Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chemotherapeutic agents, blood products and hyperalimentation solutions have been administered and recurrent diabetic ketoacidosis has been treated via vascular access procedures in 13 patients during the period from 1972 through 1977. Bovine heterograft, saphenous vein graft and the direct arteriovenous fistulae have been successfully utilized in the construction of arteriovenous fistulae in patients requiring vascular access for nonhemodialysis purposes. Operative techniques and therapeutic usefulness are discussed.
 ...
PMID:Nondialysis uses for vascular access procedures. 11 35

Hypophosphatemia with or without phosphorus depletion can be observed in various diseases--particularly diabetic ketoacidosis, respiratory alkalosis, alcoholism, parenteral nutrition and hyperalimentation--and may cause serious neurologic, muscular, and hematologic disorders. This review summarizes the knowledges about hypophosphatemia--etiological mechanisms, pathophysiology and therapeutic modalities--and suggests that some place be reserved for serum phosphate in systematic and emergency panels of blood tests.
 ...
PMID:[Hypophosphatemia. A review (author's transl)]. 11 83

Hypophosphatemia is common in hospitalized patients and occurs under a variety of circumstances other than parathyroid hormone excess. Charts of 100 inpatients with hypophosphatemia were reviewed and the patients divided into five groups on the basis of serum phosphate level: 18, 2.1 to 2.4 mg/dL; 49, 1.6 to 2.0 mg/dL; 20, 1.1 to 1.5 mg/dL; 12, 0.6 to 1.0 mg/dL; 1, 0.1 to 0.5 mg/dL. The effect of glucose ingestion on serum phosphate level was shown in one normal patient. Whenever carbohydrate was administered intravenously (45 cases), this was considered the primary cause of the hypophosphatemia. Other causes were as follows: diuretics, hyperalimentation, alcoholism, respiratory alkalosis, dialysis, insulin, corticosteroids, diabetic ketoacidosis, vomiting, phosphate-binding antacid, Gram-negative sepsis, primary hyperparathyroidism, saline, epinephrine, gastrointestinal malabsorption, and unknown. Hypophosphatemia in hospitalized patients may have multiple causes.
 ...
PMID:Hypophosphatemia in hospitalized patients. 44 90

Glucose tolerance and insulin responses have been examined over extended periods in severely obese, but otherwise healthy, subjects. Three significant points emerge from this study. First, it was shown that obese, supposedly ketosis resistant, subjects may deteriorate in a brief time span from a state of normal glucose disposal and adequate or increased insulin responses to insulin-deficient diabetes, culminating in ketoacidosis. Unusually high blood glucose levels complicating the ketoacidosis in two patients suggest hyperosmolarity obesity and added risk factor in severely obese diabetics. It appears that, after long-standing obesity and after years of hyperinsulinemia, a large weight gain due to prolonged overeating may impose an excessive challenge to islet cells of marginal competence. Such an event by itself or a superimposed stress or both may then cause acute insulin deficiency and/or insulin resistance leading to diabetic ketoacidosis. Hyperosmolarity may be exacerbated in the obese with cessation of food intake due to large losses of salt and water. Second, many symptoms and manifestations of hyperphagic obesity are similar to the early functional abnormalities of decompensated diabetes. The advent of the critical phase of uncontrolled diabetes, therefore, fails to alarm the obese patient and may escape timely recognition by the physician. Third, technical and mechanical difficulties due to severe obesity are apt to cause critical delays in therapy. These factors, when added to coexisting hyperosmolarity and ketoacidosis, probably account for the high mortality in these patients.
 ...
PMID:Evolution of diabetic ketoacidosis in gross obesity. 80 48

A 13-year-old spayed Doberman Pinscher with acute vomiting of 24 hours' duration and concurrent 2-week history of polyphagia with weight loss had diabetic ketoacidosis complicated by acute pancreatitis and exocrine pancreatic insufficiency. Diagnostic testing for exocrine pancreatic insufficiency, by determining serum trypsin-like immunoreactivity, revealed an unexpectedly high result when a low result was anticipated. High trypsin-like immunoreactivity was attributed to acute pancreatic inflammation.
 ...
PMID:High serum trypsin-like immunoreactivity secondary to pancreatitis in a dog with exocrine pancreatic insufficiency. 210 25

The hospital pharmacist is in a unique position to assist in the management and monitoring of the diabetic patient. He can alert the nurse and physician concerning medication errors involving the use of insulin and oral sulfonylureas. Medication errors may not only jeopardize the metabolic control of a person with diabetes but may also result in the development of significant hypoglycemia. Insulin orders should be written clearly and concisely. The advocation for intensive split-dose regimens and the use of insulin infusion devices require careful attention to technique, administration times and insulin doses. Inappropriate doses of insulin given to patients suffering from diabetic ketoacidosis may lead to significant morbidity. The hospital pharmacist must also carefully survey insulin orders for patients requiring hyperalimentation solutions and those persons requiring reduced caloric intake. The rational use of oral sulfonylureas requires a knowledge of potency differences and appropriate dosage adjustments in order to avoid hypoglycemic reactions.
 ...
PMID:Monitoring the patient with diabetes mellitus--how to avoid medication errors. 1031 2

