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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The continuous infusion of a concentrated, high-caloric glucose solution intravenously into underfed or 3-day-starved rats at a rate of 390 kcal/kg/day results in hypophosphatemia, muscular weakness, neuropathy, lethargy, occasional convulsions, and eventual coma and death. This sequence of events is not observed in similarly infused normal rats. It is a model of a fatal parenteral nutrition syndrome which occurs in undernourished patients. Rats in coma had an eightfold increase in the blood glucose level, a 1.6-fold increase in serum osmolarity, a 16% to 20( decrease in brain water content, and normal blood ketones. A lag phase of at least 8 hr and often 12 to 24 hr occurred following the start of the hyperosmotic glucose infusion before the blood glucose began to accumulate progressively and the syndrome developed. The onset of the syndrome could be prevented by the administration of large amounts of insulin required to keep the blood sugar from exceeding 250 mg/dl. Thus the rat model of the fatal hyperalimentation syndrome is a form of hyperglycemic, hyperosmolar, nonketotic coma caused by brain dehydration.
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PMID:Weakness, neuropathy, and coma following total parenteral nutrition in underfed or starved rats: relationship to blood hyperosmolarity and brain water loss. 21 10

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

A young man with severe multiple injuries following a motorcycle accident was admitted with head and mandible fractures, coma, fracture dislocation at C5-C6 resulting in total leg paralysis, partial paralysis of the right arm and intercostal muscles, and closed chest injury with possible pulmonary contusion. On the fourth day he developed fulminating mediastinitis and massive empyema, and was found to have a ruptured esophagus. Recovery became possible with surgical drainage of the pleural cavity and mediastinum, proximal and distal decompression of the esophagus, antimicrobial therapy, irrigation of the pleural cavity, complete intravenous hyperalimentation, and infusions of salt-poor albumin. The patient was discharged after 95 days, and 7 months after injury is neurologically intact except for a partial right wrist drop. This rare esophageal rupture should be suspected in any chest injury patients, especially those characterized by extreme cyanosis, dyspnea, shock, and prostration incompatible with thoracic cage injury.
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PMID:Rupture of the thoracic esophagus from blunt trauma. 59 47

A 61-year-old woman was admitted to our hospital because of hoarseness and abnormal shadow on chest X-ray. We diagnosed this patient as large cell carcinoma of the right upper lobe of the lung; T3N3M1 Stage IV. She was treated with OK-432, CDDP and CQ. On the 6th day after 2nd cycle chemotherapy, she was confused, and we diagnosed her as a case of hyperosmolar nonketotic coma (HNC) on the 7th day. Unfortunately, she died on the 8th day, after 20 hours of treatment for HNC. She suffered from chronic dehydration due to trouble with left recurrent nerve palsy. Although continuous intravenous hyperalimentation was used, she had severe HNC. HNC might be one complication in chemotherapy for patients with malignancy.
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PMID:[A case of hyperosmolar nonketotic coma occurring during chemotherapy in lung cancer]. 132 54

To determine the efficacy of early jejunal hyperalimentation as nutritional support in the head-injured patient, 32 head-injured patients with Glasgow Coma Scale scores less than 10 were studied for the first 7 days after injury. The experimental (E) group had nasojejunal feeding tubes placed fluoroscopically. Within 36 hours of injury, they received nutritional support equal to their measured resting energy expenditure. The control (C) group was fed gastrically when bowel sounds returned. There were no significant differences (P greater than 0.05) in age, Glasgow Coma Scale score, type of neurological injury, or associated injuries between the two groups. The mean resting energy expenditure, serum albumin, glucose, lymphocyte count, body weight, and total nitrogen loss were nearly identical for both groups. With the jejunal feedings, daily caloric (E = 2102 kcal versus C = 1100 kcal) and nitrogen intake (E = 11.1 g versus C = 5.6 g) and daily nitrogen balance (E = -4.3 g versus C = -11.8 g) improved. The incidence of bacterial infections (E = 3 versus C = 14) and days of intensive care unit hospitalization (E = 6 versus C = 10) were significantly reduced (P less than .05). Head-injured patients will tolerate early jejunal hyperalimentation despite the presence of a clinically silent abdomen, and the cost and complications of total parenteral nutrition are avoided. The increased caloric and nitrogen intake and improved nitrogen retention markedly reduced infections and days of stay in the intensive care unit.
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PMID:The benefits of early jejunal hyperalimentation in the head-injured patient. 251 99

