Non-blinded trials of pemphigus vulgaris suggest that mycophenolate mofetil (MMF) may be beneficial. In a prospective, multicenter trial, outpatients with mild or moderate pemphigus vulgaris were randomized to MMF (2 or 3 g day(-1)) plus oral corticosteroids or placebo plus oral corticosteroids for 52 weeks. The primary end point was the proportion of patients in the placebo and combined MMF groups responding to treatment (absence of new, persistent oral or cutaneous lesions, and prednisone dose < or = 10 mg day(-1) from weeks 48 to 52). Of 96 randomized patients, 94 were given treatment and 75 completed the study. Treatment responses occurred in 40 of 58 patients (69.0%) in the combined MMF group and 23 of 36 (63.9%) in the placebo group (P=0.6558, 95% confidence interval -17.4 to 27.6). MMF-treated patients showed faster and more durable responses. In post hoc analyses, more patients taking MMF showed sustained responses for 3 or 6 months than did placebo patients. MMF was well tolerated. Although MMF did not show an advantage on the primary end point, there seemed to be a beneficial treatment effect on several secondary end points, including time to response and duration of response. Thus, MMF may be a potentially useful agent in patients with mild or moderate pemphigus vulgaris.
In peritoneal biopsies from non-EOC and EOC patients, HPMCs showed different morphology but similar immunostaining characteristics, whereas cultured cells from different sources were similar in both morphology and phenotype. L-cysteine enhanced the growth of non-EOC but not of EOC-derived HPMCs, which had a maximal response to EGF and HC. The growth advantage of HPMCs from EOC in vitro suggests these cells are in a primed or activated state.
A dopaminergic system in the zona incerta stimulates LH release and may mediate the positive feedback effects of the gonadal steroids on LH release. In this study the mechanisms by which steroids might increase dopamine activity in the zona incerta were investigated. In addition, experiments were conducted to determine whether the inhibitory effects of gamma-aminobutyric acid (GABA) on LH release in the zona incerta are due to suppression of dopamine activity in this area or conversely whether the stimulatory effects of dopamine on LH release are due to suppression of a tonic inhibitory GABAergic system. Ovariectomized rats were treated s.c. with oil, 5 micrograms oestradiol benzoate or 5 micrograms oestradiol benzoate followed 48 h later by 0.5 mg progesterone, and killed 54 h after the oestradiol benzoate injection. At this time the LH concentrations were suppressed in the oestradiol benzoate group and increased in the group treated with oestradiol benzoate and progesterone. The ratio of tyrosine hydroxylase:beta-actin mRNA in the zona incerta was significantly increased by the oestradiol benzoate treatment, but the addition of progesterone resulted in values similar to those in the control group. At the same time, the progesterone treatment increased tyrosine hydroxylase activity in the zona incerta as indicated by an increase in L-dihydroxyphenylalanine (L-DOPA) accumulation after 100 mg 3-hydroxybenzylhydrazine hydrochloric acid (NSD1015) kg-1 and an increase in dopamine release as indicated by a increase in dihydroxyphenylacetic acid (DOPAC) concentrations (one of the major metabolites of dopamine). Ovariectomized rats treated with oestradiol benzoate plus progesterone were also injected i.p. with 75 mg gamma-acetylenic GABA kg-1 (a GABA transaminase inhibitor) to increase GABA concentrations in the brain. This treatment had no effect on the ratio of tyrosine hydroxylase:beta-actin mRNA but decreased L-DOPA accumulation and DOPAC concentrations in the zona incerta, indicating a post-translational inhibition of dopamine synthesis and release. Treatment of ovariectomized rats with oestradiol benzoate followed by 100 mg L-DOPA i.p. to increase dopamine concentrations in the whole brain had no effect on glutamic acid decarboxylase mRNA expression in the zona incerta, although it increased the glutamic acid decarboxylase:beta-actin mRNA ratio in other hypothalamic areas (that is, the medical preoptic area, ventromedial nucleus and arcuate nucleus). In conclusion, the steroids act to increase dopamine activity in different ways: oestrogen increases tyrosine hydroxylase mRNA expression and progesterone acts after translation to increase tyrosine hydroxylase activity and dopamine release (as indicated by increases in DOPAC concentrations). This latter effect may be due to progesterone removing a tonic GABAergic inhibition from the dopaminergic system.
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