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At least 1,315 records · Page 73Linked to original sources
PubMed2001

Symptom and health-related quality-of-life measures for use in selected gastrointestinal disease studies: a review and synthesis of the literature.

Patient-rated symptom and health-related quality-of-life (HR-QOL) outcomes are important end-points for clinical trials of medical treatments for gastrointestinal (GI) disorders. Based on this review, patient outcomes research is focused on gastroesophageal reflux disease and dyspepsia, with a growing interest in irritable bowel syndrome but little research in gastroparesis. State-of-the-art for patient-rated symptom scales is rudimentary with an abundance of scales and little attention to systematic instrument development or comprehensive psychometric evaluation. Generally, disease-specific HR-QOL measures have been more systematically developed and evaluated psychometrically, but few have been incorporated into clinical trials. More comprehensive outcome assessments are needed to determine the effectiveness of new medical treatments for functional GI disorders. Future clinical trials of GI disorders should combine clinician assessments of outcomes and symptoms with patient-rated symptom and HR-QOL end-points.

Clinical Trials as Topic↗
PubMed1995

Adolescent Human Immunodeficiency Virus Infection and Gastrointestinal Disease.

Since 1987 the presence of HIV infection among adolescents has grown dramatically. Gastrointestinal complications in HIV infection are a very diverse group of problems, all of which can cause significant morbidity and occasional mortality. This article discusses these GI disorders and recommends diagnostic studies and therapeutic options for this group of patients.

Journal Article↗
PubMed1992

Association of nonsteroidal antiinflammatory drugs with upper gastrointestinal disease: epidemiologic and economic considerations.

One of the major concerns regarding the use of nonsteroidal antiinflammatory drugs (NSAID) in the treatment of patients with arthritis is the high incidence of gastrointestinal (GI) side effects. Important issues regarding NSAID and upper GI complications include the following: (1) the magnitude of the association between NSAID therapy and clinically important gastric or duodenal ulcers or upper GI bleeding; (2) the subgroup(s) of patients who are at increased risk for upper GI side effects; and (3) the economic impact of NSAID induced upper GI toxicity. A causal association between NSAID use and the development of clinically important ulcer disease or its complications, including upper GI bleeding, is supported by available epidemiologic data. Furthermore, data suggest that up to one third of all direct costs of care may be attributed to the treatment of NSAID induced GI side effects. Approaches to this problem, such as the development of safer NSAID that are equally effective, need to be pursued.

Aged↗
PubMed2005

Probiotics and nutraceuticals: non-medicinal treatments of gastrointestinal diseases.

The demonstration that immune and epithelial cells can discriminate between different microbial and bioactive plant species has extended the known mechanism(s) of action of nutraceuticals and probiotics beyond simple nutrition and/or antimicrobial effects. The progressive unravelling of these plant and bacterial effects on systemic immune and intestinal epithelial cell function has led to new credence for the use of probiotics and nutraceuticals in clinical medicine. Level I evidence now exists for the therapeutic use of probiotics in infectious diarrhea in children, recurrent Clostridium difficile-induced infections and post-operative pouchitis. Additional evidence is being acquired for the use of probiotics in other gastrointestinal infections, irritable bowel syndrome and inflammatory bowel disease. Not all individual probiotic strains have the same efficacy, and future clinical trials may focus on multistrain preparations agents with known efficacy. The use of nutraceuticals and probiotics as therapeutic agents for gastrointestinal disorders is rapidly moving into clinical usage. Scientific studies are providing mechanisms of action to explain the therapeutic effects, and randomized controlled trials are providing the necessary evidence for their incorporation into the therapeutic armamentarium.

Colorectal Neoplasms↗
PubMed2003

Multidrug resistance 1 gene (P-glycoprotein 170): an important determinant in gastrointestinal disease?

