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,
CHARLES R. BAXTER and
C. RICHARD PARKER, JR.
Departments of Physiology and Surgery, University of Texas Southwestern Medical School Dallas, Texas 75235
The Department of Obstetrics and Gynecobgy, University of Alabama Birmingham, Alabama 35294
Address all correspondence and requests for reprints to: C. Richard Parker, Jr., Department of Obstetrics and Gynecology, University of Alabama at Birmingham, University Station, Birmingham, Alabama 35294.
The effects of burn trauma in men on the production of adrenal and testicular steroids was investigated. Whereas there were significant increases in serum cortisol levels and urinary 17-hydroxycorticosteroid excretion soon after thermal injury, there were significant decreases in serum dehydro-epiandrosterone sulfate, dehydroepiandrosterone, androstene-dione, and testosterone concentrations during the first 4 weeks following burn trauma. Serum androstenediol and androstene-diol sulfate levels also were reduced, though insignificantly, 10–23 days postburn. Serum LH levels were unchanged during the postburn interval. Since urinary 17-ketosteroid excretion was normal or below normal rather than increased, the decline in serum C19-steroid levels probably resulted from decreased glandular secretion rather than increased rates of metabolism and excretion. Low dehydroepiandrosterone sulfate and/or testosterone levels were found in some men several months after recovery from their burns. These data suggest that thermal injury leads to acute inhibition of adrenal and testicular C19-steroid secretion, but stimulation of adrenal glucocorticosteroid production, and that endocrine function in many instances is not normalized after complete healing of the burned surfaces. The mechanisms and physiological consequences of such changes in the steroid milieu of men after burn trauma are unknown.
* This work was supported by NIH Grants HD-14513/22969 and GM-21681.
Predoctoral student supported in part by NIH Training Grant HD-07062.
Received April 4, 1986.
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