Severity of Clostridium difficile-associated diarrhea in solid organ transplant patients

被引:48
作者
Gellad, Z. F.
Alexander, B. D.
Liu, J. K.
Griffith, B. C.
Meyer, A. M.
Johnson, J. L.
Muir, A. J.
机构
[1] Duke Univ, Med Ctr, Dept Med, Div Gastroenterol, Durham, NC 27710 USA
[2] Duke Univ, Med Ctr, Dept Med, Div Infect Dis & Int Med, Durham, NC 27710 USA
[3] Duke Univ, Med Ctr, Comprehens Canc Ctr Biostat, Durham, NC USA
关键词
Clostridium difficile; diarrhea; colitis; solid organ transplantation; recurrence; severity; corticosteroids;
D O I
10.1111/j.1399-3062.2007.00255.x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Clostridium difficile-associated diarrhea (CDAD) has a wide spectrum of disease severity. Studies have implicated immunosuppressants as a risk factor for severe disease. We hypothesized that solid organ transplant (SOT) patients with CDAD would be at greater risk for severe disease because of their profound immunosuppression. Adult SOT patients with CDAD seen at Duke University Medical Center between 1999 and 2003 were compared with a reference group of non-transplant patients with CDAD. The primary outcome was the development of complicated colitis defined as death, intensive care unit admission, or urgent colectomy within 30 days of diagnosis. A secondary outcome was relapse within 60 days. Eighty transplant and 86 non-transplant cases were reviewed. There was no significant difference in the development of complicated colitis (13.8% vs. 7.0%) or relapse rates (6.2% vs. 7.0%) between the 2 groups. In the entire sample, 18.5% of patients receiving corticosteroids unrelated to transplantation relapsed as compared with 4.5% not receiving corticosteroids (risk ratio 4.3, P = 0.02). In conclusion, no significant difference was found in severity of CDAD between SOT patients and non-transplant patients. Exposure to corticosteroids was significantly associated with an increased risk of relapse and may warrant a longer treatment course.
引用
收藏
页码:276 / 280
页数:5
相关论文
共 20 条
[1]  
Altman DG., 1990, PRACTICAL STAT MED R
[2]  
Apaydin S, 1998, SCAND J INFECT DIS, V30, P542, DOI 10.1080/00365549850161665
[3]   Endogenous corticosteroids modulate Clostridium difficile toxin A-induced enteritis in rats [J].
Castagliuolo, I ;
Karalis, K ;
Valenick, L ;
Pasha, A ;
Nikulasson, S ;
Wlk, M ;
Pothoulakis, C .
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY, 2001, 280 (04) :G539-G545
[4]   Clostridium difficile-associated diseases: Comparison of symptomatic infection versus carriage on the basis of risk factors, toxin production, and genotyping results [J].
Cheng, SH ;
Lu, JJ ;
Young, TG ;
Perng, CL ;
Chi, WM .
CLINICAL INFECTIOUS DISEASES, 1997, 25 (01) :157-158
[5]   Fulminant Clostridium difficile:: An underappreciated and increasing cause of death and complications [J].
Dallal, RM ;
Harbrecht, BG ;
Boujoukas, AJ ;
Sirio, CA ;
Farkas, LM ;
Lee, KK ;
Simmons, RL .
ANNALS OF SURGERY, 2002, 235 (03) :363-372
[6]  
Fleiss J. L., 1981, Statistical Methods for Rates and Proportions, V2nd
[7]   The spectrum of pseudomembranous enterocolitis and antibiotic-associated diarrhea [J].
Hurley, BW ;
Nguyen, CC .
ARCHIVES OF INTERNAL MEDICINE, 2002, 162 (19) :2177-2184
[8]   SELECTIVE NEUTRALIZATION OF A BACTERIAL ENTEROTOXIN BY SERUM IMMUNOGLOBULIN-A IN RESPONSE TO MUCOSAL DISEASE [J].
JOHNSON, S ;
SYPURA, WD ;
GERDING, DN ;
EWING, SL ;
JANOFF, EN .
INFECTION AND IMMUNITY, 1995, 63 (08) :3166-3173
[9]   Immune response to Clostridium difficile infection [J].
Kelly, CP .
EUROPEAN JOURNAL OF GASTROENTEROLOGY & HEPATOLOGY, 1996, 8 (11) :1048-1053
[10]  
Keven K, 2004, Transpl Infect Dis, V6, P10, DOI 10.1111/j.1399-3062.2004.00040.x