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

Periodic apnea and exercise hypoventilation were observed in a 14-year-old boy. Hyperphagia, obesity, serum hyperosmolality without diabetes insipidus or appropriate thirst, and retardation of growth and sexual development indicated a hypothalamic disorder. Neurologic evaluation was normal except for electroencephalographic changes induced by apnea. Pulmonary function tests, resting arterial blood gases in the wakeful state, and ventilatory response to inhaled CO2 were also normal. Acute hypoxemia and respiratory acidosis occurred with apnea during sleep and with insufficient ventilation during exercise. The central origin of sleep apneas was shown by esophageal pressure monitoring. The hypothalamic dysfunction and exercise hypoventilation distinguish this patient from others with obesity and periodic apnea.
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PMID:Periodic apnea, exercise hypoventilation, and hypothalamic dysfunction. 125 44

The hypothalamus, in addition to regulating the anterior and posterior pituitary, controls water balance through thirst, regulates food ingestion and body temperature, influences consciousness, sleep, emotion and other behaviors. Much has been learned of these effects in human disease through the clinical manifestations that occur with hypothalamic lesions. This study reviews the clinical pathologic correlations that have been made in recent years showing that regions of the hypothalamus exert functions in humans that are similar to those identified in experimental animals. Clinical pathologic correlations have not always provided precise analysis of hypothalamic function. The hypothalamus is small and often lesions that come to clinical attention achieve considerable size before their recognition, making local anatomic dissections of the effects of the lesions difficult. Nevertheless, the use of modern non-invasive techniques including CT scans and magnetic resonance imaging (MRI) have provided new information not previously available. This paper reviews several cases of hypothalamic disorder recognized recently. (1) A 33-year-old black man with hypothalamic sarcoidosis. Manifestations of hypothalamic dysfunction included panhypopituitarism, aggressive hyperphagia, polydipsia (partially due to hyperglycemia secondary to diabetes mellitus), drowsiness, depression, and irritability. (2) A 37-year-old woman with a large intrahypothalamic tumor (biopsy showed pituitary adenoma), with drowsiness, poikilothermia, lack of satiety, confusion, and memory loss. She becomes depressed when she is transiently more alert (as after hypertonic contrast-dye infusion). (3) A 60-year-old man with hypothalamic compression by a pituitary tumor, associated with syndrome of inappropriate ADH (SIADH), severe anorexia, memory loss, but preserved thirst. After surgical decompression of the tumor his appetite acutely recovered, but he developed severe hypo(poikilo)thermia. (4) A 45-year-old woman with a suprasellar craniopharyngioma presented with severe drowsiness, hyperphagia, depression, and memory loss post-operatively, which responded to antidepressants (except for the memory loss). She had extremely labile blood pressures and serum Na for about 1 week post-operatively.
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PMID:Neurologic manifestations of hypothalamic disease. 148 Jul 55

A 17-year-old adolescent had a recurrent episode of somnolence and morbid hunger (Kleine-Levin syndrome) three years after a first attack, from which he had spontaneously recovered. He was treated with 50 mg daily of clomipramine for the somnolence accompanied by disturbance of attention and memory. Under this treatment he developed thymoleptic symptoms with polyphagia, logorrhea and hyperactivity. Placed on a trial dose of at first 600 mg, then 400 mg carbamazepine daily the abnormal findings disappeared within a few days, and there has been no recurrence after some months. It is postulated, based on the observations of this case, that the Kleine-Levin syndrome, presumably a functional hypothalamic disorder, is closely related to the endogenous psychoses.
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PMID:[Kleine-Levin syndrome. The provocation of manic symptoms by an antidepressant and a therapeutic trial of carbamazepine]. 279 6

Hypothalamic disease often affects the patients' personality and this also applies to pituitary tumors with suprasellar extension. We report on a patient with a 12-year history of recurrent acromegaly, treated with three transphenoidal operations, single field radiation therapy and bromocriptine/octreotide administration. During the course of follow-up she presented with self-inflicted anemia and Kleine-Levin syndrome (hypersomnia, hyperphagia and hypersexuality). Furthermore, she developed post-radiation necrosis within the right temporal lobe. Whether her neurological and personality disorders result - at least partially - from the acromegaly or the temporal lobe necrosis remains unclear.
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PMID:Kleine-Levin and Munchausen syndromes in a patient with recurrent acromegaly. 1006 57

Obesity is a condition that results from dysregulation of energy balance. Insulin, a component of the efferent pathway of the energy-regulatory circuit, promotes storage of energy substrates in adipose tissue and is, therefore, a potential target for pharmacotherapy. Somatostatin and its analogues (octreotide and lanreotide) bind to somatostatin subtype 5 receptors on the beta-cell membrane, which limits insulin release and, consequently, may decrease adipogenesis. Somatostatin and its analogues have been used in trials in patients with paediatric hypothalamic obesity. These children have hypothalamic dysfunction, mainly due to brain tumours such as craniopharyngiomas, which are thought to generate increased vagal output, leading to hyperinsulinaemia and weight gain. Two small trials, each of 6 months' duration, in children with paediatric hypothalamic obesity showed either a minimal weight loss or stabilization of bodyweight. In children with Prader-Willi syndrome, the most common genetic hypothalamic disorder associated with hyperphagia, hyperghrelinaemia, massive obesity and other endocrine disturbances, somatostatin failed to control hyperphagia and weight gain in a small number of patients, although it lowered the levels of the anorexigenic hormone ghrelin. Long-acting release octreotide was recently used in hyperinsulinaemic obese adults without cranial pathology. Insulin suppression was associated with small decreases in the body mass indexes of obese subjects receiving the higher dosages of the drug, with an acceptable safety profile, similar to that in previous studies. In conclusion, somatostatin and its analogues, by suppressing beta-cell insulin secretion, can retard weight gain in children with hypothalamic obesity and induce a small amount of weight loss in some adults with hyperinsulinaemic obesity.
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PMID:Use of somatostatin analogues in obesity. 1877 19