Nonalcoholic fatty liver disease (NAFLD) is well described as a common cause of chronic liver disease, mostly in the obese population. It refers to a spectrum of chronic liver disease that starts with simple steatosis than progresses to nonalcoholic steatohepatitis and cirrhosis in patients without significant alcohol consumption. NAFLD in the non-obese population has been increasingly reported and studied recently. The pathogenesis of nonobese NAFLD is poorly understood and is related to genetic predisposition, most notably patatin-like phospholipase domain-containing 33 G allele polymorphism that leads to intrahepatic triglyceride accumulation and insulin resistance. Non-obese NAFLD is associated with components of metabolic syndrome and, especially, visceral obesity which seems to be an important etiological factor in this group. Dietary factors and, specifically, a high fructose diet seem to play a role. Cardiovascular events remain the main cause of mortality and morbidity in NAFLD, including in the non-obese population. There is not enough data regarding treatment in non-obese NAFLD patients, but similar to NAFLD in obese subjects, lifestyle changes that include dietary modification, physical activity, and weight loss remain the mainstay of treatment.

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Clostridium difficile infection (CDI) is a major cause of morbidity and mortality in patients with inflammatory bowel disease (IBD), especially in ulcerative colitis (UC). The incidence and severity of CDI in IBD has shown an increasing trend in the last two decades. Patients with IBD are predisposed to CDI secondary to the recurrent use of antibiotics, corticosteroids, and immunosuppressants and secondary to dysbiosis. It is clinically challenging to distinguish the symptoms of CDI from an IBD flare. The worsening of IBD symptoms demands escalation of steroids or initiation of biologics. However, the management of CDI in IBD, not responding to antibiotics, is not well described beyond a few case reports. We report two cases of CDI with active UC flare. The patients did not respond to antibiotics or intravenous corticosteroids but had rapid resolution of CDI symptoms after receiving infliximab infusion. The optimal dosing and infusion frequency of infliximab in management of CDI in UC/IBD remains to be established.

Background: The rising incidence of Clostridium difficile infection (CDI) in the general population has been recognized by health care organizations worldwide. The emergence of hypervirulent strains has made CDI more challenging to understand and treat. Inflammatory bowel disease (IBD) patients are at higher risk of infection, including CDI. Objective: A diagnostic approach for recurrent CDI has yet to be validated, particularly for IBD patients. Enzyme immunoassay (EIA) for toxins A and B, as well as glutamate dehydrogenase EIA, are both rapid testing options for the identification of CDI. Without a high index of suspicion, it is challenging to initially differentiate CDI from an IBD flare based on clinical evaluation alone. Methods: Here, we provide an up-to-date review on CDI in IBD patients. When caring for an IBD patient with suspected CDI, it is appropriate to empirically treat the presumed infection while awaiting further test results. Results: Treatment with vancomycin or fidaxomicin, but not oral metronidazole, has been advocated by an expert review from the clinical practice update committee of the American Gastroenterology Association. Recurrent CDI is more common in IBD patients compared to non-IBD patients (32% versus 24%), thus more aggressive treatment is recommended for IBD patients along with early consideration of fecal microbiota transplant. Conclusion: Although the use of infliximab during CDI has been debated, clinical experience exists supporting its use in an IBD flare, even with active CDI when needed.

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