The interface between luminal contents and intestinal epithelium constitutes the largest area of interaction between the host and the environment. There is now strong evidence that the gene product of the multidrug resistant pump (MDR) plays a critical role in host-bacterial interactions in the gastrointestinal tract and maintenance of intestinal homeostasis. This review highlights the efflux mechanism in the intestinal epithelium which is mediated by the multidrug resistant pump, also known as P-glycoprotein 170. Current studies promise to provide further insights into the contribution of the MDR1 gene in the pathogenesis of inflammatory and malignant disorders of the gastrointestinal tract.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1992

Infantile refsum disease: gastrointestinal presentation of a peroxisomal disorder.

This article describes two siblings with infantile Refsum disease (IRD) whose initial presentation was that of malabsorption and mimicked a-beta- or homozygous hypo-beta-lipoproteinemia. Failure to recognize IRD in the first-born child precluded proper genetic counseling and prenatal diagnosis in subsequent pregnancies and also caused considerable delay in diagnosing IRD in the second child. The clinical heterogeneity of peroxisomal disorders constitutes a diagnostic challenge, which demands a high degree of awareness from the part of the clinician. This is particularly the case with IRD, where protracted diarrhea with low serum cholesterol levels appears to be a frequently occurring initial feature during the 1st months of life.

Abetalipoproteinemia↗
PubMed1990

Gastrointestinal disease and oral contraception.

Oral contraceptive steroids play a major role in modern family planning. With the present tendency to decrease the doses of both estrogens and progestogens, any factor that reduces the bioavailability of the lower-dose preparations may have an impact on contraceptive protection. Although ethinyl estradiol, the most commonly used oral estrogen, is liable to an enterohepatic circulation as unchanged drug, the commonly used progestogens are not. At present, no convincing evidence exists in the human subject that disruption of the enterohepatic circulation by antibiotics or antacids does reduce contraceptive efficacy of the pill. Oral contraceptive steroids are mainly absorbed from the small bowel, and contraceptive efficacy depends on its absorptive capacity. Enhanced passage of gastrointestinal contents or impaired absorption may thus contribute to contraceptive failures in patients who have chronic inflammatory disease, diarrhea, ileostomy, or jejunoileal bypass.

Antacids↗
PubMed1998

Review article: the diagnosis and treatment of haematinic deficiency in gastrointestinal disease.

Deficiency of any of the vitamins and minerals essential for normal erythropoiesis (haematinics), including iron, copper, cobalt, vitamins A, B12, B6, C, E, folic acid, riboflavin and nicotinic acid, may be associated with defective erythropoiesis and anaemia. Iron, vitamin B12 and folate are the haematinics for which deficiency states manifest most often clinically and are the focus of this review. The normal absorption of these haematinics and gastrointestinal causes of their deficiency are described. Investigations, including the use of homocysteine metabolite levels and new techniques such as serum transferrin receptor assays, and treatment of haematinic deficiency are discussed in detail.

Deficiency Diseases↗
PubMed2001

Modulation of heme oxygenase in tissue injury and its implication in protection against gastrointestinal diseases.

Heme oxygenase (HO) is the rate-limiting enzyme in the catabolism of heme, followed by production of biliverdin, free iron and carbon monoxide (CO). There are three isoforms of HO: HO-1 is highly inducible, whereas HO-2 and HO-3 are constitutively expressed. In addition to heme, a variety of nonheme compounds, including heavy metals, cytokines, endotoxins and heat shock stress are strong inducers of HO-1 expression. Many studies indicated that induction of HO-1 is associated with a protective response due to the removal of free heme, which is shown to be toxic. However, recent studies demonstrated that the expression of HO-1 in response to different inflammatory mediators could contribute in part to the resolution of inflammation and have protective effects on brain, liver, kidney and lung against injuries. These beneficial effects seem to be due to the production of bile pigment biliverdin and bilirubin that is a potent antioxidant, as well as the release of iron and CO. However, there are few studies concerning the relationship between HO-1 and inflammation as well as injury in the gut. Interestingly, a preliminary study implicated that induction of HO-1 expression in a colonic damage model induced by trinitrobenzene sulfonic acid played a critical protective role, indicating that activation of HO-1 could act as a natural defensive mechanism to alleviate inflammation and tissue injury in the gastrointestinal tract.

