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)

Approximately 5% of all lymphomas are located in the gastrointestinal tract. These lesions may be secondary manifestations of systemic lymphomatous disease, but there are also primary lesions that are not associated with superficial lymph node enlargement mediastinal adenopathy, liver and spleen involvement or hematologic alterations. Primary lymphomas may arise in the stomach or intestine. Small intestinal lesions may or may not be preceded by other types of intestinal pathology, such as celiac or inflammatory disease. The former cases are characterized by persistent diarrhea, malabsorption and weight loss. Abdominal pain and later nausea and/or vomiting are the most common presenting symptoms of lesions that arise in an already diseased bowel, palpable abdominal masses are present in approximately one third of these cases. Gastric lymphomas often presents with non-specific symptoms: cramp-like epigastric pain, anorexia and weight loss.
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PMID:[Primary lymphomas of the gastrointestinal tract: clinical picture]. 853 64

Anorexia is associated with disorders of all systems. Anorexia represents a consistent clinical manifestation during acute and chronic pathophysiological processes (infection, inflammation, injury, toxins, immunological reactions, malignancy and necrosis). Anorexia during disease can be beneficial or deleterious depending on the timing and duration. Temporary anorexia during acute disease may be beneficial to an organism since a restriction in the intake of micro- and macro-nutrients will inhibit bacterial growth. Long-term anorexia during chronic disease, however, is deleterious to an organism and may be associated with cachexia, which can ultimately result in death. Various mechanisms participate in the anorexia observed during disease, including cytokine action. Anorexia induced by cytokines is proposed to involve modulation of hypothalamic-feeding associated sites, prostaglandin-dependent mechanisms, modifications of neurotransmitter systems, gastrointestinal, metabolic, and endocrine factors. In addition, the anorexia-cachexia syndrome is multifactorial and may involve chronic pain, depression or anxiety, hypogeusia and hyposmia, chronic nausea, early satiety, malfunction of the gastrointestinal system, metabolic alterations, cytokine action, production of other anorexigenic substances and/or iatrogenic causes (chemotherapy, radiotherapy). Cachexia may result not only from anorexia and a decreased caloric intake, but also from malabsorption and losses from the body (ulcers, hemorrhage, effusions), or a change in body metabolism. Research has focused on potential interventions to modify anorexia during disease and the anorexia-cachexia syndrome. Nutritional modifications and the use of specific steroids (such as megestrol acetate) are being tested in the clinical setting. Understanding the specific mechanisms responsible for anorexia during disease as well as their interactions is essential to develop interventions for the control of anorexia (during a critical time in a specific disease), and to devise less toxic immunotherapeutic regimens using cytokines.
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PMID:Anorexia during acute and chronic disease. 905 54

Metformin is an oral antihyperglycemic agent that is approved by the Food and Drug Administration for the treatment of noninsulin-dependent diabetes mellitus. It differs from the sulfonylureas in that it is does not enhance insulin secretion and normally does not produce hypoglycemia. Metformin acts to decrease preprandial and postprandial blood glucose concentrations by increasing skeletal muscle uptake of glucose, decreasing gluconeogenesis, and decreasing absorption of glucose. The addition of metformin to maximum dosages of a sulfonylurea may synergistically improve glucose control. The drug may offer other potential benefits, such as weight loss or minimal weight gain, improved blood flow in patients with peripheral vascular disease, reduction of tissue plasminogen activator inhibitor, and improved lipid profiles. It is relatively safe if taken appropriately. Its most common side effects are gastrointestinal (nausea, diarrhea, anorexia), metallic taste, and vitamin B12 malabsorption. Lactic acidosis may also occur, but it is rare if metformin is avoided in patients with contraindications to its use. With careful monitoring, the agent may be considered for the initial treatment of obese patients who fail dietary measures, and those whose disease is refractory to maximum dosages of sulfonylureas or who do not tolerate them.
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PMID:Metformin in noninsulin-dependent diabetes mellitus. 872 92

