Effects of haemodialysis session on plasma beta-endorphin, ACTH and cortisol in patients with end-stage renal disease.
ABSTRACT The effect of a regular haemodialysis session on the plasma concentrations of beta-endorphin, ACTH and cortisol was investigated in 14 patients with end-stage renal disease and 20 healthy controls. Blood for analysis of beta-endorphin, ACTH and cortisol was sampled before and immediately after haemodialysis. In four patients the dialysate was studied for presence of these hormones, but showed no specific activity. The predialysis beta-endorphin, ACTH and cortisol levels did not differ significantly from the control values. The postdialysis levels were significantly higher than the predialysis. Significant linear correlation was found between plasma ACTH and beta-endorphin values in the postdialysis samples. The similarity of plasma beta-endorphin, ACTH and cortisol levels in patients with end-stage renal disease before dialysis and in normal controls indicated integrity of the hypothalamic pituitary-adrenal axis. The significantly increased levels after the dialysis session and the significant correlation between postdialysis plasma beta-endorphin and ACTH suggest that the haemodialysis session was a stressful event.
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ABSTRACT: Endocrine abnormalities in chronic hemodialysis patients are in part corrected by control of anemia with recombinant human erythropoietin (rHu-EPO). We further examined the role of rHu-EPO in select hormonal abnormalities thought to be anemia related as well as the GH-insulin-like growth factor 1 (GH-IGF-1) axis that is abnormal in hemodialysis patients. We studied responses to the administration of two hypothalamic hormones, GHRH and ovine corticotropin-releasing hormone (CRH), in five anemic male patients on chronic hemodialysis before and after correction of the anemia with rHu-EPO. For comparison, five age-matched normal male volunteers were tested once. Anemic patients on chronic hemodialysis had high basal GH concentrations, an exaggerated GH response to exogenous GHRH, increased levels of IGF-1, and elevated levels of IGF-1 binding protein-3 in comparison to controls. ACTH response to CRH was comparable in dialysis patients and normal controls, but the cortisol response to endogenous ACTH release was prolonged. The cortisol binding globulin was similar to the controls. After correction of anemia, the basal elevation of GH was no longer present, but the exaggerated response of GH to exogenous GHRH persisted. IGF-1 and IGF-1 binding protein-3 levels remained elevated. The ACTH response to CRH, which was normal before correction of the anemia, became exaggerated in terms of elevated levels. Nevertheless, the prolonged cortisol response persisted. It appears that correction of the anemia in hemodialysis patients with rHu-EPO can partly correct perturbations in the GH secretory axis but may lead to new abnormalities in the CRH-ACTH axis.Journal of Clinical Endocrinology & Metabolism 02/1994; 78(1):63-9. · 6.43 Impact Factor
- New England Journal of Medicine 10/1981; 305(10):560-3. · 51.66 Impact Factor
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ABSTRACT: Several alterations are present in the hypothalamic hypophyseal regulation of many hormones in patients with chronic renal failure. Evaluation of the hypothalamic hypophyseal adrenal axis in these groups of patients demonstrated normal levels of plasma cortisol. Dexamethasone suppression is abnormal after administration of 1 mg of oral dexamethasone, but normal after 3 mg. Dexamethasone blood levels were lower than the control after administration of 1 mg of oral dexamethasone. A dexamethasone metabolic clearance showed a similar half-life between the patients and controls. Oral absorption study showed poor absorption of the drug. Therefore, there is a problem of gastrointestinal absorption producing the abnormal dexamethasone suppression test in patients with renal failure. Results of metyrapone tests were normal. Corticotropin stimulation tests elicited a normal response. Insulin-induced hypoglycemia does not produce an increment in plasma cortisol or adrenocorticotropic hormone levels.Archives of Internal Medicine 09/1982; 142(8):1448-52. · 11.46 Impact Factor