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

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

The objective of this paper is to characterize the fat cow syndrome. This condition refers to a combination of metabolic, digestive, infectious, and reproductive conditions which affects the obese periparturient cow. The condition develops primarily due to faulty feed management which permits excessive consumption of unbalanced diets. The syndrome is frequently a herd problem characterized by a high morbidity and mortality due to an increase in disease in periparturient cows. Clinical signs include depression, anorexia, ketonuria, marked decrease in production, progressive debilitation, weakness, nervous signs, and an elevation in temperature due to infectious disease. The obesity is generalized throughout the body with extensive fatty metamorphosis in the liver. Histological changes are primarily in the liver and kidney. Treatment of the condition consists of feeding a balanced diet, symptomatic treatment, and good supportive care. The condition can be prevented by feeding a balanced diet according to nutrient requirements of the National Research Council.
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PMID:Fat cow syndrome. 96 40

Propionyl CoA carboxylase deficiency was found in a 7-month-old boy who presented with attacks of vomiting, anorexia, weight loss, weakness, and hypotonia. He failed to thrive and had generalized seizures. He had propionic acidemia and hyperglycinemia; these are the manifestations of the ketotic hyperglycinemia syndrome. However, ketonuria was not a consistent part of his clinical picture, and he had at least two episodes of acute overwhelming illness, the latter one fatal, in which ketones were never found in the urine. Large amounts of pyrrolidone carboxylic acid were found in body fluids.
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PMID:Hyperglycinemia and propionyl coA carboxylase deficiency and episodic severe illness without consistent ketosis. 113 51

Calcium hopantenate (HOPA) has been widely used as an activator of cerebral metabolism in Japan. However, several cases of acute encephalopathy during HOPA administration were recently reported, which were characterized by marked metabolic acidosis and hypoglycemia. The encephalopathy in these patients was named Reye-like syndrome because of the similarity to Reye's syndrome in children. The purposes of this presentation are to report on 5 patients with acute encephalopathy developing during HOPA administration, to summarize their symptoms and clinical courses, and to discuss the pathogenesis of metabolic acidosis and hypoglycemia. Initial characteristics of the clinical course in all patients were loss of appetite, nausea and vomiting, followed by unconsciousness. Laboratory examinations revealed marked metabolic acidosis, severe hypoglycemia, hyperlactacidemia, leukocytosis, ketonuria, and increased Ht and BUN. A few days after development of the initial symptoms, mild renal and liver dysfunction, and elevation of serum amylase were observed in all patients. Hyperlactacidemia was present in 4 in the initial period. Blood concentration of HOPA was 2.131 micrograms/ml in patient 1 (8-10 hours after final administration), and 10.7 micrograms/ml in patient 5 (24 hours after final administration). These values are extremely high, because usually HOPA concentration is almost negligible 7 hours after the drug is taken. As the pathogenesis of acute encephalopathy due to HOPA administration, the failure of fatty acid beta-oxidation has been proposed by some investigators. However, the serum concentrations of CoA, pantothenic acid and carnitine during the initial stage were not reduced in our patients. Furthermore, it is very difficult to explain the severe hypoglycemia in terms of the beta-oxidation theory.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Metabolic acidosis and hypoglycemia during calcium hopantenate administration--report on 5 patients]. 258 87

An alpaca and a llama in late stages of gestation were evaluated for lethargy, anorexia, and recumbency. Both camelids had cloudy, white, turbid serum, elevated serum triglyceride (1564, 5658 mg/dL, respectively) and cholesterol (158, 297 mg/dL, respectively) concentrations, and ketonuria. Signs of fetal stress were evident ultrasonographically in the alpaca, and a live cria was delivered by Cesarean section performed under general anesthesia. The alpaca developed severe metabolic acidosis, hepatic lipidosis, and acute renal failure secondary to renal lipidosis and died 36 hours after admission despite medical therapy. Histopathology revealed renal and hepatic lipidosis and neutrophilic pancreatitis. The cria died 72 hours after birth. The llama responded to IV electrolyte, dextrose, and regular crystalline insulin therapy. The pregnancy was maintained, and the llama was discharged from the hospital 20 days after admission. Two months after discharge, the llama gave birth to a live, 5 kg cria. Findings of hypertriglyceridemia, hypercholesterolemia, elevated sorbitol dehydrogenase activity, metabolic acidosis, azotemia, and ketonuria occurred in these two camelids. Based on this report, camelids appear to be similar to both horses and cattle in their response to severe energy imbalances in late gestation.
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PMID:Hyperlipemia and ketonuria in an alpaca and a llama. 806 56

