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

In eleven cases thirteen pancreatic islet cell adenomas were found in autopsy material from 1366 adult cases. Ten of the adenomas were solitary, while 3 small adenomas were observed in a single case. Another four possible solitary adenomas were observed, but their identity was uncertain owing to marked fibrosis. All the adenomas contained A-2 (A)-1 cells but no B (B)-1 cells. Nine of them also contained A-1 (D)-1 cells. The majority of cells in the adenomas were A-2 cells or cells which did not stain with any of the techniques used. The 4 possible adenomas contained islet cells (A-1, A-2, B) in different proportions. With one exception the patients with adenomas and possible adenomas were 65 years of age or older, and in some of these cases adenomas or hyperplasias were also found in other endocrine organs. The frequency of gastroduodenal ulcers or scars in the cases with adenoma or possible adenoma did not differ notably from that found in the cases without pancreatic adenomas. Among the cases with pancreatic adenoma and possible adenoma there were 3 patients with maturity onset diabetes mellitus, but otherwise no clinical symptoms of endocrine disturbances were noted.
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PMID:Cytological differentiation of asymptomatic pancreatic islet cell tumours in autopsy material. 4 49

Familial multiple adenoma of pancreatic beta-cells is described for the first time. The occurrence of diabetes mellitus in different members of the family raises the possibility of a common genetic origin for the multiple islet-cell adenomas and the diabetic trait. The evidence suggests that this gene is autosomal and dominant, that it is not linked with the HLA antigens, and that is causes an abnormal sensitivity of the beta-cells, which become hyperplastic or hypofunctional.
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PMID:Familial islet-cell adenomatosis. 7 Jun 43

The renal oncogenic activity of streptozotocin in male Holtzman rats was significantly decreased by nicotinamide. Adenomas of the kidney were noted in 77% (21/28) of the animals treated with single iv dose of the streptozotocin, 50 mg/kg, while only 18% (5/28) of animals given nicotinamide ip, 350 mg/kg, 10 min before and 180 min after the same dose of streptozotocin had demonstrable renal tumors. Moreover, the renal adenomas induced by streptozotocin alone occurred sooner and were generally larger when compared with those in the animals treated with the nicotinamide-streptozotocin combination. The 50 mg/kg dose of streptozotocin was diabetogenic in all rats, but the diabetic state was not permanent. Spontaneous recovery from the diabetes was first noted after 8 and 10 months of followup, and after 16 months none of the surviving rats were diabetic.
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PMID:Modification of renal tumorigenic effect of streptozotocin by nicotinamide: spontaneous reversibility of streptozotocin diabetes. 17 79

A chromophobic pituitary adenoma induced on BD IX-rats has been grafted on animals of the same strain. The transplanted tumour takes in 90-100%; it grows at a slow rate (in 7 months after grafting a weight of 7-20 g is attained). Tumour-bearing animals display gigantism and hypertrophy of adrenals; moreover, in 33% of cases, diabetes is observed. With non-diabetic animals, splenomegaly and marked leukocytosis are observed; immature white and red cells are present in the peripheral blood. Spontaneous regression of the tumour never occurs. After surgical removal, tumour regrowth and the formation of metastases are observed. Diabetes is characterised by pronounced hyperglycaemia, glucosuria, polyphagia and polydipsia. Histochemically, insulin cannot be detected in pancreas. Splenomegaly is never observed in diabetic animals. Transplanted adenoma frequently tends to stop growing. No recurrence is observable after extirpation. Spontaneous regression of the tumour sometimes occurs. Gigantism, hypertrophy of adrenals and diabetes are considered as consequences of growth hormone- and ACTH-secretion of the transplanted adenoma. At present the tumour is running in the 8th passage. It did not change its characteristics over a period of 5 years.
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PMID:Transplantable, STH-producing and diabetogenic pituitary adenoma of the BD IX-strain of rats. 17 13

Hypoglycemia in diabetes can be divided into 1) spontaneous hypoglycemic reactions due to absolute or relative overproduction of endogenous insulin or some other blood glucose-lowering substance, as in islet cell adenoma or carcinoma, latent or protodiabetic conditions, (extrapancreatic) tumors and pituitary and/or adrenal disorders; and 2) hypoglycemia caused by exogenous, i.e. therapeutic, measures. The problem of hypoglycemia in insulin-treated diabetics is far from being solved. As revealed by continuous blood glucose monitoring, nocturnal hypoglycemic attacks frequently escape attention especially in juvenile diabetics. Circadian variations in peripheral glucose utilization, rather than changes in plasma insulin activity, are likely to be involved in this mechanism. At least, this was the conclusion drawn from studies carried out by means of a glucose-controlled insulin and glucose infusion system (GCIGIS) -or artificial pancreas-which delivers short-acting insulin and glucose on demand intravenously. Hypoglycemic reactions in patients being treated with oral anti-diabetic agents, on the other hand, should be regarded primarily as one of the side reactions intrinsic to the mechanism of action of some of these drugs, e.g. sulfonylureas, which act mainly via stimulation of secretion of endogenous insulin reserves not responding properly to postprandial blood glucose increments. In the case of glibenclamide, at least partial resensitization of the defective glucose receptor of the beta-cell also becomes operative. A higher incidence of a characteristic type of hypoglycemic reaction was observed soon after glibenclamide therapy was introduced. Better understanding of the drug and dissemination of the information about it to doctors and patients has reduced the number of hypoglycemic reactions caused by glibenclamide to the same proportions as for other sulfonylureas. Hypoglyoemia following therapeutic hypophysectomy retains its position as one of the main hazards of this heroic therapy.
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PMID:Hypoglycemia in diabetics. 17 24

