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Query: UMLS:C0162275 (ketonuria)
 553 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Spontaneous diabetes mellitus was diagnosed in six of 126, 13-lined ground squirrels, Citellus tridecemlineatus. Serum glucose values were significantly higher in the diabetic ground squirrels than in the non-diabetic ground squirrels, while serum insulin values of fasted diabetic squirrels were significantly lower than fasted nondiabetic ground squirrels. In addition, the classic diabetic signs of poly-dipsia, polyuria, glycosuria, ketonuria, polyphasia, and weight loss were present. The proportion of islet tissue to total pancreatic area in diabetic ground squirrels was less than 25% of that in the nondiabetic ground squirrels. Both the number and size of the islets of Langerhans in diabetic ground squirrels were less than those in nondiabetic ground squirrels.
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PMID:Diabetes mellitus in the 13-lined ground squirrel (Citellus tridecemlineatus). 33 78

It is today's general medical opinion that children's diabetes mellitus was uncommon in the past. It was generally admitted at that time the initail stages were so sudden as to make difficut its early diagnosis. It's increased incidence is at present an alarming truth; however, a parallel increase of diabetic coma or of mulminant types has rather dropped. Diabetes may be diagnosed by just considering the main symptoms at the onset which are polydipsia, polyuria and weight loss. If an early diagnosis is not made, acidosis (abdominal pain, nausea, vomiting) may appear within a few days or weeks followed by coma (Kussamul's acidotic respiration and dehydration). Coma may be avoided by an early diagnosis and a life may be saved. It must be stressed that an important percentage of children and adolescents show a slow and gradual evolution (week or months) of their diabetes: gradual weight loss, sometimes with noticeable polyphagia, occasional enuresis, but without other associated symptoms. Asymptomatic, intermittent glucosurias are also frequent; they vary in magnitude an almost always they appear without ketonuria and with fasting normal glycemia. According to our experience they may precede in weeks or months the clinical manifestations of the disease. Postprandial glycemia is a sure diagnostic resource; it is of greater trustworthines than fasting glycemia; therefore we advise it as a routine diagnostic procedure which we recommend widely. In uncertain situations, the oral glucose tolerance test is advisable.
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PMID:[Diabetes mellitus in childhood and adolescence. Clinical types]. 48 58

We have recorded clues to the clinical recognition of chronic insulin overdosage in 101 pediatric patients with diabetes mellitus, identified predisposing circumstances, and reconsidered the traditional strategy of slow reduction in insulin dose. Overtreatment occurred in 70%, overall, and in 90% of those referred for instability; mean overdose was 38% of the readjusted dose. The most common findings were frank hypoglycemic episodes, polyuria/nocturia/enuresis despite increasing insulin dosage, excessive appetite, hepatomegaly, weight gain, headaches, exercise intolerance, marked variation in glucosuria, mood swings, and frequence bouts of rapidly developing ketoacidosis. Overtreatment usually developed because of attempts to achieve metabolic control using glucosuria as principal criterion. One fourth of those observed became overtreated during periods of emotional turmoil when need for increased insulin to counter stress-induced hyperglycemia and ketosis led to chronic increase in dosage. Persistent glucosuria/ketonuria and exacerbation of hypoglycemic symptoms were more frequent with slow than with rapid reduction in insulin dosage.
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PMID:Chronic overtreatment with insulin in children and adolescents. 88 3

Very fat people die earlier than people of normal weight because hypertension, diabetes and coronary disease are more frequent among the markedly obese. Most obese subjects, however, are only slightly overweight and their mortality is not elevated. Reasons for dieting are more often psychological than somatic. 2. Reducing diets are ineffective because the obese rarely follow them. Total fasting and intestinal bypass may provide better results, but are more dangerous. 3. Atkins' diet eliminates carbohydrates from food without restricting protein and fat intake. Deprived of carbohydrates, the body uses fat for fuel. A small part of metabolized fat is eliminated in the urine as ketone bodies, and this is why such diets are called "ketogenic". They have been known at least since 1863. 4. Caloric loss due to ketonuria does not exceed 100 Cal/day in the non-diabetic. It is maximal during total fasting and cannot be increased by a ketogenic diet. 5. In the short run, such diets produce rapid weight loss due to polyuria. On the other hand, refeeding carbohydrates causes water retention and weight gain. 6. The diet decreases appetite: patients eat less without feeling severe hunger and without measuring their food intake. 7. Orthostatic hypotension, fatigue, and nausea are frequent, despite what Dr. ATKINS claims. 8. The diet increases plasma cholesterol and uric acid. It may be dangerous in diabetes (anorexia, acidosis) and in heart or kidney failure (hypokalemia). 9. The diet, though far from good, is better than the book. ATKINS' theories are at best half-truths, and the results he claims lack credibility. The obese subject's disappointment with traditional reducing diets and the book's hard-sell style account for ATKINS' success.
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PMID:[Dr. Atkins' dietetic revolution: a critique]. 89 45

