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

Hyperosmolar diabetic coma revealed the presence of a pancreatic cancer in two patients. The first case was a 59-year-old man, without a history of diabetes, treated with prednisone for jaundice and marked weight loss over the last month, and admitted in hyperosmolar coma (346 m0sm/l). After recovery from the acute episode, a diagnosis of adenocarcinoma of the head of the pancreas was established following operation. The patient died six months later. The second case, a 71-year-old man also without a history of diabetes, was admitted in hyperosmolar coma (315 m0sm/l) during the course of a pulmonary infection. Rapidly fatal cholostatic jaundice appeared one year later. An adenocarcinoma of the head of the pancreas was demonstrated at autopsy. The diagnostic criteria in both cases were those of hyperosmolar diabetic coma. Though cases of combined diabetes and pancreatic cancer are well documented, only one case of hyperosmolar coma and cancer of the pancreas has been reported in the published literature. The pathogenesis of hyperosmolar diabetic coma is discussed. The fact that it developed during the course of a pancreatic affection could be explained by a functional reduction in insulin secretion, associated with a triggering factor such as dehydration, infection, hypoglycemic agent administration, etc... The onset of hyperosmolar diabetic coma in an elderly patient without a history of diabetes, especially with associated marked weight loss, should lead to investigation for a possible pancreatic cancer.
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PMID:[Pancreatic cancer revealed by hyperosmolar coma: report on two cases (author's transl)]. 701 54

Plasma vasopressin was measured in seven insulin-treated diabetics during 24 h of insulin withdrawal to determine: 1) if abnormalities of the neurohypophysial-renal axis contribute to the dehydration of uncontrolled diabetes mellitus; and 2) the factors causing elevated levels of vasopressin in diabetic ketoacidosis. During the 24 h period of insulin withdrawal, blood glucose rose from 6.7 +/- 1.0 to 20.7 +/- 2.4 mmol/l, whereas plasma vasopressin was 3.6 +/- 0.5 pg/ml initially and in four patients showed little change. Markedly elevated levels of plasma vasopressin (17.8, 19.8 and 26.6 pg/ml) were observed in three patients following the onset of hypovolaemia, nausea and/or vomiting which are known to stimulate vasopressin release. Free water clearance was negative throughout the study in all patients. Thirst was not noted despite marked hyperglycaemia (16.9 +/- 2.5 mmol/l) until a significant fall in body weight of 0.9 +/- 0.2 kg had occurred (p less than 0.005). We concluded that marked elevation of vasopressin results from non-osmotic stimulation and that the mechanisms of body water conservation are overridden by the glycosuric diuresis.
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PMID:Plasma vasopressin during insulin withdrawal in insulin-dependent diabetes. 702 Dec 77

Accepted causes (acute insults) and risk factors for the development of acute renal failure were defined, quantitatively assessed, and tested for statistical significance in 143 patients with acute tubular necrosis. Sixty-two percent of patients had more than one acute insult, and 48 percent had more than one suspected risk factor. Hypotension, excessive aminoglycoside exposure, pigmenturia, and dehydration were identified as highly significant acute insults, while it was concluded that sepsis and administration of radiocontrast material could not be incriminated as causes of acute tubular necrosis. An additive interaction between acute insults was demonstrated, and the severity of acute renal failure was related to the number and severity of acute insults. Patients with oliguric renal failure had more severe acute insults than patients with nonoliguric renal failure. Preexisting renal disease and chronic hypertension were significant risk factors, the latter only when hypotension had been one of the acute insults. An age of more than 59 years, gout and/or chronic hyperuricemia, diabetes, and long-term diuretic administration were not found to be significant risk factors.
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PMID:Acute renal failure. Multivariate analysis of causes and risk factors. 711 78

Severe reactions to contrast media in two diabetic patients with azotemia are described. Both patients also showed signs of immunopathy. The reaction was fatal in one of them. Little is known about contrast media reactions and their natural history. Patients with diabetes mellitus and impaired renal function should be studied with caution and with careful consideration of the indication for the procedure. If an examination with contrast media is considered unavoidable, all diabetic patients with renal failure should be supervised closely to detect the development of acute renal failure. Dehydration should be avoided. Careful monitoring of blood glucose, serum electrolytes, serum creatinine and blood pressure will aid in the early detection of the adverse reaction.
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PMID:Fatal reaction following renal angiography and biopsy in diabetic patients with Azotemia. 714 9

To identify any relationship between diabetes mellitus and high salt intake in the production of hypertension, we studied the effect of a regular and high salt diet on blood pressure in rats made diabetic with alloxan. The diabetic animals developed marked hyperglycemia, glycosuria, and azotemia out of proportion to changes in glomerular filtration rate. Non-diabetic rats and diabetic rats on a high salt intake in excess of 14 mEq/day developed modest but significant increases in blood pressure, while diabetic rats on a regular diet did not. We conclude that diabetic rats have no greater susceptibility to salt-induced hypertension than rats receiving only salt. Although it is possible that dehydration may have served to attenuate blood pressure increases in our diabetic animals, the diabetic state per se does not appear to result in severe hypertension in the rat regardless of sodium intake.
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PMID:Blood pressure of alloxan diabetic rats at regular and high salt intake. 724 77

