Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Malnutrition is common among individuals suffering from hypoxemic chronic obstructive pulmonary disease (COPD), advanced HIV disease, and in patients with chronic, severe congestive heart failure. Although increased morbidity and mortality has been associated with weight loss in these conditions, the pathophysiology of malnutrition remains somewhat unclear for each. In COPD, the primary postulated mechanism is hypermetabolism resulting in elevated total caloric expenditure arising from increased airway resistance, increased O2 cost of ventilation, increased dietary induced thermogenesis, inefficient substrate use and perhaps, increased levels of proinflammatory cytokines. In AIDS, postulated mechanisms include hypermetabolism arising from increased activation of proinflammatory cytokines, along with futile cycling of fatty acids and de novo lipogenesis early in the course of HIV infection; intestinal malabsorption and anorexia also play a role in many inflicted individuals. In cardiac cachexia, dietary and metabolic factors, and levels and activity of cytokines, thyroid hormone, catecholamines and cortisol have been suggested as being responsible for causing weight loss in a most cases.
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PMID:Tissue wasting in patients with chronic obstructive pulmonary disease. 1065 78

Patients with acquired immunodeficiency syndrome (AIDS) often suffer from weight loss manifested by a loss of body cell mass (BCM). The causes of human immunodeficiency virus (HIV)-associated wasting may include anorexia, malabsorption, and a variety of altered metabolic states. Malabsorption and diarrhea may result from gastrointestinal tract opportunistic infections or from direct effects of HIV on the gastrointestinal tract. Infection with HIV may produce metabolic derangements that alter nutrient utilization, resulting in loss of BCM. Nutritional assessment of the patient with AIDS should include an evaluation of BCM and physical and psychosocial functioning. Antiretroviral therapy and eradication of opportunistic infections do not always reverse wasting. Treatment should include nutritional counseling. Total parenteral nutrition is sometimes of benefit, particularly in patients with damaged gastrointestinal tracts. Dronabinol and megestrol acetate may promote weight gain; however, dronabinol may have adverse effects, and most of the gain with megestrol acetate is in fat rather than BCM. If gonadal dysfunction is present, testosterone replacement therapy should be included in the treatment plan. Some studies suggest that oral anabolic steroids may improve muscle strength and body composition. In randomized, placebo-controlled trials, mammalian-derived human growth hormone (rhGH[m]) has produced sustained weight and BCM gains in AIDS patients. If a patient continues to lose BCM after the above factors have been addressed and corrected, a 12-week course of rhGH[m] is indicated. Halting the progression of HIV-associated wasting may improve survival, enhance physical and social functioning, and enrich quality of life.
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PMID:Treatment guidelines for HIV-associated wasting. 1076 94

Liver chronic pathologies often courses with metabolic abnormalities of macronutrients leading to or aggravating a protein-energy malnutrition status. This review raised the major pathophysiological mechanisms related to the protein-energy malnutrition in chronic liver patients. By large the reduced dietary intake is the most accepted cause particularly among alcoholic patients. Moreover during the treatment prevails the iatrogenic anorexia by unpalatable (restricted) diets interpolated with long-lasting fastings of hospitalized patients. Intestinal fat malabsorption is a common finding whereas hypermetabolism can be found associated with an acute alcoholism. Hypoglycemia or insulin resistance, hypertriglyceridemia and liver steatosis are common findings as well as lower plasma proteins along with higher levels of ammonia, aromatic and sulphur amino acids leading to neurological outcomes. The knowledge of these metabolic changes allow proper dietary interventions toward reduced morbi-mortality of those patients.
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PMID:[Nutritional consequences of metabolic impairment of macronutrients in chronic liver disease]. 1096 19

