipotriol, tacalcitol
  33. 33. • Menthol and polidocanol : • menthol (0.5-2%) • urea (2-10%) • polidocanol (3-5%)
  34. 34. • 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
  35. 35. • Cannabinoid agonists: • Topical use of the cannabinoid agonists N- palmitoylethanolamine (PEA)
  36. 36. • 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
  37. 37. 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
  38. 38. • 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
  39. 39. • 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
  40. 40. Parthenium dermatitis manifesting clinically as polymorphic light eruption and prurigo nodularis-
  41. 41. LATE ONSET NODULAR PRURIGO – THE SOLE AND INITIAL MANIFESTATION OF OCCULT HODGKIN’S DISEASE

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