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

Cataract is the major cause of blindness worldwide. It is a greater problem in third world countries than in the West and several attempts have been made to explain the excess in these countries. This paper provides an overview of the literature especially on studies designed to identify risk factors for cataract. There is an association between poverty and cataract and, more specifically, between cataract and a history of severe diarrhoea-dehydration. Recent results from a case-control-led study of cataract in Oxford are also presented with the quantitation of risks associated with a number of factors including diarrhoea, renal failure and diabetes. In this study an apparently protective effect of aspirin, paracetamol and similar drugs was observed. This protective effect applies to the risk associated with diabetes.
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PMID:Epidemiology and risk factors for cataract. 332 1

Recognized risk factors for metrizamide myelography are seizure disorder, seizure-threshold-lowering drugs, dehydration, and possibly age. After observing serious neurologic complications in diabetic patients after routine metrizamide myelography, a retrospective study was conducted to determine if diabetes should be considered another independent and important risk factor. Forty-one diabetic patients who had lumbar metrizamide myelograms were compared with a control group of 110 nondiabetic patients. A significantly higher incidence was found of severe vomiting (15% vs. 3%, p less than 0.01) and neurologic complications (20% vs. 2%, p less than 0.001) in the diabetic population. Neurologic complications included one case each of seizure, severe encephalopathy, auditory and visual hallucinations, and prolonged somnolence and four cases of confusion-anxiety. Four of the diabetic patients had major transient elevations of blood pressure. These findings suggest that diabetics are a high-risk population for metrizamide myelography. The dose of metrizamide should be minimized, whenever possible. The new nonionic myelographic agents may prove to be safer in this population, but caution and careful follow-up should be exercised in the initial trials with these patients.
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PMID:Neurologic complications in diabetics after metrizamide lumbar myelography. 348

Two male siblings with transient diabetes mellitus were of normal birth weight, were asymptomatic, and did not require treatment with insulin. This may be a previously undescribed disorder or part of the range of transient diabetes mellitus of infancy. Previously reported infants with transient diabetes mellitus of infancy have usually been small for gestational age and have presented with glycosuric dehydration, infections, or growth failure. Insulin concentrations after oral glucose challenge showed inadequate insulin secretion with respect to the degree of hyperglycaemia in these children. Autosomal dominant inheritance may occur in some families with this disorder, and parents of some affected children may also have had asymptomatic or unrecognised transient diabetes mellitus of infancy. Leucocyte histocompatibility antigen typing of this family did not show any association of specific antigens with transient diabetes mellitus of infancy in the affected children.
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PMID:A new type of transient diabetes mellitus of infancy? 351 39

Hyperosmolar hyperglycemic nonketotic diabetic coma after cardiac operations was reviewed in a total of 12 patients from the literature and from my experience in an attempt to determine the clinical features of this condition. Among the unique features of this disease were the following: The mortality is high (42%). The morbidity and mortality are higher in patients with no previous history of diabetes mellitus (67% and 50%) than in those with such a history (33% and 25%). Polyuria is usually a heralding symptom. There is an average time lag of 6 days between the onset of polyuria and the established diagnosis of hyperosmolar hyperglycemic nonketotic diabetic coma. The time lag in patients who died was 7.5 +/- 0.8 days (mean +/- standard error of the mean), significantly longer than in survivors (4.5 +/- 0.8 days). Polyuria usually emerges after the stormy immediate postoperative days have passed (on postoperative day 5.3 on the average). Polyuria is generally regarded as a favorable sign not suggestive of complicating hyperosmolar hyperglycemic nonketotic diabetic coma. Therapies known to precipitate this disorder are continued even after development of polyuria. Gastrointestinal bleeding can be a precipitating factor. Hyperalimentation or elemental diet may cause dehydration and trigger hyperosmolar hyperglycemic nonketotic diabetic coma. A high or rising serum sodium concentration and/or blood urea nitrogen level with polyuria may be a warning sign of this complication. Too hasty correction of the hyperosmolar state can be dangerous. Pulmonary dysfunction may be involved in the symptoms of hyperosmolar hyperglycemic nonketotic diabetic coma.
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PMID:Clinical features of hyperosmolar hyperglycemic nonketotic diabetic coma associated with cardiac operations. 352 Jan 59

Non-ketotic hyperosmolar diabetic coma is a complication of diabetes characterised by extreme dehydration, plasmatic hyperosmolarity and the absence of ketosis. The mortality rate is very high, especially in elderly subjects with type II diabetes. A personal series of 12 cases is reported with an assessment of general features, triggering factors, biochemical parameters at onset and treatment given. The data confirm reports in the literature and the results show the therapeutic superiority of continuous endovenous infusions of insulin at 3-10 mu/hour over other treatment protocols.
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PMID:[Nonketotic hyperosmolar coma. Clinical aspects and treatment in 12 cases]. 352 2

