Childhood obesity is a serious and urgent public health problem. In the last 10 years, there has been a concerted effort in the USA and globally to develop and implement educational, medical and public health interventions designed to attenuate its growth. The success of these efforts was probably responsible for the plateau in the prevalence rate of childhood obesity noted in the last two years. While the attenuation of the overall prevalence of childhood obesity is promising, data from the same cohort reveal a concerning upward trend in the number of children with severe obesity. The consequences of severe childhood obesity can be devastating. When compared to their moderately obese peers, children with severe obesity are at greater risk for adult obesity, early atherosclerosis, hypertension, type 2 diabetes, metabolic syndrome, fatty liver disease and premature death. The determinants for severe obesity include the same lifestyle, environmental, familial and societal risk factors reported for overweight or obesity. While all these risk factors must be screened for, genetic influences are distinct considerations that may have greater bearing especially with early-onset obesity. Treatments for severe childhood obesity include lifestyle intervention, specialised low-calorie diets and bariatric surgery. Outcomes of these treatments vary, with bariatric surgery clearly the most successful of the three for both short-term and long-term weight loss. Severe obesity in children and adolescents remains a challenging health condition. The enormous medical, emotional and financial burden these children and their families endure signals an urgent need to further investigate and standardise treatment modalities and improve outcomes.

Patients with cystic fibrosis (CF) are at increased risk of malnutrition and growth failure due to multiple factors as a result of suboptimal or absent function of the CFTR chloride channel protein. Dysfunctional CFTR contributes to increased energy expenditure, exocrine pancreatic insufficiency causing impaired dietary macronutrient digestion and absorption, intestinal dysbiosis, and impaired bile acid homeostasis. Poor nutritional status as a result of these mechanisms is associated with decreased lung function, worse clinical outcomes, and ultimately, increased mortality. Nutritional interventions addressing these mechanisms, such as pancreatic enzyme-replacement therapy and enteral caloric supplementation, have improved nutritional status and, by association, clinical outcomes. In the last decade, the advent of medications targeting defective CFTR proteins has revolutionized the care of patients with CF by reducing the overall impact of CFTR dysfunction. Below, we summarize the effects of highly effective CFTR modulators on nutritional status overall as well as specific factors including bile acid metabolism, pancreatic function, energy expenditure, and intestinal dysbiosis. The future of CF nutrition care will require a paradigm shift away from focusing on methods addressing CFTR dysfunction such as excess calorie provision and toward an individualized, holistic approach in the context of specific mutations and CFTR-directed therapy.

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Introduction. Clostridium difficile is the most common cause of healthcare associated infectious diarrhea, and its most common clinical manifestation is pseudomembranous colitis. Small bowel enteritis is reported infrequently in the literature and typically occurs only in patients who have undergone ileal pouch anastomosis due to inflammatory bowel disease or total abdominal colectomy for other reasons. Presentation of Cases. We report here two cases in which patients developed small bowel C. difficile enteritis in the absence of these underlying conditions. Discussion. Neither patient had underlying inflammatory bowel disease and both had a significant amount of colon remaining. Conclusion. These two cases demonstrate that small bowel C. difficile enteritis should be included in the differential diagnosis of patients on antibiotic therapy who demonstrate signs and symptoms of worsening abdominal disease during their postoperative course, even if they lack the major predisposing factors of inflammatory bowel disease or history of total colectomy.

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