62 research outputs found
Dexamethasone attenuation of the cortisol response to nicotine in smokers
The effect of corticosteroids upon the cortisol response to nicotine from smoking was investigated in five heavy smokers. Corticosteroid activity was manipulated by administering dexamethasone, a synthetic glucocortoicoid (1 mg orally, 14 h before), in a doubleblind, placebo-controlled procedure. Testing took place in the middle of the day and involved the smoking of two high-nicotine (2.87 mg) research cigarettes over a 15-min period. The dexamethasone condition was characterized by a pronounced suppression of baseline plasma cortisol, as expected, and by a significant dampening of the cortisol response to nicotine, indicating diminished sensitivity to nicotine under conditions of enhanced corticosteroid activity.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/46333/1/213_2005_Article_BF02244142.pd
Mode d'action des sulfamides hypoglycemiants. [Mode of action of hypoglycemic sulfanilamides]
Sulfonylureas act as hypoglycemic agents by stimulating insulin secretion and improving insulin sensibility by a post-receptor mechanism. Their long term results mainly depend on extra-pancreatic mechanisms. Moreover they indirectly decrease triglyceridemia. Glipizide and gliclazide enhance fibrinolysis. Gliclazide also inhibits platelet aggregation and adhesion. The best indication of sulfonylureas is non insulin dependent diabetes with normal weight
Association Phéochromocytome et tumeur du pancréas endocrine: d’un MEN mixte à la maladie de von Hippel-Lindau
Age-related changes in cortico-releasing factor, somatostatin, neuropeptide Y, methionine enkephalin and beta-endorphin in specific rat brain areas
We investigated the age-related changes in the tissular protein, cortico-releasing factor (CRF), somatostatin (SOM), neuropeptide Y(NPY), methionine enkephalin (M-ENK) and beta-endorphin (beta-END) levels in frontal cortex, hippocampus, striatum and hypothalamus of young (4-month-old), mature (18-month-old) and senescent (26-month-old) Wistar male rats, bred in a specific pathogen free environment. Between the age of 4 and 18 months, the tissular protein levels increased in all 4 structures studied. The CRF and SOM levels increased in the hippocampus, while the NPY levels decreased. During this time, the NPY content increased in the striatum, whereas the SOM and M-Enk striatal levels decreased. Concomitantly, the NPY and beta-End levels decreased in the hypothalamus. Interestingly, no significant variations were found to occur in the frontal cortex whatever the neuropeptide studied. Between the age of 18 and 26 months, no significant changes in the tissular protein levels were detected, except in the hippocampus. The changes in the neuropeptide concentrations observed during this period depended on the neuropeptide and the brain structure studied. The CRF and beta-End levels decreased in the frontal cortex and the hypothalamus, respectively. The NPY peptidergic systems seem to be preferentially affected by aging processes since 3 out of the 4 structures studied--the frontal cortex, the striatum and the hypothalamus--showed a decrease in their tissular NPY content. During the same period, none of the 5 neuropeptides studied were affected in the hippocampus
Ketoconazole revisited: a preoperative or postoperative treatment in Cushing's disease.
International audienceCONTEXT: Although transsphenoidal surgery remains the first-line treatment in Cushing's disease (CD), recurrence is observed in about 20% of cases. Adjunctive treatments each have specific drawbacks. Despite its inhibitory effects on steroidogenesis, the antifungal drug ketoconazole was only evaluated in series with few patients and/or short-term follow-up. OBJECTIVE: Analysis of long-term hormonal effects and tolerance of ketoconazole in CD. DESIGN: A total of 38 patients were retrospectively studied with a mean follow-up of 23 months (6-72). SETTING: All patients were treated at the same Department of Endocrinology in Marseille, France. PATIENTS: The 38 patients with CD, of whom 17 had previous transsphenoidal surgery. INTERVENTION: Ketoconazole was begun at 200-400 mg/day and titrated up to 1200 mg/day until biochemical remission. MAIN OUTCOME MEASURES: Patients were considered controlled if 24-h urinary free cortisol was normalized. RESULTS: Five patients stopped ketoconazole during the first week because of clinical or biological intolerance. On an intention to treat basis, 45% of the patients were controlled as were 51% of those treated long term. Initial hormonal levels were not statistically different between patients controlled or uncontrolled. Ketoconazole was similarly efficacious as a primary or postoperative treatment. Among 15 patients without visible adenoma at initial evaluation, subsequent follow-up allowed identification of the lesion in five cases. No adrenal insufficiency was observed. Adverse effects were rare in patients treated long term. CONCLUSIONS: Ketoconazole is a safe and efficacious treatment in CD, particularly in patients for whom surgery is contraindicated, or delayed because of the absence of image of adenoma on magnetic resonance imaging
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