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Fifth stage 

Dermatology 

Lec-16

 

 .د

  عمر

18/4/2016

 

 

Vesiculobullous diseases

 

 

CLASSIFICATION OF VESICULOBULLOUS DISEASES

CLASSIFICATION 

INTRA EPITHELIAL VESICLES: The lesion is formed within the epithelium  

  Acantholytic vesicles : This is because of the break down of  specialized attachments 

called the desmosomes  

  Nonacantholytic vesicles: It is usually in the viral infections because of the death or 

the rupture of the group of cells. 

SUB EPITHELIAL VESICLES: Lesions formed between the epithelium and the lamina propria    
eg: 

  Erthyma multifome 

  Phempegoid 

  Dermatitis herpetiformis 

  Epidermolysis bullosa 

 

PEMPHIGUS VULGARIS

  A rare autoimmune disease. 
  Common in Ashkenazi and Mediterranean jews . 
  Middle aged and older. 
  Other variants are: 

                 Pemphius  vegetans 

                 Paraneoplastic pemphigus 

 

CLINICAL FEATURES: 

  Painful erosions are formed in the oral cavity and skin. 
  The bulla is rapidly ruptured leaving a collapsed roof of grayish membrane with a red 

ulcerated base. The ulcer may look like an apthous ulcer or may be large map shaped. 

  Nikolsky sign is positive. 


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    Sometimes the ulcers are joined together to make a confluence. this condition is 

very painful. 

  It has a variable course and might involve any mucous membrane as oesophagus, 

cervix.  

  Protein/fluid,electrolyte and weight loss /secondary infections. 
  Fatal if untreated.  

 

PATHOGENESIS: 

  It is an autoimmune disease 
  There are circulating antibodies of type IgG. 
  These antibodies are reactive against the desmosomes or the tonofilament complex. 
  There destruction or disruption of these tonofilament complex ,resulting in the loss of 

attachment from cell to cell 

 

     

 

HISTOPATHOLOGY

  Intra epidermal (suprabasilar) vesicles or bulla and cleft like spaces are produced  

(acantholysis). 

  These changes are in the stratum spinosum or the prickle cell layer. 
  Inflammatory cells are very scanty however eosinophils may be seen. 

     

DIAGNOSIS

  Skin biopsy 
  Electron microscopy has shown that widening of the intercellular space is followed by 

splitting of the desmosome junctions. 


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  Direct & indirect immunofluorescence 
  ELISA 

 

DIFFRENTIAL DIAGNOSIS: 

  Bullous Pemphegoid  
  Erthema multiforme 
  Bullous lichen plannus  

 

TREATMENT: 

High mortality rates 

  Hospital admission 
  Topical potent steroids  
  Prednisolone plus azathioprine 
  Rituximab 
  Others 

 

BULLOUS PEMPHIGOID

  Bullous pemphigoid is an affliction of elderly people,with onset usually after 60 years 

of age. 

  The blister in bullous pemphigoid is subepidermal with an intact and often viable 

epidermis forming the roof. 

  Bullous pemphigoid commonly starts with itching and a non-specific rash on the limbs 

that may be either urticaria-like or occasionally eczematous and rarely may simulate 
vesicular eczema.  

                                                         

                                                                                    

               

 

 

 

 

 

 


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PEMPHGOID: 

  Blisters may arise on erythematous and on normal skin and may be associated with 

dermal edema. The blisters are tense and dome shaped, obtaining a diameter of 
many centimeteres. 

  The blisters are tough (Nikolsky sign negative) and may remain intact for several days, 

the contents often becoming jelly-like with coagulated fibrin. 

  Mucosal lesions occur less frequently (25%) and are less severe than in pemphigus 

vulgaris and are usually confined to the mouth. 

 

  Untreated bullous pemphigoid runs a chronic, self limiting course over a number of 

months or years. 

  The disease duration is usually 3-6 years, with most patients achieving complete 

remission off treatment. 

 

TREATMENT

Topical and systemic steroids are the mainstay of treatment. 

  For localized BP, very potent topical steroids are often sufficient. 
  Antibiotics 
  Systemic steroids 
  Immunsuppressives 
  IVIG 
  Plasmapheresis 

 




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