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)

Subjects with a variety of enteropathies, hemolytic anemias, acute respiratory distress syndrome, hepatitis, Gaucher's disease as well as those on TPN and hemodialysis, often have low ("deficient") blood levels of vitamin E. A deficiency of vitamin E can be manifested by accelerated red blood cell destruction and neuromuscular deficit. Supplementation of these patients may be advisable. Neurological dysfunction has been observed in adults with prolonged vitamin E deficiency resulting from lipid malabsorption. Long-term treatment with high doses of vitamin E results in improvement. Administration of 800 IU/day of vitamin E to subjects with G6PD deficiency, sickle-cell anemia and beta-thalassemia has resulted in improvement of hematological parameters. Supplementation with 300 IU/day for 3-6 months has resulted in improved walking distances and improved blood flow in patients with intermittent claudication. In a limited number of controlled studies, 300-600 IU/day resulted in improvement in premenstrual syndrome, tardive dyskinesia and also arthritis. Epidemiological studies suggest that high levels of serum vitamin E are associated with lower risk of certain cancers, cardiovascular disease and infections. In some cases the high levels are difficult to obtain by diet alone. High levels of vitamin E are contraindicated in subjects who are receiving vitamin K antagonists as anticoagulant therapy. Except for this interaction with vitamin K, there are no specific side effects associated with high doses of vitamin E. Thus, there are various reasons for supplementations with vitamin E and, with the exception noted, the risk of such supplementation is very low.
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PMID:Use and safety of elevated dosages of vitamin E in adults. 250 7

Magnesium deficiency may play a role in the pathogenesis of atherosclerosis, cardiac arrhythmias, and coronary spasm. Because less than 1% of magnesium (Mg) is extracellular, the serum magnesium (sMg) does not always accurately reflect intracellular Mg stores. To determine the frequency of Mg deficiency in patients with cardiovascular disease, we measured blood mononuclear cell Mg content (mMg) and sMg concentrations in 104 unselected patients admitted to our intensive cardiac care unit (CCU). Twenty-seven normal healthy controls and 33 hypomagnesemic patients with chronic alcoholism and/or malabsorption syndrome served as reference groups. The sMg concentration in the CCU patients was 2.05 +/- 0.03 mg/dl (mean +/- SEM), and did not differ from normal controls (mean 2.01 +/- 0.03 mg/dl). Only 8 of 104 CCU patients were hypomagnesemic (7.7%). mMg in the CCU patients, however, was significantly lower than in the normal controls (1.15 +/- 0.02 micrograms/mg protein and 1.34 +/- 0.02 micrograms/mg protein respectively, p less than 0.001). Fifty-three percent (55 of 104) of CCU patients had mMg contents less than 1.119 micrograms/mg protein, i.e., below that of the lowest normal control. mMg was significantly lower in those patients with congestive heart failure (mMg = 1.08 +/- 0.03 micrograms/mg protein) when compared to those patients without congestive heart failure (1.23 +/- 0.02 micrograms/mg protein, p less than 0.001). We conclude that the incidence of intracellular Mg deficiency in patients with cardiovascular disease is much higher than the sMg would lead one to suspect, and may contribute to clinical cardiovascular morbidity.
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PMID:Low blood mononuclear cell magnesium in intensive cardiac care unit patients. 395 55

Data continue to emerge that the low cobalamin levels often seen in the elderly and in various other settings represent a subtle cobalamin deficiency state. Even though such individuals do not have megaloblastic anemia and absorb free cobalamin normally, metabolic tests frequently document insufficiency of cobalamin that reverses after treatment with cobalamin. In many cases, malabsorption limited to food cobalamin seems responsible for the mild deficiency state. A major development related to folate has been the conclusive documentation that folate supplementation halves the risk of having a baby with neural-tube defect. The explanation for this phenomenon and the possible long-term side effects of regular folate supplementation remain to be determined. Another issue with public health implications is the association of mild homocysteinemia with premature cardiovascular disease and evidence that the homocysteinemia responds to vitamin supplementation. Important advances are being made with molecular biologic techniques in unraveling the structure of key transport proteins for cobalamin and folates.
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PMID:Megaloblastic anemias. 937 Dec 68

