Bullous pemphigoid (BP) has been suggested to be an autoimmune inflammatory disease affecting the cutaneous basement membrane zone (BMZ) [7]. Immunologic abnormalities include circulating complement-activating autoantibodies against BP antigen [6,12]. Current evidence suggests that the inflammatory
Guidelines for the management of bullous pemphigoid
โ Scribed by F. Wojnarowska; G. Kirtschig; A.S. Highet; V.A. Venning; N.P. Khumalo
- Publisher
- John Wiley and Sons
- Year
- 2002
- Tongue
- English
- Weight
- 83 KB
- Volume
- 147
- Category
- Article
- ISSN
- 0007-0963
No coin nor oath required. For personal study only.
โฆ Synopsis
These guidelines have been prepared for dermatologists on behalf of the British Association of Dermatologists. They present evidence-based guidance for treatment, with identification of the strength of evidence available at the time of preparation of the guidelines and a brief overview of epidemiological aspects, diagnosis and investigation. The guidelines reflect data available from Medline, Embase, the Cochrane library, literature searches and the experience of the authors of managing patients with bullous pemphigoid in special and general clinics for over 10 years. However, caution should be exercised in interpreting the data obtained from the literature because only six randomized controlled trials are available involving small groups of patients.
๐ SIMILAR VOLUMES
The interleukin-2 receptor (IL-2R) is mainly expressed on activated T cells. Depending on its rate of synthesis, a portion is released from the cell surface as soluble IL-2R (sIL-2R). Since the role of mononuclear cells in the pathology of bullous pemphigoid (BP) is not well understood, we determine
We have previously shown that the 180 kDa bullous pemphigoid antigen (BPAG2) is distributed on the lateral-apical (as a pool) and ventral (as hemidesmosomes) cell membranes of monolayer cultured keratinocytes and that addition of IgG purified from bullous pemphigoid (BP) patients (BP-IgG) causes the