Many factors can modify nutritional status in cancer patients, including cachexia, nausea and vomiting, decreased caloric intake or oncologic treatments capable of determining malabsorption. Cachexia is a complex disease characterized not only by a poor intake of nutrients or starvation, but also by metabolic derangement. Nausea and vomiting may limit the nutrient intake and are most often the consequences of oncologic treatments or opioid chronic therapy. Decreased caloric intake is considered to be one of the major causes of malnutrition, although the causes of anorexia remain unclear. Malabsorption is generally attributed to the consequences of oncologic treatments reducing the gastrointestinal absorption. Biochemical measurements and immunological tests may be not reliable indicators of nutritional status in cancer patients. Therefore, medical history, physical examination, estimates of daily oral intake, weight changes and an appropriate consideration of the nutritional requirements according to the stage of disease must still be assessed. The therapeutic approaches should be individualized and realistic. Whenever possible, oral nutrition is the method of choice, with due consideration for specific dietary needs. Nausea and anorexia can be reduced by different kinds of drugs. A careful decision based on good clinical judgement is necessary before deciding to start either enteral or parenteral nutrition, to avoid a useless, costly and difficult treatment. In choosing the route for administration of nutrients, availability of and access to a functioning gastrointestinal tract, compliance and comfort of the patient, gastrointestinal toxicity due to chemotherapy or radiotherapy fields, different costs, duration and place of treatment should be considered rather than the different capacity of parenteral versus enteral nutrition. However, postoperative periods after massive intestinal resection often require prolonged parenteral nutrition. The benefits of parenteral nutrition are not often demonstrable in patients with bowel obstruction. Different ethical aspects are presented. Flexibility in attempting to meet the nutrition needs of each patient is probably the most useful guide.
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PMID:Nutrition in cancer patients. 877 Dec 86

Failure to downregulate resting energy expenditure (REE) as an adaption to anorexia or malabsorption is often stated as the major cause of weight loss in individuals with AIDS. In a prospective study, REE was compared with weight changes in HIV-infected patients. The impact of altered body composition on REE was reassessed by critical review of the literature. Patients were 65 male HIV-infected patients, 28 with recent weight loss (WL), and 37 who were weight stable (WS); 50/65 patients had AIDS, and 29/65 had acute infections; 29 male healthy persons served as controls. Indirect calorimetry, prospective intake protocol, and bioelectrical impedance analysis were performed. Absolute REE was lower in WL patients than in controls (1459 +/- 309 versus 1711 +/- 151 kcal/d, p < 0.001) and in WS patients (1625 +/- 402 kcal/d, p < 0.05). REE/kg body cell mass (BCM) was higher in WL and WS than in controls (both p < 0.01) due to lower BCM in both patient groups (p < 0.001). REE (%Harris-Benedict) was not different among the three groups. Weight changes around the measurement were not correlated to REE (r2 = 0.0008, p = 0.82). REE was independent of diarrhea, acute infection, fever, or caloric intake. REE had a stronger correlation to body weight and to Harris-Benedict's prediction than to fat-free mass or BCM. REE explains < 1% of weight changes. Many patients can downregulate REE as an adaption to anorexia and/or malabsorption. Higher REE/kg BCM does not signify hypermetabolism at the cellular level but can be explained by the maintenance of energy-consuming visceral tissue within the BCM during BCM loss.
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PMID:Resting energy expenditure, weight loss, and altered body composition in HIV infection. 887 75

At least 21 genetic disorders have now been found that are linked to peroxisomal dysfunction. Whatever the genetic defect might be, peroxisomal disorders should be considered in various clinical conditions, dependent on the age of onset. The prototype of peroxisomal disorders is represented by 'classical' Zellweger syndrome (ZS) which is the most severe disorder combining all the characteristic symptoms. ZS is characterized by the association of errors of morphogenesis, severe neurological dysfunction, neurosensory defects, regressive changes, hepatodigestive involvement with failure to thrive, usually early death, and absence of recognizable liver peroxisomes. Other peroxisomal disorders (pseudo-Zellweger syndrome, neonatal adrenoleukodystrophy (NALD), pseudo-neonatal adrenoleukodystrophy, rhizomelic chondrodysplasia punctata (RCDP), and hyperpipecolic acidaemia) share some of these symptoms, but with varying organ involvement, severity of dysfunction, and duration of survival. The diagnosis should not cause difficulty when all the characteristic manifestations are present. Depending on the main presenting sign, peroxisomal disorders in neonates should be suspected in two categories of circumstances: polymalformative syndrome with craniofacial dysmorphism, and severe neurological dysfunction. During the first 6 months of life, the predominant symptoms may be hepatomegaly, prolonged jaundice, liver failure, anorexia, vomiting and diarrhoea leading to failure to thrive resembling a malabsorption syndrome; severe psychomotor retardation, hearing loss and ocular abnormalities become evident. Beyond 4 years of age, behavioural changes, intellectual deterioration, visual impairment and gait abnormalities may be the presenting symptoms. Independently of the clinical symptoms and age of onset, most peroxisomal disorders described so far can be clinically screened by recordings of electroretinogram, visual-evoked responses, and brain auditory-evoked responses, which are almost always abnormal. Nine of the 17 peroxisomal disorders with neurological involvement are associated with an accumulation of very long-chain fatty acids (VLCFA), which suggests that assay of plasma VLCFA should be used as a primary test. However, assays of plasma phytanic acid and plasma/urine bile acid intermediates should also be performed in view of the recent reports of atypical chondrodysplasia variants (without rhizomelic shortening) and isolated trihydroxycholestanoic aciduria. The differential diagnoses in various clinical conditions and age periods are discussed.
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PMID:Clinical approach to inherited peroxisomal disorders. 905 44