Diabetes mellitus was tentatively diagnosed in a black-footed ferret with polyuria, polydipsia, polyphagia, dehydration, and weight loss. Laboratory findings (marked hyperglycemia (724 mg/100 ml), glycosuria, and ketonuria) and the subsequent favorable response to insulin therapy confirmed the diagnosis. Although lesions were not observed in the pancreas, gross and histologic findings concomitant with diabetes mellitus included arteriosclerosis, with calcification of the aorta and other major vessels; mild necrotizing hepatitis; and mild proliferative glomerulonephritis. A perineal adenocarcinoma, with metastasis to an internal iliac lymph node, was an incidental finding. Special stains demonstrated adequate numbers of beta cell granules in the islets of Langerhans. Thus, the diabetes was apparently due to a lack of release of the synthesized insulin or to diminished effectiveness of the secreted insulin.
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PMID:Diabetes mellitus in a black-footed ferret. 92 62

The French incidence study has registered all new cases of Type 1 diabetic children under 20 years of age, from a population of 2.32 million, in an exhaustive and prospective manner. Three hundred and forty cases were identified between 1 January 1988 and 31 December 1989, yielding a mean annual incidence rate 7.3 per 10(5). The lowest rate was observed in the youngest age group (0-4 yr: 4.1 per 10(5)) and the highest around pubertal development (10-14 yr: 11.5 per 10(5)). Details of the previous personal and family history, and the clinical and biological pictures of the disease at diagnosis were recorded. Almost 8 per cent of the children had a first-degree relative with Type 1 diabetes. Polyuria, weight loss, fatigue and abdominal pain were the most frequently reported symptoms, which were of median duration 4.4 months. Mean weight loss before diagnosis was 9.4 +/- 6.8 (+/- SD)% of body weight and was not significantly related to age. Ketonuria was detected in 83.8 per cent and acidosis (total CO2 less than or equal to 18 mmol l-1, if measured) in 48 per cent of the cases. Ketonuria and acidosis were significantly more frequent in the younger age group than in the rest of the group (p less than 0.001).
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PMID:Clinical and laboratory features of type 1 diabetic children at the time of diagnosis. 157 13

Ten young adult cystic fibrosis (CF) patients over 16 years of age (average 21.4 years) began nighttime enteral feedings as a method of nutritional rehabilitation to regain and maintain body weight. Patients received nighttime feedings of 1,000 kcal/M2 of a low- (Pulmocare), medium- (Ensure Plus), or high-carbohydrate (Vivonex) formula for at least 2 nights each with pancreatic enzyme therapy. Five of ten young adult CF patients developed nocturnal hyperglycemia (serum glucose greater than 300 mg/dl) and glucosuria (1-3% glucose) with varying degrees of polyuria during enteral feedings. No patient developed ketonuria despite serum glucoses at times greater than 600 mg %. There was no difference between the hyperglycemic and normoglycemic groups in median age, percent of ideal body weight, NIH score, Brasfield scores, pulmonary function tests, or family history of diabetes. All normoglycemic and four of five hyperglycemic patients had normal fasting blood sugars. The percent hemoglobin A1c was greater in the glucose intolerant group than the normoglycemic patients (11.2 +/- 0.8% vs. 6.8 +/- 1.1%, mean +/- SE, p less than 0.005). Twelve to 15 units of NPH insulin prior to initiation of feedings provided adequate therapy in most hyperglycemic patients. There was no apparent difference in the elevation of early morning serum glucoses with the low- medium- and high-carbohydrate formulas. We concluded that hyperglycemia requiring insulin therapy was common in young adult CF patients using nighttime enteral feedings. A hemoglobin A1c appeared to be a useful screening test before initiating such therapy.
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PMID:Glucose intolerance with low-, medium-, and high-carbohydrate formulas during nighttime enteral feedings in cystic fibrosis patients. 249 15

