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

Consistant data drawn from animal experiments and from clinical statistics have shown the diabetic specific complications (neuropathy and microangiopathy) to be closely related to the hyperglycemic component of diabetes mellitus. Working directly or through more complicated biochemical disorders, high levels of blood glucose interfer with the metabolism of the lens, the retina and the peripheral axon (leading to cataracts, retinopahy, and neuropathy). High blood sugar also alters the metabolism of endothelial and blood cells as well as the composition of plasma proteins. Wall and content of the minute vessels are both affected resulting in disturbed local blood flows and hypoxic areas. Various intertricated mechanisms have been discovered. Some of them initiate vicious circles leading to self-supported functional and later on, morphological abnormalities of diabetic microangiopathy (retinopathy, glomerulosclerosis, etc., etc.). High blood sugar exerts its influence (directly or not) in terms of duration and intensity (hours per day, days per year). There are good reasons to believe that persistent hyperglycemia uninterrupted throughout the day is much more harmful than high peaks alternating with periods of normo- and even hypoglycemia. There is no experimental nor clinical data pointing to glycemic instability as a risk factor for the minute vessels and the nerves, and opinion still often hold in some quarters. Although undesirable, frequent bouts of hypoglycemia associated with insulin treatment are indices that a rather good glycemic control has been achieved. And this can greatly delay the development of specific complications.
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PMID:[Degenerative diabetic complications. Is persistent hyperglycemia more dangerous than wide glycemic fluctuations? (author's transl)]. 73 71

In order to determine pancreatic alpha cell function in diabetes mellitus, plasma glucagon responses to either an oral glucose load or insulin-induced hypoglycemia were investigated. Plasma glucagon in 6 normal control subjects fell significantly after the administration of glucose, whereas the levels of plasma glucagon did not decrease after glucose ingestion in patients with diabetes mellitus. In the group with severe diabetes, whose fasting blood glucose exceeded 200 mg/100 ml, the plasma glucagon level rose after glucose administration instead of decreasing. In 6 patients with diabetes mellitus, plasma glucagon did not decrease but rather increased during a glucose tolerance test which was performed after treatment with insulin and/or diet. In 6 control subjects, there was a remarkable rise of plasma glucagon in response to insulin-induced hypoglycemia. In contrast, no significant rise in plasma glucagon was demonstrated in 19 diabetic subjects undergoing intravenous insulin test. Seven patients, in whom an insulin test was repeated after treatment with insulin, sulfonylurea, or diet had a small rise in peak plasma glucagon and an increase in the integrated area under the glucagon response curve. It is concluded that the abnormal glucagon response to changes in blood glucose might be a primary defect in diabetes mellitus.
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PMID:Abnormal response of pancreatic glucagon to glycemic changes in diabetes mellitus. 75 36

In hypercalcemic patients with primary hyperparathyroidism who were fasted over a prolonged period, alcohol ingestion induced a significant fall in glucose whereas insulin remained unchanged. The hypercalcemic patients thereby differed from normocalcemic subjects, who showed a significant decline in both glucose and insulin when alcohol was ingested after a prolonged period of fasting. An increased uptake of calcium into the beta-cells appears to have been a prerequisite for the occurrence of an unchanged insulin secretion during alcohol hypoglycemia in hypercalcemic patients, since a calcium-blocking agent, verapamil, infused intravenously during and after alcohol ingestion, brought about a normalization of the insulin response to alcohol hypoglycemia in such patients.
Diabetes 1979 Jan
PMID:Effect of verapamil on insulin response to alcohol hypoglycemia in patients with primary hyperparathyroidism. 75 47

To improve plasma glucose control, we administered insulin via the subcutaneous route in seven ambulatory patients with juvenile diabetes (12 to 17 years of age), using a portable infusion pump at a basal rate with pulse-dose increments before meals. After two to four days, the mean plasma glucose (+/- 1 S.E.) of 94 +/- 5 mg per deciliter was markedly lower than when insulin was given by conventional methods in the patients' usual dose (243 +/- 28, P less than 0.01) or in a total dose equivalent to that administered with the pump (150 +/- 15, P less than 0.01). Maximal fluctuations in plasma glucose were also 50 to 150 mg per deciliter below those observed with conventional treatment (P less than 0.001). Glycosuria was eliminated in six of seven patients during pump treatment. None of the subjects had hypoglycemia. These results demonstrate that plasma glucose can be lowered to normal in ambulatory patients with brittle juvenile diabetes using a portable, subcutaneous insulin infusion system for two to four days. The feasibility and value of the long-term application of this technic need exploration.
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PMID:Reduction to normal of plasma glucose in juvenile diabetes by subcutaneous administration of insulin with a portable infusion pump. 76 70

During a six year period twelve patients with insulin dependent diabetes and end-stage renal failure received cadaveric kidney grafts. Eleven of the patients have previous to this been hemodialysed, one patient was transplanted before hemodialysis was necessary. The cumulative two year survival was thirty-seven per cent for the patients, and twenty-nine per cent for the kidney grafts. The average time of observation was eleven months, the motality was fifty per cent. The causes of death were acute myocardial infarction in two cases, sepsis in two cases, severe hypoglycemia in one case and unexpected sudden death in one case. The most prominent problems in the treatment of the diabetic patients after the renal transplantation were difficulties in the regulation of the diabetes, rejections, infections, cardiac failure and aggravation in pre-existing hypertension.
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PMID:Renal transplantation in patients with insulin requiring diabetes and renal failure. 78 7

