beneath the epidermis
? Vesicle: blister < 0.5cm
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? Bullae: >0.5cmMechanism of blister formation:
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? 1. spongiosis: extracellular fluid in epidermisEg eczema, miliaria crystallina
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? 2. Acantholysis: loss of keratinocyte cell to cell
contact........ Rounded keratinocytes......
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condensed cytoplasm...large nuclei....Peripheral condensation of chromatin and
prominent nucleoli
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Eg: pemphigus, hailey hailey ds, darriers
dis
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Tzanck smear
? Reticular degeneration ? bal ooning degeneration
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(intracel ular oedema)? eg: viral infections
? Cytolysis- friction and heat
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? Basement membrane zone destruction ?
? primary structural deficiency
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? immunological y mediated damage- BP, linearIg A disease, DH
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Based upon plane of separation? Intraepidermal-
A. subcorneal- miliaria crystallina, SSSS, P.
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foliaceous, Bullous impetigo, SCPD
B. Spinous- Eczema, Hailey Hailey, Miliaria
Rubra
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C. Suprabasal- Pemphigus vulgaris,Paraneoplastic pemphigus, Darriers
Disease
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? Subepidermal:
Bullous Pemphigoid
DH
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Linear Ig A diseasePorphyria cutanea tarda
Classification
Immunobullous disorders
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Introduction
? The immunobullous diseases are characterized by
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pathogenic autoantibodies directed at targetantigens whose function is either cell-to-cell
adhesion within the epidermis or adhesion of
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stratified squamous epithelium to dermis or
mesenchyme.
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? These diseases are often associated with significantmorbidity and some can even cause mortality, if left
untreated.
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? Adhesion between keratinocytes:
Desmosomes (transmembrane glycoproteins)
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? 1. desmogleins- 1,2,3desmoglein 3 ? in basal and suprabasal
layers and mucosae
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? 2. desmocollins? Others: non glycosylated proteins
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? Plakoglobin; desmoplakin 1 and 2; plakophilinIntraepidermal immunobullous
disorders
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Pemphigus vulgaris
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? The term pemphigus stems from the Greek`pemphix' meaning blister or bubble.
? Pemphigus is a group of autoimmune
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blistering disease of skin & mucous
membranes characterized by:
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? Histologically, intraepidermal blisters due to lossof cell-cell adhesion of keratinocytes.
? Immunopathologically, the finding of in vivo
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bound & circulating IgG autoantibodies directed
against the cell surface of the keratinocytes.
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Pemphigus vulgaris? Al patients develop painful oral erosions. More than
half of patients also have flaccid blisters and
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widespread cutaneous erosions.
? Mucosa: painful erosions over buccal & palatine mucosa.
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Intact blisters are rare. Esophagus, conjunctiva, & nasalmucosa may develop these lesions.
? Skin lesions: primary lesions are flaccid, thin walled easily
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ruptured blisters. Blisters are fragile and soon rupture to
form painful erosions.
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? Erosions often become large and partially covered with crusts.Some lesions on healing leave hyperpigmentation but no scarring.
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Skin lesions
Oral mucosal lesions
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PEMPHIGUS VULGARIS? Nikolsky sign : positive
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? Tzanck smear: Acantholytic cellsPemphigus vegetans
? Rare vegetative variant of
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pemphigus vulgaris.
? Flaccid blisters that become
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erosions and then formpapillomatous
projections especially in
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intertriginous areas and on
scalp or face.
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? Two subtypes:? Neumann type: severe
? Hal opeau type: mild
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Figure: pemphigus vegetans. Extensive
vegetating papil omatous lesions
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Pemphigus foliaceus
? Patients develop scaly, crusted cutaneous
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erosions, often on an erythematous base.? Lesions are wel demarcated and have a seborrhoeic
distribution, i.e. they favor the face, scalp and upper
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trunk
? No clinical y apparent mucosal involvement.
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? Patients are not severely il .? Disease may remain localized for years or it may
rapidly progress, in some cases to erythrodermic
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exfoliative dermatitis.
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Early disease: Scaly crustedProgressive disease: Lesions
erosions on the back
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have become confluent
PEMPHIGUS FOLIACEUS
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Pemphigus erythematosus (Senear-Usher Syndrome)
? Localized variant of pemphigus foliaceus.
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? Scaly and crusted lesions of pemphigus foliaceus appear in the
malar region of face and in other `seborrheic' areas.
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? Immunologic features of both lupus erythematosus andpemphigus.
