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].

• Exfoliation of the Skin

  […] force show an initial slight exfoliation of the skin over the involved area. [emedicine.medscape.com]

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].

Endovascular therapy increased the likelihood of a second treatment, conversion to another treatment modality, and incomplete aneurysm obliteration. [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]

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]

This content is accurate and true to the best of the author’s knowledge and does not substitute for diagnosis, prognosis, treatment, prescription, and/or dietary advice from a licensed health professional. [remedygrove.com]

Prognosis In many cases, blisters will disappear when the cause is removed or the infection has gone away, usually in a matter of days or weeks. [2minutemedicine.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]

Associated with manual labor Sites Hands and feet; sites subjected to repetitive friction Pathophysiology Shearing forces within the epidermis cause friction blisters in the areas where epidermis is thick and firmly attached to the underlying tissue Etiology [pathologyoutlines.com]

Unilateral damage of a uterine tube is characteristic of a septic etiology. [medicine-for-you.com]

고름물집건선에서 발생한 지도모양혀 1예 A Case of Geographic Tongue in Pustular Psoriasis 1조선대학교 2조선대학교 3조선대학교 4조선대학교 5조선대학교 초록 Geographic tongue is a chronic, inflammatory, and immune- mediated oral lesion of unknown etiology. [kci.go.kr]

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]

[…] clear fluid Blood blister: blister caused by excessive force, which fills with blood Hemorrhagic bullae: larger blisters (> 0.5 cm), often multiple and associated with underlying disease process, and more often deeper (suprabasilar or subepidermal) Epidemiology [pathologyoutlines.com]

[…] 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]

Because of their rarity, the natural history and pathophysiology of such aneurysms are not fully understood. [ncbi.nlm.nih.gov]

[…] underlying disease process, and more often deeper (suprabasilar or subepidermal) Epidemiology Common in athletes, dancers or those wearing poorly fitting shoes Associated with manual labor Sites Hands and feet; sites subjected to repetitive friction Pathophysiology [pathologyoutlines.com]

Cutaneous radiation syndrome Epidermolysis bullosa Pathophysiology[edit] Friction blisters[edit] Friction blisters are caused by excess shear stress between the bottom and surface of the skin and the body. [en.wikipedia.org]

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]

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]

Blister Prevention The key to preventing blisters is to eliminate friction. [sectionhiker.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.