• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.3 no.1
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• pp.98-104
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• 2000

Pseudomembranous colitis, thought to be uncommon in children, is a bacterial, toxin-mediated inflammatory process resulting in acute or chronic diarrhea and is characterized by colonic pseudomembranes. It is mediated by toxins produced by Clostridium difficile and is increasingly recognized in pediatric population. Diagnosis is based on positive culture of C. difficile in selective media and positive test of C. difficile toxin. Oral metronidazole or vancomycin are the main treatment options but avoidance of further antibiotics should also be encouraged where possible. We have experienced a case of pseudomembranous colitis in a 4-year-old female presented with septic shock and colitis. This case was diagnosed with positive test of C. difficile toxin B and confirmed by isolation of the organism on cultire in selective media. Symptoms have been ameliorated by discontinuation of antibiotics and administration of metronidazole and oral vancomycin, and ICU care.

• The Journal of Korean Medicine
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• v.22 no.3
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• pp.179-188
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• 2001

Diarrhea is the frequent passage of loose, watery stool (frequency: ${\geq}4/day$, weight: ${\geq}250g/day$) Most antibiotics can cause inflammatory change of the colon or Pseudomembranous colitis (PMC). Typical presentations of PMC are watery diarrhea, abdominal pain, fever, leukocytosis ($12,000~20,000/\textrm{mm}^3$), hypoalbuminemia, hypovolemia and recent or concurrent use of antibiotics. Diagnostic methods of PMC are stool assay, sigmoid scopy, abdominal CT, abdominal US, etc. The age-related susceptibility noted with PMC is impressive but unexplained. Two stroke patients had diarrhea, abdominal pain, fever hypoalbuminemia and a history of recent or concurrent use of antibiotics. By use of Shirhyung- Tang, we could improve clinical symptoms (diarrhea, abdominal pain, fever hypoalbuminemia, etc.) and so report clinical course of two stroke patients with antibiotics-associated PMC.

• Journal of Yeungnam Medical Science
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• v.1 no.1
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• pp.171-178
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• 1984

Many reports have been made concerning underlying and associated conditions causing pseudomembranous colitis and it has been documented that occurrence of pseudomembranous colitis is related with antibiotics administration. Recent study showed that Clostridium difficile produced enterotoxin by colonization in intestinal wall and leading into pseudomembranous colitis. Diagnosis is based on positive culture of Clostridium difficile, positive test of Clostridium difficile toxin and specific histological findings after observation of whitish plaque on colonoscopic or sigmoidoscopic examination. Authors have experienced one case of pseudomembranous colitis developing after long term ampicillin administration in a case with colon cancer associated with diarrhea and diagnosis was confirmed by typical pseudomembrane on biopsy following classical whitish plaque observation on sigmoidoscopic examination. Symptoms have been ameliorated by discontinuation of antibiotics and administration of metronidazole in four days and disappearance of whitish plaque on repeated sigmoidoscopic examination and improvement of clinical symptoms after 9 days of medication.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.1 no.1
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• pp.138-143
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• 1998

Chronic diarrhea in children is a common problem with numerous causes. Although most of these causes are benign, critical illness may present as chronic diarrhea. In a patient of chronic diarrhea, gastrointestinal infections are the most common causes in children of all ages and antibiotics may cause chronic diarrhea by altering intestinal microflora, which can result in the emergence of bacterial overgrowth. Overgrowth of Clostridium difficile may cause pseudomembranous colitis. We experienced 25-month-old boy who suffered from chronic diarrhea and partially treated with antibiotics irregularly. Colonoscopic findings of this child showed multiple plaques with white to yellowish exudate which adhere to the mucosal surface of a variable length of rectum. Histollogically, each plaque comprised a pseudomembrane of mucous debris, inflammatory cells, and exudate overlying groups of partially disrupted glands. A latex agglutination test on patient's stool was positive to toxin A of Clostridium difficile. He was recovered after stopping the antibiotics he has been prescribed, and being given vancomycin for 2 weeks. We report this case with brief review of literature.