A case report of endocrine pancreatic tumour associated with diabetes and hyperparathyroidism is presented. Some arguments are in favour of a glucagonoma. Despite the absence of beta-cells in tumour, an exceptional result was obtained by use of Streptozotocin. This case brings up the relations between endocrine pancreatic tumours and parathyroid, and may be included in polyglandular adenoma syndrome.
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PMID:[Islet cell tumor with diarrhea and diabetes (glucagonoma?) associated with hyperparathyroidism. Long-term results of local-regional treatment with streptozotocin]. 19 71

Surgical intervention in organic hyperinsulinism is based on prior accurate biochemical assessment. The emergent problems are discussed in a case with hypoglycaemic attacks, where "blind" pancreatic resections had been performed in two occasions without success. Finally, after demonstration of hyperinsulinaemia and localization of the tumour by selective angiography an adenoma was removed surgically. The postoperative complications, including the development of insulin-dependent diabetes, demonstrate the inherent risks of blind distal pancreatectomy for suspected insulinoma.
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PMID:[Therapeutic and diagnostic problems in a patient with insulinoma (author's transl)]. 19 76

Islet cell adenomas are an important consideration in infants and children with hypoglycemia due to hyperinsulinism. Between 1965 and 1977, 32 patients with hyperinsulinism were seen at the Children's Hospital of Philadelphia. Sixteen of these patients underwent surgery. Eight patients had single pancreatic adenomas, 5 of whom were infants under 1 yr of age. In 3 infants an adenoma was recognized and removed at the time of surgery. In 4 patients a subtotal pancreatectomy was successful in removing the adenoma. One infant is whom the adenoma was not included in the subtotal pancreatectomy died postoperatively with intractable hypoglycemia. Of the 7 patients cured by surgery, 6 are normal and 1 has brain damage due to delay in treatment of hypoglycemia. One child has mild diabetes. A combined medical and surgical protocol has been developed that permits rapid diagnosis of hyperinsulinism and selection of candidates for surgery. Infants under 1 yr of age who fail to respond to diazoxide should be explored. In children whose hyperinsulinism appears beyond 1 yr of age, surgery is indicated, since an adenoma is likely.
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PMID:Pancreatic adenomas in infants and children: current surgical management. 21 34

An unusual and extensive calcification of islets of Langerhans was found at autopsy in a man, 58 years old, who developed myeloma and, subsequently, hypercalcemia and diabetes. Although the islet cell calcification appears to be related to the hypercalcemia, the pathogenesis of the calcification is not clear, as primary metastatic calcification of pancreatic islets due to hypercalcemia does not occur. In support of this, a retrospective study of pancreatic tissue from 52 hypercalcemic patients with parathyroid adenoma and 34 patients with multiple myeloma, who frequently have hypercalcemia, did not reveal islet calcification. The islet calcification is ascribed to primary islet cell degeneration and necrosis, with hypercalcemia playing an augmenting but crucial role. It is considered that the combination of islet degeneration and calcification resulted in the diabetic state.
Diabetes 1978 Jun
PMID:Selective calcification of pancreatic islets of Langerhans. An unusual association with hypercalcemia and diabetes mellitus. 35 Jun 76

To our knowledge, the juvenile form of spongy degeneration of the CNS (SD-CNS); van Bogaert-Bertrand disease) has been described previously only three times. We report the case of 21 1/4-year-old Japanese woman who was first seen at the age of 11 with growth retardation, ptosis, and ophthalmoplegia. Her progressive neurodegenerative disease included retinitis pigmentosa, blindness, partial deafness, cerebellar dysfunction, hyporeflexia, and muscle wasting. Simultaneous endocrine defects were diabetes mellitus and probable hyperaldosteronism. Heart block developed later. She died of bronchopneumonia. Autopsy showed CNS stigmas typical of spongy degeneration. Additional findings included peripheral nerve demyelination, neurogenic muscle atrophy, pituitary and pancreatic atrophy, right adrenal agenesis, and a left adrenal coritcal lipid-cell adenoma. To our knowledge, our patient was the oldest survivor, the first patient of Japanese ancestry, and had a unique concurrence of certain oculoendocrine defects.
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PMID:Spongy degeneration of the CNS: an instance of the rare juvenile form. 50 59


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