Full article available at: http://www.vetsmall.theclinics.com/article/PIIS019556161200143X/abstract?rss=yes
The present report details the clinical and immunological features of a 53 year old Asian female who developed symptoms and signs of oesophageal PV during therapy with azathioprine and decreasing prednisolone dosage. Oesophageal involvement occurred during stable oral disease.
Oesophageal involvement can occur without significant oro-cutaneous lesions and immunological evidence of PV. This suggests that immunological targets for oesophageal disease may differ from those of other mucocutaneous areas, and that conventional first-line systemic therapy may not be effective for oesophageal lesions.
Full article available at: http://www.ingentaconnect.com/content/ubpl/wlmj/2012/00000004/00000002/art00001
Johns Hopkins Dermatology
I will attempt to clarify what we know about the antibody response in various forms of pemphigus and how the distribution of the targeted antigens affects the location of lesions. The synthesis of this work has been proposed by Dr. John Stanley, with key published advances from Dr. Masa Amagai and Mai Mahoney, Ph.D., P. Koch and others. John Stanley refers to his concept as the “desmoglein compensation hypothesis”. The key to this hypothesis is the desmogleins (pemphigus antigens) are key adhesion molecules that keep cells attached to each other. In some areas of the body, there are two desmogleins present, and both have to be damaged to cause cell detachment – in some areas only one desmoglein may be present at some level in the skin or mucous membrane, and there only one desmoglein has to be damaged to cause cell detachment.
By David A. Sirois, D.M.D., Ph.D.
Department of Oral Medicine
Pemphigus vulgaris is a chronic autoimmune disease affecting the mucosa and skin and resulting in epithelial acantholysis, bullae formation, and chronic ulceration.1 Skin lesions of pemphigus vulgaris present clinically with typical bullae formation and ulceration. However, oral mucosal manifestations are less characteristic, typically occurring as multiple, chronic mucosal erosions or superficial ulcerations of various sizes and rarely presenting with intact bullae.2 Although pemphigus vulgaris is widely considered a skin disease, several reports of cases and case series have described it frequently as the initial, and occasionally the exclusive, site of involvement.2, 3 Thus, the unfamiliar features of oral pemphigus vulgaris could result in longer diagnostic and treatment delays than cutaneous pemphigus, which could adversely affect treatment response and prognosis.4, 5 The present study explored the natural history and diagnostic pattern of pemphigus vulgaris among 99 patients, with specific interest in the differences between oral and cutaneous pemphigus.