? In vivo IgG and C3 deposition on cell surface of keratinocytes as well as
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basement membrane zone, in addition to circulating antinuclear
antibodies(ANA).
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Paraneoplastic pemphigus
? Associated with underlying neoplasms, both malignant and
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benign.? Most commonly associated neoplasms are non-
Hodgkin lymphoma(40%), chronic lymphocytic
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leukemia(30%), Castleman's disease , thymomas, sarcomas
? In children and adolescents, Castleman's disease is the most
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commonly associated tumor.? Most constant clinical feature is intractable stomatitis.
Cutaneous findings are pleomorphic and may present as
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macules, flaccid/tense blisters, Erythema Multiforme like
lesions, lichenoid eruption.
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PemphigusParaneoplastic pemphigus:
erythematosus: scaly
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severe stomatitis extending
crusted erosions are
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onto vermilion lipseen on the nose and
malar area.
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IgA Pemphigus = intercellular Ig Adermatosis
? Intraepidermal antikeratinocyte IgA
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? vesicopustular
1. Subcorneal pustular dermatosis (SCPD) type:
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? Presents as flaccid vesicles or pustules on eithererythematous or normal skin.
? Pustules tend to coalesce to form an annular or
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circinate pattern with crusts in the center of the
lesion.
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? Most commonly involved sites are axil a and groin.? Mucus membrane involvement is rare.
? Pruritus is a significant symptom.
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IgA Pemphigus
2. Intraepidermal neutrophilic (IEN) type:
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? Presents as flaccid vesicles or pustules on eithererythematous or normal skin.
? Pustules tend to coalesce to form an annular or
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circinate pattern with crusts in the center of the
lesion
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? Sunflower -like configuration of pustules is acharacteristic sign of the IEN type.
? Most commonly involved sites are axilla and
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groin
Subcorneal pustular
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Intraepithelial neutrophilic (IEN) type:
dermatosis(SCPD) type: pustules
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characteristic sunflower-likecoalescing in annular or circinate
configuration of pustules is seen.
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pattern with central crusting.
IgA PEMPHIGUS
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Induced Pemphigus
? Drugs: penicillamine
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captopril? Radiotherapy
? Thermal burns
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SUBEPIDERMAL IMMUNOBULLOUSDISEASES
BULLOUS PEMPHIGOID
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? Bullous pemphigoid is an acquired non-scarringautoimmune blistering disease of the elderly age
group characterized histological y by
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subepidermal bullae and immunopathological y
by deposition of antibodies and complement
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along the epidermal basement membrane zone(BMZ).
? The median age of onset ranges from 60 to 75
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years.
? tense blisters, hemorrhagic or fil ed with thick fibrinous
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fluid, on normal appearing skin or on an erythematousbase.
? The blisters range from vesicles to large bullae and may
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be seen al over the body, the commonest sites of
involvement being the lower abdomen, inner thighs,
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groin and the flexor aspects of the limbs.? The flexural and intertriginous areas are often affected.
? Vesicles may also develop on the palms and soles.
? Nikolsky's sign is negative.
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? For blisters that rupture, the resulting erosions and may
become covered with a crust.
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? The erosions heals without scarring, but transient pigmentary
changes and milia formation can occur.
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? Pruritus is generally present, but the degree is variable,ranging from none to intense.
? Mucosal lesions have been reported in 10%? 40% of patients
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? They are often mild and transient.
MUCOUS MEMBRANE PEMPHIGOID
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(SYN. CICATRICIAL PEMPHIGOID)
? Mucous membrane pemphigoid (MMP) is a group
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of chronic inflammatory, autoimmune,subepithelial blistering diseases predominantly
affecting mucous membranes and is
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characterized by linear deposition of IgG, IgA, or
C3 along the epithelial basement membrane zone
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(BMZ).? Scarring is the clinical hal mark, but is not always
obvious, particularly in the oral mucosa.
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? Mucous membrane pemphigoid is a rare diseasethat primarily affects the elderly (the peak
incidence is between the age of 60 and 80 years).
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? It affects twice as many women as men.
? The onset is usual y insidious.
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? The oral mucosa is most commonly involved(approximately 85% of patients), fol owed by the
ocular, nasal, nasopharyngeal, anogenital, skin,
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laryngeal, and esophageal mucosa in descending
order of involvement.
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? In the oral cavity, the gingival and palatal mucosae and lesscommonly the labial, glossal, and buccal mucosae are
affected.
