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)

This chapter briefly describes the physiological neural mechanisms by which diverse neurotransmitter receptor systems control several aspects of gastrointestinal functions such as motility, secretion, feeding, and emesis. The current techniques used to study the effects of cannabinoids on these gastrointestinal functions are then sequentially described, starting with isolated gastrointestinal muscle preparations and ultimately evolving to whole animal models. Both delta9-tetrahydrocannibinol (delta9-THC) and well-studied representatives of other classes of exogenous cannabinoid CB1/CB2 receptor agonists inhibit gastrointestinal motility, peristalsis, defecation, and secretions via cannabinoid CB1 receptors since the CB1 (SR141716A)- and not the CB2 (SR144528)-receptor antagonist reverses these effects in a dose-dependent manner. In addition, exogenous cannabinoids inhibit vomiting produced by diverse emetic stimuli in a SR141716A-sensitive manner in different animal models of emesis. Often these cannabinoids produce hyperphagic effects under laboratory conditions in most human and animal models of feeding. Administration of SR141716A by itself can produce effects opposite to cannabinoid agonists (e.g., increases in gastrointestinal motility and secretions, hyperphagia and vomiting), which suggests an important role for endocannabinoids in these gastrointestinal functions. Indeed, the presence of cannabinoid CB1 receptor markers, endocannabinoids such as anandamide and 2-arachidonoylglycerol (2-AG), their metabolic enzymes, and an endocannabinoid reuptake system have been confirmed in the gastrointestinal tract (GIT). The well-studied endocannabinoid anandamide also seems to reduce both gastrointestinal motility and secretion while producing hyperphagia. On the other hand, while the less well-investigated endocannabinoid 2-AG is a potent emetogen, anandamide may possess weak antiemetic activity.
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PMID:Methods evaluating cannabinoid and endocannabinoid effects on gastrointestinal functions. 1650 8

Based on the results of the clinical follow-up study of 41 female patients, diagnostic criteria of bulimia nervosa that should be used in clinical studies are suggested as follows: (1) presence of anorexia nervosa or transitory amenorrhea in the premorbid period; (2) eating attacks with losing of the control over food consumption not less than twice a week during 3 months; (3) compensatory behavior in the form of spontaneous vomiting, abuse of purgative and diuretic medications etc; (4) fear of obesity; (5) cycloid affective changes with higher impulsivity, reduction of the control over primitive drives and/or expressed anxiety disorders; inclination to alcohol and drug abuse and nicotine dependence; (6) changes of the body mass index; (7) absence of amenorrhea. The disease dynamics is characterized by formation of the pathological cycle "diet--overeating--compensatory behavior" on the background of cyclothymic affective disorders. Two types of bulimia nervosa--with and without other drive disorders--have been singled out.
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PMID:[Clinical features and diagnostic criteria of bulimia nervosa]. 1684 79

Superior mesenteric artery (SMA) syndrome (also known as Wilkie's syndrome, chronic duodenal ileus, or cast syndrome) occurs when the third portion of the duodenum is compressed between the SMA and the aorta. The major risk factors for development of SMA syndrome are rapid weight loss and surgical correction of spinal deformities. The clinical presentation of SMA syndrome is variable and nonspecific, including nausea, vomiting, abdominal pain, and weight loss. The diagnosis is based on radiographic findings of duodenal compression by the SMA. The treatment of SMA syndrome is aimed at the precipitating factor, which usually is related to weight loss. Therefore, conservative therapy with nutritional supplementation is the initial approach, and surgery is reserved for those who do not respond to hyperalimentation.
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PMID:Superior mesenteric artery syndrome. 1729 61

Hyperphagia and obesity are common features in individuals with Prader-Willi syndrome (PWS). Demographic and cause-of-death data from individuals with PWS were obtained through a national support organization. Four reports of unexpected mortality due to gastric rupture and necrosis were found in 152 reported deaths, accounting for 3% of the causes of mortality. Four additional individuals were suspected to have gastric rupture. Vomiting and abdominal pain, although rare in PWS, were frequent findings in this cohort. The physician should consider an emergent evaluation for gastric rupture and necrosis in individuals with PWS who present with vomiting and abdominal pain.
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PMID:Gastric rupture and necrosis in Prader-Willi syndrome. 1766 31

