In order to clarify the mechanism by which excess PRL inhibits gonadotropin release, in vivo and in vitro studies were performed with adult female rats. First, we examined the effect of hyperprolactinemia, produced by implantation of anterior pituitary glands under the kidney capsule, on catecholamine turnover in the medial basal hypothalamus (MBH) and on GnRH concentrations in MBH and hypophyseal portal blood. Rats bearing pituitary transplants exhibited increased turnovers of dopamine (DA) in the MBH, decreased concentrations of GnRH in the MBH and in plasma of hypophyseal portal blood and impaired gonadotropin release from the pituitary gland. Second, we examined the effects of PRL on DA release and of DA on GnRH release from rat hypothalamic cells. We observed that PRL stimulated [³H] DA release, and DA inhibited ionophore-induced GnRH release from dispersed hypothalamic cells. Third, we examined the effect of PRL on estrogen-induced LH release using the in vitro perfusion system. We found that administration of PRL suppressed estrogen-induced LH release by suppressing GnRH release from the hypothalamus. These findings suggest that chronic hyperprolactinemia may increase dopaminergic tone in the MBH that may inhibit GnRH secretion from the MBH and LH release from the pituitary and that these processes may be responsible for disturbances of cyclic hypothalamic pituitary-ovarian activity.

Background: Pemphigus is an autoimmune bullous disease characterized by the presence of antidesmoglein autoantibodies. However, the mechanism of its autoantibody production remains unknown. In previous reports, we have described rare cases of pemphigus and pemphigoid associated with silicosis. It is well known that during long-term silicosis, some autoimmune diseases, such as systemic sclerosis, systemic lupus erythematosus or rheumatoid arthritis, can occur. Objective: The aim of this study was to explore the presence of pemphigus or pemphigoid autoantibodies in silicosis patients without clinical bullous diseases or collagen diseases. Method: The presence of pemphigus antibodies was examined in 54 silicosis patients with no associated bullous diseases, using immunofluorescence, the enzyme-linked immunosorbent assay (ELISA) for desmoglein 1 and 3, and immunoblotting methods. In the antibody-positive cases, HLA genotyping of peripheral lymphocytes was performed with PCR-RFLP. Results: Seven out of the 54 patients were found to be positive for pemphigus antibodies and 1 for bullous pemphigoid by immunofluorescence. In addition, by ELISA, 6 patients were found to be positive against the desmoglein 1 antigen, 2 against the desmoglein 3 antigen and 2 against both desmoglein 1 and desmoglein 3. Conclusion: The results of the present study strongly suggest the occurrence of pemphigus and pemphigoid autoantibodies in patients with silicosis. It remains unclear whether such patients will develop an autoimmune bullous disease in the future. Accordingly, long-term follow-up of antibody-positive patients is required.

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We report a patient with primary Sjögren's syndrome who developed pyrexia, cervical lymphadenopathy, and painful indurated erythema on the forehead, back, chest, abdomen, and limbs. Laboratory data showed an elevated erythrocyte sedimentation rate, C-reactive protein and CH50 in addition to existing autoantibodies including anti-nuclear antibody, anti SS-A antibody, and anti SS-B antibody. A skin biopsy specimen showed focal infiltration of histiocytes with non-neutrophilic karyorrhetic debris in the dermis and subcutaneous fat tissue. Immunohistochemically the infiltrated cells were stained for CD68, suggesting cutaneous involvement of Kikuchi-Fujimoto disease. All symptoms and laboratory data improved within three weeks after treatment with 20 mg/day of prednisolone. The present case suggests that a pathophysiological condition similar to Kikuchi-Fujimoto disease can develop during the long-term course of Sjögren's syndrome.

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