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Results for “Adrenocortical Hyperfunction”

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At least 163 records · Page 9Linked to original sources
PubMed1979

ACTH-secreting carcinoma of the breast.

We report a case of ACTH-secreting carcinoma of the breast. Membrane-bound secretory granules were seen within the cancer cells electron microscopically. Cytoplasmic granules reacting immunochemically to anti-ACTH antisera were seen on light microscopy. Breast cancers have been shown to secrete calcitonin, parathyroid hormone, human chorionic gonadotropin, and norepinephrine in addition to ACTH. This suggests either the presence of neuroendocrine cells in the breast as a source of such neoplasms, as in the lung, or genomic derepression during neoplastic transformation.

Adrenocortical Hyperfunction↗
PubMed1981

Ectopic adrenocorticotrophic (ACTH) syndrome and small cell carcinoma of the lung-assessment of clinical implications in patients on combination chemotherapy.

Small cell carcinoma of the lung is the tumor most commonly associated with ectopic ACTH production and hypercortisolism. The relationship between this paraneoplastic endocrine syndrome and the clinical course of the tumor is examined in this review of patients with the ectopic ACTH syndrome and small cell carcinoma seen at The Johns Hopkins Oncology Center between 1973 and 1979. Five of 157 (3.2%) patients with small cell carcinoma were clinically diagnosed as having the ectopic ACTH syndrome. The onset of this endocrine syndrome appeared to coincide with a more aggressive phase of the course of small cell carcinoma. Further analysis of these cases suggests that the development of the ectopic ACTH syndrome may reflect changes in cell populations within the tumor and/or alterations in tumor behavior with time and perhaps with the effects of drug therapy.

ACTH Syndrome, Ectopic↗
PubMed1995

Adrenocortical carcinoma. A clinical study and treatment results of 52 patients.

BACKGROUND: Adrenocortical carcinoma is a rare tumor with a poor prognosis. This work was aimed at analyzing the clinical outlook and treatment results of 52 patients with this disease. METHODS: This study included patients with adrenocortical carcinoma referred to the Department of Endocrinology at the Center of Postgraduate Medical Education (Warsaw, Poland) during the last 30 years. In 11 patients, the adrenal tumor was found incidentally by ultrasonographic scan. Hormonal examinations made it possible to define the endocrine activity of the tumors, whereas imaging techniques helped to determine their staging. Forty-eight patients underwent surgery, and 36 of them received mitotane. This drug was administered to 26 patients for a range of 10 months to 10 years; 13 patients received mitotane immediately after the operation, and 13 others after a delay. The patients with severe hypercorticism were pretreated before surgery with aminoglutethimide and mitotane. RESULTS: The study comprised 10 men and 42 women; hormonally active tumors were diagnosed in 39 of them. Cushing's syndrome was the most frequent entity. At diagnosis, 17 cases were classified as localized disease, 15 as regional disease, and 20 as distant disease. Pretreatment with the inhibitors of steroidogenesis improved the survival perspectives in the early postoperative period. As of this writing, there were 12 survivors in the group of 26 patients treated by surgery and long term mitotane therapy and only 2 survivors of 7 patients treated with surgery only. CONCLUSIONS: Surgery with immediate adjuvant long term mitotane administration was the most effective form of therapy for patients with adrenocortical carcinoma.

17-Hydroxycorticosteroids↗
PubMed1976

Relationship between the adrenal cortex and thymic involution in "lethargic" mutant mice.

To determine if the adrenal gland plays a role in the thymic involution which occurs spontaneously in "lethargic" mutant mice, three different studies were made. Morphological studies were made first to determine if there was an indication of histological changes in the adrenal glands. Next, serum levels of corticosterone were measured by radioimmunoassay. Finally, mice were unilaterally adrenalectomized to see if such treatment would improve various symptoms of "lethargic" mutants. Results of the studies showed that lipid granules in the cortical cells of "lethargic"mutants were greatly reduced in number during the time of spontaneous thymic involution, and the mutant mice had a significantly higher level of serum corticosterone than the normal controls. Mutant mice unilaterally adrenalectomized at 15 days of age showed a marked improvement in their condition and their mortality rate decreased. It is concluded that spontaneous thymic involution of "lethargic" mutants is probably associated with adrenocortical hypersecretion.

Adrenal Cortex↗
PubMed1977

Hypergonadotrophic male pseudohermaphroditism due to complete 17-alpha-hyroxylase deficiency.

