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)

METHODS: Evaluated are surgical difficulties, management problems and weight loss in patients with distal gastric bypass as a revisionary procedure. Eighty patients were followed up to 3 years; four were lost to follow-up. Mean age was 43; mean prebariatric surgery weight 134 kg; height 1.65 meters; body mass index 40.1; ideal body weight 62.7 kg; excess weight 70.5 kg; per cent excess weight 214%. A 250 cm stomach-to-ileocecal valve segment of small bowel was used, and the biliopancreatic secretions were brought into the terminal ileum 100 6 in from the ileocecal valve. Mean pouch size was 63 cc; length of hospital stay 5 days; operative blood loss 616 cc; operative time 130 min. RESULTS: Intraoperative complications included three splenic injuries (without splenectomy). Early complications included one deep vein thrombosis, two marginal ulcers, one GI hemorrhage, one wound dehiscence, one pouch outlet obstruction and one pancreatitis. Late complications included: one death from protein malnutrition/ ARDS; 21 hypoproteinemia; six protein malnutrition, and of these, three had hyperalimentation; three cholecystitis; 27 anemia; 22 incisional hernia; two staple-line disruption (reoperated); 26 low serum iron; 11 prolonged (>6 months) diarrhea; three prolonged frequent vomiting; and two unrelated deaths (chronic myelogenous leukemia and amyotrophic lateral sclerosis). Mean excess weight loss was 83% at 12 months; 89% at 24 months; and 94% at 36 months. CONCLUSION: The distal gastric bypass is fraught with the operative and immediate post-operative complications experienced in any revisionary bariatric surgery. Distal gastric bypass is very effective in producing long-term weight loss. Nutritional problems are common but usually easily corrected. The most serious nutritional complication is protein malnutrition, which must be identified and corrected early. Success of this procedure is dependent upon patient compliance with proper nutrition and supplements, and regular office follow-up with monitoring of laboratory data. Patients who are noncompliant are at significant risk for complications.
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PMID:The Gastric Bypass for Failed Bariatric Surgical Procedures. 1072 55

We wished to determine whether patients with amyotrophic lateral sclerosis (ALS) show behavioural changes similar to those of frontotemporal dementia (FTD). There is accumulating evidence to suggest a link between ALS and FTD, yet there has been little systematic exploration of behaviour in ALS. An informant based semi-structured behavioural interview, sensitive to the behavioural changes of FTD, was administered to carers of 16 consecutive patients attending a motor neuron disease clinic. Findings varied across the group. At one extreme informants reported no behavioural change, whereas at the other they reported a spectrum of behaviours similar to those seen in FTD. Changes in affect and social behaviour were most common, although some patients also showed altered response to sensory stimuli, gluttony and indiscriminate eating, behavioural stereotypies and compulsions. Behavioural changes were mirrored by SPECT abnormalities in the frontal and/or temporal lobes. Thus, behavioural changes of the type seen in FTD may be present even in a small consecutive cohort of ALS patients. Detection of behavioural change is crucial for optimal management.
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PMID:Behaviour in amyotrophic lateral sclerosis. 1842 98

Dysfunction and death of motor neurons leads to progressive paralysis in amyotrophic lateral sclerosis (ALS). Recent studies have reported organism-level metabolic dysfunction as a prominent but poorly understood feature of the disease. ALS patients are hypermetabolic with increased resting energy expenditure, but if and how hypermetabolism contributes to disease pathology is unknown. We asked if decreasing metabolism in the mutant superoxide dismutase 1 (SOD1) mouse model of ALS (G93A SOD1) would alter motor function and survival. To address this, we generated mice with the G93A SOD1 mutation that also lacked the melanocortin-4 receptor (MC4R). MC4R is a critical regulator of energy homeostasis and food intake in the hypothalamus. Loss of MC4R is known to induce hyperphagia and hypometabolism in mice. In the MC4R null background, G93A SOD1 mice become markedly hypometabolic, overweight and less active. Decreased metabolic rate, however, did not reverse any ALS-related disease phenotypes such as motor dysfunction or decreased lifespan. While hypermetabolism remains an intriguing target for intervention in ALS patients and disease models, our data indicate that the melanocortin system is not a good target for manipulation. Investigating other pathways may reveal optimal targets for addressing metabolic dysfunction in ALS.
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PMID:Genetic induction of hypometabolism by ablation of MC4R does not suppress ALS-like phenotypes in the G93A mutant SOD1 mouse model. 2903 May 76