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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 cyclic excess of cortisol secretion was detected in a patient with diabetes insipidus and diabetes mellitus. The cycles of hypercortisolism were of 7 days' duration, but during the nadir of these cycles urinary excretion of corticosteroids and 17-ketosteroids was within the normal range. The radiological appearance of the sella turcica was normal; however, computerized axial tomography of the head revealed a small tumor immediately superior to the sella turcica. At operation a small chromophobe adenoma superior to the diaphragma sellae and involving the hypophysial stalk was partially resected. Postoperatively, the patient continued to have 7-day cycles of increased corticosteroid excretion, but the amounts excreted were less than they had been preoperatively. Other patients have been described in whom Cushing's disease has been due to cyclic hypercortisolism. These cycles have been remarkably regular in individual patients, but of variable duration in different patients. Furthermore, cyclic hormonogenesis probably occurs in a variety of endocrinopathies. (Neurosurgery, 5: 598--603, 1979).
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PMID:Cushing's disease with cyclic hormonogenesis and diabetes insipidus. 53 67

A study was made of 149 patients with various endocrine diseases, and 30 healthy persons. Despite the sharply increased initial level of growth hormone, somatotropic function of the adenohypophysis was considerably depressed. In patients with hypophysial, cerebral, and somatogenic nanism somatotropic function of the hypophysis proved to be lowered. In diabetes mellitus of moderate severity without any vascular affections with the normal initial blood somatotropin level reaction to insulin hypoglycemia was sharply diminished. Persons suffering from prediabetes displayed a tendency to the change of the somatotropic function of the hypophysis. With increasing adiposity there is a reduction of the initial level of blood growth hormone and of the somatotropic activity of the hypophysis in Itsenko-Cushing's disease and thyrotoxicosis was apparently connected with disturbances of the hypothalamo-hypophysial interrelations.
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PMID:[Somatotropic function of the hypophysis in endocrine diseases]. 60 Sep 25

The content of thyrotropic hormone of the hypophysis (by radioimmunological method) and the level of thyrotropic hormones in the blood plasma were studied in 178 patients with various endocrine pathology (thyrotoxicosis, hypothyroidism, diabetes mellitus, Itsenko-Cushing disease, Addison's disease, adiposity). Healthy persons (33) served as control. Thyrotropic function of the hypophysis proved to be decreased in thyrotoxicosis, diabetes mellitus, adiposity, Itsenko-Cushing disease. Comparison of the plasma level of thyrotropin and thyroid hormones led to a supposition on a different mechanism of the detected changes. A marked intensification on the thyrotropic function of the hypophysis was observed in primary hypothyroidism. A tendency to increase of thyrotropin discharge was noted in the patients suffering from thyrotoxicosis given antithyroid treatment and in Addison's disease.
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PMID:[Thyrotropic function of the hypophysis in endocrine diseases]. 81 31

According to a theory of the authors both senile osteoporosis and pathologic osteoporoses (rheumatic, in diabetes, bronchial asthma, pulmonary emphysema, portal hypertension and Cushing's disease) are due to disturbances of the circulation of the blood in bone. Every type of stasis in the sinusoids, be it due to reduced arterial supply or venous stasis or to a reduction of extravascular fluid-pressure will provoke an increase in osteoclastic activity and thus osteoporosis.
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PMID:[Osteoporosis -- due to reduced blood circulation of bone (author's transl)]. 121 86

We experienced 41 cases of Cushing's syndrome (12 males and 29 females, 15 years old - 65 years old) during the last 20 years. These included 20 patients with unilateral adrenal adenoma (Cushing's syndrome), 19 patients with bilateral adrenal hyperplasia (Cushing's disease), one patient with adrenal carcinoma and one patient with primary adrenocortical nodular dysplasia (PAND). Moreover, these cases included some special ones, i.e. 5 cases with destructive thyroiditis after treatment, 2 cases with aggravation of arthritis after treatment, a case of Carney's complex with PAND, one case with paradoxical response to dexamethasone, and one case combined with empty sella syndrome. The most specific clinical signs were moon face (95% occurrence), hypertension (95%) and subcutaneous bruising (80%). Other significant signs were eye edema (66%), buffalo hump (68%), subcutaneous purpura (63%) and osteoporosis (49%). Skin striae was not a common sign in our cases (41%). Renal stone was observed in only 20% of our patients but was a significant sign in this syndrome. There was no difference in the occurrence of each clinical sign between Cushing's syndrome and Cushing's disease. The elevation of white blood cell count (WBC) and serum sodium, a decrease of serum potassium, and a decrease of reabsorption of phosphate (%TRP) were observed. Thyroid-stimulating hormone (TSH) and human growth hormone (HGH) were suppressed in patients with Cushing's syndrome and patients with Cushing's disease. These results were consistent with those of previous reports. However, luteinizing hormone (LH), follicle-stimulating hormone (FSH) and prolactin (PRL) were high in those patients with Cushing's syndrome and those with Cushing's disease. Oral glucose tolerance test was carried out in 34 patients before and after treatment. Thirty-one percent of those had diabetes mellitus and 26% had impaired glucose tolerance (IGT). The response of IRI in this test was high in patients with Cushing's syndrome and patients with Cushing's disease, and decreased 4 weeks after treatment in those with Cushing's syndrome but remained high in those with Cushing's disease. Plasma ACTH level and urinary 17-OHCS excretion were significantly higher in Cushing's disease than in Cushing's syndrome. During an 8mg-high-dose dexamethasone suppression test, urinary 17-OHCS excretion in 13 of 14 patients with Cushing's disease (93%) was suppressed by more than 50% of baseline on the second day of testing. However, all of 18 patients with Cushing's syndrome, who had an 8mg-dexamethasone suppression test, failed to suppress urinary 17-OHCS by 50% of baseline.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Forty-one cases of Cushing's syndrome: a comparison between Cushing's syndrome (adrenal adenoma) and Cushing's disease (adrenal hyperplasia)]. 163 31