A 9-year-old spayed female Labrador Retriever was evaluated for anorexia, lethargy, and vomiting of 5 days' duration. Laboratory abnormalities included azotemia, high liver enzyme activities, hyperchloremic metabolic acidosis, glucosuria, ketonuria, proteinuria, and aminoaciduria. These laboratory abnormalities were diagnostic of proximal renal tubular acidosis and Fanconi syndrome. Results of initial and convalescent serologic tests for leptospirosis were negative. The dog was treated with amoxicillin, sodium bicarbonate, and potassium citrate at discharge. Repeated evaluations revealed resolution of the acidosis, azotemia, proteinuria, glucosuria, ketonuria, and high liver enzyme activities. Alkali administration was gradually discontinued, and the dog was clinically normal 8 months after discharge. The dog's clinical condition appeared to have been transient in nature, a phenomenon that is rarely seen in human or veterinary medicine.
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PMID:Transient proximal renal tubular acidosis and Fanconi syndrome in a dog. 1515 30

Case history The two obese mandrills (Mandrillus sphinx) showed clinical signs of depression, anorexia, hyperglycemia, hypertriglyceridemia, glucosuria, proteinuria and ketonuria. Septic bed sore wounds were noted on both fore and hind limbs. Results Histopathological study revealed severe islet amyloidosis in both mandrills. Immunohistochemical study using polyclonal anti-cat amylin antibody confirmed derivation of the islet amyloid from islet amyloid polypeptide (IAPP). Cardiomyopathy and myocardial fibrosis were also evident. Conclusions The present study documents diabetes mellitus in two obese mandrills. Diabetes in these animals had features very similar type 2 diabetes mellitus of humans, including the development of severe, IAPP-derived islet amyloidosis. The mandrill may, therefore, serve as an animal model of human type 2 diabetes mellitus.
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PMID:Spontaneous diabetes mellitus in captive Mandrillus sphinx monkeys: a case report. 1819 24

True euglycemic diabetic ketoacidosis [blood glucose <200 mg/dl (11.1 mmol/l)] is relatively uncommon and in type 1 diabetes can be caused by starvation of any cause in conjunction with an intercurrent illness. We report a case of euglycemic diabetic ketoacidosis precipitated by starvation resulting from severe depression in a patient with type 1 diabetes. He was acidotic with ketonuria, but his blood glucose was only 105 mg/dl (5.8 mmol/l). He was rehydrated, the acidosis was corrected, and his depression was later treated. This case involves the complex interplay among type 1 diabetes, depression, ketoacidosis, and starvation physiology resulting in glucose concentrations in keeping with euglycemic diabetic ketoacidosis. The case also highlights that even in the absence of hyperglycemia, acid/base status should be assessed in an ill patient with diabetes, and in cases of euglycemic diabetic ketoacidosis, the diagnosis of depression should be considered as a cause for suppressed appetite and anorexia.
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PMID:Starvation-induced true diabetic euglycemic ketoacidosis in severe depression. 1897 36

New-onset diabetes mellitus after transplant is a well-recognized complication of tacrolimus immunosuppression and commonly occurs as a form of type 2 diabetes mellitus. However, tacrolimus-associated acute pancreatitis causing diabetic ketoacidosis has not been reported in heart transplant patients. We report a 22-year-old women hospitalized owing to diabetic ketoacidosis associated with acute pancreatitis 7 months after a heart transplant. Her immunosuppression included tacrolimus. She was admitted with complaints of polydipsia, anorexia, and abdominal pain of 3 days' duration. Her initial laboratory test revealed a toxic level of tacrolimus (> 30 ng/mL), severe hyperglycemia (39 mmol/L), severe metabolic acidosis (pH 6.9), and ketonuria, although diabetes mellitus had never been diagnosed. Serum amylase and lipase levels and abdominal computed tomography suggested the presence of acute pancreatitis. After correcting the diabetic ketoacidosis and getting the tacrolimus level to the normal range, she was discharged home. Three months later, insulin was replaced with oral hypoglycemic agents. Pancreatitis can present with diabetic ketoacidosis in the recipient of a heart transplant treated with tacrolimus. Clinicians should pay more attention to tacrolimus levels and the risk of pancreatitis.
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PMID:Diabetic ketoacidosis associated with acute pancreatitis in a heart transplant recipient treated with tacrolimus. 2307 84

A case of fulminant type 1 diabetes mellitus secondary to administration of pembrolizumab in a patient with urothelial carcinoma is presented. Eight days after the third infusion of pembrolizumab, the patient presented with complaints of malaise and anorexia. The patient's laboratory data showed a blood glucose level of 1092mg/dl with ketonuria and negative for glutamic acid decarboxylase antibody. As leaving ketoacidosis by insulin therapy, pembrolizumab therapy was continued without delay. After administration of another eight infusions of pembrolizumab, the patient's disease was stable without new severe side effects.
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PMID:Fulminant type 1 diabetes mellitus induced by pembrolizumab in a patient with urothelial carcinoma: A case report. 3121 Oct 60


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