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)

Cyclospora is a coccidian parasite responsible for a syndrome of acute and chronic diarrhoea. The organism first come to worldwide attention in 1990 following the publication of three reports. The largest series of cases and the first clinical description of the illness associated with this organism came from Kathmandu where travellers and expatriates were noted to have prolonged diarrhoea with a previously undescribed organism. The organism has been identified as a coccidian both by observation of sporulation and subsequent molecular phylogenetic analysis. Cyclospora organisms appear as non-refractile double-walled spheres, 8-10 microns in diameter. The organism floats in Sheather's sucrose solution and appears variably red on the modified acid-fast stain. It can also be identified on plain wet mounts. Since its first description, Cyclospora has been noted in an increasing number of countries throughout the world. Water-borne transmission has been implicated in several studies. There is a distinct seasonality in Cyclospora outbreaks and cases. In Nepal, the organism has occurred in virtually identical seasonal outbreaks since 1989. The clinical illness associated with Cyclospora is characterized by diarrhoea, nausea, anorexia and weight loss, which may persist for weeks to months if untreated. Evidence of malabsorption of D-xylose has been noted and small bowel biopsies revealed moderately severe villous atrophy and crypt hyperplasia. Successful treatment with trimethoprim-sulfamethoxazole has been identified, but to date no alternative treatment exists for the sulfa allergic patient.
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PMID:Cyclospora infection: a review. 949 70

The unusual amino acid composition of acute phase proteins may be relevant to our understanding of the mechanism of tissue wasting in chronic inflammatory disease. During periods in which demand for amino acids outstrips dietary supply, skeletal muscle protein may be mobilized to meet this demand. An imbalance in the amino acid composition of these proteins may thus be detrimental to the body's nitrogen economy. To address this problem, we have measured the synthetic rate of fibrinogen (perhaps the major acute phase protein) and plasma amino acid profiles in a group of patients with adenocarcinoma of the pancreas and an ongoing inflammatory response (serum C-reactive protein >10 mg/L in the absence of any other obvious infective or inflammatory cause). These were also measured in a control group with no evidence of inflammation. Fibrinogen synthesis was measured after an overnight fast, using a flooding dose of 2H5-phenylalanine. The fractional rate of fibrinogen synthesis was significantly elevated in the cancer group compared with healthy controls [39.3 (20.0-49.9) and 21.9 (13.2-37.7) %/d, respectively; median (range), P < 0.05]. The absolute rate of fibrinogen synthesis was also elevated [84 (33-143) and 26 (15-43) mg/(kg.d), respectively; median (range), P < 0.01]. We calculated that, in cancer patients with anorexia-cachexia (i.e., documented ongoing weight loss in the absence of an obvious cause such as obstruction or malabsorption), aromatic amino acid supply (predominantly tryptophan) most limits fibrinogen synthesis from skeletal muscle reserves. Demand for the nonessential amino acids serine and glycine was elevated. Assuming that tryptophan is limiting, up to 2.6 g muscle protein ( approximately 12 g skeletal muscle tissue) may be wasted to synthesize 1 g fibrinogen. Interpretation of the observation that circulating free tryptophan concentrations were significantly reduced in the cancer patients will have to await flux measurements. The metabolic changes accompanying the inflammatory response suggest that down-regulation of this process may be beneficial.
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PMID:Fibrinogen synthesis is elevated in fasting cancer patients with an acute phase response. 968 56

