Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0162275 (ketonuria)
 553 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nonketotic hyperosmolar diabetic coma is a rare manifestation of juvenile diabetes, in contrast to adult onset diabetes. To date only 20 cases have been published, the majority of them infants and toddlers. This type of diabetic coma is seen with unusual frequency in children with Down's syndrome and psychomotor retardation. The clinical picture is characterised by severe dehydration, hyperglycemia with often extremely high blood sugar levels, hyperosmolarity and glucosuria without ketonuria. Mortality in children has been high (24%). This paper reports the case of a 14-month-old girl with Down's syndrome. Clinical and therapeutic as well as pathogenetic aspects are discussed.
 ...
PMID:[Hyperosmolar nonketotic diabetic coma in children]. 15 87

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.
 ...
PMID:[Diabetes mellitus in childhood and adolescence. Clinical types]. 48 58

A 85-year-old man was admitted to our hospital because of semicomatous status. Laboratory data on admission showed elevation of blood sugar (823 mg/dl) and serum osmotic pressure (345 mOsm/l), but ketonuria was not detected. Non-ketotic hyperosmolar diabetic coma was diagnosed. The insulin infusion and physiological saline improved the blood sugar level and consciousness within a day. The abdominal ultrasound examination revealed an abscess in the left kidney and right psoas muscle. The same findings were seen by abdominal computed tomography but the possibility of malignant neoplasm of the left kidney could not be ruled out because of a swelling of the left adrenal gland. Pain associated with psoas abscess and low grade fever were observed. Because of his poor general condition, drainage of the abscess was not performed and conservative therapy using antibiotics was administered. Without any improvement of the abscess, he died due to general deterioration four months later. Autopsy findings showed carcinoma of the left renal pelvis and metastasis to the right psoas muscle, left adrenal gland, liver, bilateral lungs and lymph modes. Psoas abscess is a relatively uncommon disease, especially in elderly patients. The etiology of the disease is divided into primary and secondary causes. Most secondary psoas abscess cases are caused by intestinal diseases, and Crohn's disease has been related to the highest incidence. A few cases of psoas abscess caused by colorectal carcinoma have been reported. Ultrasound and computed tomography are useful in diagnosing this disease and drainage of an abscess is necessary for therapy and proving the cause. Cancer metastasis should considered in differential diagnoses, when psoas abscess is seen in elderly patients.
 ...
PMID:[A case of psoas abscess due to renal pelvic carcinoma complicated with non-ketotic hyperosmolar diabetic coma]. 175 33

We have seen a case of "diabetic non-ketotic hyperosmolar coma" with ketosis. An 84-year-old man was brought into the hospital in a deeply comatous and dehydrated state. The initial blood glucose level was 1252 mg/dl with plasma osmolarity of 435 mOsm/l, but no ketonuria was detected by the nitroprusside method (Ketostix). However, the plasma 3-hydroxybutyrate (3-OHBA) level was 5 mM in a newly developed bedside film test. The serum ketone bodies were later found to be 5.56 and 0.82 mmol/l for 3-OHBA and acetoacetate (AcAc), respectively. A marked increase in glucagon, cortisol and ADH with renal dysfunction (creatinine 5.0 mg/dl) were noted. An abnormal electrocardiogram, occular convergence and chorea like movement disappeared after correction of metabolic disturbances. The moderate level of IRI (14 microU/ml) on admission and a good response to glucagon 2 months after admission also indicate that the present case is a typical hyperosmolar non-ketotic coma. Because of a preferential increase in 3-OHBA, ketonuria seemed to be absent in the regular nitroprusside test. Marked dehydration is thought to cause renal dysfunction, and the increase in ADH may have helped to prevent further aggravation of ketoacidosis. We propose to change the term hyperosmolar non-ketotic coma (HNC) to diabetic hyperosmolar coma (DHC), because sometimes patients with hyperosmolar non-ketotic diabetic coma are ketotic, as seen in the present case. Determination of 3-OHBA or individual ketone bodies in blood is important and essential for the differential diagnosis of diabetic coma. The diagnosis of either ketoacidotic or hyperosmolar coma should be made depending on the major expression of ketoacidosis or hyperglycemic hyperosmolarity.
 ...
PMID:A case of diabetic non-ketotic hyperosmolar coma with an increase with plasma 3-hydroxybutyrate. 184 65

It has been reported that sand rats, naturally feeding on low-caloric-value plants containing a high concentration of salt, become obese and develop hyperglycemia when fed on a standard laboratory diet. The aim of this study was to examine the long-term effects of a synthetic-chow diet on the metabolic pattern of the diabetic syndrome in a large group of sand rats. While a few animals had a fulminant reaction with markedly decreased glucose tolerance, low plasma insulin levels, and death within 3-4 wk, most sand rats developed obesity and elevated plasma insulin levels. From the third month and forward, 40% of sand rats presented with a diabetic syndrome with hyperinsulinemia, hyperglycemia, markedly decreased glucose tolerance, and insulin resistance. This diabetic syndrome can be compared with maturity-onset (type II) diabetes. When this synthetic-chow diet was given for more than 6 mo, the majority of animals lost considerable weight and showed a major depletion of fat stores. Serum immunoreactive insulin levels fell, while blood glucose rose to above 500 mg/dl with glycosuria and ketonuria. The elevated triglyceride content of plasma and the lipid deposits in the liver were greatly augmented, and no glycogen was present. Animals developed frank insulin-dependent diabetes, and diabetic animals not treated with insulin died in diabetic coma with presumed ketoacidosis. The disease was essentially confined to sand rats showing abnormal glucose tolerance, even before eating laboratory chow. This observation suggests a genetic factor. Thus, the sand rat appears to be a potentially interesting model for investigation of both maturity-onset and insulin-dependent diabetes.
 ...
PMID:Diabetes mellitus in sand rats (Psammomys obesus). Metabolic pattern during development of the diabetic syndrome. 637 52

Diabetes mellitus was diagnosed in an aged bonnet macaque (Macaca radiata). Six months later the monkey was found comatose. Laboratory findings of extreme hyperglycemia, hyperosmolality, and glycosuria without ketonuria were consistent with a diagnosis of hyperosmolar, non-ketotic diabetic coma (NKC). Further laboratory studies disclosed very low levels of immunoreactive insulin and depressed free fatty acid values. Growth hormone and cortisol levels were within normal limits.
 ...
PMID:Hyperosmolar non-ketotic diabetic coma in the nonhuman primate: a first report. 685 68

Bilateral putaminal hemorrhages rarely occur simultaneously in hypertensive patients. The association of intracerebral hemorrhage with cerebral edema (CE) has been rarely reported in diabetic patients. We present a patient with bilateral putaminal hemorrhage (BPH) and CE during the course of hyperglycemic hyperosmolar syndrome (HHS). A 40-year-old man with a history of diabetes mellitus and chronic alcoholism was admitted with acute impaired mentality. His blood pressure was within the normal range on admission. Laboratory results revealed hyperglycemia and severe metabolic acidosis without ketonuria. After aggressive treatment, plasma sugar fell to 217 mg/dl, but brain CT showed BPH and diffuse CE. Our case demonstrated that HHS should be considered as a cause of BPH with CE. Initial brain imaging study may be recommended for patients with diabetic coma.
 ...
PMID:Bilateral putaminal hemorrhage with cerebral edema in hyperglycemic hyperosmolar syndrome. 1220 43