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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a 49-year-old man and a 28-year-old woman, both of whom complained of fatigue, HFE-gen related respectively non-HFE-gen related primary haemochromatosis was diagnosed, based on the elevated serum transferrin saturation, the elevated serum ferritin levels, DNA studies and liver biopsy with qualitative respectively quantitative iron measurements. Their complaints diminished after bloodletting. Three women respectively 64, 61 and 46 years of age, were also suspected of primary haemochromatosis. The latter two presented with complaints of fatigue and malaise and chronic hepatitis C respectively. All three showed an elevated serum transferrin saturation and serum ferritin concentration. Further investigation showed the presence of secundary iron overload. Causes for it being excessive alcohol consumption, overweight and a poorly regulated diabetes mellitus type 2, and chronic hepatitis C respectively. These patients received specific therapy. Primary haemochromatosis is a common disorder of iron metabolism in individuals of Northern European descent. Diagnosis is based on an elevated serum transferrin saturation in combination with both elevated serum ferritin levels and homozygosity for the Cys282Tyr-mutation in the HFE-gen. The presence of an elevated serum transferrin saturation in combination with an elevated serum ferritin level is not always sufficient for the diagnosis, since these may be affected by other disorders. Moreover, iron overload may be caused by a form of haemochromatosis that is not HFE-related. In case of doubt as to the diagnosis, histological examination of the liver with a qualitative or quantitative iron determination is the golden standard.
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PMID:[Diagnosis of 5 patients with possible primary hemochromatosis]. 1271 48

Gonadectomy predisposes domestic cats to undesired body weight gain and obesity. The disturbance responsible for this disregulation of energy balance has not been clearly identified. Energy intake and expenditure, body composition and plasma concentrations of leptin, insulin, glucose and triacylglycerol were determined during a 36-wk period in adult male (2-5 y) gonadectomized (n = 8) and intact (n = 8) normal cats and gonadectomized (n = 8) and intact (n = 8) lipoprotein lipase (LPL)-deficient cats. Cats were housed individually in temperature- and light-controlled rooms and continuously provided a commercial dry-type diet. In normal and LPL-deficient cats, body weight increased (P < 0.05) after gonadectomy by 27 to 29%, mostly as a result of fat accretion. There was a rapid increase (P < 0.05) in food intake of approximately 12% after gonadectomy of normal and LPL-deficient cats. The metabolic rate (kJ.kg(-1).d(-1)), determined in normal intact (319 +/- 20, n = 5) and gonadectomized (332 +/- 36, n = 5) cats, did not differ after gonadectomy. After gonadectomy, plasma concentrations of glucose and triacylglycerol did not change, whereas plasma insulin and leptin concentrations increased (P < 0.05), but not coincidentally with body weight gain. A stair-step increase in energy intake, and not decreased energy expenditure, appears to drive the weight gain associated with gonadectomy. Body fat mass appears to increase until the energy intake supports no further expansion. Adiposity signaling through insulin or leptin does not appear to mediate the energy intake effect. LPL deficiency did not preclude development of the overweight body condition. Therefore, gonadectomy-induced weight gain in cats is not a result of changed adipose LPL activity, as previously suggested.
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PMID:Weight gain in gonadectomized normal and lipoprotein lipase-deficient male domestic cats results from increased food intake and not decreased energy expenditure. 1277 31

Obesity is a progressive disease of unwanted fat accumulation which has multiple, organ-specific pathological consequences. The manifestations of obesity occur within virtually every subspecialty of medicine or surgery and they interact importantly to accelerate the ageing process in many organs. Many of the hazards of obesity have multiple causes (e.g., diabetes, heart disease, stroke, colonic and breast cancer, urinary incontinence, tiredness, back pain, breathlessness). All of these conditions become more prevalent with age and are also more prevalent among overweight persons, particularly those with a central fat distribution marked by a high waist circumference. Hypertension may be caused or aggravated by weight gain. It is mediated by the physical demands of an expanded circulating volume and increased metabolic rate by metabolic mechanisms related to central fat distribution and the "metabolic syndrome", and to increased sodium consumption by overweight people (because they need more food to maintain a higher metabolic rate). Since body mass index (BMI) and waist circumference increase significantly with age there is an escalation of the burden of ill health from obesity with age. The best simple indicator of disease risk with obesity is the waist circumference since this identifies people who have a high body fat content and also those who have an increased intraabdominal accumulation of fat. The quantitative burden of ill health from overweight and obesity varies within different specialties, but up to 80% of type 2 diabetes or polycystic ovarian syndrome can be attributed to obesity. Obesity is the cause of sleep apnea syndrome in around 50% of cases and heart disease in perhaps 10-20% of cases. In Scotland 80% of people with existing cardiovascular disease are overweight compared with 57% of the general population. The financial burden to health services from overweight and obesity has been incompletely assessed, although it is estimated that around 4% of total health care budgets are attributable to people having BMI > 25 kg/m(2). This is similar to the entire cost of diabetes, epilepsy or major cancers. Obesity is therefore an extremely expensive disease based on these conservative estimates from limited evaluations. More general assessments show how obesity increases the amount of time taken off work, the number of drugs prescribed and the expenditure from social services support. Thus, obesity represents a huge burden not only on the individual patient physically, psychologically, socially and financially but also on families and careers and is a huge drain on health care resources. Overweight affects well over half of all adults worldwide, progressing to BMI > 30 kg/m(2) in around 20% outside subsistence rural communities. Its rapidly increasing prevalence now described as an epidemic demands major preventive measures, as well as better medical treatment for individuals affected.
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PMID:Obesity: burdens of illness and strategies for prevention or management. 1284 36