Synthetic arginine-vasopressin (AVP), oxytocin (OXY) and arginine-vasotocin (AVT) were labelled with radioiodine at a moderate specific activity. The purity of the labelled octapeptides was checked by descendent paper chromatography in butanol-acetic acid-water (4 : 1 : 5 v/v) after a double filtration on a Sephadex G-25 column of the labelling mixtures. The rabbit anti-AVP serum bound 125I--AVP, the highest binding belling observed on the descendent eluates from the Sephadex column. The antiserum is specific to AVP, no binding being observed will AVT or oxytocin. The sensitivity of a RIA system using 125I--AVP, commercial anti-AVP serum and polyethyleneglycol separation technique, was of 5 pg/ml in terms of AVP with a biological activity of 385 IU/mg. The validity of the assay was tested on five patients (two with diabetes inspidus (DI) and three with other endocrine diseases) submitted to dehydration of hydration tests.
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PMID:Labelling of octapeptide neurohormones for in vitro studies. Radioimmunologic assay for arginine-vasopressin. 729 46

The renal venous thrombosis is mostly produced by severe dehydration. The following, however, are also predisposing factors: infections, birth traumata, paranephritic processes, lack of oxygen, diabetes of the mother and cyanotic heart defects. The diagnosis is correctly made by means of the palpable flank tumor, the macrohematuria, together with the urogram and sonography. The most urgent therapeutic measure is the balancing of the water and electrolyte deficit to eliminate the dehydration, i.e. the existing oliguria or anuria. The therapy is primarily always conservative. In the event of a consumption coagulopathy, a therapeutical attempt can be undertaken with heparin but if this is unsuccessful, an immediate nephrectomy must be performed. A further nephrectomy will be necessary if hypertony persistent infection and renal atrophy occur. Two infants with renal venous thrombosis were used for this study on the causes and diagnosis of, and the therapy for the illness.
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PMID:[Renal venous thrombosis in the newborn (author's transl)]. 746 39

The most common nutritional problems in nursing home residents are weight loss and concomitant protein energy undernutrition. Although the causes of weight loss in these patients can usually be treated, they are rarely identified in the nursing home. Depression and adverse drug effects are the most common causes of weight loss. We discuss the appropriate use of feeding tubes in the nursing home and the early use of enteral feeding to prevent the development of severe protein energy undernutrition. Vitamin deficiencies, especially folate and pyridoxine deficiencies, frequently develop in nursing home residents. Hip fractures are often associated with vitamin D deficiency. Trace mineral deficiencies (for example, zinc deficiency) can aggravate immune deficiency and slow wound healing. Inadequate fluid intake leads to dehydration, hypotension, and, in persons with diabetes mellitus, hyperosmolarity. Finally, food intake itself can cause postprandial hypotension (which in turn may precipitate falls), produce electrolyte shifts, and result in aspiration pneumonia. Physical activity programs are an important component of nursing home care that may have an effect on nutritional status, and simple, cost-effective programs may be as beneficial as high-technology programs. Careful attention to the nutritional intake of nursing home residents is both a clinical and a quality-of-life issue.
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PMID:Nutritional issues in nursing home care. 748 69

On the basis of examination of 634 patients with acute surgical endotoxemia in patients with diabetes mellitus the following features have been revealed: hypertonic dehydration has dominant as well as hyperkalemia, marked hyperazotemia. Oliguria was detected only in 18.8% of patients. Plasmic osmolarity was 296-348 mosm/l, predominantly for account of hyperazotemia and hyperglycemia. 86.97% of patients showed ketoacidosis. The scheme of intensive therapy of surgical endotoxemia in patients with decompensative diabetes mellitus with programme applications for paternal computers is suggested.
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PMID:[The possibilities for correcting hydro ion metabolism in acute surgical pathology in diabetics]. 762 26

Postural hypotension is uncommon in diabetes but can occur secondary to autonomic neuropathy. Symptoms are rare and include dizziness, weakness, blurred vision, tiredness, and loss of consciousness. The pathophysiology of postural hypotension is not clear, but changes in intravascular volume, heart rate, cardiac output, and splanchnic vascular resistance are similar in patients and controls. The main factors producing hypotension are a blunted catecholamine response to standing, and failure of lower limb vascular resistance to increase adequately. Treatment for symptomatic postural hypotension includes avoidance of dehydration, adequate salt intake, and fludrocortisone. Other treatments are reviewed but are less helpful. Patients with postural hypotension have intermittent symptoms over the years but rarely become severely disabled. They have a poorer prognosis than patients with symptomatic autonomic neuropathy without postural hypotension.
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PMID:Postural hypotension in diabetic autonomic neuropathy: a review. 775 54


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