[Acute suppurative thyroiditis due to Streptococcus intermedius].
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Biomedical subjects
Publications and source records attributed to J Lado Abeal.
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OBJECTIVE: It is not known whether gamma-aminobutyric acid (GABA) is involved in control of pulsatile LH secretion in human beings. Previous work by our group has shown that manipulation of the GABAergic system with sodium valproate does not affect pulsatile LH secretion in normal women in the late follicular phase. However, it has been suggested that steroid levels are critical for the influence of GABA upon hormone secretion; in particular, progesterone has been said to enhance inhibition by GABA. In this work we studied the effect of sodium valproate on pulsatile LH secretion in medium-late luteal phase of normal women. DESIGN: Six normal young women were studied over an 8-hour period in two successive menstrual cycles. On each occasion blood samples were taken every 10 minutes between 1000 and 1800 h. We administered 400 mg of sodium valproate every 8 hours on the 7 days preceding their second cycle and additional 400 mg at 0900 and 1400 h on the day of the study. Ovulation day was estimated by means of serial ovarian ultrasound examinations and confirmed by serum progesterone concentrations. MEASUREMENTS: In each cycle, LH, oestradiol and progesterone were determined by radioimmunoassay and sodium valproate by repolarization fluorescence spectrophotometry. The series of LH levels was smoothed for 1-minute sampling periods by means of a spline function and analysed by means of a program developed in our laboratory and written in Fortran 77. The program deconvolved the signal and calculated the pulse area, pulse duration, interpulse interval and number of pulses. LH pulse identification on the deconvolved signals was performed using our own method based on Friedman's non-parametric statistic. The statistical significance of differences between parameters was estimated using the Mann-Whitney test and Wilcoxon signed rank test. RESULTS: There were no significant differences in LH pulse area, pulse duration, interpulse interval or number of pulses with the administration of sodium valproate. CONCLUSIONS: Activation of the GABAergic system with sodium valproate had no biologically significant effect on the mid-late luteal phase pulsatile LH secretion in normal women.
OBJECTIVE: To study whether modulation of the GABAergic system (with sodium valproate) affects pulsatile LH secretion in the late follicular phase of normal women. DESIGN: Fifteen normal women volunteers were studied over an 8-hour period in the late follicular phase of two successive menstrual cycles. On each occasion, blood samples were taken every 10 minutes between 1000 and 1800 h. Nine of the volunteers--the short treatment group--were administered 400 mg of sodium valproate every 8 hours on the two days preceding their second session, and a further 400 mg at 0900 h on the day of the session. The other six--the long treatment group--were administered 400 mg of sodium valproate every 8 hours on the seven days preceding their second session and at 0900 and 1400 h on the day of the session. MEASUREMENTS: LH, oestradiol and progesterone were determined by radioimmunoassay, and sodium valproate by repolarization fluorescence spectrophotometry. Pulse detection was carried out both by the program ULTRA and by a method developed by the authors. RESULTS: There were no significant differences in LH pulse amplitude or relative pulse amplitude between records taken in the first and second menstrual cycles, i.e. without or with prior sodium valproate treatment. Short treatment did change interpulse interval and mean secretion period, but the changes, though statistically significant, were small (about 10 minutes), so that the values for both post-treatment and control sessions were within the normal range; these parameters were unaffected by long treatment. CONCLUSIONS: Activation of the GABAergic system with sodium valproate had no biologically significant effect on the late follicular phase pulsatile LH secretion of these normal women.
The biological and clinical features and prognostic factors of 65 patients affected by alcoholic hepatitis were studied. All patients had an ethanol intake higher than 80 gr/day during at least 3 years. 22 patients were female and 43 male with a mean age of 45 +/- 11.7 years. 19 had acute hepatitis (29.2%), 2 had acute hepatic insufficiency (3%), one had acute cholestasis (1.5%), 14 had chronic hepatopathy (21.5%). 29 patients had the diagnosis (44.6%) confirmed by histologic analysis. All patients had liver enlargement, 25 had jaundice and 4 had fever. The hepatic biopsies showed steatosis in 53 cases, centrilobular sclerosis in 32 cases and cirrhosis in 19.8 patients developed hepatic encephalopathy, 3 had renal insufficiency, and 4 died. The levels of albumin (P = 0.0043), total bilirubin (P = 0.0003), prothrombin (P = 0.0001) and the development of hepatic encephalopathy or/and renal insufficiency were the parameters to define the group of patients with bad evolution, the IgA also being significant. The low mortality of our studied (6.1%) can be justified by the diagnosis at non-symptomatic stage. We recommend a liver biopsy in all patients with chronic alcoholism and liver enlargement, or biologic markers suggesting alcoholic hepatopathy.
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