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Magnetic resonance imaging of the adrenal.

Magnetic resonance imaging (MRI) of the adrenals was performed on 50 subjects: 5 normal volunteers, 6 Cushing patients with bilateral adrenal hyperplasia, 14 patients with adrenal adenomas, 3 with adrenal carcinomas, 15 with pheochromocytomas and 7 with metastatic disease to the adrenal. The normal and hyperplastic adrenal glands were imaged in all cases. Using the signal intensity of the adrenals on a T2 weighted image, various forms of adrenal pathology could be differentiated. A ratio of signal intensity of the adrenal mass to the liver was utilized and allowed the differentiation of adrenal adenomas from adrenal carcinomas, pheochromocytomas and metastases. Using the same ratio, metastases could be distinguished from pheochromocytomas as well. MRI appears to be particularly valuable in distinguishing clinically silent adrenal metastases from nonfunctioning adrenal adenomas.

Adenoma↗

Epidemiologic study of adrenal gland disorders in Japan.

A nationwide epidemiologic study of adrenal disorders was performed in Japan. To cover all the hospitals in Japan, the small-scale hospitals were selected at random, and all the large-scale hospitals were taken into the investigation. Disorders investigated in 1997 were relatively rare disorders, as follows: congenital deficiency of adrenal steroidogenic enzyme (deficiency of 21-hydroxylase, 11beta-hydroxylase, 17alpha-hydroxylase, 3beta-hydroxysteroid dehydrogenase or 18-hydroxylase, and lipoid hyperplasia), congenital Addison's disease, pseudohypoaldosteronism, and 11beta-hydroxysteroid dehydrogenase deficiency. The total number of patients with congenital deficiency of adrenal steroidogenic enzyme from 1992 to 1996 was estimated as 1,462, and 87% of these patients suffered from 21-hydroxylase deficiency. The number of patients with congenital Addison's disease (1992-1996) was estimated at 103. About one-fifth of these patients were female. The causes for these female patients are not attributed to the abnormality of DAX-1 gene, because it causes adrenal insufficiency only in males. Almost all (97.8%) of the rare adrenal diseases were under treatment or under observation. The prognosis was thus found to be quite good, although continuation of the treatment was necessary. Disorders investigated in 1998 were relatively major diseases, as follows: primary aldosteronism, Cushing's syndrome, adrenal preclinical Cushing's syndrome, Addison's disease and pheochromocytoma. The total numbers of patients in Japan in 1997 were estimated as 1,450 for primary aldosteronism, 1,250 for Cushing's syndrome, 290 for adrenal preclinical Cushing's syndrome, 660 for Addison's disease, and 1,030 for pheochromocytoma. In conclusion, for the first time, a reliable national estimation of the prevalence of disorders of adrenal hormones was conducted in this study.

Addison Disease↗

Computed tomographic evaluation of the retroperitoneum in infants and children.

With many retroperitoneal diseases in infancy and childhood, computed tomography will give information unavailable by any other single imaging technique. This maxim applies particularly to the adrenal, where the percolating nature of neuroblastoma with its propensity toward spinal involvement is exquisitely shown with computed tomography. Renal neoplasms and trauma can be illustrated effectively with computed tomography, as can pancreatic disease and spinal and paraspinal inflammatory and neoplastic disease. In addition to diagnostic studies, computed tomography may be used as guidance for invasive procedures.

Administration, Oral↗

[Heparin-induced thrombocytopenia complicated by hematoma of the adrenal glands and acute adrenal insufficiency].

Three cases of acute adrenal haemorrhage complicating heparin induced thrombocytopaenia are described. The patients were 2 men and 1 woman, respectively 62, 74 and 76-year old. They all had orthopaedic problems requiring a treatment by subcutaneous calcium heparinate. Thrombocytopaenia occurred 7 to 10 days after the beginning of treatment, with a progressive return to normal of platelet count on stopping heparin. A syndrome suggestive of adrenal failure appeared on the 10 th to 12 th day consisting of abdominal pain, hyperpyrexia, arterial hypotension, asthenia, altered consciousness. Adrenal hormone levels were decreased. Abdominal scanography demonstrated adrenal haemorrhage in 2 patients. The third patient died before further investigations could be carried out. Hormonal replacement therapy brought things back to normal. Six other similar cases have already been published. The heparin induced thrombocytopaenia probably explains the two paradoxes of adrenal haemorrhage complicating heparin therapy: its occurrence in the absence of excessive anticoagulation, and adrenal venous thrombosis. The presence of abdominal pain, fever, collapse, or hyponatraemia with heparin induced thrombocytopaenia should suggest a possible adrenal haemorrhage. Adrenal CT scans should be carried out rapidly, so that hormone treatment can be initiated without delay.

Acute Disease↗

Observations on the fine structure of propylthiouracil-induced "brown degeneration" in the zona reticularis of mouse adrenal cortex.

Propylthiouracil (6-propyl-2-thiouracil), an anti-thyroid agent, was fed to mice in a concentration equal to 0.1% of their diet for periods of 10 and 15 weeks. The cells of the inner zone of the adrenal cortex were examined with the electron microscope. In animals receiving propylthiouracil for ten weeks mitochondria were altered and the smooth endoplasmic reticulum (SER) showed a marked focal proliferation. In contrast to control animals rough endoplasmic reticulum was abundant and was frequently associated with the hyperplastic SER. After 15 weeks these alterations were no longer present but had been replaced by a spectrum of "brown degeneration." The less affected cells were characterized by increased numbers of liposomes and lysosomes and the more affected cells by liposomal and mitochondrial degeneration. These observations emphasize that "brown degeneration" is a true degenerative process and not a spontaneous proliferation of ceroid pigment. It is suggested that the changes described may be directly related to an alteration in cholesterol metabolism.

Adrenal Cortex↗

Acute, massive, haemorrhagic adrenal necrosis experimentally produced by the Shwartzman mechanism in rabbits.

Acute and severe haemorrhagic necrosis of the adrenal was produced experimentally in rabbits by means of intravenous injection of endotoxin after pretreatment by adrenocorticotropic hormone (ACTH) administration. The change occurred mainly in the zona fasciculata of the adrenal cortex, and its pathology was quite similar to that of the Shwartzman reaction. Numerous microthrombi were found in and around the lesion, but no marked changes were seen in other parts of the body. Heparin administration was very effective in preventing the necrosis. The pathogenesis of this lesion was postulated to be a univisceral Shwartzman mechanism in the adrenal. This seems to be a good experimental model for massive haemorrhagic necrosis of the adrenal in man, for example in the Waterhouse-Friderichsen syndrome, the pathogenesis of which has been assumed to involve intravascular clotting. It is suggested that hyperfunction of the adrenal cortex caused by ACTH administration could be a preparative condition for the Shwartzman reaction.

Acute Disease↗

CT in adrenal enlargement due to tuberculosis: a review of literature with five new cases.

Tubercular adrenalitis presents with adrenal enlargement prior to its atrophy and calcification. Imaging modalities like ultrasound, computerized tomography (CT), and magnetic resonance imaging have depicted adrenal enlargement due to various causes. Presented is a clinical-cum-CT review of 14 cases of tubercular adrenal enlargement with addition of five new cases and their CT follow-up.

Addison Disease↗