Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors studied serial hepatic biopsies of five patients who developed hepatic failure following jejunoileal bypass for extreme obesity, with autopsies of two. The hepatic histologic changes included centrilobular or focal alcoholic hyalin, intrasinusoidal collagenosis, fatty hydropic degeneration, and neutrophilic infiltrate. At least two of the patients were abstinent from alcohol, both prior to and after the surgical procedures. The others, after the bypass procedures, had reduced alcohol consumption from previous levels. All patients developed hepatic failure and histologically progressive hepatic disease with alcoholic hyalin and other changes indistinguishable from alcoholic hepatic disease in 21/2 to 5 months, in spite of hyperalimentation and re-establishment of intestinal continuity in four. Nausea, vomiting, abdominal pain and ascites were prominent complaints. Four of the five patients died in hepatic failure. The authors conclude that these cases of progressive hepatic disease with histologic changes simulating those found in livers of alcoholic patients offer evidence that heavy alcohol consumption may affect the liver in an indirect fashion.
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PMID:Post-jejunoileal-bypass hepatic disease. Its similarity to alcoholic hepatic disease. 4 97

The most certain symptomatic manifestation of gallstones is episodic upper abdominal pain. Characteristically, this pain is severe and located in the epigastrium and/or the right upper quadrant. The onset is relatively abrupt and often awakens the patient from sleep. The pain is steady in intensity, may radiate to the upper back, be associated with nausea and lasts for hours to up to a day. Dyspeptic symptoms of indigestion, belching, bloating, abdominal discomfort, heartburn and specific food intolerance are common in persons with gallstones, but are probably unrelated to the stones themselves and frequently persist after surgery. Many, if not most, persons with gallstones have no history of pain attacks. Persons discovered to have gallstones in the absence of typical symptoms appear to have an annual incidence of biliary pain of 2-5% during the initial years of follow-up, with perhaps a declining rate thereafter. Gallstone-related complications occur at a rate of less than 1% annually. Those whose stones are symptomatic at discovery have a more severe course, with approximately 6-10% suffering recurrent symptoms each year and 2% biliary complications. The far higher rates of symptom development reported in a few studies raise the possibility that these incidence estimates may be too low. The best predictors of future biliary pain are a history of pain at the time of diagnosis, female gender and possibly obesity. The risk of acute cholecystitis appears to be greater in those with large solitary stones, that of biliary pancreatitis in those with multiple small stones, and that of gallbladder cancer in those with large stones of any number. Drugs that inhibit the synthesis of prostaglandins may now be the treatment of choice in patients with gallstones who are suffering acute pain attacks. Persistent dyspeptic symptoms occur frequently following cholecystectomy. A prolonged history of such symptoms prior to surgery and evidence of significant psychological distress appear to be the best predictors of unsatisfactory outcome.
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PMID:Symptoms of gallstone disease. 148 6

A 39-year-old woman presented with a 2-month history of repeated severe headache, nausea and diplopia. On admission she was obese with bilateral papilledma and abducens weakness. Mass lesion and sinus thrombosis were ruled out by brain CT and angiography. CSF pressure was normal initially. CSF pressure fluctuated with menstrual cycle, sometimes showing over 600 mmH2O with worsening of the symptoms. She was diagnosed as benign intracranial hypertension (BIH). Diuretics did not improve the symptoms, and visual disturbances ensued and deteriorated. A spinal subarachnoid space-peritoneal shunt was inserted to control CSF pressure, showing rapid improvement of headache and diplopia but visual disturbances remained almost unchanged. Optic nerve sheath fenestration was performed without improvement of visual deterioration. We postulated multiple factors such as obesity, menstrual abnormality, iron deficiency anemia and analgesic drugs played important roles to produce BIH in this case. Careful quantitative perimetry should be done to decide a suitable time for surgical treatment in BIH.
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PMID:[A case of benign intracranial hypertension with fluctuated symptoms and CSF pressure synchronized with menstrual cycle]. 149 Mar 15

