Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 43-year-old man was admitted to our hospital in January, 1991 for further examination of polydipsia, polyuria and hypertension. He had had a personal history of hypertension since 1976 and of diabetes mellitus since 1982. Physical examination and routine laboratory studies showed that the patient was characterized by asymptomatic hypertension in the presence of hypokalemia and increased urinary potassium excretion. Plasma aldosterone concentrations (PAC) were elevated and plasma renin activity (PRA) was suppressed, resulting in a considerable increase in the ratio of PAC to PRA. PAC was not normally suppressed by saline infusion (2 1/2h, iv). PRA remained suppressed and PAC did not rise after stimulation with iv injection of furosemide (40 mg) in combination with walking for 60 min. PAC was increased in response to ACTH injection (0.25 mg, iv) but not suppressed by dexamethasone administration (2 and 8 mg/day, po). PAC did not rise after iv infusion of angiotensin II (20 ng/kg/min for 30 min). Venous sampling showed that PAC was considerably elevated in the bilateral adrenal vein. CT and MRI demonstrated tumor mass in the bilateral adrenal gland and the remaining normal portion in the left adrenal gland. Scintigraphic imaging with 133I-aldosterol during dexamethasone suppression provided bilateral uptake in the adrenals. Oral administration of spironolactone (375 mg/day) suppressed blood pressure and elevated PRA and serum potassium. Elevated PCA and PRA levels as well as hypertension were corrected by right-total and left-subtotal adrenalectomy performed in March, 1991. However, impaired glucose tolerance was not changed after surgery, and plasma glucose levels were well controlled with a small dose of insulin (9U/day). Pathological studies revealed adrenocortical adenoma cells of clear cell type with spironolactone bodies in the bilateral adrenal tumors. These findings indicate that this is a very rare case of primary aldosteronism due to bilateral functioning adrenocortical adenomas, which is accompanied by diabetes mellitus.
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PMID:[A rare case of primary aldosteronism due to bilateral functioning adrenocortical adenomas]. 846 28

Salivary gland enlargement by hypertrophy of normal-appearing parotid or submaxillary tissue is known as sialosis. It can be idiopathic, or may be associated with malnutrition, diabetes, bulimia, or alcoholism. When normal tissue is aspirated from an enlarged gland, one is tempted to diagnosed sialosis. We performed 26 such aspirates over a 5-yr period. In all cases, the cytology featured abundant acinar and ductal tissue in a clean (noninflammatory) background. Six cases were excluded when the records showed no return visits to the clinic. The remaining 20 patients included 9 men and 11 women, aged 24-92 yr (median 56), who harbored 12 parotid (2 bilateral) and 8 unilateral submaxillary enlargements. Clinical findings included ethanol abuse (2), diabetes (1), and previously diagnosed head and neck carcinoma (3). In six patients, the duration of the mass was described as months or years. Excision (6), reaspiration (3), radiographic evaluation (2), and clinical follow-up of patients not evaluated by other means (9 cases with median follow-up of 6 months) revealed no malignancies. One excised gland contained a pleomorphic adenoma measuring 0.5 cm in diameter. This had been diagnosed by repeat fine-needle aspiration (FNA) prior to surgery. We suggest that sialosis is a meaningful FNA diagnosis in patients who are carefully examined, skillfully aspirated, and reasonably followed.
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PMID:Fine-needle aspiration of normal tissue from enlarged salivary glands: sialosis or missed target? 859 12

To clarify the precise function of incidentally discovered adrenocortical adenoma, immunohistochemical and dispersed adrenal cell studies were performed. We have recently seen five patients with so-called nonfunctioning adrenocortical adenoma. Diurnal variation in plasma cortisol and suppression of plasma cortisol and urine 17-hydroxycorticosteroids in response to dexamethasone administration revealed adrenocortical function within normal limits in all cases, and no signs or symptoms of adrenal steroid hormone excess were evident. Since a high uptake of iodomethylnorcholesterol was recognized in each adrenal mass, it was supposed that these adrenal tumors produced steroid hormone to a certain extent, and each patient received unilateral adrenalectomy. P450c17, a key enzyme involved in cortisol production, was expressed in the tumor region in all cases in an immunohistochemical study. Upon in vitro steroidogenesis with dispersed adrenal cells in two cases, all steroid hormones measured except for aldosterone (progesterone, 17 alpha-hydroxyprogesterone, pregnenolone, 17 alpha-hydroxypregnenolone, 11-deoxycortisol, cortisol, 11-deoxycorticosterone, corticosterone, 18-hydroxydeoxycorticosterone, dehydroepiandrosterone and androstenedione) were produced in a culture medium. The results indicated that these tumors possessed the capacity for cortisol production, which was in agreement with the results of an iodomethyl-norcholesterol scintigraphy. All patients with mild hypertension or diabetes mellitus had no signs or symptoms of steroid hormone excess, but they could potentially develop a steroid excess syndrome such as Cushing's syndrome in the future.
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PMID:Incidentally discovered adrenocortical adenomas are not fully nonfunctioning: immunohistochemical and dispersed adrenocortical cell study. 873 56

