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Oral Pemphigus Vulgaris (oral + pemphigus_vulgari)
Selected AbstractsOral pemphigus vulgaris occurring during pregnancyJOURNAL OF ORAL PATHOLOGY & MEDICINE, Issue 2 2002Joseph K. Muhammad Abstract There have been few reports describing the occurrence of pemphigus vulgaris (PV) during pregnancy. The patient described in this case report is interesting because the PV that developed during her pregnancy was confined to her mouth. It has been suggested that prompt treatment with systemic steroids prevents development of PV in cutaneous tissues. In this case, early control of the condition is believed to have eliminated the need for high dose steroids throughout the remainder of the pregnancy. In addition, this therapeutic approach could have contributed to the birth of a baby free of PV. Resolution of the presenting oral symptoms allowed the mother to resume a normal diet, allaying her anxiety about the possible effects of poor nutritional intake on foetal development. Aspects of clinical management considered in this report include the choice of immunospuppressive therapy and the multidisciplinary care involving both dental and obstetric specialists. [source] Catenin dislocation in oral pemphigus vulgarisJOURNAL OF ORAL PATHOLOGY & MEDICINE, Issue 5 2001Michele Davide Mignogna Abstract: Cell-to-cell adhesion is mediated by cadherins (integral membrane proteins), which form a complex with catenins (cytoplasmatic proteins). While E-cadherin expression has been extensively studied in many human skin diseases, less is known about the expression levels of catenins in oral blistering diseases. The purpose of this study was to evaluate the role of these proteins in the pathogenesis of acantholysis in oral pemphigus vulgaris. We evaluated by immunohistochemistry beta- and gamma-catenin expression in 7 cases of oral pemphigus vulgaris (PV) at various stages of the disease and, as controls, in 18 healthy patients. Healthy cases showed, as reported in the literature, a strong reactivity with both beta- and gamma-catenins, with the intensity of staining progressively decreasing from the spinous to the keratinised layers of epithelium, which had a prevalent cellular membrane expression. In PV patients, we detected a loss of membrane expression of these molecules with a progressive displacement of the signal toward the cytosol and, for gamma-catenin, nuclear dislocation, particularly in areas with intense acantholysis. [source] Oral pemphigus: long term behaviour and clinical response to treatment with deflazacort in sixteen casesJOURNAL OF ORAL PATHOLOGY & MEDICINE, Issue 4 2000Michele D. Mignogna Abstract: Systemic corticosteroids remain the mainstay of therapy for pemphigus. Their use has transformed what was almost invariably a fatal illness into one whose mortality is now below 10%. Unfortunately, the high doses and prolonged administration of corticosteroids that are often needed to control the disease result in numerous side effects, many of which are serious or even life-threatening. Sixteen patients affected by oral pemphigus vulgaris were retrospectively examined to illustrate the natural course of the disease and to describe the efficacy of the treatment we utilised. Deflazacort, used with azathioprine, is the steroid of first choice in our therapeutic protocols, while cyclophosphamide and methylprednisolone "pulse therapy" are reserved for cases unresponsive to high doses of oral corticosteroids. In addition, the literature on oral pemphigus vulgaris was reviewed with respect to clinical history, signs and symptoms, management, and treatment outcome. [source] Neonatal pemphigus vulgaris with extensive mucocutaneous lesions from a mother with oral pemphigus vulgarisBRITISH JOURNAL OF DERMATOLOGY, Issue 4 2002A. Campo-Voegeli Summary The clinical phenotype of pemphigus is well explained by the combination of desmoglein (Dsg) 1 and Dsg3 distribution pattern and antiDsg autoantibody profile (Dsg compensation theory). It has been reported that neonatal skin has a similar Dsg distribution pattern to adult mucosal epithelia. We describe a newborn girl with mucocutaneous pemphigus vulgaris (PV) from a mother with mucosal dominant PV. The mother had had painful oral erosions for at least 7 months. Histopathological examination and direct and indirect immunofluorescence studies confirmed the diagnosis of PV and neonatal PV in the mother and daughter, respectively. The mother had a high titre of anti-Dsg3 IgG and a low titre of antiDsg1 IgG, while the neonate had only a high titre of anti-Dsg3 IgG, but no detectable antiDsg1 IgG. AntiDsg3 IgG, which caused the oral dominant phenotype in the mother, induced extensive oral as well as cutaneous lesions in the neonate. Our case provides clinical evidence for the Dsg compensation theory in neonatal PV. [source] | ||||||||||