Nonalcoholic fatty liver disease is a condition gaining increasing recognition as a cause of cirrhosis and end-stage liver disease. The condition appears identical to alcoholic liver disease histologically, yet occurs in patients with negligible alcohol intake. Nonalcoholic fatty liver disease covers a spectrum of diseases ranging from simple fatty deposition in the liver to fat and inflammation and finally to fibrosis and cirrhosis. Conditions most frequently found in association with nonalcoholic fatty liver disease include obesity, Type 2 diabetes, and hyperlipidemia. Although the exact etiology of nonalcoholic fatty liver disease is not clear, insulin resistance is thought to play an important factor. Patients typically present with asymptomatic serum aminotransferase elevations of 2-3 times normal. Symptoms may include fatigue and abdominal pain. The clinical course is difficult to predict due to a lack of research in the natural history of the disease. It is known a percentage of patients progress to end-stage liver disease and may require liver transplantation. No medical treatment has been found to be totally effective. Patients who are overweight or obese should be encouraged in gradual weight reduction that has been associated with improvement in liver test abnormalities.
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PMID:Nonalcoholic Fatty liver disease. 1292 Apr 29

Childhood obesity is currently at its highest: recent statistics show that 16% of children between the ages of 6 and 11 y are overweight [> or =95th percentile of body mass index (BMI; in kg/m(2)) for age] and that an additional 14.3% are at risk of becoming overweight (> or =85th percentile but < 95th percentile of BMI for age). As children's body weights have increased, so has their consumption of fast foods and soft drinks. The proportion of foods that children consumed from restaurants and fast food outlets increased by nearly 300% between 1977 and 1996. Children's soft drink consumption has also increased during those years, and now soft drinks provide soft drink consumers 188 kcal/d beyond the energy intake of nonconsumers. These changes in food intakes among children may partly explain the rise in childhood obesity observed in the past few years. Although the mechanism of appetite regulation will not be explored in this report, it is hypothesized that the greater energy intakes in children who consume large amounts of soft drinks and fast foods are not compensated for by increased physical activity or decreased energy intakes. Furthermore, overweight and obesity in childhood may predispose persons to morbidity in adulthood. Blood pressure and fasting insulin and cholesterol concentrations are higher in overweight children than in normal-weight children. This review focuses on current food patterns and eating habits of children, in an attempt to explain their increasing BMI. In addition, a critical review of food service and political practices regarding food choices for children at school is included.
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PMID:Changes in childhood food consumption patterns: a cause for concern in light of increasing body weights. 1466 65

The ability of insulin to stimulate glucose disposal varies more than six-fold in apparently healthy individuals. The one third of the population that is most insulin resistant is at greatly increased risk to develop cardiovascular disease (CVD), type 2 diabetes, hypertension, stroke, nonalcoholic fatty liver disease, polycystic ovary disease, and certain forms of cancer. Between 25-35% of the variability in insulin action is related to being overweight. The importance of the adverse effects of excess adiposity is apparent in light of the evidence that more than half of the adult population in the United States is classified as being overweight/obese, as defined by a body mass index greater than 25.0 kg/m(2). The current epidemic of overweight/obesity is most-likely related to a combination of increased caloric intake and decreased energy expenditure. In either instance, the fact that CVD risk is increased as individuals gain weight emphasizes the gravity of the health care dilemma posed by the explosive increase in the prevalence of overweight/obesity in the population at large. Given the enormity of the problem, it is necessary to differentiate between the CVD risk related to obesity per se, as distinct from the fact that the prevalence of insulin resistance and compensatory hyperinsulinemia are increased in overweight/obese individuals. Although the majority of individuals in the general population that can be considered insulin resistant are also overweight/obese, not all overweight/obese persons are insulin resistant. Furthermore, the cluster of abnormalities associated with insulin resistance - namely, glucose intolerance, hyperinsulinemia, dyslipidemia, and elevated plasma C-reactive protein concentrations -- is limited to the subset of overweight/obese individuals that are also insulin resistant. Of greater clinical relevance is the fact that significant improvement in these metabolic abnormalities following weight loss is seen only in the subset of overweight/obese individuals that are also insulin resistant. In view of the large number of overweight/obese subjects at potential risk to be insulin resistant/hyperinsulinemic (and at increased CVD risk), and the difficulty in achieving weight loss, it seems essential to identify those overweight/obese individuals who are also insulin resistant and will benefit the most from weight loss, then target this population for the most-intensive efforts to bring about weight loss.
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PMID:Obesity, insulin resistance, and cardiovascular disease. 1474 3

