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S N Assaad

Publications and source records attributed to S N Assaad.

5 recordsLinked to original sources
PubMed1993

Regulation of 11 beta-hydroxysteroid dehydrogenase by sex steroids in vivo: further evidence for the existence of a second dehydrogenase in rat kidney.

11 beta-Hydroxysteroid dehydrogenase (11 beta-OHSD) catalyses the reversible conversion of corticosterone to inactive 11-dehydrocorticosterone, thus regulating glucocorticoid access to mineralocorticoid and perhaps glucocorticoid receptors in vivo. 11 beta-OHSD has been purified from rat liver and an encoding cDNA isolated from a liver library. However, several lines of indirect evidence suggest the existence of at least two isoforms of 11 beta-OHSD, one found predominantly in glucocorticoid receptor-rich tissues and the other restricted to aldosterone-selective mineralocorticoid target tissues and placenta. Here we have examined the effects of chronic (10 day) manipulations of sex-steroid levels on 11 beta-OHSD enzyme activity and mRNA expression in liver, kidney and hippocampus and present further evidence for the existence of a second 11 beta-OHSD isoform in kidney. Gonadectomized male and female rats were given testosterone, oestradiol or blank silicone elastomer capsules, controls were sham-operated. In male liver, gonadectomy+oestradiol treatment led to a dramatic decrease in both 11 beta-OHSD activity (69 +/- 8% decrease) and mRNA expression (97 +/- 1% decrease). Gonadectomy and testosterone replacement had no effect on male liver 11 beta-OHSD. However, in female liver, where 11 beta-OHSD activity is approximately 50% of that in male liver, gonadectomy resulted in a marked increase in 11 beta-OHSD activity (120 +/- 37% rise), which was reversed by oestradiol replacement but not testosterone treatment. In male kidney, gonadectomy+oestradiol treatment resulted in a marked increase in 11 beta-OHSD activity (103 +/- 4% rise). By contrast, 11 beta-OHSD mRNA expression was almost completely repressed (99 +/- 0.1% decrease) by oestradiol treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed1990

Abnormal growth hormone dynamics in chronic liver disease do not depend on severe parenchymal disease.

Abnormal basal serum levels of growth hormone (GH) and abnormal GH dynamics have been observed in patients with alcoholic cirrhosis (AC). To further characterize these abnormalities, patients with AC or schistosomal hepatic fibrosis (SHF) were evaluated. The former patients have parenchymal liver disease, portal hypertension, and portosystemic shunting. SHF, in contrast, is characterized by periportal fibrosis with minimal or no parenchymal cell disease, portal hypertension, and portosystemic shunting. We studied 20 patients with SHF and normal stature and 15 patients with AC. In these two groups of patients, basal serum GH was higher than normal (P less than .01). A paradoxical increase in GH was observed during the oral glucose tolerance test (OGTT) in 55% of SHF and in 40% of AC patients. Significant GH elevation followed thyrotropin-releasing hormone (TRH) administration in 80% of SHF and 66% of AC patients, but not in normals. Serum nonsuppressible insulin-like activity (NSILA) and serum somatomedin C (Sm-C) levels were reduced significantly in both groups. In SHF patients, the paradoxical increase in GH during OGTT correlated inversely with Sm-C (r = -.6, P less than .05). We conclude that (1) abnormal GH secretion occurs in both SHF and AC, (2) serum Sm-C and NSILA are diminished in both forms of liver disease, and (3) portosystemic shunting of blood appears to be the important pathology shared by both forms of liver disease.

Adult↗
PubMedDate not supplied

Ultrasonographic and Doppler study of the thyroid gland in Graves' disease before and after treatment with antithyroid drugs.

OBJECTIVE: To determine the effects of medical treatment on the thyroid gland, peripheral circulation, and laboratory findings in patients with Graves' disease. METHODS: Twenty patients with Graves' disease were treated with either carbimazole and propranolol (group I) or carbimazole only (group II). Serum free thyroxine (FT(4)), thyroid-stimulating hormone (TSH), and thyrotropin-binding inhibitory immunoglobulins (TBII) were estimated before and after 6 weeks of treatment. Duplex Doppler ultrasonographic examination of the thyroid, inferior thyroid artery (ITA), and common carotid artery (CCA) was performed before and after 2, 4, and 6 weeks of therapy. RESULTS: Serum FT(4) and TBII decreased after treatment in both groups, whereas serum TSH increased in group I only. The volume of the thyroid gland and parenchymal blood velocity were increased in these patients and diminished only with addition of propranolol to carbimazole. A diffuse hypoechogenic pattern in the thyroid gland and increased ITA blood flow and peak velocity were observed in all patients and persisted throughout treatment. The mean CCA peak blood velocity was accelerated in Graves' disease and diminished after 6 weeks of therapy in both groups, whereas increased CCA blood flow diminished only in group I. CONCLUSION: A 6-week period of therapy with carbimazole and propranolol has no effect on the diffuse low echogenic pattern in the thyroid gland and the accelerated ITA blood flow in Graves' disease. The addition of propranolol is associated with early decrements in thyroid volume, parenchymal vascularity, and CCA blood flow as well as early recovery of TSH suppression, but it has no additional effect on thyroid hormone secretion or TBII levels.

Journal Article↗