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

The first case of Klinefelter's syndrome accompanied by diabetes insipidus and diabetes mellitus is reported. A 41-year-old man admitted for hyperosmolar diabetic coma with a past history of diabetes insipidus was diagnosed as having Klinefelter's syndrome by endocrinological examination and sex chromosome analysis. In this case, glucose tolerance test was normalized half a year later and blood glucose was well controlled with diet therapy alone.
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PMID:Klinefelter's syndrome accompanied by diabetes mellitus and diabetes insipidus. 145 May 2

A 50-year-old man presented with hyperosmolar non-ketotic diabetic coma associated with the neuroleptic malignant syndrome (NMS) after intramuscular treatment with haloperidol. It is suggested that NMS may occur as a complication of uncontrolled diabetes mellitus with dehydration. Conversely, NMS might precipitate diabetic coma in patients with previously well controlled blood glucose.
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PMID:Neuroleptic malignant syndrome presenting as hyperosmolar non-ketotic diabetic coma. 152 Nov 10

The aim of this study was to analyse the characteristics and the mortality rate of diabetic patients, in France, between 1970 and 1987, as well as the association between diabetes and other pathologies at death. These results are based on both the underlying and the associated causes of death registered on the death certificate, in contrast to most studies which use only the underlying cause. In 1987, there were 16,790 deaths in France for which diabetes was mentioned on the death certificate (as the underlying cause in 38% of cases). There was a higher mortality in male diabetic subjects then in female, for all ages except over 75 years. Between 1970 and 1987, the mortality decreased for both sexes, except for the oldest age group. The death rate varied greatly between geographical regions. A particularly high mortality occurred in the Nord-Pas-de-Calais, Lorraine and Alsace. Diabetes was significantly associated, at death, with other diseases and pathologies. The most frequent were vascular diseases (ischaemic heart disease, cerebral diseases and hypertension) and diseases of the genitourinary system. It if of note that 5% of the death certificates of these diabetic subjects indicated diabetic coma as a cause of death.
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PMID:[Analysis of diabetes-related mortality in France (1970-1987) from multiple causes of death]. 188 77

Neurosurgical patients with non-ketotic hyperosmolar diabetic coma (NHC) in our institution were analysed retrospectively. Seven cases were diagnosed as NHC being 0.47% of the number of inpatients in the last 5 years. The age ranged from 60 to 72 years old (mean 65) and there were 6 males and 1 female. Only 2 patients (29%) had a clear past history of diabetes mellitus. Prior to the NHC, systemic infection was present in 2 cases. Intravenous hyperalimentation (IVH) was performed in 5 cases, glycerol osmotherapy in 3 cases, diphenylhydantion therapy in 3 cases and tube feeding in 2 cases. The overall mortality rate in our series was 71% (5 cases), of which 2 cases died within 2 days due to cardiopulmonary failure, and 3 cases in the chronic stage died due to disseminated intravascular coagulopathy (DIC), or due to renal failure. The prognosis of NHC in neurosurgical patients is generally bad because of the presence of consciousness disturbance prior to the onset of NHC, which may mask the symptoms occurring from the NHC. Other predisposing factors could be systemic infection, IVH or tube feeding, and osmotic agents which are frequently used in neurosurgical patients. There was a tendency for NHC to occur predominantly in the chronic stage after the blood sugar had returned to normal range from the hyperglycemic state in the acute stage.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Non-ketotic hyperosmolar diabetic coma in neurosurgical cases; review of 7 cases]. 240 36

Approximately 5.8 million people in the United States have been diagnosed by a physician as being diabetic, and an additional 4 to 5 million people have undiagnosed diabetes. Although the incidence of diabetes appears to be declining from a peak of 300 per 100,000 population in 1973, to 230 per 100,000 in 1981, its prevalence continues to rise, due to a 19 percent decline since 1970 in deaths caused by diabetes. In 1982, 34, 583 deaths were attributed to diabetes, resulting in diabetes being ranked as the seventh leading underlying cause of death. Medical and surgical complications of diabetes due to macro- and microvascular disease result in 5,800 new cases of blindness, 4,500 perinatal deaths, 40,000 lower extremity amputations and 3,000 deaths due to diabetic coma (ketotic and hyperosmolar) and at least 4,000 new cases of end-stage renal disease. Hyperglycemia is a major if not sole determinant of diabetic glomerulopathy. The exact mechanism underlying diabetic vasculopathy is under intensive study. Experiments in the induced-diabetic rat and dog suggest that small vessel injury may--under defined circumstances--be associated with the polyol (sorbitol) pathway of glucose metabolism, myoinositol deficiency, capillary hypertension, plasma hyperviscosity, stiff erythrocytes, elevated circulating thromboxane, and platelet-derived growth factor(s). As yet, no single hypothesis fits these seemingly disparate pieces together into a unified formulation of the genesis of diabetic complications. Clinical experience sustains the contention that a functioning kidney transplant proffers the uremic diabetic younger than age 60 a higher probability for survival with good rehabilitation than does either peritoneal dialysis or maintenance hemodialysis. Diabetics treated by kidney transplantation require more than the routine preoperative and postoperative attention afforded to nondiabetic ESRD patients. During initial nephrologic evaluation, concurrent extrarenal vascular disease--especially ophthalmic, cardiovascular, cerebrovascular and in the extremities, often demands immediate attention. Inventory of co-morbid risk factors pre-transplant facilitates their management post-transplant, thereby improving chances for rehabilitation. Consultations with an ophthalmologist and podiatrist familiar with management of the uremic diabetic should be obtained prior to transplant surgery. When performed as a component of pre-transplant evaluation, coronary angiography permits identification and correction, in many patients, of potentially fatal coronary artery disease.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Renal failure in diabetes: a substantive problem in provision of health care. 267 7

