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At least 127 records · Page 7Linked to original sources
PubMed1992

Macronodular adrenal hyperplasia causing Cushing's syndrome: report of two cases and an overview.

Of the various entities producing adrenal hyperfunction, nodular adrenal hyperplasia is rarely described, however, recent reports have established it as a distinct cause of Cushing's syndrome. Although the etiology of this disease remains uncertain, two distinct forms are recognised, namely: macronodular hyperplasia and micronodular dysplasia. Establishing the diagnosis preoperatively is difficult but essential to ensure the correct treatment is performed. Two cases of macronodular hyperplasia are reported herein followed by a review of the available literature on this subject.

Adrenal Glands↗
PubMed1990

[The indications for the suppression of adrenal hyperfunction in a progressive course of hypertension].

The authors analyze the results of the surgical treatment of patients with progressive essential hypertension (PEN). The treatment involved cryodestruction (adrenalectomy) of the right adrenal and autotransplantation of the left adrenal on the vascular peduncle into the transverse mesentery. Before the operation the data on water-salt homeostasis, central and cerebral hemodynamics and on the renin-angiotensin-aldosterone system attested to PEH. 1 to 3 years after the operation natriuresis was revealed (210% of the initial value), as were a decrease of the total peripheral vascular resistance, amelioration of the cerebral blood flow and peripheral blood aldosterone lowering from 246 +/- 17 to 90 +/- 14 sh/ml.

Adrenal Glands↗
PubMed1974

A functioning black adenoma of the adrenal cortex: a clinico-pathological entity.

A 25-year-old woman is described who had suspected hyperfunction of the adrenal cortex. She complained of fatiguability, excessive hair growth, and attacks of swelling of the face, hands, and ankles. Moreover she had a ;moon face', hypertension, a ;buffalo hump', and livid striae of the loins and hypogastrium. Adrenal function tests yielded values which could not be clearly interpreted. Operation showed a ;black adenoma' of the adrenal cortex on the right side. As far as it is known this is the first published case of this extremely rare lesion which was operated upon and caused nearly complete remission of the endocrine disturbance.

Adenoma↗
PubMed1981

[Associated role of surgery and antimitotic o, p'-DDD treatment in hyperfunctioning adrenal cancers with diffuse metastases].

The observation of two cases of hyperworking corticosuprarenal carcinomata with diffuse metastases, has induced the authors to examine this problem on the base of the most actual bibliography of the last years. They explain in detail the 2 cases, that are a feminizing tumor in a 55 years old man and a Cushing syndrome with hypertension in a 18 years old women. The peculiar characteristic are in the first case the clinical rareness of feminizing syndrome from suprarenal carcinoma and in the second case the histopathological particularity of splenic metastases. In regard to therapy for this particular tumor, the AA. incline for the surgical removal of tumor, that can induce, in the most favourable cases, a partial or total reduction of endocrine symptomatology and for the giving in great doses of o,p'-DDD from the immediate post-operating period.

Adolescent↗
PubMed1992

Endocrinopathies of hyperfunction: Cushing's syndrome and aldosteronism.

Increased function of the adrenal cortex is a normal response in times of physiologic and psychologic stress. Adrenal cortical secretions (e.g., glucocorticoids, aldosterone) orchestrate a multitude of internal processes aimed at maintaining homeostasis and psychologic integrity. Many patients admitted to a critical care unit will manifest some increase, even minor, in adrenal function. However, excessive secretions of these hormones can have a lethal effect of fluid and electrolyte balance, energy metabolism, and immune function. Cushing's syndrome denotes a disorder characterized by increased circulating levels of glucocorticoids (primarily cortisol). An easily recognizable disorder, it may arise from pathology of the adrenal cortex or the anterior pituitary glands, ectopic secretions from a nonendocrine tumor, or from excessive doses of exogenously administered glucocorticoids. Cushing's syndrome is rarely an admitting diagnosis to critical care but is a disorder that can seriously affect recovery from coexisting illnesses if not treated. Aldosteronism, although rare, will often be diagnosed after admission to a critical care unit for management of troublesome hypertension, hypokalemia, congestive heart failure, and various dysrhythmias. Suspicion of the diagnosis should always arise when these manifestations occur, particularly when hypokalemia is refractory to potassium supplementation. Without timely diagnosis and treatment, these patients will succumb to lethal dysrhythmias.

