Transketolase abnormality in tolazamide-induced Wernicke's encephalopathy.

We studied a thiamine-dependent enzyme, transketolase, from fibroblasts of a diabetic patient who developed Wernicke's encephalopathy when treated with tolazamide, in order to delineate if this patient also had transketolase abnormality [high Km for thiamine pyrophosphate (TPP)], as previously reported in postalcoholic Wernicke-Korsakoff syndrome. In addition to this patient, we also studied this enzyme from three diabetic kindreds without any history of Wernicke's encephalopathy and from four normal controls. We found that the above-mentioned patient and one of the diabetic kindreds with no history of Wernicke's encephalopathy had abnormal transketolase as determined by its Km for TPP. These data suggest a similarity between postalcoholic Wernicke-Korsakoff syndrome and the patient with tolazamide-induced Wernicke's encephalopathy from the standpoint of transketolase abnormality.

Adrenal steroid responses to continuous intravenous adrenocorticotropin infusion compared to bolus injection in normal volunteers.

We compared the adrenal steroid responses after synthetic ACTH-(1-24) (Cosyntropin) administration given by either continuous iv infusion or bolus injection in 11 normal women and 6 normal men. Each subject received 250 micrograms Cosyntropin as a bolus iv injection on 1 occasion and as a continuous 2-h iv infusion on another occasion, in random order. There was a 1-week interval between the studies. We measured the plasma levels of cortisol, 11-deoxycortisol, 17-hydroxyprogesterone, progesterone, pregnenolone, 17-hydroxypregnenolone, dehydroepiandrosterone, dehydroepiandrosterone sulfate, delta 5-androstenediol, androstenedione, and testosterone by RIA 15 and 0 min before and 30, 45, 60, and 120 min after administering ACTH. The steroid concentrations and their increments, ratios, or areas above baseline did not differ significantly between the bolus injection and the continuous infusion. Thus, at the dose of 250 micrograms, a bolus ACTH injection stimulates adrenal steroid secretion as effectively as a 2-h continuous ACTH infusion.

Plasma and red blood cell beta-endorphin immunoreactivity in normal and complicated pregnancies: gestational age variation.

Recent observations suggest that there may be two pools of beta-endorphin-like immunoreactivity in mammalian circulation. One of these pools is present in plasma and the other is detected in association with erythrocytes. Elucidation of an erythrocyte-associated pool may explain some of the wide variability of plasma beta-endorphin levels reported in the literature. We measured beta-endorphin immunoreactivity levels in 85 normal and 33 complicated pregnancies to delineate a possible correlation between gestational age and beta-endorphin immunoreactivity levels in plasma and in erythrocytes. Our results indicate that beta-endorphin immunoreactivity levels in both plasma and erythrocytes vary systematically throughout the gestational period, reaching a peak at 31 to 32 weeks of gestation. Amniotic fluids at midgestation were also analyzed and no correlation was observed between the levels of beta-endorphin immunoreactivity and fetal sex. Compared to normal patients, diabetic patients had significantly lower levels of beta-endorphin immunoreactivity in plasma and higher levels in erythrocytes although the total beta-endorphin immunoreactivity was not statistically different from that in normal subjects. We conclude that (1) the total beta-endorphin immunoreactivity level in whole blood is much higher than that reported in plasma, (2) both plasma- and erythrocyte-associated beta-endorphin immunoreactivity levels vary with gestational age, with a peak level at 24 to 32 weeks of gestation, (3) amniotic fluid beta-endorphin immunoreactivity levels are unrelated to fetal sex, and (4) diabetic patients may have a different distribution of beta-endorphin immunoreactivity pools than normal individuals.