The aim of our study was to assess the frequency of 21-hydroxylase deficiency, a cause of congenital adrenal hyperplasia (CAH), in incidentally discovered asymptomatic adrenal masses (incidentalomas) and to compare the prevalence of this enzymatic disorder in monolateral (M) and bilateral (B) forms. Twenty-seven patients with incidentalomas (12 M and 15 B) and 16 sex and age matched controls (C) received synthetic adrenocorticotropin (ACTH, 250 μg iv). Plasma 17-OHprogesterone (17-OHP) and cortisol were collected in basal conditions and after 30, 60, 90 minutes. Basal plasma 17-OHP in C [1.25 ± 0.15 (0.61) ng/ml, mean ± SE (SD)] was not significantly different from that in patients with M [0.85 ± 0.13 (0.44) ng/ml] or B [0.94 ± 0.23 (0.90) ng/ml] incidentalomas. After ACTH, 17-OHP levels significantly (p < 0.05) increased in C, in M and B incidentalomas. However, the rise in plasma 17-OHP in C both in terms of peak [2.5 ± 0.28 (1.1) ng/ml] and of AUC values [174 ± 16 (64) ng/ml/min] was significantly lower than that observed in M [peak 6.32 ± 1.66 (5.7) ng/ml, p < 0.01; AUC 410 ± 111 (385.5) ng/ml/min, p < 0.01] and in B [peak 8.84 ± 1.98 (7.65) ng/ml, p < 0.001; AUC 613 ± 149 (579.3), ng/ml/min, p < 0.001] incidentalomas. Individual data indicated that while 17-OHP response to ACTH in C never reached 5 ng/ml (cut-off for normal response), 16 out of 27 patients with incidentalomas (59.2%) exceeded this value. Moreover, the abnormal response was more frequently observed in B (66.6%) than in M (50%) incidentalomas. Basal and stimulated plasma cortisol did not differ among the three groups. In conclusion, our data indicate that in adrenal incidentalomas the endocrine pattern of 21-hydroxylase deficiency is very common and that this enzymatic defect is more frequent in bilateral than in monolateral lesions.
17Hydroxyprogesterone response to ACTH in bilateral and monolateral adrenal incidentalomas
BERNINI, GIAMPAOLO;SALVETTI, ANTONIO
1996-01-01
Abstract
The aim of our study was to assess the frequency of 21-hydroxylase deficiency, a cause of congenital adrenal hyperplasia (CAH), in incidentally discovered asymptomatic adrenal masses (incidentalomas) and to compare the prevalence of this enzymatic disorder in monolateral (M) and bilateral (B) forms. Twenty-seven patients with incidentalomas (12 M and 15 B) and 16 sex and age matched controls (C) received synthetic adrenocorticotropin (ACTH, 250 μg iv). Plasma 17-OHprogesterone (17-OHP) and cortisol were collected in basal conditions and after 30, 60, 90 minutes. Basal plasma 17-OHP in C [1.25 ± 0.15 (0.61) ng/ml, mean ± SE (SD)] was not significantly different from that in patients with M [0.85 ± 0.13 (0.44) ng/ml] or B [0.94 ± 0.23 (0.90) ng/ml] incidentalomas. After ACTH, 17-OHP levels significantly (p < 0.05) increased in C, in M and B incidentalomas. However, the rise in plasma 17-OHP in C both in terms of peak [2.5 ± 0.28 (1.1) ng/ml] and of AUC values [174 ± 16 (64) ng/ml/min] was significantly lower than that observed in M [peak 6.32 ± 1.66 (5.7) ng/ml, p < 0.01; AUC 410 ± 111 (385.5) ng/ml/min, p < 0.01] and in B [peak 8.84 ± 1.98 (7.65) ng/ml, p < 0.001; AUC 613 ± 149 (579.3), ng/ml/min, p < 0.001] incidentalomas. Individual data indicated that while 17-OHP response to ACTH in C never reached 5 ng/ml (cut-off for normal response), 16 out of 27 patients with incidentalomas (59.2%) exceeded this value. Moreover, the abnormal response was more frequently observed in B (66.6%) than in M (50%) incidentalomas. Basal and stimulated plasma cortisol did not differ among the three groups. In conclusion, our data indicate that in adrenal incidentalomas the endocrine pattern of 21-hydroxylase deficiency is very common and that this enzymatic defect is more frequent in bilateral than in monolateral lesions.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