Despite recommendations from several bodies such as the World Health Organization and others that feeding should be continued during diarrhea, the practice of withholding food during the early stages of diarrhea is still widespread. This contributes to a deterioration in patients' nutritional state. The principal controversy in the nutritional therapy of acute gastroenteritis centers on the relative risks of cows'-milk feeds. The two things that need to be considered in determining the optimum approach to feeding the child with acute diarrhea are the optimum timing for feeding children in relation to the onset of and recovery from symptoms and, secondly, the effects of specific food ingredients in the diet. Recent studies have demonstrated that the vast majority of young children with acute diarrhea can be successfully managed with continued feeding of undiluted non-human milk. Routine dilution of milk and routine use of lactose-free formula are not necessary, especially when oral rehydration therapy and early feeding (in addition to milk) form the basic approach to the clinical management of diarrhea in children. Confounding factors are the severity of the diarrhea, coexistent malnutrition, and young age (< 1 y); such infants are much more likely to have complications from early feeding with undiluted milk and some would advocate use of specifically designed lactose-free formula in such children. Children who are fed exclusively with human milk and those who receive solid foods with or without human milk may safely continue to receive their usual diets during diarrhea. Those who are fed exclusively with non-human milk--especially when very young and with severe diarrhea or malnutrition--should be closely observed if they continue to consume milk or they should receive a special formulation (e.g., a cereal-milk mixture or fermented milk product). The use of nutrient-dense mixtures of common foods may be advisable to promote compensatory growth in those who lose weight during illness or because of anorexia or malabsorption.
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PMID:Nutritional management of acute diarrhea. 978 56

Anorexia is a common problem in HIV infection and occurs via several mechanisms, including local pathology in the oral cavity or esophagus, central nervous system disease affecting eating mechanics or the perception of hunger, or secondary anorexia due to systemic infections, malabsorption, or medications, or to nonmedical factors, such as psychosocial problems, poverty, and isolation. The etiologic diagnosis of disorders of food intake is facilitated by using a diagnostic algorithm. The consideration of nutritional management centers around the body's nutritional reserves in addition to caloric intake. The specific management of a patient with poor food intake is based on the precise cause of the problem, and may include food-based and oral supplement therapies, appetite stimulants, or nonvolitional feeding via the enteral or parenteral route. Anabolic agents, cytokine inhibitors, and other therapies, such as resistance exercise, are adjunctive therapies, and do not replace adequate caloric intake.
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PMID:Nutritional management of patients with AIDS-related anorexia. 982 81

Over the past 18 years, our laboratory has been interested in the pathogenesis of energy imbalance caused by a variety of diseases. Our view is that a clear understanding of the various factors causing negative energy balance, which in turn results in malnutrition, is the most effective way of designing preventive and therapeutic nutritional strategies. Thus, in cancer, one of the common factors is anorexia, due either to the primary tumor or to the effects of cancer therapy. Currently there is little evidence of increased resting energy expenditure in children with cancer, except in cases with very high tumor burden. Conversely, there are suggestions of a failure to down-regulate resting energy expenditure in the presence of reduced food intake in patients with cancer. Damage to the gastrointestinal tract, due to the effects either of the tumor or of tumor therapy, may result in maldigestion and/or malabsorption. Thus, as a result of a combination of reduced intake, reduced absorption and increased needs, the child with cancer may become malnourished. Prevention and treatment are dependent on the type of cancer and the pathogenesis of the negative energy balance. In broad terms, we try as far as possible to use external routes. With the advent of percutaneously placed gastrostomies and gastrojejunal tubes, we use these methods increasingly to provide nutritional support. Only in patients whose gastrointestinal tract cannot be used do we turn to i.v. feeding. In these patients, the placement of a central venous line is required, but great care must be taken to avoid infection. Whatever form of nutritional support is used, whether enteral or parenteral, we measure the body composition and energy expenditure in the patient, so that the nutritional therapy can be tailored to the child's specific needs. Using these approaches, we are having significant success in preventing and reversing malnutrition in children with cancer and those undergoing bone-marrow transplantation.
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PMID:Aggressive oral, enteral or parenteral nutrition: prescriptive decisions in children with cancer. 987 84

Protein-energy malnutrition is an inevitable consequence of chronic liver disease, particularly in the developing infant. Severe malnutrition with loss of fat stores and muscle wasting affects between 60% and 80% of infants with liver disease (Beath, 1993a; Holt et al, 1997). Reduced energy intake secondary to anorexia, vomiting and fat malabsorption, in association with a disordered metabolism of carbohydrate and protein, increased energy requirements and vitamin and mineral deficiencies, contributes towards growth failure. Reversal of malnutrition is one of the key aims of liver transplantation and is achieved in the majority of long-term survivors. The aetiology of persistent growth failure post-transplantation is multifactorial and is related to pre-operative malnutrition, glucocorticoid administration, feeding problems and post-operative complications. Strategies to prevent pre- and post-transplant growth failure include early referral for liver transplantation and a multidisciplinary approach to nutritional support, which may increase survival and improve the quality of life and outcome of liver transplantation.
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PMID:Cholestasis and end-stage liver disease. 1007 9

