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Toxin A and B frequency in mildly and moderately active inflammatory bowel disease patients

Yıl 2011, Cilt: 10 Sayı: 1, 18 - 22, 01.04.2011

Öz

Background/aims: Inflammatory bowel disease patients are at an increased risk for Clostridium difficile infection because of frequent hospitalizations and usage of immunosuppressive/immunomodulator drugs as well as antibiotics. The frequency of Clostridium difficile infection increases in parallel with the increase in disease activity. We aimed to evaluate the frequency of Clostridium difficile toxin A/B in patients with mildly and moderately active inflammatory bowel disease because a search on PubMed revealed a scarcity of literature knowledge in this regard. Methods: One hundred inflammatory bowel disease patients (48 females, 52 males) with mild and moderate activity were consecutively enrolled in the study; none of the patients had a history of hospitalization and/or antibiotic usage for the last three months. A stool sample was investigated for Clostridium difficile toxin A/B with enzyme immunoassay method by a microbiologist who was blinded to the study. Additionally, samples were evaluated for parasites and culture. Toxin A/B-positive and -negative cases were compared according to age, gender, disease type (Crohn's disease, ulcerative colitis), duration and location, extraintestinal findings, and any drugs used (azathioprine, salazopyrin, methotrexate, infliximab, adalimumab). Results were evaluated statistically. Results: Clostridium difficile toxin A/B positivity was found in only two patients (1 female, 1 male) (2%). In comparisons, we found no significant differences between the two groups. There was no growth in stool cultures and no parasite was found in stool samples. Conclusions: Clostridium difficile toxin A/B positivity in mildly and moderately active inflammatory bowel disease patients is the same as in the normal population and not higher as hypothesized.

Kaynakça

  • Issa M, Ananthakrishnan AN, Binion DB. Clostridium difficile and inflammatory bowel disease. Inflamm Bowel Dis 2008; 10: 1432- 42.
  • McFarland LV, Mulligan ME, Kwok RY, Stamm WE. Nosocomial ac- quisition of
  • Clostridium difficile infection. N Engl J Med 1989; 320: 204-10.
  • Dallal RM, Harbrecht BG, Boujoukas AJ, Sirio CA, et al. Fulminant
  • Clostridium difficile: an underappreciated and increasing cause of death and complications. Ann Surg 2002; 235: 363-72.
  • Rolny P, Järnerot G, Möllby R. Occurrence of Clostridium difficile toxin in inflammatory bowel disease. Scand J Gastroenterol 1983; 18: 61-4.
  • Bolton RP, Sheriff RJ, Read AE. Clostridium difficile associated di- arrhea: a role in inflammatory bowel disease? Lancet 1980; 1: 383- 4.
  • Trnka Y, LaMont JT. Association of Clostridium difficile toxin with symptomatic relapse of chronic inflammatory bowel disease. Gas- troenterology 1981; 80: 693-6.
  • Kressner MS, Williams SE, Biempica L, Das KM. Salmonellosis
  • complicating ulcerative colitis. Treatment with trimethoprim-sulfa- methoxazole. JAMA 1982; 248: 584-5.
  • Weber P, Koch M, Heizman WR, Scheurlen M, Jenss H, Hartmann
  • F. Microbic superinfection in relapse of inflammatory bowel disea- se. J Clin Gastroenterol 1992; 14: 302-8.
  • Szilagui A, Gerson M, Mendelson J, Yusuf NA. Salmonella infecti
  • ons complicating inflammatory bowel disease. J Clin Gastroenterol 1985; 7: 251-5.
  • Rampton DS, Salmon PR, Clark CG. Nonspecific colitis as a sequel to amebic dysentery. J Clin Gastroenterol 1983; 5: 217-9.
  • Issa M, Vijayapal A, Graham MB, et al. Impact of Clostridium diffi- cile on inflammatory bowel disease. Clin Gastroenterol Hepatol 2007; 5: 345-51.
  • Rodemann JF, Dubberke ER, Reske KA, et al. Incidence of Clostri- dium difficile infection in inflammatory bowel disease. Clin Gastro- enterol Hepatol 2007; 5: 339-44.
  • Ananthakrishnan AN, McGinley EL, Binion DG. Excess hospitalisati- on burden associated with Clostridium difficile in patients with inf- lammatory bowel disease. Gut 2008; 57: 205-10.
  • Bignardi GE. Risk factors for Clostridium difficile infection. J Hosp Infect 1998; 40: 1-15.
  • Johnson S, Clabots CR, Linn FV, et al. Nosocomial Clostridium dif- ficile colonisation and disease. Lancet 1990; 336: 97-100.
  • Meyer AM, Ramzan NN, Loftus EV Jr, et al. The diagnostic yield of stool pathogen studies during relapses of inflammatory bowel di- sease. J Clin Gastroenterol 2004; 38: 772-5.
  • Kyne L, Warny M, Qamar A, Kelly CP. Association between anti- body response to toxin A and protection against recurrent Clostri- dium difficile diarrhoea. Lancet 2001; 357: 189-93.
  • Kelly CP, LaMont JT. Clostridium difficile infection. Annu Rev Med 1998; 49: 375-390.
  • Fekety R, Shah AB. Diagnosis and treatment of Clostridium diffici- le colitis. JAMA 1993; 269: 71-5.
  • Dallal RM, Harbrecht BG, Boujoukas AJ, et al. Fulminant Clostridi- um difficile: an underappreciated and increasing cause of death and complications. Ann Surg 2002; 235: 363-72.
  • Pépin J, Valiquette L, Alary ME, et al. Clostridium difficile-associa- ted diarrhea in a region of Quebec from 1991 to 2003: a changing pattern of disease severity. CMAJ 2004; 171: 466-72.
  • McFarland LV. Alternative treatments for Clostridium difficile di- sease: what really works? J Med Microbiol 2005; 54: 101-11.
  • Özturk R, Midilli K, Ergin S, et al. İshalli olgularda ELISA yöntemiy- le Clostridium difficile toksin A aranması. 5thNational Infection Di- seases Congress, Abstract book (Turkish), p: 101 (1995).
  • Aygün G, Aslan M, Yaşar H, Altaş K. Investigation of Clostridium difficile toxin A+B in patients with antibiotic-associated diarrhoea. Türk Mikrobiyol Cem Derg 2003; 33: 39-41.
  • Clayton EM, Rea MC, Shanahan F, et al. The vexed relationship between Clostridium difficile and inflammatory bowel disease: an assessment of carriage in an outpatient setting among patients in remission. Am J Gastroenterol 2009; 104: 1162-9.

