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At least 37 records · Page 2Linked to original sources
PubMed2003

Urologic manifestations of nonurologic diseases gastrointestinal disorders.

A variety of common, gastrointestinal diseases result in significant genitourinary tract pathology. In general, knowledge of these associated disease processes permit rapid and accurate diagnosis and treatment. The underlying thread is the recognition of one pathophysiological process to explain patterns of a single disease.

Diverticulitis↗
PubMed2002

Intestinal permeation and gastrointestinal disease.

The gastrointestinal tract constitutes one of the largest sites of exposure to the outside environment. The function of the gastrointestinal tract in monitoring and sealing the host interior from intruders is called the gut barrier. A variety of specific and nonspecific mechanisms are in operation to establish the host barrier; these include luminal mechanisms and digestive enzymes, the epithelial cells together with tight junctions in between them, and the gut immune system. Disruptions in the gut barrier follow injury from various causes including nonsteroidal anti-inflammatory drugs and oxidant stress, and involve mechanisms such as adenosine triphosphate depletion and damage to epithelial cell cytoskeletons that regulate tight junctions. Ample evidence links gut barrier dysfunction to multiorgan system failure in sepsis and immune dysregulation. Additionally, contribution of gut barrier dysfunction to gastrointestinal disease is an evolving concept and is the focus of this review. An overview of the evidence for the role of gut barrier dysfunction in disorders such as Crohn's disease, celiac disease, food allergy, acute pancreatitis, non-alcoholic fatty liver disease, and alcoholic liver disease is provided, together with critical insight into the implications of this evidence as a primary disease mechanism.

Acute Disease↗
PubMed1998

[Bone changes in gastrointestinal diseases].

BACKGROUND: Gastrointestinal (GIT) diseases are a common cause of metabolic bone changes. The aim of the study was to indicate GIT diseases (lactose intolerance, non-lactose intolerance, Crohn's disease, ulcerative colitis, pancreatic insufficiency, states after gastric resection, chronic diseases of the liver, and coeliac disease) by means of literature data and the authors' own results coinciding with the detected low bone density and thus increased risk of fracture. Bone changes coinciding with GIT diseases are frequent and are commonly asymptomatic for a long period. CONCLUSION: In coincidence with GIT diseases the authors indicate the necessity of being aware of the risk of bone changes development and to investigate them actively. An early diagnosis aids to introduce preventive and therapeutical measures and to halt or at least slow down the origin of bone changes. (Ref. 21.)

Bone Diseases, Metabolic↗
PubMed2005

Mechanisms of disease: defensins in gastrointestinal diseases.

Defensins are endogenous antibiotics with microbicidal activity against Gram-negative and Gram-positive bacteria, fungi, viruses and protozoa. In the gastrointestinal tract, defensins help regulate the composition and number of colonizing microbes, and protect the host from food-borne and water-borne pathogens. In health, the normal host relationship with the commensal luminal microbiota is beneficial, but the same commensal bacteria could have a pathogenic role in inflammatory diseases. A disturbance in antimicrobial defense, as provided by Paneth cells of the small intestine, seems to be a critical factor in the pathogenesis of ileal Crohn's disease, an inflammatory disease of the intestinal tract. The disruption of the critical balance between antimicrobial peptides and luminal bacteria might also explain other gastrointestinal infections and diseases. Elucidating the underlying mechanisms involved in the regulation and biology of defensins could open up new therapeutic avenues.

Defensins↗
PubMed2000

Bone mass and gastrointestinal disease.

Several gastrointestinal and liver diseases impair the absorption of calcium, phosphate, and/or vitamin D, and are associated with an increased incidence of bone disease. Changes in bone mineral density (BMD) using dual-energy X-ray absorptiomety (DXA) have been best studied in the malabsorptive disorder, celiac disease. Celiac disease is an inflammatory condition of the small intestine triggered by ingesting gluten present in wheat, rye, or barley. Chronic inflammation leads to intestinal atrophy and nutrient malabsorption. The disease affects the proximal small bowel; the site where calcium is best absorbed. About 70% of adults with celiac disease have abnormally low BMD values. Treatment with a gluten-free diet increases BMD, but not to normal values. As celiac disease may not be detected until adult life, the failure to reach normal BMD on a gluten-free diet can be explained, at least in part, by the failure to reach peak bone mass. All individuals with malabsorptive disorders should be screened for secondary bone disease. The development of easier and less expensive methods to assess BMD will facilitate screening those at risk for bone disease.

Absorptiometry, Photon↗
PubMed2000

Association of Helicobacter pylori genotype with gastroesophageal reflux disease and other upper gastrointestinal diseases.