Rapid improvements in the understanding of the nutritional requirements of both infants and adults has led to new developments in the modification of fats and oils. Specific targets include the improvement in growth and development of infants, treatment of disease in adults, and disease prevention. Efforts have been focussed on the production of structured lipids using medium-chain acids and long-chain polyunsaturated fatty acids (PUFAs), as well as the concentration of long-chain PUFAs from new and existing sources. Short- and medium-chain fatty acids are metabolized differently than long-chain fatty acids and have been used as a source of rapid energy for preterm infants and patients with fat malabsorption-related diseases. Long-chain PUFAs, specifically docosahexaenoic acid and arachidonic acid, are important both in the growth and development of infants, while n-3 PUFAs have been associated with reduced risk of cardiovascular disease in adults. Based on the requirements for individual fat components by different segments of the population, including infants, adults, and patients, ideal fats can be formulated to meet their needs. By using specific novel fat sources and lipid modification techniques, the concentrations of medium-chain, long-chain saturated, and long-chain polyunsaturated fatty acids as well as cholesterol can be varied to meet the individual needs of each of these groups. While genetic modification of oilseeds and other novel sources of specific lipid components are still being developed, chemical and lipase-catalyzed interesterification reactions have moved to the forefront of lipid modification technology. Fractionation of fats and oils to provide fractions with different nutritional properties has potential, but little work has been performed on the nutritional applications of this method. The choice of suitable lipid modification technologies will depend on the target lipid structure, production costs, and consumer demand. A combination of some or all of the present lipid modification techniques may be required for this purpose.
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PMID:Lipid modification strategies in the production of nutritionally functional fats and oils. 985 Apr 61

A COMMON CONDITION: Vitamin B12 deficiency is common in the elderly. Search for deficiency should be undertaken whenever the clinical situation could lead to vitamin deficiency whether macrocytic anemia is present or not as its development may come late. PATHOPHYSIOLOGICAL IMPLICATIONS: The potential relationships between degenerative neuropsychiatric disorders and cerebrovascular or cardiovascular disease, mainly via hyperhomocysteinemia, emphasize the importance of searching for vitamin B12 deficiency in the elderly. SPECIFIC CAUSES: In the elderly, it is important to recognize specific causes of vitamin B12 deficiency, mainly resulting from vitamin malabsorption.
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PMID:[Vitamin B 12 deficiency in the aged]. 1056 83

The decline in duodenal ulcer disease and the established relation of peptic ulcer to Helicobacter pylori have virtually abolished the need for elective ulcer surgery. However, a substantial proportion of the population around retirement age has previously been subjected to partial gastric resection due to peptic ulcer, and the long-term outcome of these patients is of continuing relevance. Patients subjected to elective surgery could represent a selected group of healthy subjects with a lower overall morbidity, but reports indicate that patients operated on for peptic ulcer have more advanced disease associated with excess smoking and a different pattern of social behavior. The surgical procedure induces enterogastric reflux, leading to profound changes in the remnant mucosa and the formation of carcinogens in the gastric juice. In addition, metabolic abnormalities are common, especially fat malabsorption. Evaluation of the impact of these factors on morbidity and mortality is difficult. Increased mortality in gastrointestinal tumors (especially gastric stump carcinoma), respiratory diseases and other smoking-related malignancies, and suicide are found in the long-term follow-up after partial gastric resection due to peptic ulcer. However, these hazards to life are offset by a decreased mortality in cardiovascular disease. Preventive measures against suicide and especially tobacco smoking are recommended to improve th outcome for this cohort.
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PMID:Long-term prognosis after partial gastrectomy for gastroduodenal ulcer. 1065 65

The nutritional condition of children with human immunodeficiency virus (HIV) infection continues to be a problem both in developed and developing countries. HIV-infected children grow below normal standards in both height and weight when compared with HIV-exposed non-infected children. These patterns persist over time. It is possible that acute infectious episodes and increased HIV viral burden contribute to decrements in all growth variables. Potential aetiologies for abnormal growth include inadequate dietary intake, gastrointestinal malabsorption, increased energy utilization and psycho-social problems. It is likely that all these factors contribute to the growth problems of these children to some extent. With the development of protease inhibitor anti-retroviral therapy and highly-active anti-retroviral treatment regimens, children with HIV infection in developed countries are living longer with a chronic illness. New nutritional problems have arisen with the development of the fat redistribution syndrome or lipodystrophy. Emerging problems are now being recognized, with the development of insulin resistance and truncal obesity which may potentially lead to premature cardiovascular disease.
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PMID:Nutrition in paediatric human immunodeficiency virus infection. 1082 85