We studied a family with the Bardet-Biedl syndrome and diabetes mellitus. Two affected brothers and one affected sister were examined. Two older sisters with stigmata of the syndrome had died of unclear causes. The 18-year-old brother was obese, was mentally retarded, and had pigmentary retinopathy and insulin-dependent diabetes mellitus. The 16-year-old sister, who died in a diabetic coma during the course of the investigation, had polydactyly, hypogenitalism, obesity, mental retardation, and pigmentary retinopathy. The 8-year-old brother had all the features of the syndrome, but no overt diabetes mellitus. Electroretinography showed severe cone and rod dysfunction. Patients with the Bardet-Biedl syndrome should be screened for the presence of abnormalities in glucose metabolism.
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PMID:A family with the Bardet-Biedl syndrome and diabetes mellitus. 273 Apr 6

A case of central pontine myelinolysis (CPM) followed by hyperglycemia and hypoglycemia was reported. The case was 53-year-old female. Diabetes mellitus was found when she was 32 years old, insulin therapy was started at 37 years of age. Since she was 50 years old, proteinuria and ankle edema had developed and she was admitted to The Keihin Hospital. The peritoneal dialysis (PD) was performed next year, followed by the hemodialysis (HD). In January 1978, strange movements and the disturbance of her consciousness were occurred during PD, then blood glucose level showed over 1,800 mg/dl and serum osmolarity was over 390 mosm/KgH2O. Then she was diagnosed as non-ketotic hyperosmolar coma. After that, during HD and PD, hyperglycemia (approximately 1,200 mg/dl) and hypoglycemia (approximately 40 mg/dl) developed frequently. She died soon after HD on 19th December 1979. The autopsy disclosed bilateral atrophic kidneys due to diabetic changes and atrophic pancreas. Gross neuropathological findings revealed a few small infarcts at the putamen and the globus pallidus, however, other area were observed to be normal. The most remarkable change in microscopical finding was nearly symmetrical demyelinative lesion in the center of the basis pontis. The nerve cells and axon cylinders were relatively well preserved in the demyelinative lesion. The hyaline degeneration was observed in the arterial wall, however, any arterial obstruction was not found. Recent studies would suggest that the electrolyte disturbance, such as hyponatremia, may lead to CPM, particularly when this disturbance was rapidly corrected. On the other hand, CPM induced by diabetic coma has been reported, however, its pathogenesis has been unclear.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Central pontine myelinolysis followed by frequent hyperglycemia and hypoglycemia--report of an autopsy case]. 280 35

Thrombotic events may occur in patients who present with severe uncontrolled diabetes or with diabetic coma. As a possible explanation for this, platelet function was investigated at presentation with diabetic ketoacidosis and during treatment in 10 patients. Concentrations of the platelet-specific proteins, platelet factor 4 (PF4) and beta-thromboglobulin (beta TG) were elevated and fell towards normal with treatment. Despite evidence of increased aggregation in vivo, platelets from subjects with ketoacidosis were insensitive to adenosine 5'-diphosphate (ADP), sensitivity increasing with correction of ketoacidosis. Platelets from ketoacidotic diabetics were initially insensitive to the anti-aggregatory action of prostacyclin (PGI2) and became normal with treatment. Initial blood glucose concentrations correlated with log10 ADP concentrations (r = 0.72, p less than 0.01) and with log10 PGI2 ID50 (the PGI2 concentration required to half-inhibit ADP-induced aggregation) (r = 0.66, p less than 0.025). Glucose concentrations throughout the 2-week study period correlated with all log10 ADP concentrations (r = 0.32, p less than 0.005) and all log10 PGI2 ID50 concentrations (r = 0.51, p less than 0.001). The decrease in ADP sensitivity in ketoacidosis, paradoxical in view of the evidence of increased in vivo platelet aggregation, may result from an acquired platelet storage pool deficiency.
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PMID:Paradoxical platelet behaviour in diabetic ketoacidosis. 295 Nov 59

Fructosamine and glycated hemoglobin were determined in samples from 52 cadavers autopsied in the Forensic Pathology Institute of the University of Copenhagen (Denmark). The population studied comprised 15 adult subjects with history of diabetes mellitus and 37 adult non-diabetic subjects. The fructosamine/total protein ratio was 1.7 times higher in diabetic than in non-diabetic subjects, as was the case for glycated hemoglobin. Measurement of glycated serum protein appears to be a useful tool for the postmortem diagnosis of fatal diabetic coma and glucose concentration before death.
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PMID:Postmortem diagnosis of diabetes mellitus. Quantitation of fructosamine and glycated hemoglobin. 319 43

A 20-year-old woman with Kearns-Sayre syndrome (KSS) suddenly experienced two episodes of diabetic coma. She was studied to determine whether diabetes mellitus (DM) resulted from insulin resistance or from an insulin secretion abnormality, using the euglycemic glucose clamp technique and the glucagon tolerance test. She had a deficiency of insulin secretion from beta cells. It is important to recognize in practice the onset of DM in patients with mitochondrial myopathy. We would suggest that a genetic linkage or mitochondrial dysfunction may be responsible for the association of both disease states.
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PMID:Diabetes mellitus in Kearns-Sayre syndrome. 328 50


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