Malnutrition is a common finding amongst our elders. The causes of malnutrition are multifactorial and although they have been extensively studied, they are not entirely understood. Both physiological and pathological processes of aging put this population at a higher risk of being undernourished. These may be related to social, financial, psychological and/or physiological changes directly or indirectly associated to growing old. Age associated changes increase the risk of malnutrition in older individuals. These alterations range from problems in taste and smell perception, which were previously thought to be the main cause of anorexia in this population, to alterations in either the concentration or efficacy of the previously mentioned feeding modulators. Increased intestinal malabsorption together with an altered pancreatic exocrine response to different diets, further contributing to subclinical malabsorption in the elderly population aged and may account in part for the malnutrition observed in this group. Although not directly caused by the aging process, several conditions such as anorexia nervosa, cancer, infectious conditions, and inflammatory processes are associated with decreased food intake and weight loss. These conditions present with elevated levels of immunoregulatory substances known as cytokines. Each of these cytokines has multiple effects and play a leading role in the pathophysiology and maintainance of malnutrition in these situations.
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PMID:[Pathophysiology of catabolism in undernurished elderly patients]. 1044 98

Weight loss, anorexia, metabolic disorder and malabsorption are leading symptoms of HIV infection. Recent data help us to understand wasting as being intrinsically linked to immunodysregulation and enteropathy. In therapy, the role played by anabolic steroids and growth hormone has been newly defined. The new antiviral drugs may efficiently prevent clinical progression, including wasting. New metabolic side effects have, however, been encountered.
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PMID:HIV infection and malnutrition. 1056 77

In 20-60% of patients with Crohn's disease bone demineralization is found, usually osteoporosis, but also osteoporosis with malatic features. The cause is the reduced calcium intake (loss of appetite, lactose intolerance and malabsorption), reduced vitamin D intake and corticoid therapy. Nowadays the diagnosis is facilitated by the use of densitometers (ultrasonic and DEXA) and markers of osteoresorption and new bone formation. In treatment in addition to calcium and vitamin D used for a long time, fluorides are administered (only as monofluorophosphate), nasal thyrocalcitonin and bisphosphonates of the third series (alendronate). In postmenopausal women also hormonal treatment can be used unless contraindicated. However, burdening of the bones with regular exercise is a necessity. For prevention adequate calcium and vitamin D intake is important, non-smoking, and exercise.
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PMID:[Bone demineralization in Crohn's disease, its diagnosis, therapy and prevention]. 1056 30

Four cases with Capillaria philippinensis have been reported from Egypt during 1989-1992. The authors report here four other cases of severe diarrhoea caused by this parasite. A male and three female patients aged 12-45 years presented with severe diarrhoea of 1-7 months duration associated with vomiting and central abdominal colics. Stools were yellowish or greenish and voluminous. Anorexia was profound with loss of weight. Bilateral painless ankle oedema developed early in the course of the disease and two cases had ascites and bilateral pleural effusion at presentation. There was hyponatraemia, hypocalcaemia and marked hypokalaemia and hypoalbulinaemia. Small bowel series showed a rapid transit time in 3 cases and malabsorption pattern in one. Duodenal biopsies showed non-specific chronic inflammation while jejunal biopsies from one case revealed grade II villous atrophy with moderate cellular infiltration of lamina propria. The infection was diagnosed by finding the eggs, larvae and adult worms of C. philippinensis in stool. Patients were treated with mebendazole 400 mg/day in two divided doses for 28 days in addition to high protein diet and correction of electrolyte disturbance. Vomiting stopped on the second day of treatment, appetite improved and diarrhoea regressed by the fourth day. Unfortunately, one case died two days after admission due to marked hypokalaemia. Clinico-pathological and epidemiological aspects of this infection in Egypt are discussed.
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PMID:Capillaria philippinensis: an emerging parasite causing severe diarrhoea in Egypt. 1060 99


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