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)

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

Two adolescent boys with Kearns-Sayre syndrome (progressive external ophthalmoplegia, heart block, elevated CSF protein, and ragged-red muscle fibers) developed lethargy, increasing somnolence, polydipsia, polyphagia, and polyuria after a brief course of steroid therapy. Both had hyperglycemia and acidosis. Nonketotic, lactic acidosis was present in one and ketosis in the other. Severe respiratory failure developed, and both patients died. Postmortem revealed fatty infiltration of the pancreas in addition to a diffuse spongiform encephalopathy.
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PMID:Fatal metabolic acidosis, hyperglycemia, and coma after steroid therapy for Kearns-Sayre syndrome. 370 1

This paper presents the clinical and metabolic findings in two young boys with long-standing Kearns-Sayre syndrome. Following short exposure to oral prednisone, both boys developed lethargy, increasing somnolence, polydipsia, polyphagia, and polyuria. Both presented in the emergency room with profound coma, hypotension, severe hyperglycemia, and acidosis. Nonketotic lactic acidosis was present in one and ketosis without a known serum lactate level was present in the other. Respiratory failure rapidly ensued and both patients expired in spite of efforts at resuscitation. We believe these two cases represent a newly described and catastrophic metabolic-endocrine failure in the Kearns-Sayre syndrome.
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PMID:Hyperglycemic acidotic coma and death in Kearns-Sayre syndrome. 370 9

Twenty-five patients with various forms of dyskinesia were given tiapride for three months. Maximal dosage was 900 mg per day. A double-blind trial of tiapride versus placebo showed significantly better results in the group given tiapride. The forms of dyskinesia which responded best to tiapride were the following: iatrogenic dyskinesia, tics (Gilles de la Tourette syndrome), and chronic chorea (Huntington disease). Patients with complex dyskinesia resulting from neonatal encephalopathy or vascular disease were not improved. The protocol used in l-dopa-induced dyskinesia is described. Changes in dyskinesia and "on-off" effect following variations in tiapride and l-dopa dosage are detailed. An unequivocal, although minor, tiapride-induced parkinson syndrome was recorded in a few patients. No instances of tiapride-induced dyskinesia or akathisia were seen. The other side-effects were either psychic (depression, drowsiness, agitation) or endocrinologic (menstrual disorders, overeating, galactorrhea).
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PMID:[Clinical trial of tiapride in patients with dyskinesia (author's transl)]. 628 45

Seven children with advanced neuroblastoma were treated with maturation therapy. This therapy consisted of 12 hours drip infusion of papaverine (40-45 mg/kg/day) for 2 days with or without high dose cyclophosphamide (2,000-3,600 mg/m2). During maturation therapy all patients received intravenous hyperalimentation. One patient who had received papaverine alone did not respond to the therapy. Among 6 patients treated with papaverine and high dose cyclophosphamide, 3 responded to the therapy, 2 did not and one died soon after the therapy. However, similar responses were obtained in 2 of 3 responders with high dose cyclophosphamide alone. After all, papaverine infusion was evaluated to be effective only in one patient. The clinically severe complications of papaverine infusion were somnolence in all patients and extrapyramidal symptoms in 6 patients. Because of these extremely high toxicity rates with little evidence of therapeutic effect, selection for this therapy should be carefully done and the treatment plan should be reconsidered.
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PMID:[Maturation therapy for advanced neuroblastoma-therapeutic effects and problems]. 682 Sep 8

Nicotine increases the release and turnover of catecholamines in the brain, and many features of the tobacco withdrawal syndrome--such as drug craving, poor concentration, impaired motor performance, drowsiness, fatigue, increased appetite with hyperphagia--may reflect diminished central catecholaminergic tone. Support of central catecholamine synthesis with the nutrients tyrosine and glucose tolerance factor (which enhance brain tyrosine levels) may lessen tobacco withdrawal symptoms and may increase the chance of success in smoking cessation programs. Nutritional measures of this type would probably be safer and more appropriate for long-term use than central-stimulant drugs.
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PMID:Nutritional support of central catecholaminergic tone may aid smoking withdrawal. 706 62

Recent attempts to reduce weight by patients with anorexia nervosa have sometimes led to life-threatening hematologic complications. This report describes an instance in which a patient with anorexia nervosa and pancytopenia drastically improved with treatment that included administration of granulocyte colony-stimulating factor. The patient had lost 27 kg of body weight within 8 months. Even after admission, the blood cell count continued to decrease rapidly as follows: platelet, from 244 x 10(3)/microliters to 44 x 10(3)/microliters; erythrocyte, from 4.04 x 10(6)/microliters to 2.58 x 10(6)/microliters; and leukocyte, from 4.8 x 10(3)/microliters to 1.6 x 10(3)/microliters (granulocyte, 0.8 x 10(3)/microliters). Complications included pneumomediastinum, pneumothorax, purpura, petechiae, hepatomegaly, fever, gangrenous stomatitis, and somnolence. Bone marrow aspiration disclosed absence of fat cells, marrow hypoplasia, and infiltration of the mature lymphocytes. Intravenous hyperalimentation, blood transfusion, gamma-globulin, and antibiotics were administered, but leukopenia and fever remained. However, administration of recombinant human granulocyte colony-stimulating factor dramatically reversed the leukopenia and fever. With careful nutrition therapy, the patient's blood cell count and bone marrow normalized by the time of discharge. It was concluded that severe hematologic disorders may occur in patients with anorexia nervosa, and advanced treatment may be required to save the patient's life.
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PMID:Case report: reversal of severe leukopenia by granulocyte colony-stimulating factor in anorexia nervosa. 768 51

A case of Kleine-Levin syndrome, with chronic severe periodic hypersomnia is described in a 17-year-old female. The first episode started when she was 15 years old. The episodes were characterized by periodic hypersomnia accompanied by hyperphagia, lasting 5 days, and repeating at 28 to 60 day intervals. The severity of hypersomnia prevented her from attending school activities. Outside the hypersomnia periods, she was asymptomatic. EEG, brain computerized tomography and brain nuclear magnetic resonance were normal; all-night polysomnography, Multiple Sleep Latency Test (MSLT) and Epworth Sleepiness Scale (ESS) were within normal limits. During the period of hypersomnolence, polysomnography showed short sleep latency and short REM latency. MSLT mean sleep latency was 1.8 min; and REM period was present in one subtest; the ESS was markedly elevated.
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PMID:Kleine-Levin syndrome. Clinical course, polysomnography and multiple sleep latency test. Case report. 985 Jul 64

The association of Prader-Willi-syndrome with breathing disturbances such as sleep apnea syndrome and/or hypoxemia during REM sleep, REM sleep abnormalities and excessive daytime sleepiness is well known. We report the case of an 11-year-old boy who presented with Prader-Willi syndrome, obesity (body mass index [BMI] = 45.6), severe obstructive sleep apnea syndrome and significant daytime sleepiness on multiple sleep latency test. Behavioral disorders did not allowed the use of continuous positive pressure in this patient. Therefore, clomipramine (20 mg per day) was administered. Sleep examination over 8 months showed: slight weight loss (BMI = 44.4), persistence of severe obstructive sleep apnea syndrome, slight improvement in nocturnal hypoxemia, and disappearance of excessive daytime drowsiness with mean sleep latency of 15 min 37 s (less than 2 min before treatment) and no diurnal REM sleep periods. However, clomipramine had no effect on hyperphagia.
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PMID:[The effects of clomipramine on diurnal sleepiness and respiratory parameters in a a case of Prader-Willi syndrome]. 989 31


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