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Blisters are fluid filled lesions in the skin. Some types of blister are caused by friction during physical exercise, while others are precipitated by allergic or drug reactions; the most severe symptoms are caused by the blisters formed due to genetic and autoimmune diseases.


Blisters (fluid-filled pockets between layers of the skin) develop under various conditions, the most common being physical exercise during which the skin is repeatedly rubbed when the frictional forces eventually separate the epidermal cells [1]. Blisters due to friction occur most frequently in the palms of the hands and on the soles of the feet [1]. Although common, blisters are not trivial; many conditions leading to blister formation may cause infection [2].

Much more severe are the blistering diseases caused by autoimmune or genetic bullous conditions [2]. The autoimmune blistering diseases are a collection of conditions that can be divided into two groups. In pemphigus diseases, the separation of layers occurs within the epidermis, because antibodies against desmosomal proteins are present that weakens contacts between epidermal cells [3]. In subepidermal (pemphigoid) diseases, the separation is between the epidermis and the dermis, caused by autoantibodies against hemidesmosomal proteins; this situation also occurs in epidermolysis bullosa acquisita [3].

Several diseases have been identified in both groups. In the pemphigus disease group, pemphigus vulgaris affects the mucous membranes and pemphigus foliaceus affects only the skin, whereas mucocutaneous diseases cause problems in both mucous membranes and skin. The different varieties have antibodies against different isotypes of a desmosomal adhesion protein [4]. Paraneoplastic pemphigus is associated with neoplasia and is characterized by debilitating skin lesions, including stomatitis [3] [5].

Among the subepidermal diseases, bullous pemphigoid (BP) and pemphigoid gestationis are associated with severe itching [3]. Linear IgA dermatosis is a disease of children. Epidermolysis bullosa acquisita, which is characterized by the presence of anti-collagen antibodies [6], has two variants: one is the inflammatory type that closely resembles BP and the other presents with blisters developing at mechanically exposed locations. Dermatitis herpetiformis is the cutaneous manifestation of celiac disease [3].

A large group of inherited subepidermal blistering diseases is called epidermolysis bullosa. Currently, mutations affecting ten genes have been identified that result in the blistering seen in the various forms of this disease [7].

  • Thrombosis, aneurysm rupture, and other complications did not develop in any case. Angiographic follow-up showed complete aneurysm exclusion without aneurysm recurrence in any patients.[ncbi.nlm.nih.gov]
Exfoliation of the Skin
Wide Neck
  • Nevertheless, they often present a diagnostic challenge because of the characteristic morphological features of a wide neck and shallow outpouching of the medial wall.[ncbi.nlm.nih.gov]


Friction blisters are caused by a split in the stratum spinosum. The keratinocytes forming the top of the blister are normal and necrotic. The floor of the blister also has these types of keratinocytes, but in addition, it has edematous ones also. The blister is filled with clear serum unless infected.

For autoimmune blistering diseases, the best diagnostic tool is direct immunofluorescence microscopy. This can show the presence of bound autoantibodies on the skin or on mucous membranes of the patient in both pemphigus and pemphigoid (subepidermal) diseases.

Indirect immunofluorescence microscopy identifies circulating antibodies by testing for the binding of these proteins to monkey, guinea pig, or normal human skin substrates. The antibodies will bind to the target antigens in the test skin samples [3].

These assays are followed up by tests using western blot and enzyme-linked immunosorbent (ELISA) assays. There are commercially available ELISA kits for antibodies against several of the target antigens (transglutaminase, and components of desmosomes and hemidesmosomes). These tests can also be used to monitor the disease during immunosuppressant treatment [3].

Some of the blistering autoimmune diseases can be differentiated from each other based on indirect immunofluorescence. Others need the consideration of all available information for diagnosis, including clinical, histopathological, and immunofluorescence results [8].

  • CT scan revealed a mesenteric infiltration surrounding a thickened wall bowel agglomeration; inside, a dense 2 cm foreign body with no pneumoperitoneum or peritoneal effusion.[ncbi.nlm.nih.gov]


  • Endovascular treatment with the pipeline embolization device (PED) has been described as a new treatment strategy for these lesions.[ncbi.nlm.nih.gov]
  • Endovascular therapy increased the likelihood of a second treatment, conversion to another treatment modality, and incomplete aneurysm obliteration.[ncbi.nlm.nih.gov]
  • Open surgical treatment is associated with high rates of complications, morbidity, and mortality; endovascular treatment is a promising alternative.[ncbi.nlm.nih.gov]
  • Detection and treatment of blister-like intracranial aneurysms as a source of subarachnoid hemorrhage (SAH) can be challenging. In the past the results of both microsurgical and endovascular treatment were difficult.[ncbi.nlm.nih.gov]
  • […] highly dangerous method, was used as the treatment of last resort.[ncbi.nlm.nih.gov]