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? There may be swollen, bright, erythematous, focal or
generalized, mildly painful erosions on the gingiva (termed
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`desquamative gingivitis')? The presentation may also be as fluid- or sometimes blood-
filled blisters.
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? The lips are rarely involved.
? The eyes are affected in about two-thirds of patients, most often by
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a unilateral chronic cicatricial conjunctivitis with symptoms of
burning, irritation and excessive lacrimation.
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? Genital involvement has been observed in about 20% of cases, asblisters and erosions on the glans and prepuce or the labia.
? Skin lesions occur in 10%?30% of patients, and are of two types:
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scarring and nonscarring.
? Flaccid blisters develop on erythematous plaques on the head, neck
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and upper trunk, and heal with atrophic scars.? This eruption tends to be localized and recurrent.
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PEMPHIGOID GESTATIONIS
? Pemphigoid gestationis (PG), also known as herpes
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gestationis, is a rare autoimmune pruriticpolymorphic dermatosis of pregnancy and
puerperium.
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? pemphigoid gestationis is undoubtedly under
hormonal influence since it occurs only with
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pregnancy, menstruation, oral contraceptiveingestion, hydatidiform mole or choriocarcinoma.
? The PG antigen is the 180 kDa BP antigen (BP180 or
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BPAG2),that is present in the hemidesmosomes of
the basement membrane.
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? PG may occur in the first or any subsequent pregnancy.? It usual y begins in the second or third trimester,
though it can begin at any time between the first
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trimester and the immediate postpartum period.
? Intense pruritus usual y accompanies but occasional y
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precedes a polymorphic eruption of erythematousurticarial papules and plaques, vesicles or bul ae arising
on inflamed or normal skin.
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? Classical y, there are erythematous urticarial plaques
rimmed by blisters, and crusts that enlarge peripheral y
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to form annular or polycyclic patterns.? The eruption usually begins on the abdomen,
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especially around the umbilicus, or on theextremities and then spreads to the rest of the trunk,
palms and soles.
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? Facial and mucosal lesions are rare.
DERMATITIS HERPETIFORMIS
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? Dermatitis herpetiformis is a rare chronic blistering
skin disease characterized clinically by intensely
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pruritic grouped vesicles arising on an erythematousbase, by granular IgA deposits in the dermal papillae
on direct immunofluorescence, and associated with
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gluten-sensitivity and a mostly asymptomatic
enteropathy.
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? It presents most often in the second or thirddecades, but the disease can occasionally occur in
children also.
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? A slight male predominance has been reported.
? Onset may be acute or gradual.
? The eruption is characteristical y polymorphous,
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although at a given time any one type of lesion (e.g.
papular, urticarial, vesicular or bul ous) may
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predominate.? The primary lesion is classical y, a smal vesicle on an
? erythematous, edematous base, or an erythematous
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papule, or an urticarial plaque.
? The vesicles may be grouped in a herpetiform manner
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on an erythematous plaque.? Intense itching or a burning or stinging sensation is a
common
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? If the rash is chronic, there are often lichenified
plaques at the sites of involvement.
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? The areas of predilection are the elbows, knees,buttocks, sacrum, shoulders, posterior hairline and
scalp.
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? The lesions are symmetrically distributed over the
extensor surfaces of the limbs.
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? The face is occasionally affected, but the mucousmembranes, only rarely.
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LINEAR IgA DISEASE? Linear IgA disease can be clinical y categorized into two
disorders with two distinct presentations: CBDC, which
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begins in childhood, and adult LAD, which begins in
adult life.
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? In children, the disease usual y starts below the age of5.
? The onset is usual y abrupt, with large tense bul ae
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fil ed with clear or hemorrhagic fluid on or near the
genitalia.
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? They gradual y involve other areas such as thebuttocks, scalp and
? face, especial y the perioral and periocular areas.
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? Blisters may also appear in a generalized butasymmetric distribution.
? Typical features include herpetiform clustering of
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blisters, formation of bizarre, irregularly shaped bul ae
as they enlarge and coalesce, and `rosettes' or `clusters
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of jewels' which represent the annular arrangementsof new, smal , tense blisters around a crusted healing
erythematous plaque (the `string of pearls' sign) .
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? Pruritus is variable in intensity.
? In adults, the onset may be insidious or abrupt, with
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symptoms varying from mild pruritus to severe pruritusand burning.
? There may be flexural and truncal involvement with
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scattered vesicles and tense blisters similar to BP.
