Septic Shock and Sepsis: A Comparison of Total and Free Plasma Cortisol Levels
Autor: | T. Quach, John G. Lewis, J. T. Ho, Marianne J. Chapman, David J. Torpy, H. Al-Musalhi, P. Thomas, Christopher J. Bagley |
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Rok vydání: | 2006 |
Předmět: |
Male
endocrine system medicine.medical_specialty Hydrocortisone Microdialysis Endocrinology Diabetes and Metabolism Clinical Biochemistry Context (language use) Biochemistry Sepsis Endocrinology Internal medicine Severity of illness Adrenal insufficiency medicine Humans Prospective Studies Serum Albumin Aged Transcortin Critical illness-related corticosteroid insufficiency business.industry Septic shock Biochemistry (medical) Reproducibility of Results Middle Aged medicine.disease Shock Septic Cortisol binding Cosyntropin Female business hormones hormone substitutes and hormone antagonists Adrenal Insufficiency medicine.drug |
Zdroj: | The Journal of Clinical Endocrinology & Metabolism. 91:105-114 |
ISSN: | 1945-7197 0021-972X |
Popis: | Severe systemic infection leads to hypercortisolism. Reduced cortisol binding proteins may accentuate the free cortisol elevations seen in systemic infection. Recently, low total cortisol increments after tetracosactrin have been associated with increased mortality and hemodynamic responsiveness to exogenous hydrocortisone in septic shock (SS), a phenomenon termed by some investigators as relative adrenal insufficiency (RAI).Free plasma cortisol may correspond more closely to illness severity than total cortisol, comparing SS and sepsis (S).This was a prospective study.This study took place in a tertiary teaching hospital.Patients had SS (n = 45) or S (n = 19) or were healthy controls (HCs; n = 10).The aim of the study was to compare total with free cortisol, measured directly and estimated by Coolens' method, corticosteroid-binding globulin (CBG), and albumin in patients with SS (with and without RAI) and S during acute illness, recovery, and convalescence.Comparing SS, S, and HC subjects, free cortisol levels reflected illness severity more closely than total cortisol (basal free cortisol, SS, 186 vs. S, 29 vs. HC, 13 nmol/liter, P0.001 compared with basal total cortisol, SS, 880 vs. S, 417 vs. HC, 352 nmol/liter, P0.001). Stimulated free cortisol increments varied greatly with illness category (SS, 192 vs. S, 115 vs. HC, 59 nmol/liter, P = 0.004), whereas total cortisol increments did not (SS, 474 vs. S, 576 vs. HC, 524 nmol/liter, P = 0.013). The lack of increase in total cortisol with illness severity is due to lower CBG and albumin. One third of patients with SS (15 of 45) but no S patients met a recently described criterion for RAI (total cortisol increment after tetracosactrinor = 248 nmol/liter). RAI patients had higher basal total cortisol (1157 vs. 756 nmol/liter; P = 0.028) and basal free cortisol (287 vs. 140 nmol/liter; P = 0.017) than non-RAI patients. Mean cortisol increments in RAI were lower (total, 99 vs. 648 nmol/liter, P0.001; free, 59 vs. 252 nmol/liter, P0.001). These differences were not due to altered CBG or albumin levels. Free cortisol levels normalized more promptly than total cortisol in convalescence. Calculated free cortisol by Coolens' method compared closely with measured free cortisol.Free cortisol is likely to be a better guide to cortisolemia in systemic infection because it corresponds more closely to illness severity. The attenuated cortisol increment after tetracosactrin in RAI is not due to low cortisol-binding proteins. Free cortisol levels can be determined reliably using total cortisol and CBG levels. |
Databáze: | OpenAIRE |
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