Biomedical subjects
E Cecchin
Publications and source records attributed to E Cecchin.
[Low T4 syndrome in alcoholism: role of the decrease in TBG].
Controversial data concerning thyroid function in chronic alcoholics prompted us to evaluate some aspects of thyroxine transport and metabolism in these patients. We studied 45 patients with a history of alcohol consumption of at least 160 g a day for 10 years or more. Only patients without clinical and histopathological evidence of chronic liver disease have been included in the study. All patients were clinically euthyroid and there was no history of thyroid disease. Serum thyroxine (T4), free thyroxine (FT4) and thyroxine-binding globulin (TBG) were measured by radioimmunoassay methods within 48 hours of admission and after 30 day of alcohol abstinence. At admission the mean values of T4 and TBG in alcoholics were significantly reduced when compared to those of healthy controls (6.8 +/- 1.4 vs 8.4 +/- 1.2 micrograms/dl; p less than 0.01 and 17.5 +/- 3.2 vs 20.5 +/- 1.2 micrograms/ml; p less than 0.01). Contrarily FT4 levels did not differ significantly between the groups (9.8 +/- 1.6 vs 10.8 +/- pg/ml). A close relationship between T4 and TBG (r = 0.684; p less than 0.0001) demonstrated that the decrease of T4 in alcoholics depended on a decrease in circulating TBG. We could not find any correlation between TBG and serum albumin, gamma-glutamyl-transpeptidase, aspartate aminotransferase, alanine aminotransferase and mean corpuscular volume. Indeed there was a strong relationship between TBG and mean daily alcoholic intake (r = 0.712; p less than 0.0001). T4 and TBG increase rapidly during withdrawal and after 30 days of abstinence their values did not differ significantly from those of healthy controls. In conclusion these data provide evidence that alcohol abuse causes a decrease in T4 which depends on a decrease in circulation TBG and is not associated with a reduction of FT4. Such "low TBG syndrome" seems to be due more probably to a primary effect of alcoholic on TBG synthesis that to the liver injury secondary to the alcohol abuse.
Are orthostatic hypotension and impaired blood pressure control common features of the alcohol withdrawal syndrome?
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Immunological abnormalities and renal tubular disorders: a puzzling association.
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Relation between plasma aldosterone concentration and renal handling of sodium and potassium in alcoholics during the withdrawal phase.
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Intraocular pressure and hemodialysis.
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Ethanol-induced water diuresis: one of a spectrum of renal defects resulting from ethanol toxicity.
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Calcium and alcohol-associated hypertension.
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Reduced renal phosphate threshold concentration in chronic alcoholics: one component of a more complex tubule dysfunction?
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Alcohol withdrawal and hypertension: evidence for a kidney abnormality.
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Chemotherapy and/or removal of the peritoneal catheter in the management of fungal peritonitis complicating CAPD?
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Reversible tubular dysfunction in alcohol abuse.
The discovery of an unexplained alkaline urine pH in a significant percentage of chronic alcoholic patients prompted us to evaluate some aspects of their tubular function. We studied 60 patients with a history of alcohol consumption of at least 160g daily for 10 years or more. Only patients without clinical and histopathological evidence of chronic liver disease were included in the study. The endogenous creatinine clearance was in the normal range in all patients. On the first day of hospitalisation 22 patients (36.6%) had a urine pH greater than 6.4 and a daily bicarbonate excretion ranging from 5.8 to 25.9mmol. The fractional urinary excretion of beta 2-microglobulin, sodium, potassium, chloride, calcium, phosphorus and uric acid were significantly increased compared with those of 38 alcoholic patients with urine pH less than 6.4 and those of 50 healthy controls. All these indices of tubular function improved during withdrawal, and after 30 days of abstinence their values did not differ from those of controls. This data provides evidence that in one-third of heavy drinkers alcohol abuse causes a complex tubular dysfunction which, at least in this stage of alcoholic disease, recovers with abstinence.
Fractures and hypercalciuria: two markers of severe dependence in alcoholics.
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Torulopsis glabrata peritonitis complicating continuous ambulatory peritoneal dialysis: successful management with oral 5-fluorocytosine.
We report two cases of fungal peritonitis caused by Torulopsis glabrata, an uncommon opportunistic pathogen, in patients with end-stage renal disease receiving continuous ambulatory peritoneal dialysis (CAPD). The general clinical characteristic of T glabrata peritonitis was comparable to previously reported cases of Candida peritonitis. Although appropriate therapy of fungal peritonitis in patients undergoing CAPD still remains controversial, both for the drug of choice and for the dosage to be used, our study indicates that a 5-week course of oral 5-fluorocytosine (5-FC) may obviate the need to remove the peritoneal catheter during the management of peritonitis caused by susceptible strains of T glabrata.
Close genetic linkage between HLA and renal glycosuria.
Renal glycosuria is an inherited disorder of renal tubule function in which significant amounts of glucose are excreted in the urine in the simultaneous presence of normal blood glucose levels. Renal glucose titration analyses and HLA genotypes were performed in 5 unrelated affected families with a total of 25 patients and 40 healthy relatives. In each family the gene responsible for renal glycosuria segregates with the HLA complex suggesting a close genetic linkage. 2 cases carry intra-HLA recombinant haplotypes; in these subjects our findings indicate that the abnormal gene is closer to the HLA-A locus than the HLA-B locus. No HLA-A, HLA-B or HLA-C specific antigen is selectively increased among the 5 unrelated families affected with renal glycosuria.
Fungal peritonitis in ambulatory peritoneal dialysis.
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Relative contribution of glucose intolerance, hyperazotemia and uremic acidosis to hemoglobin A1 levels in chronic renal failure.
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