A 9-year-old male Doberman Pinscher was referred to the Department of Clinical Sciences of Companion Animals, Faculty of Veterinary Medicine, Utrecht University, for polyuria/polydipsia, anorexia, and vomiting. Laboratory examination of blood and urine revealed hyperglycemia, glucosuria, and acidosis. Diabetes mellitus was diagnosed but was very resistant to subsequent insulin treatment. At the owners' request, the dog was euthanatized and a postmortem examination was performed. In addition to hepatic, pancreatic, and renal changes compatible with diabetes mellitus, an acidophilic adenoma of the adenohypophysis was found. Immunohistochemical staining for growth hormone, adrenocorticotropic hormone, and prolactin showed a strong immunolabeling for growth hormone within the cytoplasm of the tumor cells. Although growth hormone level was not measured in the plasma, our findings suggest that the diabetes mellitus in this dog was caused by excess growth hormone secreted by the pituitary neoplasm.
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PMID:Diabetes mellitus in a dog with a growth hormone-producing acidophilic adenoma of the adenohypophysis. 881 49

A case of acromegaly associated with variegated spinal disorders was reported. The spinal disorders were multiple cervical disc herniations, spinal epidural cavernous angioma, multiple ossification of the spinal ligament and lumbar canal stenosis. A 51-year-old woman with acromegaly, complaining of disturbances of delicate hand movement and gate, consulted our department. Her past history included diabetes mellitus, hypertension and progressing enlargement of her extremities. Serum growth hormone level was 65.7 ng/ml and somatomedin-c level was 746 ng/ml. Brain MRI showed a pituitary tumor extending to the right cavernous sinus. Cervical MRI revealed disc herniations at C5/6 and C6/7. Thoracic MRI revealed osteoporosis, ossification of the posterior longitudinal ligament and multiple ossification of yellow ligament. Lumbar MRI disclosed ossification of yellow ligament and canal stenosis. Anterior fusion of C5-C7 and an intracapsular removal of the pituitary tumor were performed. Its pathology was that of eosinophilic adenoma. After 3 months, she suffered from paraparesis. On repeating MRI examination with Gd-DTPA, a spinal epidural mass was found at T4. Under laminectomy of Th3-5 and Th8-11, the epidural mass and ossified yellow ligament were removed. The epidural mass was cavernous angioma. She was able to walk without any assistance. An association of spinal canal stenosis with acromegaly is well known. But the association of disc herniation and with the ossification of spinal ligaments is rather rare in the literature. Spinal epidural cavernous angioma is very rare. We discussed the etiological aspects and the management of spinal disorders with acromegaly.
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PMID:[A case of acromegaly associated with variegated spinal disorders]. 891 52

This paper presents a 59-year-old man who was admitted to our hospital because of abdominal pains in 1973. He had pancreatic calcification and showed high levels of serum amylase, Ca, and PTH. He was diagnosed as primary hyperparathyroidism with chronic pancreatitis. After excision of an ectopic parathyroid adenoma, serum Ca levels were decreased and normalized by dihydrotachysterol p.o. At the same time his symptoms disappeared. The exocrine and endocrine pancreatic functions, however, decreased gradually. Diabetes mellitus appeared in 1975 and he required insulin injection since 1983. In spite of the treatment, his diabetic control was poor. Seventeen years later in 1992, he showed hypertension and edema (nephrotic syndrome). Because of renal failure, he underwent hemodialysis and passed away due to myocardial infarction in 1993. Autopsy findings showed existence of diabetic nephropathy as the cause of renal failure. Clinical course of this patient suggests that severe complications occur even in pancreatic diabetes and that we have to control diabetes strictly in pancreatic diabetes as well as in primary diabetes.
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PMID:[An autopsy case of renal failure as its cause of death in a patient with primary hyperparathyroidism associated with chronic pancreatitis]. 894 Aug 1