The cachexia-anorexia syndrome occurs in chronic pathophysiologic processes including cancer, infection with human immunodeficiency virus, bacterial and parasitic diseases, inflammatory bowel disease, liver disease, obstructive pulmonary disease, cardiovascular disease, and rheumatoid arthritis. Cachexia makes an organism susceptible to secondary pathologies and can result in death. Cachexia-anorexia may result from pain, depression or anxiety, hypogeusia and hyposmia, taste and food aversions, chronic nausea, vomiting, early satiety, malfunction of the gastrointestinal system (delayed digestion, malabsorption, gastric stasis and associated delayed emptying, and/or atrophic changes of the mucosa), metabolic shifts, cytokine action, production of substances by tumor cells, and/or iatrogenic causes such as chemotherapy and radiotherapy. The cachexia-anorexia syndrome also involves metabolic and immune changes (mediated by either the pathophysiologic process, i.e., tumor, or host-derived chemical factors, e.g., peptides, neurotransmitters, cytokines, and lipid-mobilizing factors) and is associated with hypertriacylglycerolemia, lipolysis, and acceleration of protein turnover. These changes result in the loss of fat mass and body protein. Increased resting energy expenditure in weight-losing cachectic patients can occur despite the reduced dietary intake, indicating a systemic dysregulation of host metabolism. During cachexia, the organism is maintained in a constant negative energy balance. This can rarely be explained by the actual energy and substrate demands by tumors in patients with cancer. Overall, the cachectic profile is significantly different than that observed during starvation. Cachexia may result not only from anorexia and a decreased caloric intake but also from malabsorption and losses from the body (ulcers, hemorrhage, effusions). In any case, the major deficit of a cachectic organism is a negative energy balance. Cytokines are proposed to participate in the development and/or progression of cachexia-anorexia; interleukin-1, interleukin-6 (and its subfamily members such as ciliary neurotrophic factor and leukemia inhibitory factor), interferon-gamma, tumor necrosis factor-alpha, and brain-derived neurotrophic factor have been associated with various cachectic conditions. Controversy has focused on the requirement of increased cytokine concentrations in the circulation or other body fluids (e.g., cerebrospinal fluid) to demonstrate cytokine involvement in cachexia-anorexia. Cytokines, however, also act in paracrine, autocrine, and intracrine manners, activities that cannot be detected in the circulation. In fact, paracrine interactions represent a predominant cytokine mode of action within organs, including the brain. Data show that cytokines may be involved in cachectic-anorectic processes by being produced and by acting locally in specific brain regions. Brain synthesis of cytokines has been shown in peripheral models of cancer, peripheral inflammation, and during peripheral cytokine administration; these data support a role for brain cytokines as mediators of neurologic and neuropsychiatric manifestations of disease and in the brain-to-peripheral communication (e.g., through the autonomic nervous system). Brain mechanisms that merit significant attention in the cachexia-anorexia syndrome are those that result from interactions among cytokines, peptides/neuropeptides, and neurotransmitters. These interactions could result in additive, synergistic, or antagonistic activities and can involve modifications of transducing molecules and intracellular mediators. Thus, the data show that the cachexia-anorexia syndrome is multifactorial, and understanding the interactions between peripheral and brain mechanisms is pivotal to characterizing the underlying integrative pathophysiology of this disorder.
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PMID:Central nervous system mechanisms contributing to the cachexia-anorexia syndrome. 1105 8

Parasite infection of the gastrointestinal tract with helminths or protozoa induces detrimental effects on host tissues and host physiology, which have been extensively studied and reviewed. However, parasitism of the digestive system is also associated with adaptive, compensatory phenomena based on changes in host physiology or structures and which tend to counterbalance the negative consequences. The objective of this review is to describe these adaptive processes and their possible underlying mechanisms. Different processes which tend to attenuate the effect of either the loss of appetite, the intestinal malabsorption or the increased tissue losses have been assessed. These processes have been reported both for helminth and protozoan infections, where they present similar characteristics. The mechanisms involved in the adaptation to parasitism remain largely unidentified. The role of feedback mechanisms based on host regulation, possibly through gastrointestinal hormones, has been raised. On the other hand, some data support the proposal that parasites themselves may initiate some of the adaptive processes and consequently favour their own survival. These adaptive phenomena appear to be an essential component in the dynamic balance between host and parasites. Also, parasite infections represent unique models to study the adaptation of the gastrointestinal tract to aggressors.
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PMID:Adaptive physiological processes in the host during gastrointestinal parasitism. 1122 49

Cardiac cachexia is divided into two types, i.e., the classic type, which occurs in patients with severe heart failure, and the nosocomial type, which develops in the postoperative state. Cardiac cachexia is due both to a decrease in nutrient intake (anorexia, malabsorption) and to specific metabolic alterations (hypercatabolism with increased energy expenditure, response to hypoxia, inflammatory status, etc). Among the various mechanisms involved in the pathogenesis of cachexia, cellular hypoxia has long been recognized. The chronic activation of the endogenous neurohormonal system is another specific feature of such patients; a striking relationship was found between cardiac cachexia and hormonal levels which correlate better than the classical parameters of cardiac failure severity. Finally, inflammatory syndrome has been known to occur frequently in patients with cardiac cachexia. Several studies have shown that tumor necrosis factor-alpha was significantly increased in cachectic patients and that chronic activation of the systemic immune response might be a common and unifying factor.
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PMID:Metabolic and nutritional disorders in cardiac cachexia. 1152 73

There are various potential explanations for weight-loss and poor physical performance in patients with chronic pancreatitis: In severe chronic pancreatitis the decline in enzyme secretion is an important cause for the malassimilation syndrome frequently seen in these patients. Occasionally, difficulties may arise in establishing this decline and in quantifying the secretory capacity of the gland. Many patients limit their food intake because of the pain caused by eating. In untreated patients with diabetes, glucosuria may contribute to their malnutrition. Insufficient funds for food due to alcoholism and anorexia may also be of some significance. Concomitant gastrointestinal diseases and malabsorption following gastrointestinal surgery are frequently found in patients with chronic pancreatitis. Neurological complications and traumatic lesions after accidents - often in connection to the underlying alcoholism - are joined by physical inactivity and thus contribute to the development of muscular atrophy and decreased physical performance. Consequently, rehabilitation of patients with chronic pancreatitis is challenging: They not only need expert medical treatment of both the symptoms of chronic pancreatitis and the concomitant disorders. Therapy must also include dietary support, careful physical training, and - in cases caused by alcoholism - psycho-social support. So far, the multi-professional competence required for these purposes can only be expected in a specialized rehabilitation centre.
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PMID:[Chronic pancreatitis: weight loss and poor physical performance - experience from a specialized rehabilitation centre]. 1174 23

