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At least 739 records · Page 41Linked to original sources
PubMed1997

Functional adrenocortical adenoma in a case with B cell chronic lymphoproliferative disorder.

We describe a B cell chronic lymphocytic leukemia/lymphoma (B-CLL) patient with an adrenocortical adenoma. He was treated initially with oral cyclophosphamide and prednisolone for 2 months, followed by low-dose prednisolone for an additional 2 years, which resulted in the prompt disappearance of CLL cells. After a period of 2 years without therapy, a functional adrenocortical adenoma was found. After adrenalectomy, the CLL cells rapidly increased. Progression of the disease and clinical-hematological relapse was well controlled by low doses of steroids alone, and the patient's condition stabilized. Considering the recent data that corticosteroids can induce apoptosis of CLL cells, the above clinical course suggests that augmented glucocorticoid production from the tumor may have suppressed disease progression.

Adenoma↗
PubMed2004

Impaired cerebral autoregulation in patients with malignant hypertension.

BACKGROUND: In patients with a malignant hypertension, immediate parenteral treatment with blood pressure-lowering agents such as intravenous sodium nitroprusside (SNP) is indicated. In this study, we evaluated static and dynamic cerebral autoregulation (CA) during acute blood pressure lowering with SNP in these patients. METHODS AND RESULTS: In 8 patients with mean arterial pressure (MAP) >140 mm Hg and grade III or IV hypertensive retinopathy at hospital admission, middle cerebral artery blood velocity (MCA V) and blood pressure were monitored. Dynamic CA was expressed as the 0.1-Hz MCA V(mean) to MAP phase lead and static CA as the MCA V(mean) to MAP relationship during SNP treatment. Eight normotensive subjects served as a reference group. In the patients, the MCA V(mean) to MAP phase lead was lower (30+/-8 degrees versus 58+/-5 degrees , mean+/-SEM; P<0.05), whereas the transfer gain tended to be higher. During SNP treatment, target MAP was reached within 90 minutes in all patients. The MCA V(mean) decrease was 22+/-4%, along with a 27+/-3% reduction in MAP (from 166+/-4 to 121+/-6 mm Hg; P<0.05) in a linear fashion (averaged slope, 0.82+/-0.15% cm x s(-1) . % mm Hg(-1); r=0.70+/-0.07). CONCLUSIONS: In patients with malignant hypertension, dynamic CA is impaired. An MCA V(mean) plateau was not detected during the whole SNP treatment, indicating loss of static CA as well. This study showed that during the whole rapid reduction in blood pressure with SNP, MCA V(mean) decreases almost one on one with MAP.

Adrenal Cortex Hormones↗
PubMed2005

Expression profiles for steroidogenic enzymes in adrenocortical disease.

CONTEXT: Excess production of aldosterone or cortisol has profound effects on cardiovascular function and impacts other major organ systems. The mechanisms leading to the autonomous hypersecretion of aldosterone or cortisol in aldosterone-producing adenoma (APA) or cortisol-producing adenoma (CPA) are unknown. OBJECTIVE: The objective of this study was to compare the expression profiles of several steroid-metabolizing enzymes and transcription factors from normal adrenal (NA), APAs, and CPAs. DESIGN: RNA from NAs, APAs, and CPAs were analyzed by microarray and real-time RT-PCR. SETTING: This study was performed at academic research laboratories. PATIENTS: At least nine normal controls and 12 patients with APA or CPA were studied. INTERVENTION: There was no intervention procedure. MAIN OUTCOME MEASURE: The main outcome measure was the expression of steroidogenic enzymes in adrenocortical disease. RESULTS: A microarray indicated a greater than 3-fold increase in the expression of CYP11B2 (aldosterone synthase) in APA, whereas 11beta-hydroxysteroid dehydrogenase type 2 (HSD11B2) and HSD17B1 had greater than 3-fold increases in expression in CPA compared with NA. Real-time RT-PCR showed that APAs produced higher levels of HSD3B2, CYP21 (21-hydroxylase), and CYP11B2 mRNA, whereas CPAs produced higher levels of CYP11A (cholesterol side-chain cleavage), CYP17 (17alpha-hydroxylase/17-20 lyase), HSD3B2, and CYP11B1 (11beta-hydroxylase) mRNA compared with normal adrenal. Steroidogenic factor-1, DAX-1 (dosage-sensitive sex reversal, adrenal hypoplasia congenita, critical region on the X chromosome gene 1), and GATA-6 were expressed at higher levels in APAs and CPAs, whereas NURR1 was expressed at higher levels in APAs than in CPAs or NAs. CONCLUSION: Elevated production of aldosterone in APAs and of cortisol in CPAs is associated with increased expression of enzymes needed for corticosteroid production along with alterations in transcription factors that enhance the expression of steroid-metabolizing enzymes.

Adenoma↗
PubMed1982

Steroid enzyme activities in extraadrenal pheochromocytomas.

