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)

Liver disease, alcohol and malnutrition are combinations usually associated with micronutrient impairment. Chronic liver disease courses with lower storage and activation of vitamin-coenzymes related to their malabsorption. Alcohol worsens the picture by reducing food intake, increasing micronutrients utilization and decreasing their absorption secondary to either intestinal or pancreatic injuries. Other concurrent causes would be drug treatments, urinary losses, protein deficiency and oxidative stress. As consequences the clinical signs are anemia, liver steatosis, oxidative stress and immunosuppression.
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PMID:[The impact of alcohol and chronic liver disease of micronutrients metabolism]. 1114 14

Regardless of the type and dose of beverage involved, alcohol facilitates the development of gastroesophageal reflux disease by reducing the pressure of the lower esophageal sphincter and esophageal motility. Fermented and nondistilled alcoholic beverages increase gastrin levels and acid secretion. Succinic and maleic acid contained in certain alcoholic drinks also stimulate acid secretion. Low alcohol doses accelerate gastric emptying, whereas high doses delay emptying and slow bowel motility. Alcohol facilitates the development of superficial gastritis and chronic atrophic gastritis--though it has not been shown to cause peptic ulcer. Alcoholic beverages, fundamentally wine, have important bactericidal effects upon Helicobacter pylori and enteropathogenic bacteria. The main alcohol-related intestinal alterations are diarrhea and malabsorption, with recovery after restoring a normal diet. Alcohol facilitates the development of oropharyngeal, esophageal, gastric, and colon cancer. Initial research suggests that wine may be comparatively less carcinogenic.
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PMID:The effects of alcohol consumption upon the gastrointestinal tract. 1115 64

The classic signs of vitamin deficiency only occur in states of extreme depletion and are unreliable indicators for early treatment or prophylaxis of alcoholic patients at risk. Post-mortem findings demonstrate that thiamine (vitamin B1) deficiency sufficient to cause irreversible brain damage is not diagnosed ante mortem in 80-90% of these patients. The causes of vitamin deficiency are reviewed with special attention to the inhibition of oral thiamine hydrochloride absorption in man caused by malnutrition present in alcoholic patients or by the direct effects of ethanol on intestinal transport. As the condition of the patient misusing alcohol progresses, damage to brain, liver, gastrointestinal tract, and pancreas continue (with other factors discussed) to further compromise the patient. Decreased intake, malabsorption, reduced storage, and impaired utilization further reduce the chances of unaided recovery. Failure of large oral doses of thiamine hydrochloride to provide an effective treatment for Wernicke's encephalopathy emphasizes the need for adequate and rapid replacement of depleted brain thiamine levels by repeated parenteral therapy in adequate doses.
Alcohol Alcohol Suppl
PMID:Mechanisms of vitamin deficiency in chronic alcohol misusers and the development of the Wernicke-Korsakoff syndrome. 1130 71

In this review the effects of lifestyle factors, especially alcohol consumption, on vitamin bioavailability are summarized and discussed. Alcohol effects are clearly dose-dependent. Excessive chronic alcohol intake is generally associated with vitamin deficiency (especially folate, thiamine, and vitamin B6) due to malnutrition, malabsorption, and ethanol toxicity. Effects of moderate alcohol use are mainly explained by a lower vitamin intake. In the case of vitamin A and beta-carotene, effects on post-absorptive (lipoprotein) metabolism have been demonstrated. In one diet-controlled crossover study, alcohol consumption resulted in an increase in the plasma vitamin B6 (PLP) content, especially after beer consumption (containing vitamin B6), but also after wine and spirit consumption (not containing vitamin B6). Smoking is also associated with a lower dietary vitamin intake. In the case of vitamin C, B12, folate, and beta-carotene, evidence has been presented for effects on postabsorptive metabolism, due to smoke-induced oxidative stress and/or vitamin inactivation. For vitamin E a direct effect of smoking on absorption has been demonstrated. There is no convincing evidence that low-fat diets negatively affect fat-soluble vitamin absorption, but cholesterol-lowering compounds (diets), or unabsorbable fat substitutes, may do so. Vitamin bioavailability may be compromised from certain vegetables (particularly raw), and/or from high-fiber foods, because of limited digestion and inefficient release of vitamins from the food matrix.
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PMID:Influence of lifestyle on vitamin bioavailability. 1188 54

