Context: Primary adrenal insufficiency (Addison's disease) is a rare autoimmune disease. Until recently, life expectancy in Addison's disease patients was considered normal. Objective: To determine the mortality rate in Addison's disease patients. Design and methods: i) Patients registered with Addison's disease in Norway during 1943-2005 were identified through search in hospital diagnosis registries. Scrutiny of the medical records provided diagnostic accuracy and age at diagnosis. ii) The patients who had died were identified from the National Directory of Residents. iii) Background mortality data were obtained from Statistics Norway, and standard mortality rate (SMR) calculated. iv) Death diagnoses were obtained from the Norwegian Death Cause Registry. Results: Totally 811 patients with Addison's disease were identified, of whom 147 were deceased. Overall SMR was 1.15 (95% confidence intervals (CI) 0.96-1.35), similar in females (1.18 (0.92-1.44)) and males (1.10 (0.80-1.39)). Patients diagnosed before the age of 40 had significantly elevated SMR at 1.50 (95% CI 1.09-2.01), most pronounced in males (2.03 (1.19-2.86)). Acute adrenal failure was a major cause of death; infection and sudden death were more common than in the general population. The mean ages at death for females (75.7 years) and males (64.8 years) were 3.2 and 11.2 years less than the estimated life expectancy. Conclusion: Addison's disease is still a potentially lethal condition, with excess mortality in acute adrenal failure, infection, and sudden death in patients diagnosed at young age. Otherwise, the prognosis is excellent for patients with Addison's disease.

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Sleep and waking in cats and rats were studied 6-10 hours following acute administration of zimeldine, alaproclate or saline. The effects on slow wave sleep of the two compounds markedly differed in the cats. Following zimeldine, sleep with a high amount of synchronized slow waves (SWS-2) was increased, and total sleep was unchanged. Following alaproclate, SWS-2 did not increase, and total sleep was reduced. In the rats, zimeldine increased SWS-2 during the first 4 hours after administration, while there was no change in SWS following alaproclate. Both zimeldine and alaproclate increased REM latency and reduced REM sleep in both species with somewhat more pronounced effects in cats than in rats. The results on SWS-2 following zimeldine are consistent with earlier results following serotonin depletion in both species. The differential effects on SWS-2 are discussed in terms of regional differences in uptake inhibition and other differences between the two uptake inhibitors. The results on REM sleep confirm earlier results involving serotonin uptake inhibitors and serotonin precursor loading and indicate that increased synaptic serotonin concentrations suppress REM sleep.