Animals↗
PubMed1999

Slow-transit constipation: solitary symptom of a systemic gastrointestinal disease.

INTRODUCTION: Autonomic neuropathy is thought to play a role in the pathogenesis of slow-transit constipation, but other gastrointestinal organs may also be involved, even if they are symptom-free. We investigated whether motility in gastrointestinal organs other than the colon was impaired in patients with slow-transit constipation and whether the autonomic nervous system was involved. METHODS: Twenty-one consecutive patients (18 females; median age, 46 years) with severe chronic constipation (< or = 2 defecations/week and delayed colonic transit time) were studied. Autonomic neuropathy function was tested with esophageal manometry, gastric and gallbladder emptying (fasting and postprandial motility) by ultrasonography, orocecal transit time (H2-breath test), colonic transit time (radiopaque markers), and anorectal volumetric manometry. The integrity of the autonomic nervous system was assessed by a quantitative sweat-spot test for preganglionic and postganglionic fibers, tilt-table test, and Valsalva electrocardiogram R-R ratio. RESULTS: Esophageal manometry showed gastroesophageal reflux or absence of peristalsis in five of the seven patients examined. Gallbladder dysmotility (i.e., increased fasting, postprandial residual volume, or both) was observed in 6 of 14 (43 percent) patients. Gastric emptying was decreased in 13 of 17 (76 percent) patients. Orocecal transit time was delayed in 18 of 20 (90 percent) patients; median transit time was 160 (range, 90-200) minutes. Median colonic transit time was 97 (range, 64-140) hours. Anorectal function showed abnormal rectoanal inhibitory reflex and decreased rectal sensitivity in 11 of 19 (58 percent) patients. Signs of autonomic neuropathy of the sympathetic cholinergic system were found in 14 of 18 (78 percent) patients. Only one of nine patients had vagal abnormalities detected with the Valsalva test and four of five patients with a history of orthostatic hypotension had a positive tilt-table test. CONCLUSIONS: Slow-transit constipation may be associated with impaired function of other gastrointestinal organs. More than 70 percent of patients with slow-transit constipation present some degree of autonomic neuropathy. Severe constipation may be the main complaint in patients with a systemic disease involving several organs and possibly involving the autonomic nervous system. This should be considered in the management of such cases.

Adolescent↗
PubMedDate not supplied

Nonsteroidal anti-inflammatory drugs and gastrointestinal disease: pathophysiology, treatment and prevention.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are a common cause of gastrointestinal ulceration. Chronic NSAID use increases the risk of ulcer bleeding or perforation 3- to 4-fold. NSAID-induced injury results from both local effects and systemic prostaglandin inhibition. New evidence suggests that the systemic effects on prostaglandin production may vary between NSAIDs. The majority of NSAID-induced ulcers are asymptomatic. They may be treated by discontinuing the NSAID and using standard ulcer therapy. Patients taking NSAIDs who are at a high risk for a GI complication should also receive therapy to decrease their risk for ulceration. In this review the epidemiology, pathogenesis, risks, treatment and prophylaxis of NSAID-induced gastrointestinal complications are discussed.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2006

Association of H pylori cagA and vacA genotypes and IL-8 gene polymorphisms with clinical outcome of infection in Iranian patients with gastrointestinal diseases.

AIM: To find out if a functional promoter polymorphism in the IL-8 gene along with cagA status and polymorphisms in vacA gene influence the type of diseases in Iranian patients infected by H pylori. METHODS: IL-8 -251 A/T polymorphism was genotyped by oligonucleotide allele specific PCR (ASO-PCR) in a sample of 233 patients with H pylori infection undergoing upper gastrointestinal endoscopy. The presence of cagA gene and polymorphisms in vacA gene was also determined by PCR. Association of these genetic polymorphisms with the development of gastritis, peptic ulcers as well as gastric cancer was tested. RESULTS: When the patients with different clinical manifestations were compared according to the presence of cagA gene or various vacA genotypes, only the vacA genotypes were significantly different among gastritis, peptic ulcer and gastric cancer patients (chi 2 = 17.8; P = 0.001). Furthermore, there was a significant difference in the frequency of IL-8 -251 A/T genotypes between patients with gastric cancer and benign diseases (chi 2 = 10.47; P = 0.005). CONCLUSION: The IL-8 -251 A/T polymorphism and the polymorphisms in H pylori vacA gene are involved in limiting the infection outcome to gastritis and peptic ulcer or in favoring cancer onset in Iranian patients.

