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This study was carried out to investigate the clinical and biochemical factors which might be of importance in predicting the outcome of patients with myxoedema coma. Eleven patients (ten female) aged 68.1+/-19.5 years attended our institution over a period of 18 years.Glasgow and APACHE II scores and serum free thyroxine and TSH were measured in all the patients on entry. Patients were selected at random to be treated with two different regimens of l-thyroxine.Four patients died with the mortality rate being 36.4%. The patients in coma at entry had significantly higher mortality rates than those with minor degrees of consciousness (75% vs 14.3% respectively, P=0.04). The surviving patients had significantly higher Glasgow scores than those who died (11.85+/-2.3 vs 5.25+/-2.2 respectively, P<0.001). Comparison of the mean values of APACHE II scores between the surviving group and those who died was significantly different (18.0+/-2.08 vs 31.5+/-2.08 respectively, P<0.0001).The degree of consciousness, the Glasgow score and the severity of the illness measured by APACHE II score on entry were the main factors that determined the post-treatment outcome of patients with myxoedema coma.

Fetuses with intrauterine growth restriction (IUGR) have high concentrations of catecholamines, which lowers the insulin secretion and glucose uptake. Here, we studied the effect of hypercatecholaminemia on glucose metabolism in sheep fetuses with placental insufficiency-induced IUGR. Norepinephrine concentrations are elevated throughout late gestation in IUGR fetuses but not in IUGR fetuses with a bilateral adrenal demedullation (IAD) at 0.65 of gestation. Euglycemic (EC) and hyperinsulinemic–euglycemic (HEC) clamps were performed in control, intact-IUGR, and IAD fetuses at 0.87 of gestation. Compared to controls, basal oxygen, glucose, and insulin concentrations were lower in IUGR groups. Norepinephrine concentrations were five-fold higher in IUGR fetuses than in IAD fetuses. During the EC, rates of glucose entry (GER, umbilical + exogenous), glucose utilization (GUR), and glucose oxidation (GOR) were greater in IUGR groups than in controls. In IUGR and IAD fetuses with euglycemia and euinsulinemia, glucose production rates (GPR) remained elevated. During the HEC, GER and GOR were not different among groups. In IUGR and IAD fetuses, GURs were 40% greater than in controls, which paralleled the sustained GPR despite hyperinsulinemia. Glucose-stimulated insulin concentrations were augmented in IAD fetuses compared to IUGR fetuses. Fetal weights were not different between IUGR groups but were less than controls. Regardless of norepinephrine concentrations, IUGR fetuses not only develop greater peripheral insulin sensitivity for glucose utilization but also develop hepatic insulin resistance because GPR was maintained and unaffected by euglycemia or hyperinsulinemia. These findings show that adaptation in glucose metabolism of IUGR fetuses are independent of catecholamines, which implicate that hypoxemia and hypoglycemia cause the metabolic responses.