Hafif ve orta aktiviteli inflamatuvar barsak hastalarında toksin A/B sıklığı

Yıl 2011, Cilt: 10 Sayı: 1, 18 - 22, 01.04.2011

Öz

Giriş ve Amaç: İnflamatuvar barsak hastalığı olan hastalar sık hastaneye yatış ve immünsüpresif/immünmodülatör ilaç ve antibiyotik kullanımı nedeniyle Clostridium difficile enfeksiyonu açısından artmış riske sahiptir. Clostridium difficile enfeksiyonu sıklığı hastalık aktivitesiyle paralel olarak artar. Bu çalışmadaki amacımız hafif ve orta aktiviteli inflamatuvar barsak hastalarında toksin A/B sıklığını araştırmaktır. Gereç ve Yöntem: Son üç ayda hastaneye yatış ve/ya antibiyotik kullanım öyküsü olmayan 100 inflamatuvar barsak hastası (48 kadın, 52 erkek) çalışmaya alındı. Her hastadan bir adet dışkı örneği alınıp EIA metoduyla Clostridium difficile toksin A/B açısından çalışıldı. Ek olarak dışkı örnekleri parazit açısından incelendi ve örneklerin kültürü yapıldı. Toksin A/B açısından pozitif ve negatif olan hastalar yaş, cinsiyet, hastalık tipi (Crohn hastalığı, ülseratif kolit), lokalizasyonu ve süresi, ektsraintestinal bulgular ve kullanılan ilaçlar (azatioprin, salazoprin, metotreksat, infliximab ve adalimumab) açısından karşılaştırıldı. Bulgular: Clostridium difficile toksin A/B pozitifliği sadece iki hastada saptandı (1 erkek, 1 kadın). İki grup arasında karşılaştırılan parametreler açısından anlamlı bir fark saptanmadı. Dışkı örneklerinde parazit saptanmadı ve dışkı kültürlerinde herhangi bir üreme olmadı. Sonuçlar: Hafif ve orta aktiviteli inflamatuvar barsak hastalarında Clostridium difficile toksin A/B pozitifliği normal popülasyonla benzerdir ve sıklığı daha önce düşünüldüğü kadar yüksek değildir.

