prurigo
DESCRIPTION
Prurigo: Types & managementTRANSCRIPT
Prurigo
Dr Yugandar
• 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.
• chronic inflammatory skin disorder characterized by severe pruritus and papules and nodules with excoriations and ulcerations due to scratching.
• 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.
Pruriginous dermatoses
• Nodular prurigo
• chronic prurigo
• prurigo pigmentosa
• prurigo of pregnancy
• actinic prurigo.
• 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
• Chronic prurigo: prurigo chronica
multiformis,with aggregated individual
papules that tend to form a lichenoid lesion;
• prurigo nodularis, with large nodular
papules that form sparsely and individually.
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 remissions
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.
• history of atopic dermatitis
• Aetiology : unknown, Hyde is
credited with being the first describe
• Hyde’s prurigo, prurigo simplex
chronica,
and lichen obtusus corneus
• 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
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 nerves.
• 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
• Keratinocyte and fibroblast
activation: acanthosis,
parakeratosis,and hyperkeratosis of
the epidermis
• Thes changes are due to the chronic
stimulation of keratinocytes by
scratching
• 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
• 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
• 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.
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
• 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
• 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
• 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
• 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
• 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.
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
• 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,
• 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
• gross accentuation of the changes of lichenifi cation.
• The epidermal downgrowth is pseudoepitheliomatous in extent.
• mixed inflammatory cell infi ltrate in the dermis
• sclerosis of the dermal collagen
Differential Diagnosis
• 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.
• 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
• Calcineurin inhibitors :• topical tacrolimus• antipruritic effect of calcineurin
inhibitors can possibly be explained by their anti-inflammatory effect and direct effect on nerve fibers
• Vitamin D3 analogues : topical therapy
calcipotriol, tacalcitol
• Menthol and polidocanol : • menthol (0.5-2%)• urea (2-10%)• polidocanol (3-5%)
• 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
• Cannabinoid agonists: • Topical use of the cannabinoid
agonists N-palmitoylethanolamine (PEA)
• 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
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
• 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
• 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
Parthenium dermatitis manifesting clinicallyas polymorphic light eruption and prurigo
nodularis-
LATE ONSET NODULARPRURIGO – THE SOLE AND INITIAL
MANIFESTATION OF OCCULTHODGKIN’S DISEASE