In a recent editorial, Kapur described perioperative nausea and vomiting as "the big 'little problem' following ambulatory surgery."257 Although the actual morbidity associated with nausea is relatively low in health outpatients, it should not be considered an unavoidable part of the perioperative experience. The availability of an emesis basin for every patient in the postanesthesia recovery unit is a reflection of the limited success with the available therapeutic techniques.257 There had been little change in the incidence of postoperative emesis since the introduction of halothane into clinical practice in 1956. However, newer anesthetic drugs (e.g. propofol) appear to have contributed to a recent decline in the incidence of emesis. Factors associated with an increased risk of postoperative emesis include age, gender (menses), obesity, previous history of motion sickness or postoperative vomiting, anxiety, gastroparesis, and type and duration of the surgical procedure (e.g., laparoscopy, strabismus, middle ear procedures). Anesthesiologists have little, if any, control over these surgical factors. However, they do have control over many other factors that influence postoperative emesis (e.g., preanesthetic medication, anesthetic drugs and techniques, and postoperative pain management). Although routine antiemetic prophylaxis is clearly unjustified, patients at high risk for postoperative emesis should receive special considerations with respect to the prophylactic use of antiemetic drugs. Minimally effective doses of antiemetic drugs can be administered to reduce the incidence of sedation and other deleterious side effects. Potent nonopioid analgesics (e.g., ketorolac) can be used to control pain while avoiding some of the opioid-related side effects. Gentle handling in the immediate postoperative period is also essential. If emesis does occur, aggressive intravenous hydration and pain management are important components of the therapeutic regimen, along with antiemetic drugs. If one antiemetic does not appear to be effective, another drug with a different site of action should be considered. With the availability of new antiserotonin drugs, the incidence of recurrent (intractable) emesis could be further decreased. Research into the mechanisms of this common postoperative complication may help in improving the management of emetic sequelae in the future. As suggested in a recent editorial, improvement in antiemetic therapy could have a major impact for surgical patients, particularly after ambulatory surgery. Patients as well as those involved in their postoperative care look forward to a time when the routine offering of an emesis basin after surgery becomes a historical practice.
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PMID:Postoperative nausea and vomiting. Its etiology, treatment, and prevention. 843 45

Fluoxetine is a highly specific serotonin reuptake inhibitor. In studies that used a dose of 60 mg once daily, fluoxetine-treated patients consistently had greater weight loss than placebo-treated patients. In six double-blind, placebo-controlled studies of 6-8 wk duration, mean weight changes on fluoxetine were approximately 0.5 kg/wk. Longer term studies have shown maximum mean weight loss to occur at 12-20 wk of therapy. Studies have consistently shown improvements in indices of glycemic control as well as weight loss in obese diabetic patients. Safety analysis has been performed on data from 3491 obese patients in controlled clinical trials of up to 52 wk duration. Adverse events with an incidence of greater than 5%, which were reported significantly more frequently by fluoxetine-treated patients, were headache, asthenia, nausea, diarrhea, somnolence, insomnia, nervousness, sweating, and tremor. Fluoxetine is effective, well tolerated, and safe in the treatment of obesity and obese diabetics.
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PMID:Clinical studies with fluoxetine in obesity. 172 31

We retrospectively reviewed the records of 60 patients who had been referred for gastrointestinal manometry because of stasis after gastric surgery. Nausea, vomiting, bloating, abdominal pain, and weight loss were the most common symptoms. Two thirds of these patients had a well-documented history of peptic ulcer before their initial operations; in others, surgery was performed for other reasons, such as obesity (5%) or reflux esophagitis (8%). Twelve patients had undergone truncal vagotomy and a "drainage operation" and 48 had received a partial gastrectomy with a gastroenterostomy: Billroth I (n = 8), Billroth II (n = 11), Roux-en-Y (n = 29). All patients had recordings of gastrointestinal manometry; 16 also had a scintigraphic measurement of gastric emptying. Measurements were compared with data from healthy controls. Gastric manometry, which could be assessed only in the group with an intact antrum, was characterized by antral hypomotility (p less than 0.05). Gastric emptying studies showed rapid early emptying of liquids and delayed emptying of solids (both p less than 0.05). In the whole group, fasting jejunal motility was characterized by absence of phase II in 13, presence of bursts of phasic activity in 18, and abnormal propagation of phase III in 8. A significantly increased frequency of phase III of MMC was noted in the patients after Billroth II and Roux-en-Y operations. Postprandially, 19 patients failed to develop a "fed pattern."(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Stasis syndromes following gastric surgery: clinical and motility features of 60 symptomatic patients. 222 93