The adrenal medulla and tumors derived from it have been shown to be capable of converting radioactive steroid intermediates into glucocorticoid end products in vitro. This capacity for partial steroid synthesis was explored in two large extraadrenal pheochromocytomas and compared to the results of parallel studies with intraadrenal pheochromocytomas and adrenal cortex; in one experiment, all three types of tissue were obtained from a single patient and studied simultaneously. Slice preparations of extraadrenal pheochromocytoma transformed 14C-labeled pregnenolone (3 beta-hydroxypregn-5-en-20-one) into corticosterone and cortisol. Incubations of subcellular fractions demonstrated that, as in the adrenal cortex and intraadrenal chromaffin tissue, delta 5-3 beta-hydroxysteroid dehydrogenase-isomerase, 17 alpha-hydroxylase, and 21-hydroxylase activities in extraadrenal pheochromocytomas were associated with the microsomes and 11 beta-hydroxylase was associated with the mitochondria, where metyrapone was an effective inhibitor, these findings tend to dissociate steroid-metabolizing activity in the adjacent chromaffin tissue perfused by glucocorticoid intermediates in high concentrations.

Adenoma↗
PubMed1998

Variable expression of the V1 vasopressin receptor modulates the phenotypic response of steroid-secreting adrenocortical tumors.

We studied the putative role of the vasopressin receptors in the phenotypic response of steroid-secreting adrenocortical tumors. A retrospective analysis of a series of 26 adrenocortical tumors responsible for Cushing's syndrome (19 adenomas and 7 carcinomas) showed that vasopressin (10 IU, i.m., lysine vasopressin) induced an ACTH-independent cortisol response (arbitrarily defined as a cortisol rise above baseline of 30 ng/mL or more) in 7 cases (27%). In comparison, 68 of 90 patients with Cushing's disease (76%) had a positive cortisol response. We then prospectively examined the expression of vasopressin receptor genes in adrenocortical tumors of recently operated patients (20 adenomas and 19 adrenocortical carcinomas). We used highly sensitive and specific quantitative RT-PCR techniques for each of the newly characterized human vasopressin receptors: V1, V2, and V3. The V1 messenger ribonucleic acid (mRNA) was detected in normal adrenal cortex and in all tumors. Its level varied widely between 2.0 x 10(2) and 4.4 x 10(5) copies/0.1 microgram total RNA, and adenomas had significantly higher levels than carcinomas, although there was a large overlap. Among the 6 recently operated patients who had been subjected to the vasopressin test in vivo, the tumor V1 mRNA levels were higher in the 4 responders (9.5 x 10(3) to 5.0 x 10(4)) than in the 2 nonresponders (2.0 x 10(2) and 1.8 x 10(3)). One adenoma that had a brisk cortisol response in vivo, also had in vitro cortisol responses that were inhibited by a specific V1 antagonist. In situ hybridization showed the presence of V1 mRNA in the normal human adrenal cortex where the signal predominated in the compact cells of the zona reticularis. A positive signal was also present in the tumors with high RT-PCR V1 mRNA levels; its distribution pattern was heterogeneous and showed preferential association with compact cells. RT-PCR studies for the other vasopressin receptors showed a much lower signal for V2 and no evidence for V3 mRNA. We could not establish whether the V2 mRNA signal observed in normal and tumoral specimens was present within adrenocortical cells or merely within tissue vessels. We conclude that the vasopressin V1 receptor gene is expressed in normal and tumoral adrenocortical cells. High, and not ectopic, expression occurs in a minority of tumors that become directly responsive to vasopressin stimulation tests.

Adenoma↗
PubMed1993

Significance of steroidogenic enzymes in the pathogenesis of adrenal tumour.

We examined both activities and amounts of steroidogenic cytochrome P-450s at the posttranslational protein level and steroid contents in the adrenocortical adenoma from patients with primary aldosteronism and Cushing's syndrome. Aldosterone synthase cytochrome P-450 (human P-450aldo) was detected in the tumour portion of aldosterone-producing adenoma, but not in the normal control adrenals, at the protein level. Neither the activities nor the amounts of other P-450s in the tumour portion of aldosterone-producing adenoma were significantly different from those in the non-tumour portion in the adenoma and the normal control adrenals. The aldosterone content was significantly elevated, while the androstenedione content was significantly decreased in the tumour portion of the adenoma compared with that in the normal control adrenals. In Cushing's syndrome, both the activities and amounts of P-450(17 alpha) and P-450c21 were significantly elevated in the tumour portion compared with the non-tumour portion of the adenoma and the normal control adrenals, while those of P-450scc and P-450(11 beta) in the tumour portion were not significantly different from the normal control adrenals. The cortisol content was significantly elevated, while the amounts of aldosterone and 18-hydroxydeoxycorticosterone in the tumour portion of the adenoma were significantly decreased compared with those in the normal control adrenals. These results demonstrate that overexpression of P-450aldo in aldosterone-producing adenoma, and those of P-450(17 alpha) and P-450c21 in cortisol-producing adenoma may play some role in the pathogenesis of primary aldosteronism and Cushing's syndrome, respectively.

Adenoma↗