With the increasing prevalence of recurrent/refractory Clostridium difficile infection (CDI), alternative treatments to the standard antibiotic therapies are being sought. One of the more controversial of such alternative treatments is fecal microbiota transplantation (FMT). Although the notion of FMT is foreign-even startling-and not esthetic to most people, the concept has been around for many decades. Its benefit and efficacy dates back >50 years to its use for staphylococcal pseudomembranous colitis, and now FMT is showing a great promise as an inexpensive, safe, and highly efficient treatment for recurrent and refractory CDI. Moreover, with a better understanding of the intricacies of the colonic microbiome and its role in colonic pathophysiology, FMT has the potential to become the standard of care for CDI treatment, and a potential answer to other intestinal disorders in years to come.
The prevalence of Clostridium difficile infection (CDI) in inflammatory bowel disease (IBD) has become a focus of increased attention, as the C. difficile epidemic continues to grow. Although first documented more than 20 years ago, only in recent years has the relationship between these 2 entities been better clarified, and recent epidemiologic studies have shown that IBD patients are at increased susceptibility for CDI compared with the general population. Despite this increased attention, much still remains unknown, and the overlapping clinical presentations of CDI and IBD pose barriers to diagnosis and standardized treatment. Moreover, given the relationship between mortality and severity of CDI in IBD patients, early recognition of those who are at increased risk for infection is of paramount importance to improve patient outcome.
BackgroundThe development of left ventricular systolic dysfunction (LVSD) after liver transplant (LT) can result in increased morbidity and mortality in the immediate period following liver transplant. The aim of this study was to evaluate low muscle mass due to chronic liver disease, as a potential risk factor for LVSD after LT.Material/MethodsA retrospective chart review was completed for all adult patients who received a liver transplant between January 2002 and January 2015 at a single academic LT center. Collected data included patient demographics, medical history, laboratory data, radiology results, and pathology. Echocardiograms were reviewed for patients identified as having LVSD diagnosed within 1 year after LT (left ventricular ejection fraction <55%). The total psoas area (TPA), a marker of low muscle mass, was determined by measuring the average cross-sectional area of the psoas muscle on MRI or CT scans before transplant at the level of L4 vertebra.ResultsOf the 503 post-LT patients reviewed, 144 (28.6%) had pre-and post-LT echocardiograms. Of these 144 patients, 17 developed LVSD, of which 15 (88.2%) occurred within 1 year after LT. The average age at transplant of those with LVSD was 58.9±6 years, with a mean MELD score of 30.7±6. The mean TPA normalized for height for patients with LVSD was 297.68±86.99 mm2/m2 compared to 382.1±104.2 mm2/m2 for those with normal EF (p= 0.002). BMI, MELD score, and etiology of cirrhosis were not significant risk factors for post-LT LVSD in our study population. During the study period, 35.2% (n=6) of LVSD patients died within 1 year after LT.ConclusionsAlthough LVSD is thought to be a rare complication after LT, those with muscle loss as predicted by mean TPA measurements normalized for height may be at highest risk.
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