? The bullae may be somewhat linear, sausage- shaped
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and hemorrhagic.? A few patients of LAD may present with a DH like
itchy eruption with grouped papulovesicles involving
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the extensor surfaces.
? Perineal and perioral involvement is less common
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than in children.? Approximately 80% of adults and children with LAD
have mucosal lesions
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Treatment of Immunobul ous
disorders
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? Management includes-
1. Investigations
2. Treatment
INVESTIGATIONS
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1-Routine
?
Full blood count and differential
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?
Fasting blood sugar
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?Liver function tests
?
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Renal function tests
? Chest x-ray
? Urinalysis
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2-Specific ?for diagnosis
? Tzanck smear
? Histopathological examination
? DIF
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? I F? Immunoblotting
? Immunoelectron microscopy
? ELISA
TREATMENT
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? The treatment of immunobul ous diseases consists of
three phases: control, consolidation, and maintenance.
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? control phase- intense therapy is given to suppressdisease activity until no new lesions appear.
? consolidation phase during which drugs and doses are
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maintained until complete clearance of lesions.
? Final y, medications can be gradual y tapered in the
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maintenance phase, aiming for the lowest dose thatprevents new lesions from appearing .
? Aim of therapy is to prevent the appearance of new lesions &
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produce healing of existing lesions.
? The choice of therapy
? Severity of the disease at presentation.
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? Patient-related? age
? general health
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? associated medical illnesses
? Drug-related
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? onset of action? efficacy
? adverse effects
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? cost
TREATMENT PHASES
? GENERAL THERAPY
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? PHARMACOLOGICAL THERAPY-A. TOPICAL
B. SYSTEMIC
General measures
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? It includes-
1. General nursing care-
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? Proper and regular dressing of the raw area is doneuntil re-epithelization takes place.
? This is performed with sterile petroleum gauze or
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gauge impregnated with topical antibiotics.
2.Adequate Nutrition ?
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? Oral supplementation with protein and high caloriefluids.
? Soft easily chewable diet in case of oral lesions
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3. control of secondary infection-antibiotics should begiven preferably following culture and sensitivity
report.
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4. restoring fluid and electrolyte equilibrium
Topical therapy
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? Is indicated in more local oral lesion with lessaggressive behaviour.
? Skin lesions-
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1. clobetasol propionate .05% may reduces therequirement of oral steroid.
2. Potassium permanganate and antiseptics to reduce
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the risk of secondary infection.
q Oral lesions-
? soft diets, soft toothbrushes help to minimize local trauma.
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? Topical analgesics or anaesthetics - benzydamine
hydrochloride 0.15% (Oral Rinse) are useful in alleviating
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oral pain, particularly prior to eating or tooth brushing.? Tooth brushing should be encouraged and antiseptic
mouthwashes may be used such as
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- chlorhexidine gluconate 0.2%
- hexetidine 0.1%
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-01:4 hydrogen peroxide solutions.? Patients are susceptible to oral candidiasis which
should be treated.
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? Topical Corticostreoid therapy may help to reduce
the requirement for systemic agents.
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? It include application of clobetasol gel .05%? Clobetasol gel may be used with occlusive vehicle
mainly in desquamative gingivitis
? Soluble betamethasone sodium phosphate 0.5 mg
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tablet dissolved in 10 mL water may be used up to four
times daily, holding the solution in the mouth for about
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5 minutes.? Isolated oral erosions could be treated with application
of triamcinolone acetonide 0.1% in adhesive paste
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? 2.5 mg hydrocortisone lozenges or sprayed directly
with an asthma aerosol inhaler, for example
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beclomethasone dipropionate 50-200 micrograms orbudesonide 50-200 micrograms.
? Topical ciclosporin (100 mg/mL) in oral pemphigus
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has been described and may be of some benefit but
is expensive
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? Tetracyclines are successful in pemphigus vulgarisand cicatricial pemphigoid
? Tacrolimus is indicated in oral resistant cicatricial
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pemphigoid
SYSTEMIC THERAPY
? Corticosteroids:
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? Oral
? Pulse IV
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? Adjuvant drugs? Azathioprine
? Oral cyclophosphamide
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? Pulsed cyclophosphamide and dexamethasone
? MMF
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? Gold? Methotrexate
? Ciclosporin
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? Tetracyclin and nicotinamide
? Dapsone
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? ChlorambucilNewer treatment modalities
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? IVIG? Cholinomimetic drugs
? Plasma exchange
? Extracorporeal photophoresis
? Biologicals
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? ImmunoadsorptionTHANKS