Thyrotrophin (TSH) secretion was studied in 63 patients with Cushing's syndrome (53 patients with pituitary dependent Cushing's disease, eight with adrenocortical tumours, and two with the ectopic ACTH syndrome). Prior to treatment, TSH response to 200 micrograms of TRH intravenously was significantly decreased compared to controls; TSH response was 'flat' (increment less than 2 mU/l) in 34 patients (54%). Patients with a flat response to TRH had significantly higher morning and midnight cortisol levels than patients with a TSH response of 2 mU/l and more; this was not due to differences in serum thyroid hormone levels. Basal TSH, TSH increment after TRH, and stimulated TSH value, but not serum triiodothyronine, were correlated with cortisol measurements (0800 h serum cortisol, midnight cortisol, and urinary free corticoid excretion). After exclusion of 40 patients with additional disease (severe systemic disease, diabetes mellitus, or goitre), cortisol-TSH correlations were even more pronounced (r = -0.73 for midnight cortisol and stimulated TSH levels), while in the patients with additional complications, these correlations were slight or absent. Successful treatment in 20 patients was associated with a rise in thyroid hormone levels and the TSH response to TRH. These results indicate that (1) the corticoid excess but not serum T3 is the principal factor regulating TSH secretion in Cushing's syndrome, (2) a totally flat response to TRH is rare, and (3) TSH suppression and lower than normal serum thyroid hormone levels are reversible after treatment. Since factors like severe systemic disease, diabetes mellitus and goitre also affect TSH secretion, they tend to obscure the statistically significant correlations between cortisol excess and TSH secretion.
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PMID:TSH secretion in Cushing's syndrome: relation to glucocorticoid excess, diabetes, goitre, and the 'sick euthyroid syndrome'. 212 25

Basal immunoreactive serum trypsin (RIT) was determined in comparative study of 46 patients with adrenocortical hyperfunction and 24 patients with hypocorticism for specifying the potentialities of the diagnostic test. Excess of endogenous corticosteroids is accompanied by a marked increase in the RIT serum concentration, this increase is particularly pronounced in Itsenko-Cushing syndrome and in exacerbations of Itsenko-Cushing disease in comparison with its level in Itsenko-Cushing disease remission. The presence of steroid diabetes had no significant RIT changes in Itsenko-Cushing disease. Attendant chronic pancreatitis that developed in patients with adrenocortical hyperfunction had no influence on blood serum RIT content. In patients with adrenal steroid deficiency who did not take glucocorticoids the serum RIT concentration was lower than that in those who constantly used hormones. RIT is increased in cases of chronic pancreatitis combined with chronic adrenal insufficiency. Measurement of the basal serum RIT may contribute to the diagnosis of pancreatitis in patients with hypocorticism but provides no information on this pathology in patients with endogenous hypercorticism.
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PMID:[Immunoreactive trypsin in the blood serum of patients with endogenous hypercorticism]. 277 53

Type 2 diabetes is a familial disease and studies of both Caucasian and Japanese families have raised the possibility that a major susceptibility gene is involved. The majority of patients have both beta cell dysfunction and impaired insulin sensitivity but studies of relatives of Type 2 diabetic patients suggest that beta cell dysfunction is an early feature of the disease. Impaired insulin sensitivity, from acromegaly, Cushing's disease or steroid therapy, induces diabetes only in a small proportion of the population, and they may be those who have an inherited cell defect. We postulate that a single beta cell defect gene, on its own, may be insufficient to cause overt diabetes and would lead to life-long glucose intolerance unless associated with other defects such as impaired insulin sensitivity. The nature of such a postulated beta cell defect is uncertain. Whilst it has been reported to be specific to glucose, and not to non-glucose stimuli, this feature may be secondary to hyperglycaemia. The occurrence of islet amyloid in 70-90% of Type 2 diabetic patients, and rarely in the normal population, raises the possibility that amyloid deposition causing disruption of the islet is a factor which might affect beta cell function. Amyloid formation may be a primary abnormality or could be secondary to beta cell dysfunction induced by hyperglycaemia. A major susceptibility gene might predispose a proportion, perhaps 10-15%, of a Caucasian population towards diabetes. The subsequent development of diabetes in a particular patient is likely to depend on many factors including other genetic factors, a sedentary life style and obesity. In different populations different genetic influences may operate, including abnormalities of insulin receptor genes and glucose transporter genes, which may allow a beta cell abnormality to become expressed clinically.
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PMID:Pathogenesis of NIDDM--a disease of deficient insulin secretion. 307 95

Examination of 13 untreated patients with Itsenko--Cushing disease and syndrome showed an increase in total Ig as well as IgA, IgM and IgG, a decrease in the number of O-cells, and the absence of significant change in in the blood content of T-lymphocytes. A decrease in the amount of B-lymphocytes was noted in this group of patients with GTT of diabetic type or mild diabetes mellitus. Repeated examination of 7 of these patients 1-1.5 mos. after the resection of one adrenal gland showed that the content of O-cells had returned to normal, tension of the system of humoral immunity was on a decrease and combined with a decrease in the excretion of 17-OCS fractions though they were still above normal. Hyperlymphocytosis with a high level of T- and B-lymphocytes and the normal content of O-cells was noted in 11 patients after bilateral adrenalectomy for Itsenko--Cushing disease receiving maintenance doses of cortisone.
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PMID:[Immunologic indices in Itsenko-Cushing disease and syndrome]. 342 33


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