Pseudomembranous Colitis: An Update

Abstract

Clostridium difficile is the most common nosocomial infection of the gastrointestinal tract. Most cases are associated with antibiotic therapy that alters the fecal flora, allowing overgrowth of C difficile with production of its toxins. Diagnosis is made by detection of the organism or toxin in the stools. A variety of different tests can be used, but none is perfect. A stool culture can be positive in someone without diarrhea, ie, a carrier. While the cytotoxin is the gold standard, it is expensive, and there is a delay before results are available. Thus, many laboratories use the enzyme-linked immunoassay tests to detect toxin of C difficile because they are a more rapid screen. Depending on the specific test used, they can detect toxin A, toxin B or occasionally both. Sensitivity and specificity rates vary. First line therapy for C difficile disease should be metronidazole 250 mg qid for 10 days. Vancomycin should be reserved for severe cases where metronidazole has failed or where metronidazole cannot be tolerated or is contraindicated. Recurrent C difficile disease is a particularly vexing clinical problem. A variety of biotherapeutic approaches have been used. Retreatment with antibiotics is almost always necessary. In addition, the nonpathogenic yeast Saccharomyces boulardii has been showed to be of benefit as an adjunct in preventing further recurrences.

Outcome After Colectomy for Clostridium Difficile Colitis

“…difficile is the most commonly identified microbial agent in nosocomial diarrhea and accounts for nearly 20 percent of antibiotic-associated diarrhea. [15][16][17][18] With increasing antibiotic usage, C. difficile colitis is becoming more common. The use of vancomycin or metronidazole yields a favorable clinical response observed in three to four days in most patients.…”

Gastric cancer incidence and mortality is associated with altitude in the mountainous regions of Pacific Latin America

“…The logistic regression showed that decreased selenium was a risk factor for gastric cancer: OR 0.90 (95 % CI, 0.85–0.96), when adjusted for age, sex, H. pylori status, and host IL-1β and IL-10 risk allele status [16]. Another possible factor is differences in the content of salt (NaCl) in the diet of people living in the mountains versus those living in the coast, since salt has been associated with gastric cancer risk in many countries [36]. …”

Twenty-Five Years of Research on Saccharomyces boulardii Trophic Effects: Updates and Perspectives

“…Antibiotic-associated diarrhea [2][3][4] Acute infectious [5,6] Amebiasis [7] Acute and subacute giardiasis [8] Clostridium difficile enterocolopathies [9][10][11] Pseudomembranous enterocolitis [12] Traveler's diarrhea [13,14] Acute Helicobacter pylori [15,16] Chronic persistent diarrhea [9,17] Chronic protracted diarrhea [9] AIDS-associated diarrhea [18] IBD Crohn's disease [19] Ulcerative colitis [20] Continuous enteral feeding [21] Critically ill tube-fed patients [22] Hirschsprung's disease, enterocolitis [23] Pediatric age group [9,[24][25][26] Prematures [27] Infants, children [24][25][26] Autism and diarrhea [28] Irritable bowel [29] Since S. boulardii given orally is a shuttle delivering several substances to the endoluminal compartment, it becomes of major importance to elucidate the molecular pathways stimulated by the yeast and their metabolic or physiological effects in the host. Beside the molecular transduction pathways of insulin, IgF-1, and other trophic peptides, the MAPK/ERK 1-2 cascades and the PI-3 kinase signaling pathway represent two molecular transduction pathways of major interest for the understanding of how the yeast cell works (Fig.…”