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Biomedical subjects

S De Marchi

Publications and source records attributed to S De Marchi.

At least 55 records · Page 3Linked to original sources
PubMed1990

Severe metabolic acidosis and disturbances of calcium metabolism induced by acetazolamide in patients on haemodialysis.

1. To investigate mechanisms of extrarenal buffering in uraemic acidosis, we studied the effects of the carbonic anhydrase inhibitor, acetazolamide, in normal subjects and in patients with end-stage kidney disease on maintenance haemodialysis with virtually no urine output. 2. Acetazolamide (500 mg) was administered daily for 7 days, after pretreatment for 1 month with 1,25-dihydroxyvitamin D (n = 12) or placebo (n = 12); only placebo was administered to a third group (n = 12) of haemodialysis patients. In addition, acetazolamide was administered to normal control subjects (n = 12). 3. Treatment with acetazolamide resulted in a more marked metabolic acidosis in haemodialysis patients than in normal control subjects and the effect in haemodialysis patients was attenuated by prior treatment with 1,25-dihydroxyvitamin D. 4. The administration of acetazolamide to haemodialysis patients led to an increase in serum inorganic phosphorus, bone isoenzyme of alkaline phosphatase and parathyroid hormone, and a reduction in serum calcium, whereas acetazolamide had no effect on these variables in normal subjects. In contrast, in the haemodialysis patients previously treated with 1,25-dihydroxyvitamin D, acetazolamide increased serum inorganic phosphorus, bone isoenzyme of alkaline phosphatase, parathyroid hormone and serum calcium. 5. We hypothesize that the metabolic acidosis induced by acetazolamide in haemodialysis patients may result from interference with the mechanisms of extrarenal buffering. 6. As parathyroid hormone, 1,25-dihydroxyvitamin D and carbonic anhydrase are thought to be involved in bone buffering, we suggest that the marked acidosis seen in haemodialysis patients treated with acetazolamide may be due to impaired parathyroid hormone-mediated bone buffering.

Acetazolamide↗
PubMed1989

Intraocular pressure changes during hemodialysis: prevention of excessive dialytic rise and development of severe metabolic acidosis following acetazolamide therapy.

The response of intraocular pressure (IOP) to hemodialysis was investigated in 55 patients with end-stage kidney disease enrolled in a chronic dialysis program. The mean level of IOP, measured by the Goldman applanation tonometer, before dialysis was slightly lower than that of a control group of 50 healthy subjects (14.9 +/- 2 mm Hg vs 15.6 +/- 1.9 mm Hg. p = .07). During dialysis IOP underwent an excessive rise (7.8 to 12.5 mm Hg) in 10 patients (group 1), remained unchanged (variations below 2 mm Hg) in 41 patients (group 2), and decreased (3.1 to 5.1 mm Hg) in 4 patients (group 3). In group 1 patients, gonioscopy showed a narrow angle between iris and lateral cornea. Conversely, the anterior chamber angle was normal in patients of groups 2 and 3. The effect of a 7-day course of acetazolamide therapy (500 mg per day orally) on IOP was investigated in group 1 patients. Acetazolamide was capable of preventing the excessive IOP rise during dialysis. The mean reduction of such a dialytic rise was 8.1 mm Hg. However, despite this effect, in these patients the IOP level after dialysis still remained significantly higher than that of patients of group 2 (18.1 +/- 1 mm Hg vs 14.9 +/- 0.8 mm Hg. p less than .0001). Acetazolamide therapy precipitated in all patients a severe metabolic acidosis (blood pH fell from 7.38 +/- 0.02 to 7.24 +/- 0.03, p less than .0001; and bicarbonate concentration from 21 +/- 2.5 mmol/liter to 12.3 +/- 2.4 mmol/liter, p less than .0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Acetazolamide↗
PubMed1987

Rheological abnormalities of erythrocyte deformability and increased glycosylation of hemoglobin in the nephrotic syndrome.

This report is an attempt to gain more complete knowledge of the causes of the tendency to thrombosis in the nephrotic syndrome. Our purpose was to detect some rheological abnormalities in a group of nephrotic patients having normal renal function. Plasma and blood viscosity, erythrocyte filtration flow (EFF) and some indices of the carbohydrate metabolic state (glycosylated hemoglobin A1c; HbA1c, fasting glycemia and oral glucose tolerance test) were investigated in 10 patients with newly diagnosed primary nephrotic syndrome and 10 healthy subjects. EFF was determined in order to avoid variables depending upon plasma, white cells and hematocrit. The mean level of HbA1c was higher in the nephrotic group, in which we found 4 patients with impaired glucose tolerance according to the criteria of the National Diabetes Data Group. EFF was lower in nephrotic patients than in controls and correlated inversely with HbA1c. These findings indicate that nephrotic patients have a reduced red cell deformability which seems to be related to the abnormal carbohydrate metabolism commonly observed in this syndrome.

Adult↗
PubMed1987

Serum reverse T3 assay for predicting glucose intolerance in uremic patients on dialysis therapy.

Sixty patients with end stage chronic renal failure (CRF) enrolled in a dialysis program underwent studies of serum thyroid hormones and carbohydrate metabolic state. The aim of the study was: 1) to evaluate whether the glucose intolerance per se represents a factor for the alteration of circulating thyroid hormones; and 2) to explore the potential usefulness of specific thyroid hormones and particularly reverse T3 (RT3) as indicators for predicting glucose intolerance. Forty-two patients received hemodialysis and 18 were on intermittent peritoneal dialysis (IPD). CRF patients had reduced serum total T4 and T3 levels, slightly decreased RT3 and TBG concentrations and normal TSH values. There was no significant difference in serum thyroid hormone indices between HD and IPD patients. Glucose intolerance was found in 25 patients. Ten had fasting hyperglycemia and diabetic response to oral glucose tolerance test (OGTT), 15 had an impaired glucose tolerance according to the criteria of the National Diabetes Data Group. In CRF patients with glucose intolerance, serum T3 and T3/T4 molar ratio were significantly lower than in those with a normal OGTT response, whereas serum RT3 and RT3/T4 molar ratio were found to be higher. In the whole group of CRF patients these serum thyroid hormones closely correlated with glucose tolerance indices. To investigate the usefulness of serum RT3 assay in predicting glucose intolerance we compared the outcome of the OGTT and serum RT3 values. Using the results of the OGTT as the true diagnosis of glucose intolerance, serum RT3 assay showed a diagnostic specificity of 94.2% and a sensitivity of 100%. In conclusion these results suggest that: 1) the glucose intolerance, which frequently occurs in uremia, may influence circulating thyroid hormones probably leading to a shift in the peripheral tissue conversion of T4 from T3 to RT3; and 2) serum RT3 assay could assume a clinical interest in assessing carbohydrate metabolic state in treated end stage renal failure independently of the type of dialysis therapy.

Adult↗
PubMed1986

[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.

Adult↗