Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “GASTROINTESTINAL DISEASE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 757 records · Page 42Linked to original sources
PubMed1995

[Tactivin in combined treatment of patients with pulmonary tuberculosis associated with gastrointestinal diseases].

Tactivin was tried in combined therapy of 49 new-onset cases with destructive pulmonary tuberculosis and gastrointestinal lesions. 52 controls received antibacterial drugs alone. Tactivin increased T-lymphocyte count and improved their subpopulations proportion in a shorter period of time. Immunochemotherapy contributed to efficacy of the main and associated disease treatment. Healing of the destruction foci occurred in 87% versus 70% in controls, side effects of antibacterial drugs and exacerbations of gastrointestinal diseases arose 2-2.5 times less frequently.

Adjuvants, Immunologic↗
PubMed2003

Gastrointestinal diseases in the elderly.

PURPOSE OF REVIEW: The subject of gastrointestinal disorders in the elderly is timely and important because of the demographic reality that soon over 20% of our population will be older than 65 years of age, utilizing perhaps 50% of our total healthcare costs. The purpose of this review is to draw attention to some areas of clinical information that point in the direction of better clinical care for the elderly. Medicine is finally advancing from the era when most symptoms in older patients were ascribed to the aging process itself. Indeed, within gastroenterology there are few changes that occur inevitably as part of aging. RECENT FINDINGS: Progress has been made in several areas of gastrointestinal pathophysiology. These include: the pathophysiology of swallowing and evacuation disorders and the beginning of the application of techniques derived from physiological studies to improve function; recognizing the importance of reflux esophagitis and its complications and improving treatment; understanding the importance of disorders of malabsorption and their impact upon nutrition in the elderly; major issues in the diagnosis and management of inflammatory bowel disease in this age group; and approaches to the prevention and treatment of gastrointestinal cancer, particularly colorectal cancer. SUMMARY: As we pay more attention to these areas and encourage clinical research we expect to improve the treatment of older patients with these diseases and to reduce the burden of morbidity in this population.

Aged↗
PubMed1999

Inactivation of the gene (cpe) encoding Clostridium perfringens enterotoxin eliminates the ability of two cpe-positive C. perfringens type A human gastrointestinal disease isolates to affect rabbit ileal loops.

Previous epidemiological studies have implicated Clostridium perfringens enterotoxin (CPE) as a virulence factor in the pathogenesis of several gastrointestinal (GI) illnesses caused by C. perfringens type A isolates, including C. perfringens type A food poisoning and non-food-borne GI illnesses, such as antibiotic-associated diarrhoea and sporadic diarrhoea. To further evaluate the importance of CPE in the pathogenesis of these GI diseases, allelic exchange was used to construct cpe knock-out mutants in both SM101 (a derivative of a C. perfringens type A food poisoning isolate carrying a chromosomal cpe gene) and F4969 (a C. perfringens type A non-food-borne GI disease isolate carrying a plasmid-borne cpe gene). Western blot analyses confirmed that neither cpe knock-out mutant could express CPE during either sporulation or vegetative growth, and that this lack of CPE expression could be complemented by transforming these mutants with a recombinant plasmid carrying the wild-type cpe gene. When the virulence of the wild-type, mutant and complementing strains were compared in a rabbit ileal loop model, sporulating (but not vegetative) culture lysates of the wild-type isolates induced significant ileal loop fluid accumulation and intestinal histopathological damage, but neither sporulating nor vegetative culture lysates of the cpe knock-out mutants induced these intestinal effects. However, full sporulation-associated virulence could be restored by complementing these cpe knock-out mutants with a recombinant plasmid carrying the wild-type cpe gene, which confirms that the observed loss of virulence for the cpe knock-out mutants results from the specific inactivation of the cpe gene and the resultant loss of CPE expression. Therefore, in vivo analysis of our isogenic cpe mutants indicates that CPE expression is necessary for these two cpe-positive C. perfringens type A human disease isolates to cause GI effects in the culture lysate:ileal loop model system, a finding that supports CPE as an important virulence factor in GI diseases involving cpe-positive C. perfringens type A isolates.

Animals↗