Adult↗
PubMed1989

Campylobacter pylori-related gastrointestinal disease in children. Incidence and clinical findings.

Over a one-year period, 95 children and adolescents presenting with epigastric pain and/or vomiting, and without associated risk factors for development of peptide disease, underwent endoscopic antral biopsies for pathologic diagnosis and to detect presence of Campylobacter ss. pylori (C. pylori). Additional biopsies of the esophagus, stomach, and duodenum were obtained for histologic evaluation. C. pylori was identified in 16 patients (16.8%), all of whom had evidence of acute and/or chronic gastritis. Significant discriminating factors between C. pylori-positive and -negative subjects included age at presentation (positive vs negative = 14.6 vs 9.9 years, P less than 0.01), biopsy-confirmed gastritis (100% vs 30.4%, P less than 0.001), and diagnosis of duodenitis alone (0% vs 46.8%, P less than 0.001). Risk for bacterial colonization was significantly higher in the presence of endoscopic gastritis (P less than 0.001). Among C. pylori-positive patients, none responded to standard antiulcer therapy (H2-receptor antagonists, antacids). Symptomatic and histologic remission was achieved utilizing combined therapy with bismuth subsalicylate and antibiotics. Seven of 79 C. pylori-negative patients with biopsy-proven gastritis who responded poorly to antisecretory therapy had the organism identified in follow-up antral biopsies; these patients improved clinically following treatment for C. pylori. These data suggest that C. pylori is a significant factor in the etiology of upper gastrointestinal tract inflammatory disease in pediatrics, and presence of the organism should be evaluated, particularly in children with evidence of acute and/or chronic gastritis.

Adolescent↗
PubMed1991

The epidemiology of NSAID associated gastrointestinal disease.

Many problems make it difficult to estimate the exact risk of peptic ulceration and its complications, perforation and bleeding, in patients receiving NSAIDs. Nevertheless the association of these events and treatment is now beyond dispute. Deaths are a particular problem in the elderly since mortality from peptic ulcer disease rises steeply after age 60. Risk factors identified with hospitalisation for gastrointestinal problems in patients receiving NSAIDs include age, previous gastrointestinal symptoms, corticosteroid use and disability. The risk of death is highest in elderly females and is substantial.

Adolescent↗
PubMed2001

[Substantiation of the need of fortification with vitamins of the diet of children with gastrointestinal diseases].

Surveys of 28 children have shown that 64 per cent of the children suffering from ulcerous disease of the stomach and the duodemun or chronic duodenitis have a combined deficiency of vitamin E, vitamins of the B group and beta-carotene. Diet No. 1 and No. 5 could not provide daily needs for vitamins. The patients were found to have a lower antioxidant activity of the blood serum, whereas the contents of hydroperoxides, double bonds and malonic dialdehydes were higher than in healthy children. The POL index in children with high beta-carotene deficiency was significantly higher than that in ailing children supplied with this carotenoid. Correlation analysis has revealed a reverse relationship between concentration of vitamin E and beta-carotene in blood serum and POL products, i.e. the better a child is supplied with these vitamins, the lower is the level of POL products. When the drink with the whole set of vitamins and an oil solution of beta-carotene was included in the diet of the children, it was found that hypovitaminosis frequency lowered with positive effects on their clinical condition and improved POL indexes. So there is a reason to fortify diets of children suffering from gastrointestinal disorders with vitamins-antioxidants.

Adolescent↗