No abstract

Day-of-admission sera from myocardial infarction patients (MI) and patients with cardiopathies other than MI (non-MI) were analysed for total and unbound cortisol (F), progesterone (P4), oestrone (E1), and corticosteroid binding activities (CBG). The MI who survived (n = 28) showed high increases of F, P4 and E1 compared to healthy controls. By contrast, the MI who died within 10 days of admission (n = 6) had unchanged F and less increased P4 and E1 than survivors. The non-MI (n = 6) had higher F and E1 than controls but normal P4. The unbound steroids were increased in all patients: however, the MI who died showed much smaller rises than survivors (P less than 0.001 for unbound F and E1 increases in survivors vs. deceased). The CBG activity was in all MI lower than in normals (P less than 0.001) but unchanged in non-MI. These results are discussed in terms of the potential significance of unbound plasma steroids as predictors of MI severity.

The cortisol binding ability of transcortin (corticosteroid binding globulin or CBG) was found to be virtually absent from the sera of patients in a state of shock associated with high levels of antibodies to candida albicans.At the same time the serum proteins of the patients in shock displayed a number of the classical responses seen in acute inflammation: increased haptoglobin (28 \m=+-\10 vs 10.8 \m=+-\7.7 \g=m\m in normals), reduced prealbumin (1.7 \m=+-\ 0.6 vs 3.6 \m=+-\0.1 \g=m\m in normals) and albumin (485 \m=+-\78 vs 600 \ m=+-\200 \ g=m\ m in normals).The shock sera also showed increases in levels of endogenous cortisol (610 \ m=+-\ 260 vs 395 \ m=+-\ 192 nM in normals) and progesterone (2.40 \ m=+-\ 0.7 vs 1.4 \ m=+-\ 1.2 nM in normals) similar to those seen in inflammatory conditions.In sera from patients with superficial chronic candidiasis no significant variation of cortisol binding was observed. Haptoglobin was increased (26.4 \ m=+-\8.2 \g=m\m) and prealbumin decreased (2 \m=+-\0.8 \g=m\m), while the other serum indices tested retained essentially normal levels.Compared with previous studies from this laboratory which demonstrate a fall of CBG in septic shock of bacterial origin and lack of this response in acute inflammation, these results suggest that the loss of serum CBG acitivity is a specific marker for shock of fungal or bacterial aetiology. Possible endocrine or immune implications and clinical applications of our findings are discussed.Uow transcortin (CBG) values have been described in a few cases of liver, adrenal or renal disease (Brien 1981) or as a result of surgery (Hamanaka et al. 1970). Until recently, however, no consistent decrease of this corticosteroid binding activity has been reported in human disease states.Studies from this laboratory have shown that a severe and highly reproducible fall of CBG activity occurs in the rat as a result of turpentine-induced inflammation (Savu et al. 1980) and in man during the early phase of septic shock of bacterial aetiology (Savu et al. 1981). In man, this response resulted in virtual disappearence of the glucocorticoid binding activity of the serum ; this seemed specific for septic shock, since sera from patients with shock or acute inflammation displayed similar responses of their classical acute phase reactants (APRs), and endo¬ genous cortisol or progesterone levels, whereas the CBG fall was only seen in the shock sera.We have now extended our observations to shock associated with severe acute infection by the fungus candida albicans and shown that this dis¬ order brings about an almost complete loss of CBG activities similar to that caused by bacterial septic shock.In addition, to further delineate the specificity of the CBG fall in various shock and inflammatory conditions, we have examined the serum levels of typical APRs, steroids, and thyroid hormones, in patients with severe or superficial candidiasis.The physiological and practical implications of our findings are discussed.