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Query: UMLS:C0011849 (diabetes)
277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In examination of 123 patients with diabetes mellitus. Itsenko-Cushing disease, Addison's disease, thyrotoxicosis and adiposity there was revealed an increase in the content of the adrenocorticotropic hormone (ACTH) in the blood. Comparison of the ACTH and cortizol concentration in the blood permitted to suppose a different mechanism of the derangements revealed. An increase of the adrenocorticotropic function of the hypophysis in diabetes mellitus, Itsenko-Cushing disease and thyrotoxicosis was accompanied by a rise in the blood cortizol level. A fall of glucocorticoid function of the adrenal glands in Addison's disease and a relative hypocorticism in the patients with adiposity caused a compensatory intensification of the ACTH secretion.
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PMID:[Adrenocorticotropic function of the pituitary gland in endocrine diseases]. 19 3

A rare case of pancreatic exocrine carcinoma with an endocrine component secreting adrenocorticotropic hormone (ACTH) is reported and discussed in relation to other cases previously published. The patient initially presented with a severe form of diabetes, which was treated accordingly. Persistence of hyperglycemia, along with other metabolic alterations and marked hypokalemia, led to the suggestion of abnormal ACTH secretion. In this patient, however, a florid Cushing's syndrome was not observed. The patient also developed hematological alterations, mainly leukopenia and thrombocytopenia, whose origins were unclear. At autopsy, a poorly-defined mass was discovered between the body and tail of the pancreas. Standard histology showed a moderately-differentiated adenocarcinoma. Immunohistochemical analysis of the tumor specimen demonstrated the presence of some neoplastic cells immunoreactive for chromogranin A, neuron-specific enolase and ACTH. These findings are consistent with the existence of an endocrine component within the exocrine carcinoma with ACTH differentiation.
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PMID:Pancreatic exocrine carcinoma producing adrenocorticotropic hormone. 131 74

A 57-year-old obese woman with hypertension, diabetes mellitus, osteoporosis, and a 40-year history of secondary amenorrhea was diagnosed with corticotropin-dependent Cushing's syndrome. Dynamic endocrine testing and radiological evaluation did not reveal definitively the source of the excess corticotropin. Bilateral adrenalectomy was performed with resolution of the signs and symptoms of hypercortisolism. Four years later, the patient was noted to have rising serum corticotropin levels and an enlarging pituitary mass; hyperprolactinemia also was documented. A diagnosis of Nelson-Salassa syndrome was made, and she underwent a transsphenoidal adenomectomy. A histological examination of the specimen revealed two distinct, albeit contiguous, adenomas: a corticotroph adenoma and a lactotroph adenoma. Postoperatively, the serum prolactin and corticotropin levels decreased significantly. Although the stalk section effect resulting from compression by a pituitary adenoma can raise serum prolactin levels, a concurrent lactotroph adenoma should be considered in patients with nonfunctional or functional pituitary adenomas of other types associated with significantly elevated prolactin levels. The mechanisms underlying simultaneous adrenocorticotropic hormone and prolactin excess are discussed.
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PMID:Coexisting corticotroph and lactotroph adenomas: case report with reference to the relationship of corticotropin and prolactin excess. 131 62

We compared insulin-dependent diabetic outpatients with and without retinopathy for plasma indices of hypothalamo-pituitary-adrenal (HPA) axis activity. Diabetic patients with moderate-to-severe retinopathy had significantly higher postdexamethasone plasma levels of adrenocorticotropic hormone than patients with minimal or no retinopathy. However, when duration of diabetes was taken into account this difference was no longer significant. These data suggest that dysregulation of the HPA axis and retinal microvascular complications found in diabetic patients may both be a function of duration of diabetes.
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PMID:Dysregulation of the hypothalamo-pituitary-adrenal axis and duration of diabetes. 166 54

We compared insulin-requiring diabetic outpatients (n = 49) with normal controls (n = 42) for indices of hypothalamic-pituitary-adrenal (HPA) axis activity. Diabetic patients showed significantly elevated 9 a.m. plasma levels of cortisol as well as significantly elevated plasma levels of cortisol and adrenocorticotropic hormone (ACTH) at both 4 p.m. before and 4 p.m. after dexamethasone. Also, there was a significant correlation between postdexamethasone plasma levels of ACTH and duration of diabetes. These results suggest that HPA-axis dysregulation is found among diabetic outpatients. The possible psychiatric implications are discussed.
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PMID:Hypothalamic-pituitary-adrenal axis dysregulation among diabetic outpatients. 215 75

offlated hypoaldosteronism with or without hyperkalemia in patients with diabetes mellitus has been shown to exist occasionally without hyporeninemia. To assess in detail the adrenal function in this disorder, the responses of plasma aldosterone (PA) and its precursor steroids to angiotensin II (AII) infusion and adrenocorticotropic hormone (ACTH) injection were studied in seven patients with asymptomatic normoreninemic hypoaldosteronism (ANH) and 11 age-matched normal subjects. The ANH diabetic patients had, by definition, a low PA level after furosemide (80 mg orally) plus upright posture (4 hours) stimulation, low PA and high plasma renin activity (PRA) increases after the stimulation (a low delta PA/delta PRA ratio), and normokalemia. Plasma inactive renin and the inactive renin/total renin ration were similar in the ANH diabetic patients and in the normal subjects. Under the pre-AII condition, plasma DOC and corticosterone levels tended to be low, and the plasma 18-OHB and PA levels were low in the ANH diabetic patients compared with the normal subjects. The ratio of plasma 18-OHB to PA was similar in the two groups. All infusion produced no increases in plasma 18-OHB and PA in the ANH diabetic patients, whereas the infusion caused dose-dependent increases in these steroids in the normal subjects. Plasma DOC and corticosterone levels remained unchanged during AII infusion in the two groups. ACTH injection produced appropriate PA increases relative to the basal PA in the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Unresponsiveness of plasma mineralocorticoids to angiotensin II in diabetic patients with asymptomatic normoreninemic hypoaldosteronism. 298 80