Epidemiological evidence for prenatal carcinogenesis includes associations between cancer in young people and intrauterine exposure to X-rays, drugs and hormones and prezygotic events such as specific chromosomal aberrations associated with specific cancers. Recent findings suggest that the hormonal environment during early gestation can result not only in the development of clear-cell adenocarcinoma of the vagina but also in the development of germ cell tumours of the testes and ovary. Hormone-related risk factors for testicular germ cell neoplasms include maternal use of exogenous oestrogens during early gestation and, possibly, maternal nausea, maternal obesity and race as well. Ovarian germ cell tumours also appear to be related to maternal use of hormones and obesity. Several epidemiological studies of cancer in young people have been directed towards suggested associations with parental occupational exposures, parental cigarette smoking and household exposures to electric and magnetic fields (EMF). The findings of the many studies of parental occupational exposures are inconsistent and are often nonspecific with respect to the type of childhood cancer and the job exposure implicated. Parental cigarette smoking has been associated in some studies with an increased risk for cancer among children and young adults, and in other studies with an increased risk among mature adults, but the findings are not consistent across studies. Three studies of all types of childhood cancer found risk to be related to household exposures to EMF; in all three, the risk for central nervous system tumours was increased, and in two of the three leukaemia risk as well. A fourth study showed no association between childhood leukaemia and EMF. A hypothesis is proposed which suggests that prenatal and early childhood exposure to N-nitroso compounds (NOC) may be related to the development of primary tumours of the brain in children. Experimentalists have shown that various NOC are potent nervous system carcinogens, particularly when animals are exposed transplacentally. This experimental model and findings from a Los Angeles case-control study (209 pairs) of brain tumours in young people led to the proposed epidemiological hypothesis. Although this and other epidemiological studies of NOC have major limitations, findings from epidemiological studies of congenital defects and of other childhood cancers lend the hypothesis some support. A large international collaborative case-control study of childhood brain tumours was begun recently. This study has a major advantage over most case-control studies in adults because the exposure period of greatest interest (gestation) is clearly defined.
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PMID:Epidemiological studies of perinatal carcinogenesis. 268 Sep 50

CCK appears to regulate short-term control of food intake by acting as a satiety signal. Larger doses of CCK may decrease food intake by aversive actions (malaise, nausea, cramps), presumably by effects on gastrointestinal motility. In rats and most likely humans CCK is released from the upper intestine after a mixed meal and appears to activate afferent vagal fibers by causing pyloric contraction with resultant gastric distention or directly binding to the gastric afferent vagus which courses to the nucleus solitarius with further projections to the paraventricular nucleus and ultimately the ventromedial hypothalamus. Peripherally released CCK may also bind to CNS receptors in the area postrema overlying the nucleus solitarius. Central nervous system CCK released from the paraventricular nucleus may also exert a satiety effect. The satiety effect of CCK appears to be a physiologic action of the peptide since antibodies to CCK and CCK receptor antagonists can increase food intake. CCK is probably just one of several satiety signals but can cause a profound decrease in food intake when administered exogenously in pharmacologic doses. Administration of exogenous CCK, as well as endogenous CCK released by oral protease inhibitors, can decrease food intake in humans. Studies designed to examine the effect of chronic administration of CCK on food intake will be necessary to determine if the peptide has a role in the management of obesity and bulimia.
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PMID:Role of cholecystokinin in the control of food intake. 269 51

The mechanism by which intragastric balloons induce weight loss is not known, although they may act simply by reducing the amount of food needed to induce satiety. The knowledge that a balloon is present may influence the patients' eating patterns and reduce caloric intake and weight. In order to test whether the balloon or the secondary psychological effect caused weight loss, a double blind balloon versus sham procedure was devised with both groups receiving identical outpatient dietary advice (800 kcal/day). Twenty four obese women with body mass index greater than 30 kg/m2 from an obesity clinic were studied. Twelve had the balloon and 12 the sham procedure. The balloon was removed after three months and the patients were followed for a further three months. There was significantly greater weight loss in the balloon group, mean weight loss (SD) of 7.33 (6.12) kg compared with the sham group, mean weight loss (SD) of 3.33 (3.9) kg (p less than 0.05). Weight loss was not maintained in all patients after balloon removal. Side effects were more common in the balloon group (abdominal pain, nausea, and vomiting) but resolved by the second week. We conclude that the intragastric balloon is a safe and effective method of inducing weight loss in well motivated obese patients.
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PMID:Effect of the gastric balloon versus sham procedure on weight loss in obese subjects. 276

Seven patients developed acute hepatitis after receiving Plethoryl for obesity for 4 to 16 weeks. Jaundice was generally associated with or preceded by asthenia, nausea and pruritus. Serum aminotransferase activities were markedly increased whereas alkaline phosphatase and gamma-glutamyltransferase activities were moderately elevated. There was no hepatic failure. In all cases, Plethoryl administration was promptly discontinued. In 6 cases, jaundice disappeared within 2 to 4 weeks, and recovery occurred within 2 to 5 months. In one case, however, jaundice disappeared within 12 weeks and recovery took 10 months.
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PMID:[Hepatitis probably caused by Plethoryl. Apropos of 7 cases]. 337 97


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