This is a case report of a 43 years old phaenotypic female (karyotype 46 XY) with congenital adrenal hyperplasia and male pseudohermaphroditism presenting with severe hypertension and hypokalaemic alkalosis. Evaluation of the steroid biosynthesis of the adrenals as well as of the intraabdominal testes demonstrated a severe degree of 17-alpha-hydroxylase deficiency in this patient. This defect was associated by a complete lack of deoxycortisol and cortisol as well as of testicular testosterone synthesis, and by an overproduction of DOC and corticosterone. Sruvival of the patient in spite of severe cortisol deficiency was due to the glucocorticoid activity of corticosterone. This compound and DOC account also -- due to their mineralocorticoid properties -- for the hypertensive state of this male pseudohermaphrodite.

Adrenocortical Hyperfunction↗
PubMed1977

Application of glass capillary gas chromatography to the study of urinary steroid excretion in normal children and in patients with various endocrinopathies.

A method of gas chromatography on glass capillary columns (g. c. c. c.) is presented which allows the determination of 26 urinary C19 and C21 steroid metabolites in one procedure. Hundredthirtyseven normal individuals of both sexes from 6 months through 32 years of age were studied regarding their urinary steroid patterns. These were compared to the excretion patterns of patients with congenital adrenal hyperplasia before and during treatment and of a child with virilizing adrenal carcinoma. From the results it is concluded that g. c. c. c. may be considered a valuable tool in the study of steroid production and metabolism.

Adolescent↗
PubMed1996

Persistent and recurrent hypercortisolism after transsphenoidal surgery for Cushing's disease.

After transnasal operations in Cushing's syndrome persisting hypercortisolism either due to negative pituitary exploration or due to subtotal tumor removal, and recurrence of the disease after successful surgery still are challenging. We report on the therapeutic failures among 310 consecutive patients who underwent primary transsphenoidal microsurgery for Cushing's disease. In 287 patients an ACTH-producing pituitary adenoma could be detected (finding rate: 92.6%). In 264 cases remission of hypercortisolism could be attained (remission rate with adenoma 92.0%, for the whole series of primary operations 85.2%). In 23 patients no adenoma could be found despite extensive pituitary exploration (7.4%). Here, we will focus on the management of the 23/287 patients with persistent hypercortisolism after transnasal tumor operation (8.0%) and those 29 cases of the 264 patients with a remission who developed a recurrence of hypercortisolism (11.0%). In recurrent hypercortisolism we recommend transsphenoidal reoperation even when no tumor is visible in MRI. Seventeen of 24 reoperations in recurrent Cushing's disease were successful (70.8%). In persistent hypercortisolism we perform a reoperation during the same hospital stay. Nine of 16 early reoperations led to remission of hypercortisolism (56.3%). If transsphenoidal reoperation fails we indicate radiation therapy of different modalities depending on the extension and location of the tumor remnants. Bilateral adrenalectomy is proposed by us only if all other therapeutic measures failed.

Adrenalectomy↗
PubMed1983

Morphometric investigations into the mechanism of the compensatory hypertrophy of the rat adrenal zona fasciculata after unilateral adrenalectomy.

Compensatory hypertrophy of the remaining gland in unilaterally adrenalectomized rats was investigated by morphometric techniques. It was observed that compensatory adrenal growth occurred in both dexamethasone-treated and hypophysectomized rats, receiving maintenance doses of ACTH. However, it was only half that found in intact animals. These results support the view that activation of the hypothalamo-hypophyseal axis is not the unique mechanism underlying adrenal compensatory hypertrophy in the rat.

Adrenal Glands↗
PubMed1977

Use of 131I-19-cholesterol in functional dynamic studies of the adrenals in vivo. II. Clinical application.

Functional dynamic studies of the adrenal in vivo employing 131I-19-cholesterol were carried out as a further screening test, according to the method previously described (Pavonia and Magrini, 1977), on seven patients in whom hyperadrenocorticism was suspected on the basis of clinical symptoms. The data obtained in basal conditions, under ACTH stimulation, and under dexamethasone suppression, compared with each other and supported by the results of conventional examinations, demonstrate that the quantitative information provided by this radioisotope test is correlated with the functional state of each adrenal, thus confirming the potential value of the method for diagnostic purposes. The functional dynamic test proposed does not require a higher dose of tracer than morphologic studies and the radiation risk (approximately 2.5 rad to the ovaries or gonads) seems acceptable in adult subjects.