The goals and objectives of these studies, conducted over the past 30 y, were to determine: a) how chronic alcoholism leads to folate deficiency and b) how folate deficiency contributes to the pathogenesis of alcoholic liver disease (ALD). The intestinal absorption of folic acid was decreased in binge drinking alcoholics and, prospectively, in volunteers fed alcohol with low folate diets. Monkeys fed alcohol for 2 y developed decreased hepatic folate stores, folic acid malabsorption and decreased hepatic uptake but increased urinary excretion of labeled folic acid. Micropigs fed alcohol for 1 y developed features of ALD in association with decreased translation and activity of intestinal reduced folate carrier. Another study in ethanol-fed micropigs demonstrated abnormal hepatic methionine and DNA nucleotide imbalance and increased hepatocellular apoptosis. When alcohol feeding was combined with folate deficiency, micropigs developed typical histological features of ALD in 14 wk, together with elevated plasma homocysteine levels, reduced liver S-adenosylmethionine and glutathione and increased markers for DNA and lipid oxidation. In summary, chronic alcohol exposure impairs folate absorption by inhibiting expression of the reduced folate carrier and decreasing the hepatic uptake and renal conservation of circulating folate. At the same time, folate deficiency accelerates alcohol-induced changes in hepatic methionine metabolism while promoting enhanced oxidative liver injury and the histopathology of ALD.
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PMID:Metabolic interactions of alcohol and folate. 1216 94

To determine the natural history of chronic pancreatitis (CP), we retrospectively studied 193 consecutive patients who had at least one hospitalization for the control of pain or a complication of CP by examining the hospital records and by using a standard questionnaire. Alcohol (66%) was the major cause of CP and the cause was unknown in 21%. Pain was the presenting symptom in 93%. Pancreatic calcification was observed in 41% (alcoholic 54% vs. nonalcoholic 19%; OR = 6.7, CI = 2.7, 14.3; p < 0.0001). Diabetes (28%), malabsorption (16%), pseudocysts (21%) and pancreatic (3%) or extrapancreatic malignancy (5%) were the main complications. 43% had surgical intervention for pain relief, 10% had either endoscopic sphincterotomy or surgical sphincteroplasty and 16% had surgery for complications. Surgical or endoscopic intervention was more commonly performed in nonalcoholics compared with alcoholics (OR = 12.8, CI = 3.6, 53.9; p < 0.0001). However, if sphincterotomy and sphincteroplasty were excluded, the total number of surgical procedures for pain relief was similar in both groups. Complete follow-up information was available in 107 patients with a mean duration of follow-up of 10 years (range, 1-28 years); 27 patients died during the follow-up; 5, 10 and 15 year mortality was 14%, 18% and 20% respectively. The mortality was significantly higher in patients with alcoholic CP than in nonalcoholic CP (35% vs. 10%; OR = 1.4, 18.7; p = 0.005). Of the 80 patients who were alive and had complete long-term follow-up, pain improved in 62 patients, remained unchanged in 17 and worsened in one. Pain improved in 34 of 41 (83%) patients who had surgical intervention for pain, 7 of 9 patients (78%) who had surgery for complications, 4 of 7 (57%) who had sphincter ablation and 17 of 23 patients (74%) who had nonprocedural treatment. Long-term pain relief was similar in patients with alcoholic and nonalcoholic pancreatitis.
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PMID:Chronic pancreatitis. Long-term pain relief with or without surgery, cancer risk, and mortality. 1254 89

Coeliac disease (CD), a gastrointestinal illness characterized by intestinal malabsorption, results from gluten intolerance accompanied with immunological responses towards gliadin, an ethanol-soluble protein fraction of wheat and other cereals. The role of gliadin in eliciting immune responses in CD is still partly unclear; however, the occurrence of anti-gliadin in the sera of patients suffering from CD correlates well with clinical symptoms. In this work we report the construction of isotype-specific, phage-displayed scFv libraries from peripheral blood lymphocytes of a patient with CD and from a healthy control individual. VH and VL chains were amplified by reverse transcription-polymerase chain reaction (RT-PCR) using a set of oligonucleotides recognizing all human variable gene families. The three scFv libraries (IgA, IgG and IgM) were selectively enriched for gliadin-binding phage. After four rounds of affinity selection, polyclonal enrichment of gliadin-binding phage was observed in all libraries from the CD patient but in none from the healthy donor. Phagemid particles generated from single clones were demonstrated to be gliadin-specific, as shown by strongly positive enzyme-linked immunosorbent assay (ELISA) and BiaCore signals. The VH and VL chains from samples of these monoclonal isotype-specific phage were sequenced to identify the most common variable regions used by the immune system to elicit antibody responses against gliadin.
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PMID:Phage display of human antibodies from a patient suffering from coeliac disease and selection of isotype-specific scFv against gliadin. 1451 Dec 41