Adrenocortical Hyperfunction↗
PubMed1987

Familial hypersecretion of adrenal androgens transmitted as a dominant, non-HLA linked trait.

Clinical evidence of adrenal androgen hyperfunction (premature pubarche, hirsutism, amenorrhea) occurred in the studied proband, her mother, maternal aunt (twin sisters), and maternal great-grandmother. The basal levels of androgen in the first three were variably elevated. In all the members of this family who were tested, the response of 17-hydroxyprogesterone and progesterone to adrenocorticotropic hormone stimulation was either normal or of the type seen in heterozygotes for congenital adrenal hyperplasia due to 21-hydroxylase deficiency. Of particular importance is the fact that neither the proband nor her mother or maternal aunt had the type of response seen in homozygotes presenting the attenuated form of congenital adrenal hyperplasia. The disorder appears to be a familial condition resulting in excessive levels of adrenal androgens beginning during childhood years, causing hirsutism and amenorrhea and interfering with normal pubertal and adult ovarian function. Glucocorticoid therapy suppresses adrenal androgen levels; in two individuals, conception occurred twice in each during such treatment in otherwise amenorrheic individuals. The pattern of transmission of the disorder appears to be either autosomal or X-linked dominant, and not linked to the homologous leucocytic antibodies (HLA) region of the sixth chromosome.

Adolescent↗
PubMed1978

The diagnosis of Leydig cell tumors in childhood.

We report the clinical and hormonal findings in two boys with isosexual precocity secondary to Levdig cell tumor of the testis. The hormonal profile at the initial evaluation was quite different in the two cases suggesting differences in steroid biosynthesis by the tumors. These differences indicate that a dexamethasone suppression test may be required to differentiate between Leydig cell tumors and congenital virilizing adrenal hyperplasia with adrenal rest tissue located within the testes.

Adrenocortical Hyperfunction↗
PubMed1978

Preadolescent and adolescent endocrinology: physiology and physiopathology. II. Hormonal changes during abnormal pubertal development.

Based on the knowledge of the physiology of regulation of gonadotropins and gonadal steroids, basal levels of these hormones might be indicative of the etiologic factors of abnormal pubertal development. In addition, stimulatory tests may help in the diagnosis of such conditions. It is interesting that the pubertal maturation of the adrenal cortex is independent of the hypothalamic-pituitary-gonadal axis. The role of the adrenal cortex for the pubertal development remains questionable: adrenal androgens are low in isosexual precocious puberty, low in delayed adolescence, and normal in hyper- or hypogonadotropic hypogonadism. The importance of this role is doubled in congenital virilizing adrenal hyperplasia. When the disease is untreated, although adrenal androgens in excess advance bone age and hypothalamic maturation, girls remain prepubertal. When the therapeutic control is good, normal puberty occurs. The action of the adrenal androgens on growth and puberty remains to be determined.

Adolescent↗
PubMed1989

Hypercortisolism among socially subordinate wild baboons originates at the CNS level.

Recent studies suggest that the hypercortisolism and dexamathasone resistance of depression arise, at least in part, at the level of the brain, ie, cortisol-releasing factor (CRF) and/or other corticotropin-secretagogues are hypersecreted. This article suggests a similar cause of the hypercortisolism of social subordinance. Two troops of wild olive baboons, living freely in the Serengeti Ecosystem of East Africa, have been under long-term study. Consistently, in stable dominance hierachies, subordinate males are hypercortisolemic relative to dominant animals. Furthermore, hypercortisolemic males are dexamethasone resistant. There are no rank-related difference in cortisol clearance or adrenal sensitivity to corticotropin, suggesting a pituitary and/or neural locus of the hypercortisolism. Subordinate males were shown to secrete less corticotropin in response to a CRF-challenge than did dominant males. Following the logic used in similar studies with depressives, if subordinate males were hypercortisolemic despite decreased pituitary sensitivity to CRF, then this implies that the hyperactivity of the adrenocortical axis is driven at the level of the brain. Furthermore, subordinate males were hyporesponsive to CRF after administration of metyrapone, which blocks cortisol secretion and disinhibits the pituitary from feedback inhibition. Thus, the pituitary appears to have lost sensitivity to CRF itself in these low-ranking males. These observations are interpreted in light of behavioral data suggesting that these subordinate males are under sustained social stress.

Adrenocortical Hyperfunction↗
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↗
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↗