Kaynakça

  • Issa M, Ananthakrishnan AN, Binion DB. Clostridium difficile and inflammatory bowel disease. Inflamm Bowel Dis 2008; 10: 1432- 42.
  • McFarland LV, Mulligan ME, Kwok RY, Stamm WE. Nosocomial ac- quisition of
  • Clostridium difficile infection. N Engl J Med 1989; 320: 204-10.
  • Dallal RM, Harbrecht BG, Boujoukas AJ, Sirio CA, et al. Fulminant
  • Clostridium difficile: an underappreciated and increasing cause of death and complications. Ann Surg 2002; 235: 363-72.
  • Rolny P, Järnerot G, Möllby R. Occurrence of Clostridium difficile toxin in inflammatory bowel disease. Scand J Gastroenterol 1983; 18: 61-4.
  • Bolton RP, Sheriff RJ, Read AE. Clostridium difficile associated di- arrhea: a role in inflammatory bowel disease? Lancet 1980; 1: 383- 4.
  • Trnka Y, LaMont JT. Association of Clostridium difficile toxin with symptomatic relapse of chronic inflammatory bowel disease. Gas- troenterology 1981; 80: 693-6.
  • Kressner MS, Williams SE, Biempica L, Das KM. Salmonellosis
  • complicating ulcerative colitis. Treatment with trimethoprim-sulfa- methoxazole. JAMA 1982; 248: 584-5.
  • Weber P, Koch M, Heizman WR, Scheurlen M, Jenss H, Hartmann
  • F. Microbic superinfection in relapse of inflammatory bowel disea- se. J Clin Gastroenterol 1992; 14: 302-8.
  • Szilagui A, Gerson M, Mendelson J, Yusuf NA. Salmonella infecti
  • ons complicating inflammatory bowel disease. J Clin Gastroenterol 1985; 7: 251-5.
  • Rampton DS, Salmon PR, Clark CG. Nonspecific colitis as a sequel to amebic dysentery. J Clin Gastroenterol 1983; 5: 217-9.
  • Issa M, Vijayapal A, Graham MB, et al. Impact of Clostridium diffi- cile on inflammatory bowel disease. Clin Gastroenterol Hepatol 2007; 5: 345-51.
  • Rodemann JF, Dubberke ER, Reske KA, et al. Incidence of Clostri- dium difficile infection in inflammatory bowel disease. Clin Gastro- enterol Hepatol 2007; 5: 339-44.
  • Ananthakrishnan AN, McGinley EL, Binion DG. Excess hospitalisati- on burden associated with Clostridium difficile in patients with inf- lammatory bowel disease. Gut 2008; 57: 205-10.
  • Bignardi GE. Risk factors for Clostridium difficile infection. J Hosp Infect 1998; 40: 1-15.
  • Johnson S, Clabots CR, Linn FV, et al. Nosocomial Clostridium dif- ficile colonisation and disease. Lancet 1990; 336: 97-100.
  • Meyer AM, Ramzan NN, Loftus EV Jr, et al. The diagnostic yield of stool pathogen studies during relapses of inflammatory bowel di- sease. J Clin Gastroenterol 2004; 38: 772-5.
  • Kyne L, Warny M, Qamar A, Kelly CP. Association between anti- body response to toxin A and protection against recurrent Clostri- dium difficile diarrhoea. Lancet 2001; 357: 189-93.
  • Kelly CP, LaMont JT. Clostridium difficile infection. Annu Rev Med 1998; 49: 375-390.
  • Fekety R, Shah AB. Diagnosis and treatment of Clostridium diffici- le colitis. JAMA 1993; 269: 71-5.
  • Dallal RM, Harbrecht BG, Boujoukas AJ, et al. Fulminant Clostridi- um difficile: an underappreciated and increasing cause of death and complications. Ann Surg 2002; 235: 363-72.
  • Pépin J, Valiquette L, Alary ME, et al. Clostridium difficile-associa- ted diarrhea in a region of Quebec from 1991 to 2003: a changing pattern of disease severity. CMAJ 2004; 171: 466-72.
  • McFarland LV. Alternative treatments for Clostridium difficile di- sease: what really works? J Med Microbiol 2005; 54: 101-11.
  • Özturk R, Midilli K, Ergin S, et al. İshalli olgularda ELISA yöntemiy- le Clostridium difficile toksin A aranması. 5thNational Infection Di- seases Congress, Abstract book (Turkish), p: 101 (1995).
  • Aygün G, Aslan M, Yaşar H, Altaş K. Investigation of Clostridium difficile toxin A+B in patients with antibiotic-associated diarrhoea. Türk Mikrobiyol Cem Derg 2003; 33: 39-41.
  • Clayton EM, Rea MC, Shanahan F, et al. The vexed relationship between Clostridium difficile and inflammatory bowel disease: an assessment of carriage in an outpatient setting among patients in remission. Am J Gastroenterol 2009; 104: 1162-9.
Toplam 30 adet kaynakça vardır.

Ayrıntılar

Birincil Dil Türkçe
Bölüm Makaleler
Yazarlar

Ali Tüzün İnce Bu kişi benim

Ebubekir Şenateş Bu kişi benim

Seniha Şenbayrak Akçay Bu kişi benim

Zeynep Satı Tekin Bu kişi benim

Mesut Sezikli Bu kişi benim

Süleyman Çoşgun Bu kişi benim

Mustafa Erhan Altunöz Bu kişi benim

Yayımlanma Tarihi 1 Nisan 2011
Yayımlandığı Sayı Yıl 2011 Cilt: 10 Sayı: 1

Kaynak Göster

APA İnce, A. T., Şenateş, E., Akçay, S. Ş., Tekin, Z. S., vd. (2011). Hafif ve orta aktiviteli inflamatuvar barsak hastalarında toksin A/B sıklığı. Akademik Gastroenteroloji Dergisi, 10(1), 18-22.

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