Insulin resistance is a well-known phenomenon in diabetic patients. Its occurrence in Type 1 (insulin-dependent) diabetes is thought to be due both to metabolic and immunological disturbances. In this context, a key role is attributed to the augmented release of the 'diabetogenic' hormones, adrenaline, glucagon, cortisol and growth hormone, as well as to hypertonic dehydration and to the presence of insulin-binding antibodies. In this connection it is noteworthy that among the 'diabetogenic' hormones adrenaline exerts the strongest insulin-antagonistic effect and that hypertonic dehydration is associated with impairment of insulin action and of non-insulin-dependent hepatic glucose uptake (in vitro), while hypotonic rehydration reduces the elevated hepatic glucose production in dehydrated Type 1 diabetic patients. By contrast, the generally only slightly elevated serum insulin-binding capacity in insulin-treated diabetics is probably of least importance in the development of insulin resistance, unless excessively high insulin antibody titres prevail.
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PMID:[Causes of insulin resistance in type 1 diabetes]. 399 44

The etiology, epidemiology, pathophysiology, and complications, therapy, and prognosis of hypernatremic (hypertonic) dehydration in infants are briefly discussed. The most likely causal condition for hypernatremic states in infants is enteric disease, because the symptoms of diarrhea and vomiting result in water loss and inability to take in water for replenishment. Other causes include dubious feeding practices, diabetes mellitus, diabetes insipidus, and maladroit diagnostic and therapeutic maneuvers, including administration of radiologic contrast medium or hypertonic sodium bicarbonate or mannitol infusions, or the use of salt solutions as an emetic. Epidemiologically, 2 factors are apparent: high saline diet and winter season. The clinical hallmarks of hypernatremic disturbance are relative preservation of circulation and early presence of neurologic symptomatology. Renal tube necrosis is also occasionally encountered. Therapy is rehydration, but the bone of contention is the technique for replacing water in the face of the fact that water administered without electrolyte causes the brain to swell and frequently results in convulsions. The management of hypernatremic dehydration begins with a replenishment phase if neither shock nor apparent anuria is present. The principle is to replenish the body slowly, and 48 hours has been chosen as the target, so that for volume the deficit plus 2 days of ongoing losses should be allocated. However, the sodium and other ion contents are derived solely from the deficit, without factoring the 2-day maintenance period. A recipe for rehydration fluid is presented.
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PMID:Hypernatremic (hypertonic) dehydration in infants. 457 33

The name juvenile tropical pancreatitis syndrome (JTPS) is proposed for a disease which affects young people of both sexes in certain parts of the tropics and which is characterised by abdominal pain, diabetes, steatorrhoea, and pancreatic calcification. The condition seems to start with blockage of the pancreatic ducts by laminated secretions or inspissated mucus plugs which later calcify. Chronic pancreatitis follows. The hypothesis is that plugs are the result of pancreatic stasis due to prolonged lack of food in the stomach and/or gastroenteritis and dehydration. Most plugs are probably dislodged during convalescence when protein-containing foods are eaten and stimulate vigorous flow of pancreatic juice. The sluggish pancreatic flow produced by very-low-protein diets may not dislodge plugs. Repeated infection and anorexia can enlarge the plugs which ultimately calcify. JTPS therefore occurs in Third-World areas with a high rate of childhood infections, and where low-protein staples are taken. Cereal staples seem to reduce the incidence of JTPS in endemic areas because of their protein content.
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PMID:Pathogenesis of juvenile tropical pancreatitis syndrome. 610 87

Thirteen cats with diabetes mellitus were evaluated. Clinical signs included polydipsia, polyuria, polyphagia, lethargy, and weight loss. Results of physical examination included obesity, hepatomegaly, mild seborrhea sicca, muscle wasting, and dehydration. One cat walked plantigrade and was suspected of having a diabetic neuropathy. Persistent hyperglycemia, glucosuria, high liver enzyme activities, hypercholesterolemia, hyperproteinemia, and low electrolyte concentrations were the common laboratory findings. In 3 cats diabetes mellitus developed after megestrol acetate therapy; 2 of these cats required only temporary insulin treatment. In a 3rd cat, which had no history of receiving diabetogenic drug therapy, remission of diabetes mellitus also was observed. Serum insulin and plasma glucose concentrations were determined in 6 cats after administration of an intermediate-acting insulin (isophane insulin) and in 3 cats after administration of a long-acting insulin (protamine zinc insulin). The insulin concentration peaked 2 to 6 hours after the injection of intermediate-acting insulin and 6 to 12 hours after the injection of long-acting insulin. The lowest glucose concentration was recorded 4 to 8 hours after injection of intermediate-acting insulin, and 6 to 12 hours after injection of long-acting insulin. It was concluded that, although insulin therapy must be adjusted to the individual, the diabetic cat usually requires twice-daily administration of isophane insulin; however, the protamine zinc insulin can be given once daily for satisfactory control.
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PMID:Insulin therapy in cats with diabetes mellitus. 629 64

The physiopathology and clinical picture of hyperosmolar diabetic coma are described, and four personal cases are presented. This form of coma is a rare, but particularly serious complication of diabetes mellitus. Since its prognosis is poor, even when suitable treatment is provided, the greatest possible care should be devoted to preventing its main cause, namely dehydration.
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PMID:[Hyperosmolar diabetic coma. Case reports and review of the literature]. 633 18


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