Bullous dermatoses of pregnancy

Honeyman, J. F.

doi:10.1001/archderm.117.5.264

Cited by 16 publications

(6 citation statements)

References 2 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In many cases, pemphigus seems to occur when environmental factors combine with genetic ones. The exogenous factors include: drugs, in particular thiol drugs, 11 physical agents such as burns, 12 ultraviolet radiation, 13 , 14 X‐rays, 15 viruses, 16 , 17 neoplasms, 18 , 19 hormones and pregnancy, 20 , 21 nutritional factors 22 , 23 and emotional stress. 24 , 25 Various reports have pointed to the possible part played by viral infections, in particular herpesvirus infections.…”

mentioning

confidence: 99%

Detection of herpesvirus DNA in peripheral blood mononuclear cells and skin lesions of patients with pemphigus by polymerase chain reaction

et al. 1999

View full text Add to dashboard Cite

Pemphigus is an autoimmune disease where both endogenous (genetic) and exogenous (environmental) factors play a part. Viral infections, in particular herpesvirus infections, have been identified as a possible triggering factor for pemphigus. In this study, using the polymerase chain reaction, we studied peripheral blood mononuclear cells (PBMC) and skin biopsies from patients with pemphigus, and in some of these were able to demonstrate the presence of DNA sequences of herpes simplex virus 1/2 (50% in PBMC and 71% in skin biopsies), Epstein-Barr virus (15% in PBMC and 5% in skin biopsies) and human herpesvirus 6 (20% in PBMC only). However, the inability to detect herpesvirus DNA consistently in these cases suggests that viral infection may only be an occasional factor triggering the outbreak or exacerbation of the disease. The possible role of interferons and interleukins in the pathogenesis of virus-induced pemphigus is discussed.

show abstract

mentioning

confidence: 99%

Detection of herpesvirus DNA in peripheral blood mononuclear cells and skin lesions of patients with pemphigus by polymerase chain reaction

et al. 1999

View full text Add to dashboard Cite

show abstract

“…Pemphigus vulgaris (PV) is a well‐established, autoimmune, intraepidermal, blistering disorder of the skin and mucous membranes characterized by circulating autoantibodies directed against the 130‐ and 85‐kDa antigens on the keratinocyte cell surface. Several reports of its coexistence with other autoimmune diseases, such as rheumatoid arthritis, Sjogren's syndrome, systemic lupus erythematosus (SLE), and scleroderma, neoplasms, such as thymomas, lymphoreticular malignancies, etc., and therapeutic agents, such as penicillamine, captopril, progesterone, or vaccines, have been documented in the literature 1–5 . In vivo and in vitro studies performed in these cases have suggested various etiologic mechanisms, including the dysregulation of the immune response by the drug or disease, with an increased tendency to antibody formation in genetically predisposed individuals 6,7 …”

Section: Discussionmentioning

confidence: 99%

An unusual association of pemphigus vulgaris with hyperprolactinemia

Khandpur¹,

Reddy²

2002

Int J Dermatology

View full text Add to dashboard Cite

A 21‐year‐old unmarried woman presented with oral ulcerations and generalized, itchy, fluid‐filled, skin lesions of 10 days’ duration. The lesions ruptured spontaneously, resulting in extensive denuded areas covered by crusts. One month prior to this, she experienced pain and enlargement of both breasts with galactorrhea. Her menstrual cycles were normal initially, but later she developed menstrual irregularities. No past history suggestive of any other systemic or skin disease, including atopy or drug allergies, could be obtained. Her family history was not contributory. Dermatologic examination revealed multiple, flaccid bullae and extensive denuded areas of skin covered with crusts over the scalp, face, trunk, and upper and lower limbs (Fig. 1). Bulla spread sign and Nikolsky's sign were positive. The oral mucosa, including the lips, buccal surface, tongue, and palate, showed multiple erosions covered with necrotic slough. The rest of the mucocutaneous and systemic examination was within normal limits. 1 Extensive erosions and flaccid bullae over the trunk with breast enlargement The patient's diagnostic work‐up revealed: hemoglobin, 11.2 g%; total leukocyte count, 7400/mm3; differential leukocyte count, P62L34E2M2; erythrocyte sedimentation rate, 34 mm/h. A peripheral blood smear examination, urinalysis, blood sugar, and renal and liver function tests were normal. Venereal Disease Research Laboratory (VDRL) test and enzyme‐linked immunoabsorbent assay (ELISA) for human immunodeficiency virus (HIV) were nonreactive. Antinuclear antibody, lupus erythematosus (LE) cell, rheumatoid factor, and anti‐dsDNA levels were normal. Serum protein electrophoresis demonstrated increased levels of immunoglobulin G (IgG) antibody. The serum prolactin level was significantly raised to 139.49 ng/mL (normal, 3.6–18.9 ng/mL). The sex hormone levels, however, including follicle‐stimulating hormone (FSH), luteinizing hormone (LH), estradiol, and progesterone, were within normal limits. The thyroid hormone profile was also unaltered. Chest X‐ray was normal. Ultrasound of the abdomen and pelvis revealed no visceral abnormality and computerized tomography (CT) scan of the pituitary sella showed no adenoma. Mammography was negative for breast malignancy. A Tzanck smear prepared from the base of the erosion showed multiple acantholytic cells and lymphocytes. Histologic examination from an intact vesicle was suggestive of pemphigus vulgaris (PV), showing a suprabasal cleft with acantholytic cells and the basal layer demonstrating a “row of tombstones” appearance (Fig. 2). Direct immunofluorescence (DIF) revealed the intercellular deposition of IgG and C3 throughout the epidermis in a “fishnet pattern.” Indirect immunofluorescence (IIF) test performed on rat esophagus for circulating IgG antibody was positive in a titer of 1 : 120. 2 Photomicrograph showing suprabasal cleft with “row of tombstones” appearance, suggestive of pemphigus vulgaris (hematoxylin and eosin, × 40) Based on the clinical and immunohistological features, a diag...

show abstract

“…It is well established that the development of pemphigus is the result of the interaction between endogenous, genetic factors (the soil) and exogenous factors (the seed). The latter include drugs; 1 − 5 nutritional factors; 6 − 9 physical agents such as burns, UV radiation, and X‐rays; 10 − 13 infections, in particular viral; 14,15 neoplasms; 16 hormones and pregnancy; 17,18 contact dermatitis; 19 − 22 and emotional stress 23,24 . Studies have shown that these factors may affect only genetically predisposed individuals.…”

Section: Introductionmentioning

confidence: 99%