OBJECTIVE: Helicobacter pylori (H. pylori) is a recognized pathogen, but it may also have a protective effect for gastroesophageal reflux disease (GERD). We compared the prevalence of potential virulence factors (cagA, cagE, vacA genotypes) in GERD to other upper gastrointestinal diseases and controls. METHODS: A total of 405 patients underwent gastroscopy with H. pylori isolation and serum testing. Patient diagnostic subgroups were prospectively defined. Genotypes were determined by amplification using polymerase chain reaction. CagA antibodies were determined by western blot, enzyme-linked immunosorbent, and flow microsphere immunofluorescent assays. RESULTS: Patients were grouped as follows: nonulcer dyspepsia (26%), GERD (20%), gastric ulcer (17%), duodenal ulcer (12%), gastric cancer (6%), or controls (19%). The cagA gene was present in 94-97% of subjects in all categories, but the cagA antibody was less prevalent in nonulcer dyspepsia (69%, 95% CI: 48-86%, p = 0.02) and GERD (69%, CI: 39-91%, p < 0.05) than in those with gastroduodenal pathology including gastric ulcer, duodenal ulcer, and gastric cancer (92%, CI: 81-98%). The cagE gene and vacA S1 genotype were more frequent in patients with gastroduodenal pathology (p < 0.01). GERD was associated with a significantly lower rate of vacA S1 genotype than controls (29% (CI: 10-56%) versus 80% (CI: 59-93%), p < 0.01). The vacA S1 genotype was associated with the presence of cagA antibodies. CONCLUSIONS: The cagE and vacA S1 genotypes are more prevalent in patients with peptic ulcer or gastric cancer, suggesting a potential function in virulence for these genes. However, the vacA S1 genotype was also more prevalent in controls than GERD, suggesting a potential protective effect against GERD.

Antigens, Bacterial↗
PubMed1977

Drug-induced gastrointestinal disease.

The gastrointestinal tract is a common target for adverse drug reactions. The resultant changes are often nonspecific (e.g., mucosal ulceration, intestinal infarction, motility disturbance) and in many cases no radiographically detectable lesion may occur. A comprehensive review of the reported drug-induced disorders of the digestive organs is herein presented and their radiographic manifestations are described.

Adult↗
PubMed1994

Gastrointestinal disease in the immunocompromised patient.

Gastrointestinal (GI) disease is frequent in all types of immunocompromised patients but occurs with greatest frequency in patients with acquired immunodeficiency syndrome (AIDS). Thus, much of this review deals with human immunodeficiency virus (HIV)-related GI diseases. Gastrointestinal diseases in other immunocompromised patients are compared with those in patients with AIDS. Conditions unique to transplant recipients, such as graft-versus-host disease (GVHD) and posttransplant lymphoproliferative disorders (PTLDs), are discussed separately. We have divided these GI diseases into four main categories: (1) HIV-related inflammatory conditions other than opportunistic infections (HIV-related enteropathy, proctocolitis, and CD8 lymphocytosis); (2) inflammatory conditions unrelated to HIV or opportunistic infections (neutropenic enterocolitis, regional enteritislike enteropathy, and GVHD); (3) opportunistic infections (illnesses caused by herpesvirus, cytomegalovirus, and miscellaneous other viruses; Mycobacterium, Candida, Histoplasma, Cryptococcus, Cryptosporidium, Microsporida, Isospora, Leishmania, Toxoplasma and Strongyloides organisms as well as Pneumocystitis carinii; and (4) neoplasias (Kaposi's sarcoma [KS], AIDS-related non-Hodgkin's lymphoma [NHL], HIV-related Hodgkin's disease [HD], PTLDs, and miscellaneous neoplasms). The prevalence, pathogenesis, clinical manifestations, gross pathological findings, and microscopic features of each disease entity are discussed.

AIDS-Related Opportunistic Infections↗
PubMed2003

Nutritional management of gastrointestinal disease.

The gastrointestinal (GI) tract is primarily responsible for acquiring and digesting food, absorbing nutrients and water, and expelling wastes from the body as feces. A proper diet and normally functioning GI tract are integral for the delivery of nutrients, prevention of nutrient deficiencies and malnutrition, repair of damaged intestinal epithelium, restoration of normal luminal bacterial populations, promotion of normal GI motility, and maintenance of normal immune functions (eg, both tolerance and protection from pathogens). The amount of food, its form, the frequency of feeding, and the composition of diet each have important effects on GI function and may be used to help ameliorate signs of GI disease. Although both nutrients and nonnutritional components of a diet are important to GI health, they also may cause or influence the development of GI pathology (eg, antibiotic responsive diarrhea, inflammatory bowel disease, dietary intolerance, or sensitivity and/or allergy). The appropriate diet may have a profound effect on intestinal recovery and successful management of chronic or severe GI disease.

Animal Nutritional Physiological Phenomena↗
PubMed1998

Gastrointestinal diseases in women.

Gastrointestinal disorders are among the most common disorders for which women seek medical attention. Most gastrointestinal diseases in women are not inherently different from those that occur in men. There are several disorders, however, that occur more frequently or manifest themselves differently in women. This article reviews common gastrointestinal disorders affecting women. The pathophysiology, clinical manifestations, management, and gender-specific issues of gastroesophageal reflux disease, peptic ulcer disease, irritable bowel syndrome (IBS), and inflammatory bowel disease (IBD) are discussed.

Contraceptives, Oral↗
PubMedDate not supplied

Prevention of gastrointestinal diseases.

The prevalence of gastrointestinal diseases markedly differs between developed and developing countries because of the poor sanitation, hygiene, impure water and food ingestion, widespread illiteracy and poverty in the developing world. The incidence of gastrointestinal diseases such as diarrhoea, cholera, typhoid, dysentery, viral hepatitis (A and E virus) can be substantially reduced by providing clean water and food to the population. Restricting consumption of tobacco and nonsteroidal anti-inflammatory drugs will reduce diseases and/or complications of the upper gastrointestinal tract. Diminishing alcohol intake and overuse of blood transfusion and improving blood banks would prevent many acute and chronic liver diseases. Costly passive and active immunoprophylaxis will become unnecessary if these measures are undertaken.

Esophageal Diseases↗