Drug therapy may become difficult when a significant amount of the small intestine is resected, as happens in patients with a short small bowel. Drug absorption from the gastrointestinal tract is altered in these patients; however, this effect is variable in patients and differs with each drug. Literature regarding clinical outcomes of normal or alternative administration routes in patients with a short small bowel is limited. We explored what is written about the normal absorption of commonly used drugs and what difference the resection of different but substantial parts of the small intestine makes. Changes in the gastrointestinal tract after resection of >50% of the small intestine causes malabsorption of macronutrients and micronutrients, and may alter the drug absorption process. The metabolic activity of the abundantly present intestinal lactobacilli can also affect the enteral drug absorption in patients with short small bowel as this results in the production of lactic acid, gaseous CO(2), ethanol and an increased bile acid deconjugation. Accelerated intestinal luminal transit time causes a reduction in absorption of certain antimicrobial agents, digoxin, hydrochlorothiazide, ciclosporin, cimetidine, mesalazine (5-aminosalicylic acid), oral contraceptives and levothyroxine. Gastric hypersecretion and lack of sufficient contact time with the intestinal mucosa in patients with short small bowel leads to insufficient absorption of drugs such as omeprazole. Successful treatment with warfarin, tricyclic antidepressants, metronidazole, fluconazole, procainamide, sotalol and pindolol are reported in several studies. Many different factors cause this variability in drug absorption in such patients. Monitoring the serum drug concentration in these patients may ease dealing with the management problems.
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PMID:Enteral drug absorption in patients with short small bowel : a review. 1553 Jan 27

Nutrition is an important "modifiable" factor in the development and maintenance of bone mass and in the prevention of osteoporosis. The improvement of calcium intake in prepuberal age translates to gain in bone mass and, with genetic factor, to achievement of Peak Bone Mass (PBM), the higher level of bone mass reached at the completion of physiological growth. Individuals with higher PBM achieved in early adulthood will be at lower risk for developing osteoporosis later in life. Achieved the PBM, it is important maintain the bone mass gained and reduce the loss. This is possible adopting a correct behaviour eating associated to regular physical activity and correct life style. The diet is nutritionally balanced with caloric intake adequate to requirement of individual. This is moderate in protein (1 g/kg/die), normal in fat and the carbohydrates provide 55-60% of the caloric intake. A moderate intake of proteins is associated with normal calcium metabolism and presumably does'nt alter bone turnover. An adequate intake of alkali-rich foods may help promote a favorable effect of dietary protein on the skeleton. Lactose intolerance may determinate calcium malabsorption or may decrease calcium intake by elimination of milk and dairy products. Omega3 fatty acids may "down-regulate" pro-inflammatory cytokines and protect against bone loss by decreasing osteoclast activation and bone reabsorption. The diet is characterized by food containing high amount of calcium, potassium, magnesium and low amount of sodium. If it is impossible to reach the requirement with only diet, it is need the supplement of calcium and vitamin D. Other vitamins (Vit. A, C, E, K) and mineral (phosphorus, fluoride, iron, zinc, copper and boron) are required for normal bone metabolism, thus it is need adequate intake of these dietary components. It is advisable reduce ethanol, caffeine, fibers, phytic and ossalic acid intake. The efficacy of phytoestrogens is actually under investigation. Some drugs may interfere with calcium and other nutrients and produce an unfavourable effect on bone health.
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PMID:[Diet, nutrition and bone health]. 1608 Jun 61

Nonunions and delayed unions have been classically defined by Bassett as an arrest of the fracture healing process at an intermediary stage of repair, at which time the fracture gap is bridged by fibrocartilage. It is estimated that approximately 10-20 % of long bone fractures in the United States will result in delayed unions when compared to the average rate of healing for the location and type of fracture. Many of these will go on to a nonunion if biological or biomechanical factors are not optimized to enhance healing. Additional commorbities such as smoking, ethanol abuse, malnutrition, malabsorption and altered neurologic conditions can contribute to delayed unions or nonunions. Even despite appropriate and aggressive early management of long bone fractures, a certain percentage still lack progression of healing and go on to nonunion. Classical surgical management of nonunions includes obtaininjg fracture stabilization with ORIF techniques and bone grafting, with reported clinical successes ranging from 50-80%. Those that fail to achieve union despite classical management are indeed recalcitrant nonunions.
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PMID:Successful treatment of recalcitrant nonunions with combined magnetic field stimulation. 1616 Oct 3


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