Although a high prevalence of overweight is present in elderly people, the main concern in the elderly is the reported decline in food intake and the loss of the motivation to eat. This suggests the presence of problems associated with the regulation of energy balance and the control of food intake. A reduced energy intake causing body weight loss may be caused by social or physiological factors, or a combination of both. Poverty, loneliness, and social isolation are the predominant social factors that contribute to decreased food intake in the elderly. Depression, often associated with loss or deterioration of social networks, is a common psychological problem in the elderly and a significant cause of loss of appetite. The reduction in food intake may be due to the reduced drive to eat (hunger) resulting from a lower need state, or it arises because of more rapidly acting or more potent inhibitory (satiety) signals. The early satiation appears to be predominantly due to a decrease in adaptive relaxation of the stomach fundus resulting in early antral filling, while increased levels and effectiveness of cholecystokinin play a role in the anorexia of aging. The central feeding drive (both the opioid and the neuropeptide Y effects) appears to decline with age. Physical factors such as poor dentition and ill-fitting dentures or age-associated changes in taste and smell may influence food choice and limit the type and quantity of food eaten in older people. Common medical conditions in the elderly such as gastrointestinal disease, malabsorption syndromes, acute and chronic infections, and hypermetabolism often cause anorexia, micronutrient deficiencies, and increased energy and protein requirements. Furthermore, the elderly are major users of prescription medications, a number of which can cause malabsorption of nutrients, gastrointestinal symptoms, and loss of appetite. There is now good evidence that, although age-related reduction in energy intake is largely a physiologic effect of healthy aging, it may predispose to the harmful anorectic effects of psychological, social, and physical problems that become increasingly frequent with aging. Poor nutritional status has been implicated in the development and progression of chronic diseases commonly affecting the elderly. Protein-energy malnutrition is associated with impaired muscle function, decreased bone mass, immune dysfunction, anemia, reduced cognitive function, poor wound healing, delayed recovery from surgery, and ultimately increased morbidity and mortality. An increasing understanding of the factors that contribute to poor nutrition in the elderly should enable the development of appropriate preventive and treatment strategies and improve the health of older people.
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PMID:Eating habits and appetite control in the elderly: the anorexia of aging. 1283 2

In human immunodeficiency virus (HIV) disease, symptoms of underlying illness may promote weight loss through decreased caloric intake, increased metabolic needs, or nutrient malabsorption. We evaluated disease symptoms as predictors of acute weight loss (i.e., loss of > or =5% of weight). HIV-infected men and women (n=415) were telephoned every 5 weeks to obtain information about weight and recent symptoms. Weight change between each pair of consecutive calls (telephone intervals, 2814) was calculated. Acute weight loss occurred across 4.5% of intervals and among 24% of individuals. Patients reported > or =1 symptom before 58% of telephone intervals. The most common symptoms or symptom complexes before intervals were diarrhea (21% of patients), anorexia (17%), upper respiratory symptoms (16%), skin symptoms (12%), and abdominal pain (12%). Trouble swallowing (6%) and oral symptoms (7%) were less common. Risk of acute weight loss was significantly increased when oral symptoms or trouble swallowing were present, and it was decreased when highly active antiretroviral therapy (HAART) was used or when diarrhea was not present. Even when HAART is being administered, clinicians should remain vigilant regarding weight loss, oral symptoms, and trouble swallowing.
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PMID:Difficulty swallowing and lack of receipt of highly active antiretroviral therapy predict acute weight loss in human immunodeficiency virus disease. 1458 69

Villous atrophy in an infant immediately suggests food intolerance. We report a case with an unusual cause. This female infant was first examined at 5 months for anorexia and failure to thrive. Intestinal biopsy showed total villous atrophy. A diet excluding gluten and cow milk proteins failed to improve her condition and the infant was hospitalized at 7 months for further investigations. The infant was hypotonic with a head lag. No other clinical sign was noted. Serum transaminases were increased 5- to 10-fold and CSF proteins concentration was increased. Metabolic investigations revealed hyperlactacidaemia and an increased lactate/pyruvate ratio during fasting and feeding, suggesting a mitochondrial cytopathy. Respiratory chain enzymatic activity measurements confirmed the diagnosis and showed severely decreased activities of complexes I, III and IV in both the liver and muscle. Molecular analysis demonstrated depletion of mitochondrial DNA in the liver (75%) and in muscle (97%). The infant was discharged under continuous enteral nutrition. Improvement was of short duration and the infant died at 1 year of age of massive hepatic failure. This is the first report of a mitochondrial DNA depletion with total villous atrophy and malabsorption as early clinical onset. A mitochondrial cytopathy should be considered in such conditions when food exclusion diets fail.
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PMID:[Mitochondrial cytopathy: an unusual infantile cause of total villous atrophy]. 1476 33


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