Diabetes mellitus is associated with coronary artery disease, and diabetic patients are frequently referred for coronary bypass graft surgery. It is well known that HbA1c, which reflects long-term glycemic control, is related to diabetic morbidity and mortality. It is not known whether HbA1c is related to postoperative length of stay among patients who undergo coronary artery bypass surgery. The authors evaluated 135 patients who underwent bypass surgery at the Westchester Medical Center (Valhalla, NY). HbA1c was measured in all patients preoperatively; a value of 7% or greater was used as a threshold for uncontrolled hyperglycemia. A postoperative length of stay of 6 days or more was used as the cutoff for an extended length of stay. Linear regression was used to assess the relationship between HbA1c, adjusted for age, and length of stay in days. Logistic regression, with length of stay a binary variable <6, > or =6 days, was used to assess the accuracy of HbA1c <7%, > or =7%, adjusted for age, in predicting length of stay. An HbA1c of 7% or greater was found to be a strong predictor of a length of stay of 6 days or longer. These data suggest that HbA1c can be used as a surrogate marker for cardiac and noncardiac morbidity that prolongs hospitalization after coronary artery bypass surgery.
The activity and kinetics of delta 5-3 beta-dehydrogenase and 17 alpha-hydroxylase, using labeled pregnenolone as substrate, were measured in gonadal homogenates from rats fed alcohol or isocalorically substituted carbohydrate for 40 days. There was no difference in the rate or reaction kinetics for either enzyme noted between control and alcohol-treated animals when the assays were carried out in the presence of saturating amounts of exogenous pyridine nucleotide cofactors. However, when exogenous cofactors were omitted from the reaction mixture, there was decreased activity of the delta 5-3 beta-dehydrogenase system and increased activity of the 17 alpha-hydroxylase reaction. Furthermore, a cofactor-specific inhibiting effect on delta 5-3 beta-dehydrogenase activity by NADH and NADPH was found. Incubation of gonadal homogenates from the alcohol-treated animals with pyruvate on lactate (in the absence of exogenous cofactors) resulted in an increase and a decrease, respectively, in enzyme activity. These studies indicate that chronic alcohol use decreases gonadal delta 5-3 beta-dehydrogenase activity and that this is most likely due to an effect of the agent on the concentration and/or availability of pyridine nucleotide cofactors rather than to a direct effect on the enzyme. This phenomenon may account for the mechanism by which alcohol decreases testosterone secretion in these animals.
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