• Journal of Microbiology and Biotechnology
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• v.27 no.4
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• pp.694-700
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• 2017

Clostridium difficile, which causes pseudomembranous colitis, releases toxin A and toxin B. These toxins are considered to be the main causative agents for the disease pathogenesis, and their expression is associated with a marked increase of apoptosis in mucosal epithelial cells. Colonic epithelial cells are believed to form a physical barrier between the lumen and the submucosa, and abnormally increased mucosal epithelial cell apoptosis is considered to be an initial step in gut inflammation responses. Therefore, one approach to treating pseudomembranous colitis would be to develop agents that block the mucosal epithelial cell apoptosis caused by toxin A, thus restoring barrier function and curing inflammatory responses in the gut. We recently isolated an antimicrobial peptide, Periplanetasin-2 (Peri-2, YPCKLNLKLGKVPFH) from the American cockroach, whose extracts have shown great potential for clinical use. Here, we assessed whether Peri-2 could inhibit the cell toxicity and inflammation caused by C. difficile toxin A. Indeed, in human colonocyte HT29 cells, Peri-2 inhibited the toxin A-induced decrease in cell proliferation and ameliorated the cell apoptosis induced by this toxin. Moreover, in the toxin A-induced mouse enteritis model, Peri-2 blocked the mucosal disruption and inflammatory response caused by toxin A. These results suggest that the American cockroach peptide Peri-2 could be a possible drug candidate for addressing the pseudomembranous colitis caused by C. difficile toxin A.

• Tuberculosis and Respiratory Diseases
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• v.49 no.6
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• pp.774-779
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• 2000

Pseudomembranous colitis, although uncommon, is an important complication of antibiotics that is related to a variety of deleterious effects on the gastrointestinal tract. Rifampicin is one of the 1st line agents in the treatment of tuberculosis and a large number of patients are exposed to its potential adverse effects. We report upon a patient that had diarrhea due to pseudomembranous colitis after receiving antitubeculous medication, and which was probably caused by rifampicin. A 77-year-old man was admitted with diarrhea of three weeks duration. One month previously, he suffered from left pleuritic chest pain and left pleural effusion was noticed at chest X-ray. One week prior to the onset of diarrhea, he was started on empirically isoniazid, rifampicin, ethambutol and pyrazynamide as antituberculous medication. On admission, he complained of diarrhea, left pleuritic chest pain, dyspnea and sputum. On physical examination, breathing sound was decreased in the left lower lung field and bowel sound increased. Pleural biopsy revealed chronic granulomatous inflammation, which was compatible with tuberculosis, Sigmoidoscopy showed whitish to yellowish pseudomembrane with intervening normal mucosa, and his stool was positive for C.difficle toxin. He was diagnosed as pseudomembranous colitis and treated with oral metronidazole and vancomycin. The diarrhea did not recur after reinstitution of the anti-tuberculous medication without rifampicin inpatients with severe diarrhea receiving anti-tuberculous medication, rifampicin induced pseudomembranous colitis should be excluded.

• The Journal of the Society of Stroke on Korean Medicine
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• v.8 no.1
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• pp.58-62
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• 2007

Objective : Stroke patients tend to take antibiotics due to infection resulting from complication. One of many side effects from using antibiotics is diarrhea, which infact causes anaerobic organism dysfunction resulting Pseudo-Membranous Colitis (P.M.C). To treat P.M.C, antibiotics and antibacterial agents are usually used. But they may cause other side effects, therefore extreme caution must be taken. Methods : We treated an antibiotic induced P.M.C patient who diagnosed by sigmoid scopy with only Yijoong-tang (Lizhong-tang) without antibiotics and observed patients stool aspects. Results and Conclusion : Patiensts symptom was improved after 7days, and we can see the improvement by follow-up sigmoid scopy. This case may give us a possibility of that oriental medical treatments as complementary and alternative medicine to standard antibiotic treatment.