Phagophobia is a disorder characterized by a conditioned excessive fear of eating and is initiated by an event such as vomiting or choking. During childhood, vomiting often occurs as a result of infection or overeating, and painful experiences bring about maladaptive eating behavior like food refusal. There have been few reports of phagophobia, and patients have sometimes been misdiagnosed with anorexia nervosa (AN). The objective of this study was to elucidate the psycho-pathology and current treatment of patients with phagophobia by analyzing case studies. We describe 6 cases with phagophobia. Patients with strong obsessions were refractory to treatment, indicating that evaluation of premorbid personality is crucial to the prognosis. It is important to classify this disorder according to psycho-pathology into "post-traumatic type" and "gain-from-illness type" to make a treatment plan. A solution focused approach is also effective for patients and their family. Paying close attention to these conditions and to the diagnostic concept referred as "hagophobia" is useful in achieving these aims.
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PMID:A study of psycho-pathology and treatment of children with phagophobia. 1797 43

Cyclic vomiting syndrome (CVS) is a disorder characterized by recurrent, stereotypic episodes of incapacitating nausea, vomiting, and other symptoms, separated by intervals of comparative wellness. Associated symptoms include nausea, abdominal pain, headache, and motion sickness. Recently, CVS was categorized as a migraine. Case 1 was a girl aged 4 years and 11 months, who had frequent and severe episodes of vomiting since she was 3 years old. The diagnosis of CVS was established on the basis of clinical symptoms and laboratory data. Her electroencephalogram was normal. Prophylactic therapy using a single drug such as amitriptyline, carbamazepine, phenytoin, cyproheptadine, valproate sodium or phenobarbital was not effective. However, her recurring vomiting disappeared with prophylactic therapy using valproate sodium and phenobarbital. Case 2 was a boy aged 10 years and 7 months, who had frequent episodes of vomiting since he was 1 year and 10 months old. He had been receiving intravenous hyperalimentation therapy at home since infancy because of frequent vomiting and failure to thrive. His electroencephalogram showed no abnormality. Prophylactic therapy using a single drug such as diazepam, phenytoin, valproate sodium or phenobarbital was not effective. However, his recurring vomiting disappeared with prophylactic therapy using valproate sodium and phenobarbital. There were no adverse effects in both patients. The combination therapy with valproate sodium (20 - 26 mg/kg/day) and phenobarbital (4 - 5 mg/kg/day) was effective as a prophylactic therapy in these two patients. The combination therapy with valproate sodium and phanobarbital for prophylaxis of vomiting may be helpful in patients with intractable CVS.
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PMID:[The effect of prophylactic therapy with valproate sodium and phenobarbital in two patients with cyclic vomiting syndrome]. 1880 88

Medical records of 16 cats diagnosed with exocrine pancreatic insufficiency (EPI) were reviewed. The diagnosis was confirmed with either a serum feline trypsin-like immunoreactivity (fTLI) concentration <or=12 microg/l or a fecal proteolytic activity (FPA) <6mm for three consecutive days. The majority of cats were castrated male domestic shorthairs. The median age of cats affected was 7 years. The most common clinical sign was weight loss followed by diarrhea, polyphagia and vomiting. Concurrent disease was present in 10/16 (63%) cats. The most common laboratory abnormalities were normocytic normochromic anemia, lymphopenia, neutrophilia, increased alanine transferase activity, hyperglycemia and increased bilirubin concentrations. All 10 cats that were tested for serum cobalamin levels were found to be deficient. All 10 cats that were tested for serum folate concentrations had normal or increased levels. Ten out of 11 cats had at least a partial response to treatment. All cats were discharged from the hospital alive. Results suggest that EPI should be considered a differential diagnosis in any cat with weight loss or poor growth after more common diseases have been ruled out. Concurrent disease is common in feline EPI. Cobalamin deficiency is common in cats with EPI and cats should receive cobalamin supplementation to improve response to treatment. Cats in this study had a good prognosis.
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PMID:Feline exocrine pancreatic insufficiency: 16 cases (1992-2007). 1955 51

