However, most commonly, drug can be one of the cause of bullous pemphigoid, such as thiazide diuretics, antibiotics (e.g., penicillins, vancomycin), nonsteroidal anti-inflammatory drugs (NSAIDs) and angiotensin-converting enzyme (ACE) inhibitors (e.g., captopril) and possibly angiotensin receptor blockers (ARBs, e.g., valsartan).The implicated drugs include penicillin derivatives, sulfasalazine, ibuprofen, phenacetin, enalapril, captopril, lisinopril, gabapentin, novoscabin, levobunolol ophthalmic solution, tetracoq, influenza, tetanus, and other vaccinations, a homeopathy regimen, nifedipine, 5-aminosalicylic acid, doxazosin, serratiopeptidase, losartan, cephalexin, bumetanide, fluoxetine, chloroquine, antipsychotic drugs, enoxaparin, ciprofloxacin, furosemide (frusemide), neuroleptics, penicillamine, gliptin plus metformin, intravenous iodine, etanercept, levofloxacin, and topical fluorouracil. Influenza vaccination does not appear to be an important trigger for bullous pemphigoid. Trauma, burns, lymphedema, phototherapy, and radiation have been implicated in a very small number of cases. Pathophysiology
The pathophysiology of bullous pemphigoid consists of two major components, which are immunologic and inflammatory. In the immunologic component, autoantibodies act against the hemidesmosomal bullous pemphigoid antigens BP230 (BPAg1) and BP 180(BPAg2 or type XVII collagen) which are located at the lamina lucida of the basement membrane zone. These antigens play an important role in the adhesion complexes that promote epithelial-stromal adhesion. The predominant subclass of antibodies that acts against the antigens is IgG4. IgG1 and IgG2 antibodies are less frequently detected compared to IgG4 antibodies, while IgG3 antibodies are usually absent. When the autoantibodies bind specifically to the target antigens, the complement system and mast cells are activated, thereby representing the inflammatory component. Inflammatory cells such as neutrophils and eosinophils are then attracted to the affected area.
Azathioprine or Cyclosphosphamide are the choices of immunosuppressive drugs that can be used. Sometimes, immunosuppressive agents and prednisolone can be combined if dapsone fails to improve the condition. Lastly, in patients who do not respond to the conventional therapy, rituximab may be an option.There is insufficient evidence that cyclophosphamide combined with corticosteriods are effective in treating mucous membrane pemphigoid.Other than that, oral hygiene instructions should be given to patients as oral care is a critical part in treating mucous membrane pemphigoid. Before meals, patients are advised to rinse with hydrogen peroxide (diluted with water to a concentration of 1:4 or 1:6) and diphenhydramine to reduce the pain. Patient would then rinse with hydrogen peroxide to remove food particles and debris and later rinse with dexamethasone for anti-inflammatory effect. Hydrogen peroxide, elixir of dexamethasone and elixir of diphenhydramine are each diluted with water to a concentration of 1:4 or 1:6 and are instructed not to swallow in the end. Epidemiology
MMP mainly affect the elderly population of ages between 60 and 80 years and rarely children. Women are affected twice as frequently than in men. There is no known racial or geographic predilection, but several studies have suggested that there is an association of specific immunogenetic haplotype HLA-DQB1*0301 with MMP. See also
List of cutaneous conditions
List of target antigens in pemphigoid

References
Further reading


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