  • Endovascular treatment benefits more for Tibetan BLA patients in reducing cerebral infarctions and improving neurological functional recovery prognosis. Copyright 2017 Elsevier B.V. All rights reserved.[ncbi.nlm.nih.gov]
  • No patient experienced recurrence or rebleeding, and all patients had a good prognosis. We conclude that this suturing technique is an optional safe and reliable method to treat BBAs.[ncbi.nlm.nih.gov]
  • CONCLUSIONS: BBAs are challenging vascular lesions with poor prognosis. Endovascular treatment may be more effective and safer with better outcomes than surgical approaches. Copyright 2017 Elsevier Inc. All rights reserved.[ncbi.nlm.nih.gov]
  • However, this grim prognosis is based on results that indiscriminately group all blister aneurysms together without taking into account the heterogeneous appearance of these lesions.[ncbi.nlm.nih.gov]
  • Call your dentist or physician right away if: Lip or mouth sores persist longer than one week The sores make it hard for you to talk or swallow You develop a fever You have a second outbreak of blisters Prognosis HSV-1 infection is a lifelong problem.[colgate.com]


  • A traumatic etiology is implicated in a large proportion of these cases, leading to the formation of both 'false' and 'true' aneurysms.[ncbi.nlm.nih.gov]
  • Technology such as thermographic images may facilitate assessment of traumatically damaged foot skin. [5] Etiology Poorly fitting shoes are the most common cause.[emedicine.medscape.com]


  • We review the epidemiology, pathophysiology and diagnostic considerations of these lesions. The endovascular and surgical management of these complex non-branching supraclinoid ICA aneurysms is also discussed.[ncbi.nlm.nih.gov]
  • […] individuals prone to blisters to be at variance from less predisposed to this finding. [6] Baseball pitchers suffer repeated trauma between the baseball seams and the fingers of the pitching hand, most often at the tips of the index and long fingers. [7] Epidemiology[emedicine.medscape.com]
Sex distribution
Age distribution


  • Because of their rarity, the natural history and pathophysiology of such aneurysms are not fully understood.[ncbi.nlm.nih.gov]
  • Because of specific peculiarities such as different pathophysiology, fragility of the aneurysmal wall, high risk of intraoperative bleeding, and high probability of losing parent vessel patency, their treatment is controversial, and both endovascular[ncbi.nlm.nih.gov]
  • We review the epidemiology, pathophysiology and diagnostic considerations of these lesions. The endovascular and surgical management of these complex non-branching supraclinoid ICA aneurysms is also discussed.[ncbi.nlm.nih.gov]
  • Pathophysiology The influence of epidermal hydration on the friction of human skin against textiles was studied.[emedicine.medscape.com]


  • Friction Management Interfaces : ENGO Blister Prevention Patches allow athletes to lower friction forces in areas where hot spots and blisters commonly form; effectively preventing blisters altogether.[web.archive.org]
  • A complete shutdown of blood flow to the BBA by ICA trapping is essential for the permanent prevention of BBA recurrence.[ncbi.nlm.nih.gov]
  • Blister prevention Hot-spot management Blister treatment Best case scenario is you start at blister prevention . It's your best chance of a no-fuss and pain-free experience.[blisterprevention.com.au]
  • Prevention and even early intervention can save you huge headaches! Prevent Foot Blisters! Most blisters can be avoided altogether by taking preventative measures instead of waiting to treat a situation that is already bad.[bodyglide.com]
  • One study showed that Blist-O-Ban bandages not only stayed on sweaty feet but also prevented the formation of blisters (when the instructions were followed closely) Efficacy of a new blister prevention plaster under tropical conditions.[greatist.com]



  1. Knapik JJ, Reynolds KL, Duplantis KL, Jones BH. Friction blisters. Pathophysiology, prevention and treatment. Sports Med. 1995 Sep;20(3):136-147.
  2. Jurj G, Waisse S. Blisters and homeopathy: case reports and differential diagnosis. Homeopathy. 2011 Jul;100(3):168-174.
  3. Schmidt E, Zillikens D. The diagnosis and treatment of autoimmune blistering skin diseases. Dtsch Arztebl Int. 2011 Jun;108(23):399-405.
  4. Amagai M, Tsunoda K, Zillikens D, Nagai T, Nishikawa T. The clinical phenotype of pemphigus is defined by the anti-desmoglein autoantibody profile. J Am Acad Dermatol. 1999;40:167–170.
  5. Anhalt GJ, Kim SC, Stanley JR, et al. Paraneoplastic pemphigus. An autoimmune mucocutaneous disease associated with neoplasia. N Engl J Med. 1990 Dec 20;323(25):1729-1735.
  6. Yancey KB. The pathophysiology of autoimmune blistering diseases. J Clin Invest. 2005 Apr;115(4):825-828.
  7. Schmidt E, Zillikens D. Autoimmune and inherited subepidermal blistering diseases: advances in the clinic and the laboratory. Adv. Dermatol. 2000;16:113–157
  8. Wojnarowska F, Kirtschig G, Highet AS, Venning VA, Khumalo NP, and British Association of Dermatologists. Guidelines for the management of bullous pemphigoid. Br J Dermatol. 2002 Aug;147(2):214-221.

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Last updated: 2019-07-11 22:51