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

The data generated from the human genome project offers unprecedented opportunities to elucidate the etiology of chronic diseases and developmental anomalies that arise from deleterious genome-diet interactions. Folate metabolism is an attractive system to explore such relationships. Folate is necessary for the synthesis of purine and thymidine deoxyribonucleotides and S-adenosylmethionine, a cofactor required for DNA methylation. Impaired folate metabolism results from primary folate deficiency, alcohol, gastrointestinal disorders that result in malabsorption, single nucleotide polymorphisms, increased folate catabolism and secondary nutrient deficiencies in vitamin B-6, vitamin B-12 and iron arising from a variety of pathologies. Any of these conditions singly or in combination influence DNA synthesis, DNA integrity, allelic-specific gene expression, chromatin structure and DNA mutation rates. Biochemical manifestations of impaired folate metabolism include increased uracil uptake into DNA, altered DNA methylation status and elevated homocysteine and S-adenosylhomocysteine in serum and tissues. These biochemical changes are associated with risk for cancer, cardiovascular disease, neural tube defects and some neuropathies and anemia, although direct causative mechanisms have not been established in all cases. Interactions between folate and the genome are reciprocal; polymorphisms in key genes influence folate nutritional requirements, indicating that dietary folate adequacy likely exerts selective pressure and thereby influences genetic variation. Other studies indicate that exposure to excess folate, perhaps at levels that occur at the upper end of the intake distribution curve, may have unintended consequences in promoting embryo viability. Therefore individualizing folic acid dietary recommendations necessitates a detailed understanding of all genetic and physiological variables that influence the interaction of folate with the genome and their relationship to the disease process.
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PMID:Bringing individuality to public health recommendations. 1216 15

Obesity is considered a primary risk factor for cardiovascular disease and related mortality. The current study aimed to investigate the efficacy of minimal invasive gastric banding (GB) surgery for reducing caloric intake in morbid obesity, and to analyze the effects of weight loss on body composition and metabolic and psychosocial outcomes. Twenty-six adult severely obese patients (mean body mass index [BMI], 48.1 kg/m(2); range, 42 to 56) underwent adjustable silicone laparoscopic GB. Nine additional obese patients who declined surgery were treated with metformin (2 g daily) and served as a small additional group (BMI, 50.5 kg/m(2); range, 41 to 68). Presurgery and 17 +/- 2.2 months postoperatively, body composition (fat mass [FM], lean body mass [LBM], body water) and serum parameters (lipids, glucose, thyrotropin-stimulating hormone [TSH]) were determined. Quality of life (QoL) was evaluated by a standardized self-rating questionnaire (Short Form-36 [SF-36]), and supplemented by measures of physical complaints and psychological distress. After GB, weight loss was 21 +/- 14.9 kg (14%, P <.001). It was associated with a decrease in FM by 14 +/- 8.6 kg (18%, P <.001), LBM by 4 +/- 2.7 kg (5%, P <.001), body water by 4 +/- 3.4 L (7%, P <.01), systolic blood pressure by 16 +/- 26.3 mm Hg (10%, P <.05), total cholesterol by 0.69 +/- 1.29 mmol/L (12%, P <.05), and low-density lipoprotein cholesterol (LDL-C) by 0.38 +/- 0.39 mmol/L (10%, P <.05). Highly significant interactions between surgery and time were noted for weight (P <.005), BMI (P <.005), and FM (P <.007, analysis of variance [ANOVA]). Preoperatively, 14 of 26 patients (54%) had high fasting blood sugar levels (type 2 diabetics) and 11 (42%) had impaired glucose tolerance, whereas postoperatively, for baseline glucose levels a trend to decrease was noted. Neither malabsorption nor anemia was observed. QoL improved after GB; in particular, physical functioning and well being increased (P <.01), and somatic complaints (eg, dyspnea and heart complaints, pain in legs and arms) markedly decreased (P =.008). In the metformin group, neither relevant weight loss nor a significant decrease of biochemical values was observed. Minimal invasive GB is a successful therapeutic tool for reducing FM in morbidly obese patients. Weight loss resulted in improved metabolic parameters, suggesting a lowered atherogenic risk.
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PMID:Metabolic and psychosocial effects of minimal invasive gastric banding for morbid obesity. 1466 54


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