The cardiovascular and metabolic responses to severe head injury were studied in the acute phase after severe head injury with the object of determining if a common response was present and, if so, its significance in the management of the patients' intracranial and systemic physiological states. The cardiovascular response to head injury was studied by measurement of cardiac output, pulmonary capillary wedge pressure, arterial blood pressure, arterial and mixed venous blood gases and arterial and mixed venous epinephrine and norepinephrine serially in 15 patients during the first three days after injury. A hyperdynamic state was found characterized by increased cardiac output and cardiac work, moderate hypertension, tachycardia, decreased or normal systemic and pulmonary vascular resistance, increased pulmonary shunting and increased oxygen delivery and utilisation. Arterial E and NE levels correlated well with the cardiac output, cardiac work, blood pressure, heart rate, oxygen delivery, and oxygen utilization but not with vascular resistance or pulmonary shunt. The magnitude of the hyperdynamic state did not correlate with intracranial pressure, Glasgow Coma Score, or findings on CT scan. The metabolic response to head injury was studied by measurement of resting metabolic expenditure (RME) in 14 comatose head-injured patients in the first nine days after injury. During this period patients were fed with a continuous parenteral infusion of a formula containing 2 Kcal/cc and 10 mg nitrogen/liter. Indirect calorimetry was carried out for 102 patient-days. The mean resting metabolic expenditure (RME) for nonsedated, nonparalyzed patients was 138 +/- 37% of that expected for a non-injured resting person of equivalent age, sex, and body surface area. Nitrogen excretion was measured for 109 patient-days. The mean excretion was 20.2 +/- 6.4 mg/day. The mean protein caloric contribution was 23.9 +/- 6.7% and was greater than 25% for six patients, compared to normal values of 10-15%. Despite hyperalimentation, positive nitrogen balance for any 3-day period was achieved in only seven patients, and required replacement of 161% to 240% of RME with the parenterally administered formula. Head-injured patients had a metabolic response similar to that reported for patients with burns of 20-40% of the body surface.
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PMID:Cardiovascular and metabolic responses to severe head injury. 281 17

Metabolic effects of 3 different sites of transplantation of cultured tumour cells from a radiation induced insulinoma (28 X 10(6) viable cells per rat) were examined in 15-18 weeks old male NEDH rats. Subscapular implantation consistently produced a highly vascularised encapsulated tumour associated with hyperinsulinaemia, hyperphagia and hypoglycaemia by 21 days, which progressed to fatal neuroglycopaenic coma at 37 +/- 3 days (mean +/- SEM). Implantation of tumour cells into the hepatic portal vein resulted in a multilobular hepatic tumour in two out of nine rats, with hyperinsulinaemia and fatal hypoglycaemia by 49-54 days. Irregularities of glucose homeostasis were observed in a further three rats by 62 days. Intrapancreatic implantation consistently produced a similar tumour to that observed at the subscapular site. Implantation into the pancreas produced the most rapid onset of hyperinsulinaemia, hyperphagia and hypoglycaemia, with survival for only 28 +/- 3 days. The results demonstrate an important effect of transplantation site on the function and metabolic consequences of the NEDH rat insulinoma.
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PMID:Metabolic effects of radiation induced rat insulinoma at pancreatic, hepatic and subscapular transplantation sites. 287 15

