Plasma dehydroepiandrosterone sulfate levels in patients with hyperfunctioning and non-hyperfunctioning adrenal tumors before and after adrenal surgery.
To investigate the clinical significance of plasma dehydroepiandrosterone sulfate (DHEAS) measurements, 175 patients with histologically confirmed adrenal tumors, 10 cortisol-producing adenomas, 59 aldosterone-producing adenomas, 56 non-hyperfunctioning adenomas, 13 adrenocortical carcinomas, 13 adrenal cysts, and 24 adrenomedullary tumors were studied. Plasma DHEAS levels were expressed as percentage of the mean of sex- and age-matched groups of healthy, normal subjects (DHEAS %). We found that before adrenal surgery, DHEAS % values were significantly reduced in patients with cortisol-producing (mean, 15.2% of control; 95% confidence interval (CI), 9.4-24.7%), non-hyperfunctioning (28.4%; 22.4-36.0%) as well as aldosterone-producing adrenocortical adenomas (55.4%; 47.1-65.1%) compared with controls, while values were normal in patients with adrenal cysts and in those with adrenomedullary tumors. Plasma DHEAS % values exhibited a great variability in adrenocortical carcinomas (mean, 84.0%; 95% CI, 33.2-212.5%). Death from adrenocortical carcinoma was more frequent in patients with high plasma DHEAS % values compared with those with low DHEAS %. During long-term postoperative monitoring, we found that plasma DHEAS levels of patients with aldosterone-producing and non-hyperfunctioning adenomas returned to normal in the second and fourth postoperative year respectively. In patients with cortisol-producing adenomas, plasma DHEAS remained suppressed for as long as 8 years after the operation. These findings show that except in adrenocortical carcinomas and cysts, plasma DHEAS levels are significantly decreased in all groups of adrenocortical tumors, including non-hyperfunctioning and aldosterone-producing tumors. The extent of this decrease and the postoperative persistence of suppressed plasma DHEAS levels may be related to the glucocorticoid production of adrenocortical tumors.
Tóth
M
M
2nd Department of Medicine, Semmelweis University Medical School, Budapest, Hungary.
Rácz
K
K
Varga
I
I
Adleff
V
V
Jakab
C
C
Fútó
L
L
Kiss
R
R
Gláz
E
E
D000236:Adenoma / Q000097:blood* / Q000378:metabolism / Q000601:surgery*; D000306:Adrenal Cortex Neoplasms / Q000097:blood / Q000378:metabolism / Q000601:surgery; D000307:Adrenal Gland Diseases / Q000097:blood / Q000601:surgery; D000310:Adrenal Gland Neoplasms / Q000097:blood* / Q000378:metabolism / Q000601:surgery*; D000313:Adrenal Medulla; D000328:Adult; D000368:Aged; D000450:Aldosterone / Q000096:biosynthesis; D002277:Carcinoma / Q000097:blood* / Q000378:metabolism / Q000601:surgery*; D003560:Cysts / Q000097:blood / Q000601:surgery; D019314:Dehydroepiandrosterone Sulfate / Q000097:blood*; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000096:biosynthesis; D008297:Male; D008875:Middle Aged; D011184:Postoperative Period
D000450:Aldosterone; D019314:Dehydroepiandrosterone Sulfate; D006854:Hydrocortisone