Branched-chain ketoacid dehydrogenase deficiency results in complex and volatile metabolic derangements that threaten brain development. Treatment for classical maple syrup urine disease (MSUD) should address this underlying physiology while also protecting children from nutrient deficiencies. Based on a 20-year experience managing 79 patients, we designed a study formula to (1) optimize transport of seven amino acids (Tyr, Trp, His, Met, Thr, Gln, Phe) that compete with branched-chain amino acids (BCAAs) for entry into the brain via a common transporter (LAT1), (2) compensate for episodic depletions of glutamine, glutamate, and alanine caused by reverse transamination, and (3) correct deficiencies of omega-3 essential fatty acids, zinc, and selenium widespread among MSUD patients. The formula was enriched with LAT1 amino acid substrates, glutamine, alanine, zinc, selenium, and alpha-linolenic acid (18:3n-3). Fifteen Old Order Mennonite children were started on study formula between birth and 34 months of age and seen at least monthly in the office. Amino acid levels were checked once weekly and more often during illnesses. All children grew and developed normally over a period of 14-33 months. Energy demand, leucine tolerance, and protein accretion were tightly linked during periods of normal growth. Rapid shifts to net protein degradation occurred during illnesses. At baseline, most LAT1 substrates varied inversely with plasma leucine, and their calculated rates of brain uptake were 20-68% below normal. Treatment with study formula increased plasma concentrations of LAT1 substrates and normalized their calculated uptakes into the nervous system. Red cell membrane omega-3 polyunsaturated fatty acids and serum zinc and selenium levels increased on study formula. However, selenium and docosahexaenoic acid (22:6n-3) levels remained below normal. During the study period, hospitalizations decreased from 0.35 to 0.14 per patient per year. There were 28 hospitalizations managed with MSUD hyperalimentation solution; 86% were precipitated by common infections, especially vomiting and gastroenteritis. The large majority of catabolic illnesses were managed successfully at home using 'sick-day' formula and frequent amino acid monitoring. We conclude that the study formula is safe and effective for the treatment of classical MSUD. In principle, dietary enrichment protects the brain against deficiency of amino acids used for protein accretion, neurotransmitter synthesis, and methyl group transfer. Although the pathophysiology of MSUD can be addressed through rational formula design, this does not replace the need for vigilant clinical monitoring, frequent measurement of the complete amino acid profile, and ongoing dietary adjustments that match nutritional intake to the metabolic demands of growth and illness.
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PMID:Classical maple syrup urine disease and brain development: principles of management and formula design. 2006 Nov 71

Thyroid disease is common, and its effects on the gastrointestinal system are protean, affecting most hollow organs. Hashimoto disease, the most common cause of hypothyroidism, may be associated with an esophageal motility disorder presenting as dysphagia or heartburn. Dyspepsia, nausea, or vomiting may be due to delayed gastric emptying. Abdominal discomfort, flatulence, and bloating occur in those with bacterial overgrowth and improve with antibiotics. Reduced acid production may be due to autoimmune gastritis or low gastrin levels. Constipation may result from diminished motility, leading to an ileus, megacolon, or rarely pseudoobstruction. Ascites in myxedema is characterized by a high protein concentration. Graves' disease accounts for 60% to 80% of thyrotoxicosis. Hyperthyroidism is accompanied by normal gastric emptying with low acid production, partly due to an autoimmune gastritis with hypergastrinemia. Transit time from mouth to cecum is accelerated, resulting in diarrhea. Steatorrhea is due to hyperphagia and stimulation of the adrenergic system. Diarrhea in medullary carcinoma of the thyroid (MCT) may be due to elevated calcitonin, prostaglandins, or 5-hydroxyindoleacetic acid. Ileal or colonic function may be abnormal. The esophagus may be compressed by benign processes, but more often by malignancies. MRI and CT scans are the best diagnostic modalities. The gastrointestinal manifestations of thyroid disease are generally due to reduced motility in hypothyroidism, increased motility in hyperthyroidism, autoimmune gastritis, or esophageal compression by a thyroid process. Symptoms usually resolve with treatment of the thyroid disease.
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PMID:The thyroid and the gut. 2035 69

Previous reports of true pancreatic cysts in cats have suggested that pancreatic cysts in cats are benign incidental findings. This case report describes the progressive clinical course and diagnostic findings in a cat with multiple recurrent pancreatic cysts. The presenting clinical signs included diarrhea, intermittent vomiting, polyphagia, and marked weight loss. Pancreatic cysts were identified via abdominal ultrasound and computed tomography (CT). An exploratory celiotomy and lesion histopathology confirmed multiple true pancreatic cysts of unknown etiology. One month after surgery the cat presented for lethargy and decreased appetite. Clinical re-evaluation was diagnostic for diabetes mellitus and an abdominal ultrasound confirmed recurrence of the pancreatic cysts. The recurrent nature of the pancreatic cysts and the concurrent development of diabetes mellitus were suggestive of progressive loss of pancreatic function or insulin resistance. This is the first described case of multiple recurring pancreatic cysts in a cat associated with pancreatic inflammation, atrophy and endocrine dysfunction.
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PMID:Multiple recurrent pancreatic cysts with associated pancreatic inflammation and atrophy in a cat. 2081 26


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