The majority of thyroid adenomas have been shown to be of clonal origin. In a portion of them, somatic or germline point mutations leading to altered TSH receptor or Gs alpha-proteins have been found. The constitutive activation of these proteins consecutively stimulate cAMP-levels. Expression of the TSH receptor mutants in mammalian cells leads to increased cAMP-production compared to cells transfected with the wild type receptor. Presently, the role of these mutations in the development and growth of such tumours is still unclear. In our own investigations we made an attempt to evaluate the functional significance of these observations. In nodular tissue derived from patients with functioning autonomous adenoma we found significantly higher basal and TSH stimulated thyroid hormone releasing activity than in the surrounding paranodular tissue and in thyroid tissue derived from patients with euthyroid goiter. These findings indicate a functional relevance of constitutively activated intracellular signal transducing cascade in thyroid adenomas that may lead to hyperthyroidism in the presence or absence of external thyroid stimulators.
Exp Clin Endocrinol Diabetes 1996
PMID:Enhanced functional activity in thyroid adenomas in vitro. 898 Sep 99

Mouse transgenic models that develop thyroid diseases were generated. All transgenes were driven by the thyroid specific promoter of the thyroglobulin gene. The tissue specificity of the promoter was investigated by using the bacterial chloramphenicol acetyl transferase gene as reporter. The expression of an adenosine A2a receptor resulted in the permanent activation of the cAMP cascade. As a consequence, the transgenic mice developed severe hyperthyroidism and a large goiter, demonstrating in vivo the role of the cAMP cascade in the promotion of both function and proliferation of the thyroid cell. These mice constitute a model for autonomous hyperfunctional adenoma and non-autoimmune familial hyperthyroidism, where mutant thyrotropin receptors stimulate the cAMP cascade constitutively. In another transgenic model, the function of the retinoblastoma susceptibility gene product RB1 (and of related proteins) was inhibited by expression of the E7 oncoprotein of human papillomavirus type 16. The result was the development of a differentiated and normofunctional colloid goiter, with the progressive development of differentiated malignant lesions. This model suggests the essential role of RB1 and related proteins in the negative control of proliferation that characterizes thyroid cells in the adult. Other transgenic models of thyroid diseases are discussed.
Exp Clin Endocrinol Diabetes 1996
PMID:Transgenic models for proliferative and hyperfunctional thyroid diseases. 898 22

A 56-year-old woman presented with diabetes mellitus and primary hyperparathyroidism simultaneously. Initial random blood glucose was recorded at 20.8 mmol l-1, serum calcium was 3.07 mmol l-1 (normal range 2.10-2.55 mmol l-1), and plasma parathyroid hormone estimation by intact assay was 110 ng l-1 (normal range 10-65 ng l-1). Initial glycated haemoglobin was 9.4% (non-diabetic range < 7.5%). Left lower parathyroidectomy was carried out and pathology confirmed the presence of a chief cell adenoma. The gland measured 10 x 5 x 5 mm. Following parathyroidectomy serum calcium normalized, glucose tolerance improved, and a subsequent 75 g oral glucose tolerance test was normal. The patient weighted 80 kg at presentation but the post-operative weight had risen to 81.5 kg. The most recent glycated haemoglobin was 4.6%. Primary hyperparathyroidism may have a reversible effect on glucose tolerance.
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PMID:Remission of non-insulin-dependent diabetes mellitus following resection of a parathyroid adenoma. 901 58

We have previously demonstrated in short-term experiments that altered hepatocytes in liver acini draining the blood from intraportally transplanted pancreatic islets in streptozotocin-induced diabetic rats with mild persisting diabetes resemble those in preneoplastic foci of altered hepatocytes. We now present the results of long-term studies (up to 22 months) in this animal model. Glycogen-storing foci (which were the first parenchymal alteration observed some days after transplantation) persisted at least for 6 months, when the first mixed-cell foci and the first hepatocellular adenoma emerged. After 15 to 22 months, 86% of the animals exhibited at least one hepatocellular adenoma and four animals (19%) showed a hepatocellular carcinoma. The transplants were found in a close spatial relationship with the preneoplastic foci and the hepatocellular neoplasms. The mitotic indices, the 5-bromo-2'-desoxyuridine labeling indices and the apoptotic indices showed significant differences between the unaltered liver parenchyma, different types of preneoplastic foci, and hepatocellular neoplasms. The immunohistochemical expression of transforming growth factor-alpha increased during the stepwise development from glycogen-storing liver acini to hepatocellular carcinomas. Hepatocarcinogenesis in this new animal model is probably due to the hormonal and growth-stimulating effects of insulin secreted by the intraportally transplanted islets of Langerhans in diabetic rats.
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PMID:Hepatocellular neoplasms induced by low-number pancreatic islet transplants in streptozotocin diabetic rats. 906 Aug 43


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