The growth and metabolic effects of a transplantable radiation-induced rat insulinoma were examined in intact male and female New England Deaconess Hospital (NEDH) rats, and in parathyroidectomised or adrenalectomised male NEDH rats. Subscapular transplantation of insulinoma fragments in intact male rats consistently produced a highly vascularised encapsulated tumour associated with hyperphagia, hyperinsulinaemia and hypoglycaemia which progressed to fatal neuroglycopaenic coma by 30 +/- 0.8 days (mean +/- SEM) and 19 +/- 0.5 days for slow-growing and fast-growing tumour sublines respectively (P less than 0.001). In intact female rats transplanted with the slow-growing subline, the onset of hyperphagia was advanced by 4 days and the severity of hyperinsulinaemia and hypoglycaemia increased (21% and 36%; P less than 0.01 and P less than 0.001, respectively), resulting in a 10% decrease of survival time (P less than 0.05) and a 65% reduction of tumour weight (P less than 0.01). Transplantation of the fast-growing subline into parathyroidectomised male rats, which exhibited a 15-24% (P less than 0.05 - less than 0.01) decrease of plasma calcium, did not modify either the growth or metabolic effects of the tumour. In contrast, transplantation of this subline into adrenalectomised male rats decreased survival time by 32% (P less than 0.001) and reduced final tumour weight by 88% (P less than 0.02) without markedly affecting the onset or magnitude of the hyperinsulinaemia. These results indicate that the growth and metabolic effects of the transplantable NEDH rat insulinoma are modified by the presence of ovarian hormones and by adrenal hormones.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hormonal modification of the growth and metabolic effects of a transplantable rat insulinoma. 302 Aug 53

Subcutaneous implantation of small fragments of a radiation-induced transplantable rat insulinoma into the subscapular region of 16- to 17-week-old male NEDH rats resulted, over a 22-day period, in the progressive development of marked hyperinsulinaemia and severe hypoglycaemia, despite a compensatory increase in food intake. Diurnal changes were examined at 3-hourly intervals for 24 h in control rats and tumour-bearing rats at 20-21 days after transplantation. The control animals exhibited distinct diurnal changes of food intake, glucose and insulin concentrations. Food intake was greatest between 17.00 and 23.00 h; plasma insulin was greatest between 20.00 and 23.00 h, and plasma glucose was raised at 20.00, 02.00 and 05.00 h, compared with the other times. In contrast, insulinoma-bearing rats displayed no diurnal changes other than a small decrease in food intake between 05.00 and 11.00 h. Plasma glucose and insulin concentrations were significantly different from control rats at all times, and food intake was significantly increased between 23.00 and 17.00 h. These observations demonstrate that the transplantable insulinoma not only causes hyperinsulinaemia and hypoglycaemia but results in hyperphagia and defective diurnal changes of food intake, plasma glucose and insulin concentrations. Interruption of nutrient intake by withdrawal of food for 6 h exacerbated the hypoglycaemia of insulinoma-bearing rats leading to coma.
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PMID:Defective diurnal changes of food intake, plasma glucose and insulin in rats with a transplantable islet cell tumour. 304 May 62

Fifty-nine patients with both clinical evidence of thyroid dysfunction and patent diabetes mellitus were investigated in our diabetology department. Patients with euthyroid goitre and iatrogenic or pituitary hypothyroidism were excluded from the study. Among the 45 diabetics with hyperthyroidism, 32 had Graves' disease and 13 had toxic adenoma; 71% were insulin-treated. Hyperthyroidism had passed unnoticed in 7 of these 32 patients because fatigue and loss of weight, which initially were the predominant or sole symptoms, are extremely frequent in uncontrolled diabetes. These symptoms, as well as polyuria, polyphagia and even sweating are common to both diseases. Considerable deterioration in the control of glycaemia was observed in 63% of the insulin-treated patients when hyperthyroidism developed, with a 17 to 212% (mean 82%) increase in insulin dosage in 53%. There was no correlation between the degree of hyperthyroidism and the loss of control. Following treatment of the hyperthyroidism, control was improved in 63%, with an 11-83% (mean 44%) decrease in insulin dosage in 59% of them. Insulin therapy could be withdrawn in only one of the 32 insulin-treated patients. Non-iatrogenic primary hypothyroidism was found in 0.2% of the diabetics investigated. This incidence was significantly higher than the calculated probability of the two diseases occurring by chance in the same patient. Eleven out of 14 patients were insulin-treated. When hypothyroidism developed, 73% of them had their insulin dosage reduced, with a high frequency of hypoglycaemic disorders: repeated "malaise" in 55% and coma in 27%. A higher proportion of vitiligo was also noted: 14% in the total patient population reported, and 18% in insulin-treated patients.
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PMID:[Effect of clinical hyperthyroidism and hypothyroidism on patent diabetes. 59 cases]. 315 40


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