Despite efforts to achieve a desirable weight, two-thirds of the population has an elevated body weight. Medications are useful in supporting weight loss, but produce adverse effects. This study compared the effects of amphetamine and modafinil on food intake and cardiovascular activity in healthy men and women. Participants (n = 11) completed 11 sessions. In random order, participants received placebo on five separate sessions and single oral doses of modafinil (1.75, 3.5, or 7.0 mg/kg) and amphetamine (0.035, 0.07, 0.14 mg/kg). Free time between hourly performance testing intervals gave participants the opportunity to eat. Like amphetamine, modafinil reduced the amount of food consumed and decreased energy intake, without altering the proportion of macronutrients consumed. Although both medications significantly increase heart rate and blood pressure at higher doses, the dose of modafinil that was efficacious in decreasing food intake did not significantly increase heart rate. Modafinil may be well suited for the treatment of obesity, although further studies with repeated dosing in overweight populations are warranted. Modafinil may have less adverse health consequences than some anorectic agents and greater treatment efficacy.
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PMID:Wake-promoting agents with different mechanisms of action: comparison of effects of modafinil and amphetamine on food intake and cardiovascular activity. 1501 Jan 83

Several recent studies have found greater weight loss at 6 months among participants on a very-low-carbohydrate (VLC) weight-loss diet compared with a low-fat (LF) weight-loss diet. Because most of these studies were not matched for calories, it is not clear whether these results are caused by decreased energy intake or increased energy expenditure. It is hypothesized that several energy-consuming metabolic pathways are up-regulated during a VLC diet, leading to increased energy expenditure. The focus of this study was to investigate whether, when protein and energy are held constant, there is a significant difference in fat and weight loss when fat and carbohydrate are dramatically varied in the diet. The preliminary results presented in this paper are for the first four of six postmenopausal overweight or obese participants who followed, in random order, both a VLC and an LF diet for 6 weeks. Other outcome measures were serum lipids, glucose, and insulin, as well as dietary compliance and side effects. Our results showed no significant weight loss, lipid, serum insulin, or glucose differences between the two diets. Lipids were dramatically reduced on both diets, with a trend for greater triglyceride reduction on the VLC diet. Glucose levels were also reduced on both diets, with a trend for insulin reduction on the VLC diet. Compliance was excellent with both diets, and side effects were mild, although participants reported more food cravings and bad breath on the VLC diet and more burping and flatulence on the LF diet.
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PMID:A randomized trial comparing low-fat and low-carbohydrate diets matched for energy and protein. 1560 61

The term 'non-alcoholic fatty liver disease' (NAFLD) includes cases with steatosis alone and those with non-alcoholic steatohepatitis (NASH). Usually there are no signs or symptoms, sometimes fatigue or pain, and apart from hepatomegaly the condition is revealed by abnormal liver biochemistry or by abdominal ultrasound. Most cases are associated with overweight or diabetes. Liver enzymes are usually elevated, especially GGT, ASAT and ALAT. Other conditions, including alcohol abuse and autoimmune hepatitis, have to be excluded. The diagnosis of steatosis can be made with ultrasound or CT scan. A liver biopsy is often needed to exclude other disease and to assess inflammation and fibrosis. Cirrhosis can develop. NAFLD is usually caused by two 'hits': the 'first hit' is peripheral insulin resistance, causing steatosis. The 'second hit' is caused by reactive oxygen species, inducing vicious cycles leading to inflammation. Weight loss, metformin or thiazolidinediones can improve NAFLD by increasing insulin sensitivity. Radical scavengers such as vitamin E, betaine and perhaps also urodeoxycholic acid may improve the hepatitis component. Further studies on treatment are needed.
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PMID:Non-alcoholic fatty liver disease: a brief review. 1569 51

The efficacy of topiramate in migraine prevention (prophylaxis) was established in two multicenter, randomized, double-blind, placebo-controlled, pivotal trials. Topiramate has received regulatory approval for use in adults for migraine prophylaxis (prevention) in the US and numerous other countries, including France, Ireland, Switzerland, Brazil, Taiwan, Spain, and Australia. Treatment with 100 or 200 mg per day of topiramate was associated with significant reductions in the frequency of migraine headaches, number of migraine days, and use of acute medications. No increase in efficacy was observed between 100 and 200 mg per day of topiramate. Based on efficacy and tolerability, 100 mg per day of topiramate should be the initial target dose for most patients. The most common adverse events were paresthesia, fatigue, decreased appetite, nausea, diarrhea, weight decrease, and taste perversion. Topiramate is a first-line migraine preventive drug and should especially be considered as a preferred treatment for all patients who are concerned about gaining weight, who are currently overweight, or who have coexisting epilepsy.
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PMID:Topiramate in migraine prevention. 1583 91


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