• Intestinal research
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• v.13 no.1
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• pp.80-84
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• 2015

The rates and severity of Clostridium difficile infections, including pseudomembranous colitis, have increased markedly. However, there are few effective treatments for refractory or recurrent C. difficile infections and the outcomes are poor. Fecal microbiota transplantation is becoming increasingly accepted as an effective and safe intervention in patients with recurrent disease, likely due to the restoration of a disrupted microbiome. Cure rates of >90% are being consistently reported from multiple centers. We cured a case of severe refractory C. difficile infection with fecal microbiota transplantation in a patient colonized by vancomycin-resistant enterococcus.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.18
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• pp.7673-7677
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• 2014

Background: Patients with long-standing inflammatory bowel disease (IBD) have an increased risk of developing colorectal cancer (CRC). Colon cancer risk in IBD increases with longer duration and greater anatomic extent of colitis, the presence of primary sclerosing cholangitis, family history of CRC and degree of inflammation of the bowel. This study aimed to characterize the histopathological pattern of benign colorectal diseases among Saudi patients and to highlight age and gender variations of lesions as base line data for future studies to investigate the link between benign/IBD and colorectal cancers in the local population. Materials and Methods: The materials consisted of 684 biopsies, reported as benign (excluding malignancies and polyps) at the Department of Pathology, King Fahad Hospital, Madinah, Saudi Arabia from January 2006 to December 2013. Data collected and entered in MS-Excel and were analyzed using SPSS-20. Results: Of 684 colorectal tissues reviewed, 408 specimens (59.6%) were from male patients and 276 specimens (40.4%) were from females giving a male: female ratio of 1.5:1. Age of the patients ranged from 4 to 75 years with a mean of 39.6 years. The most frequent histologic diagnosis was a chronic non specific proctocolitis followed by ulcerative colitis, accounting respectively for 52.6% and 31.7% of all cases. These were followed by Crohn's disease 22 (3.2%), ischemic bowel disease 20 (2.9%), diverticular disease 14 (2%), eosinophilic colitis 12 (1.7%) and solitary rectal ulcer 12 (1.7%). A minority of 21 patients (3.1%) were cases of acute nonspecific proctocolitis, schistosomiasis, tuberculosis, volvulus and pseudomembranous colitis. Conclusions: These data show that although chronic non specific proctocolitis and ulcerative colitis were the dominant diagnoses, Crohn's disease, ischemic bowel disease and diverticular disease also existed to a lesser extent and should be considered in the differential diagnosis of benign colorectal diseases. This study provides a base line data for future studies which would be taken up to investigate the link between benign/IBD and colorectal cancers in the local population.

• Journal of Life Science
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• v.28 no.9
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• pp.1016-1021
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• 2018

Clostridium difficile toxin A causes pseudomembranous colitis. The pathogenesis of toxin A-induced colonic inflammation includes toxin A-dependent epithelial cell apoptosis, resulting in the loss of barrier function provided by epithelial cells against luminal pathogens. Toxin A-dependent epithelial cell apoptosis has been linked to toxin A-induced production of reaction oxygen species and subsequent p38MAPK activation; $p21^{CIP1/WAF1}$ upregulation-dependent cell cycle arrest; cytoskeletal disaggregation; and/or the induction of Fas ligand on epithelial cells. However, the molecular mechanisms underlying toxin A-induced apoptosis remain poorly understood. This study tested whether toxin A could block the Wnt signaling pathway, which is involved in gut epithelial cell proliferation, differentiation and antiapoptotic progression. Toxin A treatment of nontransformed human colonocytes (NCM460) rapidly reduced ${\beta}$-catenin protein, an essential component of the Wnt signaling pathway. Exposure of mouse ileum to toxin A also significantly reduced ${\beta}$-catenin protein levels. MG132 inhibition of proteasome-dependent protein degradation resulted in the recovery of toxin A-mediated reduction of ${\beta}$-catenin, indicating that toxin A may activate intracellular processes, such as $GSK3{\beta}$, to promote degradation of ${\beta}$-catenin. Immunoblot analysis showed that toxin A increased active phosphorylation of $GSK3{\beta}$. Because the Wnt signaling pathway is essential for gut epithelial cell proliferation and anti-apoptotic processes, our results suggest that toxin A-mediated inhibition of the Wnt signaling pathway may be required for maximal toxin A-induced apoptosis of gut epithelial cells.