We report a rare case of Klebsiella pneumoniae meningitis associated with liver abscess, which was successfully treated with cefotaxime (CTX), one of the third-generation cephalosporins. A 53-year-old man was admitted to Keio University Hospital on June 13, 1988, because of a fever and a headache. On June 3, he suddenly started shivering and his temperature rose to 39 degrees C. He then began to complain of polydipsia, polyuria, and a weight loss of 4 kg a week. On June 11, he developed a severe headache. Four years prior to this incident, he had been diagnosed as having diabetes after a routine medical examination, but had neglected to undergo medical treatment. On admission, laboratory data showed leukocytosis, hyperglycemia (394 mg/dl) and ketonuria (4+). A lumbar puncture yielded cloudy cerebrospinal fluid (CSF) containing 500/3 cells/mm8, of which about 70% were neutrophils. A diagnosis of diabetic ketoacidosis and purulent meningitis was made. A treatment with ampicillin (ABPC) and CTX, (12 g/day, each) was begun. On the third day, cultures of a blood specimen and CSF yielded both K. pneumoniae. The MICs of CTX to K. pneumoniae isolated from blood and CSF were both 0.05 microgram/ml. ABPC was discontinued, gentamicin was administered for 2 days, CTX was continued at the same dosage level and an administration of prednisolone 40 mg daily was begun.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Klebsiella pneumoniae meningitis associated with liver abscess: a case report]. 269 13

The BB rat model of spontaneous diabetes mellitus was discovered in 1974 in Ottawa in a colony of specific pathogen-free Wistar rats. Investigations to determine the cause of rapid weight loss and death in a few weanling rats from this colony revealed polydypsia, polyuria, glucosuria, ketonuria, and hyperglycemia. These signs regressed and normal weight gain occurred when daily insulin therapy was given. Histologic studies of the pancreas of affected animals showed fibrosis and absence of beta cells. The original colony was established by crossbreeding the clinically normal parents of the diabetic animals. Approximately 10% of the offspring of these matings became diabetic. This incidence was increased to approximately 25% by father-daughter mating, suggesting a genetic component in the etiology.
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PMID:The discovery and development of the BB rat colony: an animal model of spontaneous diabetes mellitus. 686 71

When glucose utilisation is impaired due to decreased insulin effect, ketones are produced by the liver from free fatty acids to supply an alternate source of energy. This adaptation may be associated with severe metabolic acidosis and tends to occur in patients with type I (insulin-dependent) diabetes mellitus. In addition, hypovolemia is an almost invariable finding with marked hypoglycemia and is primarily induced by the associated glucosuria. Ketoacidosis stimulates both the central and peripheral chemoreceptors controlling respiration, resulting in alveolar hyperventilation (Kussmaul's respiration). With the ensuing fall in pCO2 the patient tries to raise the extracellular pH. A fruity odor of acetone on the patient's breath sometimes suggests that ketoacidosis is present. The classical triad of symptoms associated with hyperglycemia are polyuria, polydipsia, and weight loss. Circulatory insufficiency with hypotension is not uncommon due to the marked fluid loss and acidemia. In more severely affected patients, neurologic abnormalities may be seen, including lethargy, seizures or coma. Some patients also have marked vomiting and abdominal pain. The history and physical examination may provide important clues to the presence of uncontrolled diabetes mellitus. Once suspected, the diagnosis can be easily confirmed by measuring the plasma glucose concentration. Glucosuria and ketonuria can be semiquantitatively detected with reagent sticks. Blood gas analysis and anion gap give objective information as to the severity of the metabolic acidosis. Therapy must be directed toward each of the metabolic disturbances: hyperosmolality, ketoacidosis, hypovolemia and potassium, and phosphate depletion. The mainstays of therapy are the administration of low-dose insulin and volume repletion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Ketoacidotic diabetic metabolic dysregulation: pathophysiology, clinical aspects, diagnosis and therapy]. 817 67


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