Diurnal metabolic profiles in hyperthyroidism.
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Biomedical subjects
Publications and source records attributed to A J McCulloch.
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To investigate the influence of thyroid hormones on intermediary metabolism in man, hormone and metabolite profiles were obtained over a 12-h period of normal meals and activity in eight hypothyroid subjects before and during thyroxine replacement therapy, and in sixteen matched controls. The fasting blood glucose concentration and the mean 12-h blood glucose concentration were normal in hypothyroid subjects but the blood glucose response to breakfast was exaggerated. Fasting blood lactate and pyruvate levels were normal but post-prandial hyperlactataemia and hyperpyruvicaemia were found and mean 12 h values for lactate (hypothyroid 1.80 +/- 0.06 v. control 0.77 +/- 0.03 mmol/l, P less than 0.01) and pyruvate (0.10 +/- 0.01 v. 0.08 +/- 0.003 mmol/l, P less than 0.01) were elevated. Blood alanine concentrations were elevated only in the evening. Although plasma non-esterified fatty acid levels were normal, fasting blood glycerol levels were decreased (0.06 +/- 0.01 v 0.08 +/- 0.01 mmol/l, P less than 0.001) and this decrease persisted throughout the 12-h period. Blood total ketone body concentrations did not differ from controls, but, as for plasma NEFA and blood glycerol, the normal preprandial rise in concentration was absent. Serum insulin, glucagon and growth hormone concentrations did not differ from control values at any time. Six months of thyroxine (T4) treatment produced a rise in blood glycerol concentration (mean 12 h value during T4 therapy, 0.06 +/- 0.01; before T4 therapy, 0.04 +/- 0.005 mmol/l; P less than 0.01) but not to control values (0.08 +/- 0.01 mmol/l). Concentrations of glucose and other gluconeogenic precursors were unaltered by therapy but the insulin response to meals and the mean 12 h serum insulin concentration were increased.
Nodular regenerative hyperplasia of the liver is an uncommon disorder, the main consequence of which is portal hypertension, hepatocellular decompensation being uncommon. A case associated with membranous glomerulonephritis is reported, in which death was caused by fulminant hepatic failure.
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The antihypertensive and metabolic effects of a new calcium antagonist nisoldipine (10 to 20 mg at night) were investigated in 14 mild to moderately hypertensive non-insulin-dependent diabetic patients (median age 62, range 50-70 years). In a 12-week placebo controlled single blind study, sitting and standing blood pressure were significantly lowered (p less than 0.001). Heart rate was unchanged as were blood urea, creatinine, bilirubin, mmol/l (mean +/- SEM) and uric acid concentrations. Plasma sodium levels fell during active therapy (142 +/- 0.5 mmol/l (mean +/- SEM) versus 139 +/- 0.5 (p less than 0.001) and remained lower during the washout period. Plasma calcium concentrations increased during nisoldipine therapy (2.41 +/- 0.02 versus 2.51 +/- 0.03 mmol/l, p less than 0.001) and returned towards baseline during the washout period. Plasma ionized calcium concentrations showed similar changes but plasma sodium and calcium remained within the normal laboratory ranges in all patients at all times. Serum triglyceride concentrations fell (placebo 1.9 +/- 0.02 mmol/l vs nisoldipine 1.6 +/- 0.2, p less than 0.05), but fasting cholesterol was unchanged. Fasting blood glucose, and the blood glucose response to oral glucose challenge (75 g) showed no differences though HbA1 concentrations fell (10.6 +/- 0.7 versus 9.2 +/- 0.05%, p less than 0.05) and tended to rise when the drug was withdrawn. Haemoglobin concentrations also fell during active therapy (14.7 +/- 0.4 vs 14 +/- 0.32 g/dl p less than 0.001) and also remained lower after the washout period (13.9 +/- 0.03 g/dl).(ABSTRACT TRUNCATED AT 250 WORDS)
The efficacy of structured education for 158 Type 2 diabetic patients in primary care (80 male, mean age 63 yr, median diabetes duration 3 yr) was assessed with respect to change in knowledge of diabetes, weight, and haemoglobin A1 over a 6-month period. The programme supplemented a primary care initiative in our semi-rural population. Teaching was carried out by a Diabetes Nurse Educator within primary care health centres (141 patients) and a hospital diabetes clinic (17 patients). For all patients mean baseline questionnaire score (maximum possible 12) was 6.2 rising after the programme to 10.5 (p < 0.01). At 6 months mean score fell to 9.5 (p < 0.01 compared to end of the programme), but still significantly better than baseline (p < 0.01). For patients on the primary-care-based programme mean haemoglobin A1 at baseline was 10.7% (normal range 6%-9%) decreasing after 6 months to 9.6% (p < 0.01). No significant changes were found in mean weight. Unlike many previous studies, these results demonstrate a highly beneficial effect not only on knowledge but also on metabolic control in patients who received their education in the primary-care setting. These results have obvious implications for patients residing in rural or semi-rural populations.
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