Adenoma↗
PubMedDate not supplied

Point mutations of ras genes in human adrenal cortical tumors: absence in adrenocortical hyperplasia.

Point mutations of ras genes (K-, H-, and N-ras) at codons 12, 13, and 61 and of the Gi2 alpha gene at codons 179 and 205, were studied in 56 primary adrenal cortical tumors and 6 adrenal cortical hyperplasias. Of 56 tumors, 24 were carcinomas and 32 were benign. The 24 carcinomas and 20 of the benign tumors were from American patients; the 12 remaining adenomas were from Japanese patients. Of the benign tumors 12 were cortisol-producing adenomas, 15 were aldosterone-producing adenomas, 3 were nonfunctioning adenomas, and 2 were adenomas that produced a virilizing syndrome. Tumor DNA obtained from archival formalin-fixed, paraffin-embedded tissue or fresh frozen tissue was amplified by polymerase chain reaction; and point mutations were detected by sequence-specific oligonucleotide hybridization. Activating ras mutations were found in 7 of 56 (12.5%) of all tumors: 3 of 24 (12.5%) carcinomas and 4 of 32 (12.5%) adenomas. Of adenomas from an American population, 4 of 20 (20%) exhibited positive ras mutations, whereas none was present in the Japanese tumors. All mutations detected were adenine to guanine transitions at the second position of N-ras codon 61, resulting in a conversion from glutamine to arginine. No mutations were found in K-ras or H-ras genes. Furthermore, no mutations of the Gi2 alpha gene were identified. These findings demonstrate that N-ras mutations at codon 61 may contribute to the genesis of both benign and malignant human adrenal cortical tumors. Finally, no mutations of the ras or Gi2 alpha genes were identified in hyperplastic adrenocortical tissues.

Adenoma↗
PubMed1977

Congenital adrenal hyperplasia: renin and steroid values during treatment.

Plasma renin activity (PRA), aldosterone (Aldo), 17alpha-hydroxyprogesterone (17-OHP) and testosterone (T), together with urine sodium, pregnanetriol, 17-oxosteroids and the 11-oxygenation index (11-OH) were estimated in 23 patients (age 5.7--18 yrs.) with congenital adrenal hyperplasia (CAH) due to 21-hydroxylase deficiency during glucocorticoid treatment. Elevated PRA levels (1400--17200 ng Al/l/hr) were found in 13 out of 15 patients with a history of salt loss. Three non-salt losers showed high PRA levels and in the remaining 5 the levels were in the upper normal range (540--900 ng Al/l/hr). Plasma Aldo levels were normal (25--620 pmol/l) in 18 patients and slightly elevated (690--2360 pmol/l) in 5. While these results indicate persistent impairment of sodium homeostasis in CAH patients, no significant correlations between log. PRA, log. Aldo and urinary sodium excretion were found. Mid-day 17-OHP levels ranged from 9 to 117 nmol/l and T from 0.3 to 18.0 nmol/l. Neither the 17-OHP nor the T results correlated well with the clinical assessment of therapeutic control. The results of the urinary steroid determinations showed better agreement with the clinical assessment of treatment and the 17-oxosteroid, pregnanetriol and 11-OH index results appeared to be better discriminants between good and poor control. Twelve of the patients with a history of early salt loss were reinvestigated after one month's treatment with oral 9 alpha-flurohydrocortisone (0.05 mg/day). PRA was reduced in 7 patients and 17-OHP fell in 10 patients. No consistent changes were found in Aldo, T, or urinary sodium and steroid excretion during this low-dose mineralocorticoid treatment.

17-Ketosteroids↗
PubMed1976

A test for heterozygocity of 21-hydroxylase deficiency: preliminary report.

The urinary excretion of steroids was studied in 8 parents of children with congenital adrenal hyperplasia due to 21-hydroxylase deficiency of the simple virilizing and of the salt-losing type. Eight parents of normal children served as controls. 24-hour urines before and after the injection of 40 IU of ACTH were fractionated using gas liquid chromatography on glass capillary columns. Before stimulation no excretion of pregnanetriolone was detected in heterozygous and in normal parents. Following ACTH only heterozygotes showed an excretion of pregnanetriolone in the urine. This averaged 289 mug per 24 h. Employing gas liquid chromatography on glass capillary columns heterozygous carriers of congenital adrenal hyperplasia due to 21-hydroxylase deficiency may reliably be detected by their increased urinary excretion of pregnanetriolone following ACTH.

Adrenocortical Hyperfunction↗