The prevalence of diabetes due to chronic pancreatitis would appear to be increasing. In western countries this is associated with the known increase in alcohol consumption and AIP. Malnutrition may be etiologic in tropical areas. The incidence of diabetes in chronic pancreatitis is dependent on a number of factors. It is more common in alcohol-induced pancreatitis, rarely occurs after the first attack but tends to increase with time and rises markedly in calcific pancreatitis. Abnormal glucose tolerance occurred in 91% of patients with calcific pancreatitis and 70% of patients with noncalific AIP in our follow up of five to 12 years. This stresses the importance of serial regular glucose tolerance tests in these patients (Table I). The insulin-reserve is severely depleted in most patients who do not yet demonstrate abnormal glucose tolerance, indicating that pancreatitis regularly affects the islets and that nearly all patients are potential diabetics. The beta cells appear to respond better to oral glucose, glucagon or secretin than to i.v. glucose suggesting a selective glucose receptor loss or block to hyperglycemia in chronic pancreatitis. The alpha cells seem to be more resistant to the effects of chronic pancreatitis but true hypoglucagonemia was found in 16% of patients. In addition, stimulated growth hormone secretion may be deficient in pancreatic diabetes. These last two factors, among others, may be responsible for the protracted and even fatal hypoglycemia to which some patients with AIP on insulin therapy are liable. The danger of drug-induced hypoglycemia, coupled with the infrequency of vasculopathy, retinopathy and nephropathy in pancreatic diabetes has induced us to keep these patients hyperglycemic and glycosuric rather than in a sugar-free state, as long as symptoms are contained. Recurrent abdominal pain, marked weight loss and associated steatorrhea often raise special problems in the management of the pancreatic diabetic.
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PMID:Clinical and hormonal aspects of pancreatic diabetes. 80 21

Seventeen new cases of diabetes in childhood were given an initial mean dose of insulin of 0-29 unit/kg body weight by intramuscular injection (mean age of patient 7-4 years). This resulted in a fall in blood glucose over the first 2 hours at a mean rate of 88 mg/100 ml per hour. Over the same time the mean total blood ketones fell from 3-23 to 2-3 mmol; and plasma insulin levels rose from a mean of 6 muU/ml to a mean of 65 muU/ml. Thus, with this small initial dose of insulin the 2-hour plasma insulin values were within the range which in adults has been associated with a maximum fall in blood glucose concentration. Three children with established diabetes presenting with ketoacidosis were also treated with a small initial dose of intramuscular insulin, 0-1 unit/kg in 2 of the patients and 0-5 unit/kg in the third. In 2 during a period of rehydration before insulin was given, blood glucose fell at a rate of 100 mg/100 ml per hour. Over the 2 hours after the initial dose of insulin the mean rate of fall of blood glucose for all 3 patients was 73 mg/100 ml per hour. None of these children developed hypoglycaemia nor hypokalaemia during treatment. We conclude that an initial intramuscular injection of soluble insulin in the dose range of 0-1-0-5 units/kg body weight may be more appropriate and possibly safer for the treatment of diabetic ketoacidosis in children than the currently recommended larger doses divided between intravenous and intramuscular routes. Adequate rehydration must, however, remain the first priority in the management of such cases.
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PMID:Immediate metabolic response to a low dose of insulin in children presenting with diabetes. 81 Nov 77

We describe a genetic defect in a kindred in whom proinsulin or a proinsulin-like material constitutes the major fraction of circulating insulin immunoreactivity in both the fasting and stimulated states. The defect, familial hyperproinsulinemia, affects eight males and 10 females in four generations of the kindred, with an autosomal dominant mode of transmission. Familial hyperproinsulinemia is asymptomatic in the affected progeny, with no apparent relation to hypoglycemia or to the development of diabetes mellitus. This genetic defect may represent either a deficiency in the proinsulin cleaving enzyme (or enzymes) within the beta cell, or more probably, an abnormal species of proinsulin.
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PMID:Familial hyperproinsulinemia. An autosomal dominant defect. 81 12

For children with diabetes and their families, education should start immediately upon diagnosis of the disease or recovery from the initial episode of ketoacidosis and should be directed specifically toward childhood diabetes. The physician or nurse should be accessible by phone at all times in case of severe hypoglycemia or ketoacidosis. Nonemergency problems are handled during routine office visits, which should be scheduled regularly every three months. Measures important to good control include accurate daily testing of urine, proper choice and careful regulation of insulin, and maintenance of a well-balanced diet consistent in total intake and meal and snack times. Children who stay involved with peer groups and activities maintain a healthier attitude toward living with their disease.
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PMID:Pediatrics: office management of diabetes mellitus in children. 81 78

We report 18 consecutive phenformin-treated diabetic patients admitted to this Medical Service acutely ill with metabolic acidosis. Lactic acidosis was anticipated, and documented, in all. Also, however, though most of the patients had only weakly positive, or even negative, serum reactions with the nitroprusside reagent, all were found to have coexisting ketoacidosis, plasma 3-hydroxybutyrate averaging 7.1 mmol/L. +/- 3.9 (S.D.). This finding suggest that treatment of these patients should include insulin, and often also glucose, because most do not have marked hyperglycemia and some have hypoglycemia. The lactic acidosis in the nine patients who survivied was, on average, less severe than in the nine who died, but the difference was not statistically significant. Surivival correlated closely with the absence of shock on arrival. Only eight patients had a identifiable acute illness other than the metabolic acidosis. The other 10 patients had no discernible cause for the acute illness apart from their treatment with phenoformin. This finding raises serious doubts about whether phenformin should be used to treat patients with diabetes.
Diabetes 1976 Apr
PMID:Phenformin-associated metabolic acidosis. 81 51


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