A case of a 58-year-old woman with an unusual variant of malignant islet-cell tumor showing oncocytic features is described. Using the light microscopy technique, the tumor appeared comprised of solid nests of uniform cells with abundant, eosinophilic cytoplasm and round nuclei with granular chromatin. Ultrastructurally, the cells contained numerous abnormal mitochondria, dilated rough endoplasmic reticulum, and scattered dense-core neurosecretory granules, often associated with cytoplasmic filaments. Tumor cells were focally immunoreactive for insulin, glucagon, and somatostatin and diffusely immunoreactive for alpha 1-antitrypsin as assayed by the avidin--biotin technique. The tumor was immunonegative for human chorionic gonadotropin, gastrin, adrenocorticotropic hormone, and serotonin. The patient exhibited some of the clinical features associated with glucagonoma syndrome, including diabetes mellitus and chronic diarrhea. The tumor behaved in a malignant fashion, with widespread lymphatic involvement and bony metastases at the time of presentation. This report of an oncocytic islet-cell carcinoma supports the concept of oncocytic differentiation in islet-cell tumors in a fashion analagous to oncocytic carcinoids.
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PMID:Functioning oncocytic islet-cell carcinoma. Report of a case with electron-microscopic and immunohistochemical confirmation. 300 44

A sensitive assay method for pituitary cell antibodies (PitCA) was established by a biotin/avidin system using rat pituitary. Results in 24 cases out of 81 insulin-dependent diabetic patients and 10 cases of 21 adrenocorticotropic hormone (ACTH) deficient patients were positive for autoantibodies to anterior pituitary cell cytoplasm. PitCA observed in the sera of insulin-dependent diabetic patients were suspected of being pituitary specific and independent with islet cell antibodies (ICA) and islet cell surface antibodies (ICSA). In the sera of ACTH deficient patients, PitCA were frequently absorbed with liver acetone powder. Populations of insulin-dependent diabetes mellitus (IDDM) are almost equal in males and females. A total of 16 cases out of 21 ACTH deficient patients were female. These results suggest that heterogenous PitCA are involved in the sera of those patients with IDDM and ACTH deficiency.
Diabetes Res 1986 Mar
PMID:Heterogeneity of anterior pituitary cell antibodies detected in insulin-dependent diabetes mellitus and adrenocorticotropic hormone deficiency. 301 44

Autoantibodies for anterior pituitary cell surface membrane (PitCSA) were assayed by immunofluorescence method using GH3 cells (rat GH and prolactin secreting cell) and AtT-20 cells (mouse adrenocorticotropic hormone secreting cell) as antigens. Out of 18 insulin dependent diabetic patients who were positive for antibodies to islet cell surface membrane (ICSA), 3 cases (16.7%) were positive for antibodies to GH3 cells and 12 cases (66.7%) were positive for antibodies to AtT-20 cells. Moreover, out of 18 insulin dependent diabetic patients who were negative for ICSA, 2 (11.1%) and 6 cases (33.3%) were positive for antibodies to GH3 cells and AtT-20 cells, respectively. Among 5 adrenocorticotropic hormone (ACTH) deficient patients, all of the sera were positive for antibodies to AtT-20 cells. These results suggested that PitCSA and ICSA have independent features, though both are closely related, and that PitCSA was one of the significant immunological markers often observed in the sera of the patients with insulin dependent diabetes mellitus (IDDM) and ACTH deficiency.
Diabetes Res 1987 Feb
PMID:Detection of antibodies to anterior pituitary cell surface membrane with insulin dependent diabetes mellitus and adrenocorticotropic hormone deficiency. 303 74

The characterization of the hyperandrogenism of two sisters with type A insulin-resistant diabetes and hirsutism is presented. Testosterone (T) and androstenedione levels were elevated in peripheral serum. These were not markedly affected by infusion of adrenocorticotropic hormone. In patient 1 glucocorticoid suppression decreased T levels by 50% and androstenedione levels by 30% but had no effect on them in patient 2. Estrogen-progestin suppression markedly reduced testosterone levels in both patients. The blood production of T in patient 1 was 0.8 mg/day and in patient 2 was 4.5 mg/day, both of which are elevated. Selective venous catheterization in patient 2 revealed markedly elevated testosterone levels in the ovarian veins, and polycystic ovaries were found at subsequent laparotomy. These endocrine studies have shown that the source of excessive testosterone in these patients is excessive production by the ovaries, and it can be suppressed by oral contraceptives.
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PMID:Characterization of hyperandrogenism with insulin-resistant diabetes type A. 624 39


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