We report a 15-year-old Muslim boy with insulin-dependent diabetes mellitus (IDDM) who presented with diabetic ketoacidosis (DKA) during the Muslim Ramadan month of day-time fasting. DKA apparently occurred due to omitting pre-lunch insulin combined with dehydration and overeating during the permitted sunset-to-sunrise meals. It is well-known that fasting accelerates development of lipolysis and ketosis and increases glucagon levels. Thus, these pathophysiological aberrations related to fasting in ketosis-prone patients, in conjunction with fasting, endanger metabolic control in IDDM.
 ...
PMID:[Diabetic ketoacidosis during the Ramadan fast]. 1086 72

We report a 43-year-old man who presented diabetic ketoacidosis 1 year after receiving kidney transplantation. He was a recipient of renal transplantation treated with metyl-prednisolone and tacrolimus regimen. The serum level of tacrolimus was 12.4 ng/ml, and he showed hyperphagia before a month of admission. A week before admission, he was aware of polydipsia, polyuria, and general fatigue. He visited our hospital and was found to have severe hyperglycemia (925 mg/dl), significant ketosis and mild metabolic acidosis (pH 7.341), although he had not been diagnosed as diabetes mellitus. He administrated in our hospital, and was treated with insulin for 5 weeks. He was not obese (BMI = 18.2 kg/m(2)) and had no family history of type 2 diabetes. He was finally treated with diet therapy alone. The 24 h urine C-peptide secretion on the third hospital day was low (8.4 microg per day). However, no autoantibodies against pancreatic islets were positive, and his insulin secretion was recovered at discharge suggesting that he was not type 1 diabetes. Although, tacrolimus has been reported to cause or worsen diabetes mellitus, the present case suggests that it could cause severe decrease in insulin secretion which leading to diabetic ketoacidosis in lean subject without previous history of diabetes mellitus.
 ...
PMID:Sudden onset of diabetes with ketoacidosis in a patient treated with FK506/tacrolimus. 1187 16

Craniopharyngioma management is challenging. Although histology is benign, the tumour can be clinically aggressive with local invasion and frequent recurrences. Extensive morbidity may be present at diagnosis and furthermore, occurs as a consequence of neurosurgery and radiotherapy. Hypothalamic symptoms can have a devastating effect on quality of life and may reduce life expectancy. This case highlights both the challenge of managing hyperphagia and morbid obesity and the importance of initial treatment preserving existing hypothalamic function and the need to avoid tumour recurrence and further surgery. A 11-year old boy presented with hydrocephalus secondary to a craniopharyngioma (he had visual failure and hypopituitarism but few hypothalamic symptoms). He underwent radical resection followed by radiotherapy. Following this treatment, he developed psychological and behavioural problems and hyperphagia. Weight gain in the first year (an increase from +1.4 to +3.7 s.d.) resulted in poor mobility and a fall which caused a slipped femoral epiphysis. In the next year, there was a 6-month period of unexpected weight loss (+4.2 to +3.8 s.d.) that culminated in emergency treatment for diabetic ketoacidosis secondary to severe insulin resistance. He developed a left hemiplegia, and a subsequent cerebral angiogram identified multiple stenoses of the Circle of Willis with a Moyamoya appearance secondary to radiotherapy. Weight gain has continued (+3.8 to +5.5 s.d.) so that bariatric surgery is a management option.
 ...
PMID:'Do no harm': management of craniopharyngioma. 1877 78

Diabetic ketoacidosis is characterized by a serum glucose level greater than 250 mg per dL, a pH less than 7.3, a serum bicarbonate level less than 18 mEq per L, an elevated serum ketone level, and dehydration. Insulin deficiency is the main precipitating factor. Diabetic ketoacidosis can occur in persons of all ages, with 14 percent of cases occurring in persons older than 70 years, 23 percent in persons 51 to 70 years of age, 27 percent in persons 30 to 50 years of age, and 36 percent in persons younger than 30 years. The case fatality rate is 1 to 5 percent. About one-third of all cases are in persons without a history of diabetes mellitus. Common symptoms include polyuria with polydipsia (98 percent), weight loss (81 percent), fatigue (62 percent), dyspnea (57 percent), vomiting (46 percent), preceding febrile illness (40 percent), abdominal pain (32 percent), and polyphagia (23 percent). Measurement of A1C, blood urea nitrogen, creatinine, serum glucose, electrolytes, pH, and serum ketones; complete blood count; urinalysis; electrocardiography; and calculation of anion gap and osmolar gap can differentiate diabetic ketoacidosis from hyperosmolar hyperglycemic state, gastroenteritis, starvation ketosis, and other metabolic syndromes, and can assist in diagnosing comorbid conditions. Appropriate treatment includes administering intravenous fluids and insulin, and monitoring glucose and electrolyte levels. Cerebral edema is a rare but severe complication that occurs predominantly in children. Physicians should recognize the signs of diabetic ketoacidosis for prompt diagnosis, and identify early symptoms to prevent it. Patient education should include information on how to adjust insulin during times of illness and how to monitor glucose and ketone levels, as well as information on the importance of medication compliance.
 ...
PMID:Diabetic ketoacidosis: evaluation and treatment. 2354 50


1 2 Next >>