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A group of 24 patients underwent a 7–14‐day course of continuously infused Cyclosporin A (2 mg · kg‐1 · day‐1) to treat a severe attack of ulcerative colitis. In 19 of them, including eight treated with total parenteral nutrition, we retrospectively analyzed the serum aminotransferase (AST/ALT) levels at the beginning and at the end of Cyclosporin infusion. The baseline levels of AST/ALT in the group were 19.9±3.2 and 31.4±6.4; on stopping Cyclosporin infusion, they were 43±15.8 and 119±56, respectively. Six patients showed an ALT change above 1.5 times the upper limit of reference. They included five of the eight patients treated with total parenteral nutrition (62.5%). In one of the six, ALT rose to 1000 U/l and was accompanied by full‐blown febrile cholangitis (proven by liver biopsy). This episode was preceded by excessive accumulation of Cyclosporin in blood. The development of liver toxicity was independent of the length of Cyclosporin treatment, nor did it impair drug efficacy. Thus, in these patients total parenteral nutrition and Cyclosporin were synergistic, causing twice the frequency of liver damage (62.5%) reported for ulcerative colitis patients on total parenteral nutrition alone (37%). Total parenteral nutrition should not be used to support patients needing Cyclosporin for autoimmune disease. However, too high a dose of Cyclosporin may cause liver disease per se.

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Six comatose patients hospitalized in an intensive care unit immediately following an acute trauma with severe brain injury (road or industrial accident) were examined through out three consecutive 24-h cycles in the first week after trauma, when receiving intramuscularly 12 mg daily of dexamethasone-21-phosphate. Intravenous or enteral nutrition was supplied continuously. Plasma cortisol and aldosterone were measured on blood samples drawn at 4-h intervals. Data were analyzed both by conventional chronograms and by rhythmometric analysis according to the Cosinor procedures. A normally-synchronized circadian pattern of plasma cortisol was recognizable in all cases in the face of the lack of consciousness and of the pharmacological administration of dexamethasone. Acrophase was located at 08:56, with a 95% confidence region vastly overlapping the corresponding region of the controls. By contrast, the circadian pattern of plasma aldosterone appeared to be disrupted; irregular fluctuations were recorded along the entire day. The Cosinor analysis did not detect a significant rhythm of plasma aldosterone during the examined 24-h cycles. Data obtained with the present investigation demonstrate that comatose patients within a few days after severe head injury and given high-dose corticoid treatment do maintain the normal circadian organization of the plasma cortisol, whereas loose that of the plasma aldosterone. Our findings are compatible with the concept that glucocorticoid rhythmicity is particularly resistant to acute injury; the mineralocorticoid rhythmicity appears more labile probably as a consequence of the plurifactorial modulation.