Interactions between undernutrition, infection, and growth and development are complex, and are reviewed in this article, giving particular emphasis on the importance of diarrheal infection in this process. The effects of diet, nutrition and infection on the nutritional status of a child can vary according to the disease ecology, the age of the child, patterns of feeding and types of food consumed. There are two possible ways in which this relationship can begin; one in which poor nutritional status leads to impaired immunocompetence and reduced resistance to infection, and the other in which exposure to infectious disease can lead to appetite loss and anorexia, malabsorption, and elevated metabolism of energy and other nutrients. Once started, the interactions between these two major environmental stressors becomes increasingly complex, with the nature of the disease ecology influencing the balance of immunoparesis and adaptive immunity and its effect on subsequent disease experience. Furthermore, the disease ecology influences the type and extent of associated physiological phenomena including anorexia, fever, and malabsorption, all of which have an impact on nutritional status. Of disease categories, diarrhea has particularly potent effects in this relationship. The predicted impact of HIV infection among newborn infants is the earlier onset of the undernutrition-infection cycle, as low CD4+ T lymphocyte counts soon after birth are likely to predispose such infants to earlier opportunistic infection.
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PMID:Transdisciplinarity in the study of undernutrition-infection interactions. 922 95

A documented association exists between nutritional status and immunologic function, development, and outcome of infectious processes, and treatment-related toxicity and vital organ function. In persons with AIDS, nutritional deficits precipitate a cycle that results in a downward spiral of weight lost, malabsorption, diarrhea, anorexia, body image disturbance, and increased risk for morbidity and mortality. This article presents an overview of the malnutrition in HIV/AIDS patients. It critiques the current Centers for Disease Control's definitions of wasting syndrome, describes the incidence of weight loss, delineates the implications of untreated malnutrition, and traces the etiology of weight loss and contributing factors. This article serves as an introduction to HIV/AIDS related malnutrition. A subsequent article will review nursing implications and clinical management programs.
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PMID:Malnutrition associated with HIV/AIDS. Part One: Definition and scope, epidemiology, and pathophysiology. 924 67

In those who are infected with human immunodeficiency virus, poor nutritional status can result from numerous causes, including anorexia, catabolism, chronic infection, fever, poor nutrient intake, nausea, vomiting, diarrhea, malabsorption, metabolic disturbances, lack of access to food, depression, and side effects of drug, radiation, and chemotherapy treatments. A compromised immune system may not be reversed by any medical treatments at this time, but malnutrition may be prevented and reversed by using current therapies, including medical nutrition therapy that includes nutrition assessment, the development of an individualized nutrition therapy plan, and implementation of the therapy. There is substantial evidence that medical nutrition therapy saves lives, reduces morbidity, improves health outcomes, reduces costs, and shortens hospital stays.
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PMID:HIV and medical nutrition therapy. 933 81

A 22-year-old Nepali man presented with a 2-month history of fever, ill health, anorexia, loss of weight and diarrhoea. Apart from an ill-defined lower abdominal mass, physical examination was unremarkable. Investigations showed the picture of malabsorption syndrome with no evidence of structural gastro-intestinal tract involvement on barium meal, small bowel and large bowel enema, upper gastro-intestinal endoscopy, colonoscopy and mucous membrane biopsy. Laparoscopy showed typical features of tuberculous peritonitis. Liver biopsy showed tuberculous granulomatous hepatitis, and peritoneal biopsy showed caseating granulomata. The patient responded rapidly to antituberculosis chemotherapy.
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PMID:Malabsorption syndrome complicating tuberculous peritonitis. 944 Oct 65


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