The appetite and weight regulating peptide leptin was associated recently with alcohol craving during withdrawal. Nevertheless, correlations were only significant with craving displayed on the visual analogue scale for maximum craving during the previous week (VAS), and not if assessed with the highly validated Obsessive Compulsive Drinking Scale (OCDS). The objective of the following study, therefore, is to elucidate further the associations between the leptin system and craving concepts during alcohol withdrawal. A sufficiently large sample size should allow multiple statistical subgroup and confounder analyses. We prospectively investigated 102 chronic alcoholic inpatients (23 females, 79 males) during withdrawal on days 0 (admission), 1, 2 and days 7-10. In addition to the statistical analysis of the total sample, females and males were to be analysed separately. For detecting associations between leptin levels and craving scores multiple regression analysis was performed. Plasma leptin levels were determined, and craving for ethanol was assessed by both the OCDS and the VAS. Leptin plasma levels significantly increased during alcohol withdrawal compared to day 0, while all craving scores decreased. Body mass corrected leptin plasma levels predicted craving on day 0 in the OCDS total score (R=0.55, F=7.91, df=1.19, p<0.05) and in the OCDS obsessive subscore (R=0.57, F>=8.48, df=1.19, p<0.05) in females. Neither in males nor in the total population did multiple regression analysis reveal any significant results. Leptin levels seem to change during inpatient alcohol withdrawal. In a multivariate model, correlations between leptin levels and the highly validated craving scores of the OCDS can only be assumed in females. Hence, gender differences have to be taken into account when searching for neurobiological models of alcohol craving.

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PubMedDate not supplied

Effects of sleep on endotoxin-induced host responses in healthy men.

OBJECTIVE: To examine whether increased sleep during viral or bacterial infections supports host defense mechanisms. METHODS: To test this assumption in humans, healthy male subjects were assigned either to sleep from 2300 to 0700 hours (n = 10) or to stay awake through the night (n = 10). In the sleeping subjects Salmonella abortus equi endotoxin (0.4 ng/kg) or placebo were intravenously injected in balanced order during the first SWS episode. The age-matched, sleep-deprived subjects were injected at the same time point. RESULTS: As expected, endotoxin significantly increased rectal temperature, the plasma levels of cortisol, tumor necrosis factor-alpha (TNF-alpha), the soluble TNF receptors p55 and p75, Interleukin (IL)-6, the IL-1 receptor antagonist (RA), leukocyte, and granulocyte counts in both sleeping and sleep-deprived subjects, whereas lymphocyte and monocyte counts were transiently reduced. Time courses of endotoxin-induced host responses did not differ between the sleep and sleep deprivation groups. Endotoxin did not affect the amount of nocturnal wakefulness, nonrapid-eye-movement (NREM) sleep, or rapid-eye-movement (REM) sleep across the total night compared with placebo, but significantly increased electroencephalogram-arousals (EEG-arousals) in stage 2 and decreased arousals in SWS. In addition, the amount of SWS, spectral EEG-delta and -theta power was increased at the beginning and at the end of the sleep period, respectively, when the degree of immune activation was relatively low. CONCLUSION: The present results support the notion that short-term sleep deprivation is unlikely to harm the immune system as far as unspecific acute responses are concerned. The effects of endotoxin on sleep in this case support prior observations that in humans, enhanced SWS and intensified NREM sleep occur when host defense activation is subtle.

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PubMedDate not supplied

Emergency carotid endarterectomy.

OBJECTIVE: Evaluation of the therapeutical efficacy of emergency carotid endarterectomy (CEA) in neurologically unstable patients. PATIENTS AND METHODS: Three groups of a consecutive series of 71 emergency CEAs performed from 1980 to July 1998 were classified: (1) acute onset of severe stroke (n = 16), (2) progressive stroke/stroke in evolution (n = 34), and (3) crescendo transient ischemic attacks (n = 21). Cerebral coma, cerebral haemorrhage, and major ischemic stroke established in cranial computed tomography scans were contraindications for surgery. The neurological outcome was assessed by the modified Rankin scale. Long-term survival and long-term stroke recurrences were analyzed. RESULTS: The recovery/minor stroke rates (Rankin 0-3) in acute stroke, progressive stroke, and crescendo transient ischemic attacks were 56.3, 76.4 and 80.9%, respectively; the combined major stroke/mortality rates (Rankin 4-6) were 43.7, 23.6 and 19.1%, respectively. Intraoperative angiography in 39 patients detected early carotid reocclusions in 2 and intracranial embolism in 7 patients. Local application of thrombolytic agents (n = 5) may contribute to a better neurological outcome in emergency CEA. Life table probabilities of major strokefree survival were 74.5, 71.6, and 53.7% after 1, 2, and 5 years, respectively (including perioperative strokes). Life table probabilities to suffer no stroke recurrence during follow-up were 96.7, 96.7 and 85.3%, respectively (perioperative strokes excluded). CONCLUSIONS: Emergency CEA may be worthwhile in selected patients. Completion angiography is mandatory. Emergency CEA should be included in therapeutic strategies for ischemic stroke.

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