Oral glucose tolerance tests (OGTT) were performed on eighteen patients with suspected obstructive sleep apnoea who also completed a whole-night polygraphic recording with oximetry. Insulin resistance indices (IRI) were calculated as the product of areas under glucose and insulin curves. In the resulting multiple regression analysis the dependent variable was IRI and the independent variables were age, body mass index (BMI) and the number of nocturnal hypoxic episodes with over 4% desaturation per hour (ODI4). ODI4 was between 4.6 and 70 (median 22.3); IRI ranged from 2.20 to 33.55 (median 7.50). In the regression model the coefficient of determination (R2) for IRI was 0.441 (F-ratio = 3.681, P = 0.038). The strongest determinant of IRI was ODI4 and the regression coefficient of BMI was not significantly different from zero even when possible outliers were excluded. It was found that insulin resistance is related to the severity of sleep anoea. This may be due to a hypoxia-induced hormonal stress reaction which decreases tissue insulin sensitivity. Since upper body obesity is associated with both insulin resistance and sleep apnoea, the distribution of fat should be taken into account in future studies.

In patients on antiepileptic drugs, bone loss has been mainly demonstrated at radial sites using old technology and has been ascribed to drug-induced vitamin D deficiency rather than to any direct effects of the treatment on bone cells. We examined 38 epileptic patients (24 women and 14 men) aged 20-49 years who were using either carbamazepine or phenytoin or both. Bone mineral density (BMD) at the lumbar spine and three femoral sites was measured by dual-energy x-ray absorptiometry (DXA) and serum and urine markers of bone and mineral metabolism were determined. The latter included the C-terminal extension peptide of type I procollagen (PICP), a putative serum marker of bone formation, and the cross-linked carboxyl-terminal telopeptide of human type I collagen (ICTP), a novel serum marker of bone matrix degradation. In female patients on phenytoin, weight- and height-adjusted BMD was reduced at the femoral neck and the Ward's triangle (p < 0.05) but was at the control level in the other patient groups at all four measurement sites. Compared with controls, the serum concentrations of 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D were reduced by 26% (p < 0.01) and by 27% (p < 0.001) in female patients. These changes were independent of the therapy used. They were not present in male patients. For both genders the serum levels of vitamin D binding protein were normal. Both female and male patients had hypocalcemia, but women only showed hypocalciuria.(ABSTRACT TRUNCATED AT 250 WORDS)

This study focused on eyeblink duration as a measure of sleepiness in on-road driving and on the driving performance of professional bus drivers with polysomnographically confirmed mild obstructive Sleep Apnea Syndrome (OSAS). Ten bus drivers with OSAS and their matched controls participated in the study. The Maintenance of Wakefulness Test (MWT) and a monotonous on-road driving task were completed. Eyeblink duration and frequency and speed control were measured while driving. Lane-keeping was evaluated by the supervisor in the car. Subsequent to these tasks, drivers with OSAS received continuous positive airway pressure treatment (nasal CPAP). After nine weeks of treatment, the tasks were repeated. Prior to treatment the average blink duration in the driving task was significantly longer and sleep latency in the MWT was significantly shorter for bus drivers with OSAS than for controls (mean blink duration 82.3 ms; 51.9 ms and mean sleep latency 23.2 min; 35.4 min), indicating increased daytime sleepiness. Subsequent to treatment both measures in drivers with OSAS decreased to the level of the controls. Treatment effects in MWT and blink duration in on-road driving also correlated significantly. No significant differences between the groups appeared in average blink frequency or driving performance in terms of maintenance of speed. No significant lane drifting appeared either. These results support earlier findings on blink duration as an indicator of increased sleepiness and have important implications for those involved in the transport technological industry. The findings also suggest that nasal CPAP treatment is effective in reducing excessive daytime sleepiness.

Thyroid hormone concentrations and measures reflecting thyroid function were studied in sera from 35 patients receiving long-term phenytoin (PHT) or carbamazepine (CBZ) therapy. The mean concentrations of T4, FT4, FT3, and rT3, but not T3, of these patients were significantly lower than those of 19 controls of similar age and sex distribution. The mean serum thyrotropin (TSH) concentration was slightly but significantly higher in patients than in controls, but the serum TSH response to TRH was not significantly increased. In patients, the higher mean clinical diagnostic index of hypothyroidism (CDI-HT: -20.3 +/- 19.1 vs. -33.7 +/- 8.5, p < 0.05) and higher ratio of preejection period to left ventricular ejection time (PEP/LVET: 0.343 +/- 0.065 vs. 0.334 +/- 0.030, p < 0.05) than in controls were compatible with tissue hypothyroidism. However, comparison of the mean levels of alanine aminotransferase (ALAT), creatine kinase (CK), creatinine, triglycerides, cholesterol, high-density lipoprotein (HDL) cholesterol, osteocalcin, procollagen type III aminoterminal propeptide, and somatomedin-C showed no significant differences between patients and controls. The increased mean angiotensin convertase and sex hormone-binding globulin (SHBG) levels, typical of hyperthyroidism, were probably caused by drug effects. Fourteen patients with a subnormal FT4 concentration in serum participated in a double-blind thyroxine treatment cross-over study. Neither the mean CDI-HT score, nor the systolic time intervals were significantly different between the thyroxine and placebo periods. Five patients benefited subjectively from the treatment. On the basis of all data from the cross-sectional and thyroxine treatment studies, we conclude that patients receiving anticonvulsant drugs chronically are eumetabolic and do not need thyroxine supplementation.

Oral thyroxine produces a rise in serum IGFBP-1 levels without a change in serum IGF-I concentration.