Serial estimations of activities of creatine kinase and its MB isoenzyme, aspartate aminotransferase, alanine aminotransferase, and lactate dehydrogenase and of concentrations of alpha1-acid glycoprotein were performed in 15 healthy well-trained male marathon runners. Estimations were made initially within three days before a race and then one, 24, and 96 hours after the race. Technetium-99m pyrophosphate myocardial scintigraphy was carried out at the initial prerace assessment and repeated 48 to 96 hours after the race. None of the subjects developed cardiac symptoms during or after the race. Activities of creatine kinase and creatine kinase MB became maximal 24 hours after the race. One and 96 hours after the race two and five subjects, respectively, showed amounts of creatine kinase MB totalling 5% or more of total creatine kinase. Lactate dehydrogenase activity peaked at one hour after the race, and activities of aspartate and alanine aminotransferases peaked at 24 and 96 hours after the race, respectively. Activities of all these enzymes showed a significant increase from prerace values during the rest of the study. Electrocardiographic features noted were similar to those reported elsewhere in athletes under similar conditions. They included first-degree heart block, incomplete right bundle-branch block, left ventricular hypertrophy, pseudoischaemic T-wave changes, and early repolarisation of variant ST-segment elevations in precordial leads. Technetium-99m pyrophosphate myocardial scintigraphy did not show evidence of myocardial damage before or after the race. Alpha1-acid glycoprotein concentrations were normal throughout. These data suggest that reliance on standard enzyme estimations and electrocardiographic criteria may yield false-positive indicators of myocardial injury during prolonged strenuous exercise. Technetium-99m pyrophosphate scintigraphy and alpha1-acid glycoprotein measurements offer additional information and may usefully be employed in evaluating circulatory collapse associated with such exercise.
A case of dilated cardiomyopathy in a young boy secondary to type II 3-methylglutaconic aciduria is described. A metabolic cause for his dilated cardiomyopathy was suspected because of the development on the electrocardiogram of an unusual "camel's hump" shape of the T waves, and of progressive thickening with increasing echogenicity of the left ventricular wall. He initially improved on digoxin treatment, but did not maintain the response with conventional dietary treatment for this condition. Supplementation with L-carnitine was associated with rapid deterioration in cardiac state, and may be contraindicated in this condition. At a point when the patient was moribund, large doses ofpantothenic acid, a precursor of coenzyme A, produced a dramatic and sustained improvement in myocardial function and in growth, neutrophil cell count, hypocholesterolaemia, and hyperuricaemia, which suggests that limitation of availability of coenzyme A is a fundamental pathological process in this condition. The clinical improvement has been maintained for 13 months, and myocardial function is now nearly normal. Oral pantothenol, unlike pantothenic acid, is not efficacious.
Objectives: To determine the dependence of plasma leptin concentrations upon circulating noradrenaline (NA) and thyroid hormones (TH) in humans. Design: Cross-sectional study in 40 newly diagnosed untreated patients with primary thyroid disease, and 69 lean and obese euthyroid control subjects. Measurements: Plasma leptin, NA, free T3 (fT3) and TSH in the fasting state. Anthropometry and % body fat (electrical bioimpedance). Results: Leptin levels were highest in 37 obese euthyroid and 22 hypothyroid (median [interquartiles]31.5 [19.0 ± 48.0], 19.2 [11.5 ± 31.5] ng ml 71 ), and lowest in 32 lean euthyroid and 18 hyperthyroid subjects (6.6 [3.9 ± 14.4], 8.9 [5.5 ± 11.1]; ANOVA, P`0.0001). Plasma NA was similar in all groups (P n.s.). In obese controls, TSH correlated with % body fat and leptin (r 0.67, r 0.61; P`0.001). Treatment of hypothyroidism (n 10) with T4 reduced leptin from 20. 8 [11.8 ± 31.6] to 12.9 [4.6 ± 21.2] (P 0.005) with no change in BMI. Conclusions: Thyroid status modi®es leptin secretion independently of adiposity and NA. The data suggest leptin ± thyroid interactions at hypothalamic and adipocyte level.
Studies were carried out to investigate whether the administration of oestradiol to laying hens induced fatty liver-haemorrhagic syndrome (FLHS). Short term oestradiol administration (up to 6 d) significantly increased liver size and plasma lipid concentration but had no effect on liver lipid concentration or hepatic lipogenic enzyme activities. Longer-term hormone treatment (up to 28 d) again significantly increased liver size and plasma lipid concentration. Liver lipid concentration was substantially reduced and lipogenic enzyme activity significantly reduced in oestradiol-treated birds. These effects had some similarities to those seen in oestrogenised immature birds and were additive to the effects of endogenous oestrogen in the laying bird. There were no deaths from FLHS and oestradiol treatment did not cause liver haemorrhages or affect egg production.
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