G. Vincoli

Small Intestine Contrast Ultrasonography in Pediatric Crohn's Disease

OBJECTIVEnTo evaluate the diagnostic accuracy of small intestine contrast ultrasonography (SICUS) in pediatric Crohns disease (CD).nnnSTUDY DESIGNnA total of 51 consecutive patients (median age 15 years; range 3-20, 31 male patients), 21 with suspected and 30 with proven CD, were studied. All patients underwent standard ultrasonography (ie, transabdominal ultrasonography [TUS]), SICUS, small bowel follow-through, and upper and lower endoscopy. SICUS was performed in patients after they ingested an oral contrast solution. TUS and SICUS were compared with small bowel follow-through and endoscopy via use of the final diagnosis as reference standard.nnnRESULTSnIn undiagnosed patients, the sensitivity and specificity of TUS and SICUS in detecting CD small bowel lesions were 75% and 100% and 100% and 100%, respectively. In patients with proven CD, the sensitivity and specificity of TUS and SICUS were 76% and 100% and 96% and 100%, respectively. The agreement (k) with radiology for site of lesions was almost perfect for SICUS (0.93), both for jejunal and ileal lesions, and it was fair (0.40) for jejunal and substantial (0.68) for ileal lesions for TUS. Compared with radiology SICUS correctly assessed the length of lesions, whereas TUS underestimated it (P = .0001).nnnCONCLUSIONSnThe radiation-free technique SICUS is comparable with radiology and more accurate than TUS in assessing small bowel lesions in pediatric CD, mainly in the detection of proximal small bowel disease.

Two-hour postload glycemia is associated to an increased risk of NAFLD in healthy subjects with family history of type 2 diabetes: a case control study

Nonalcoholic fatty liver disease (NAFLD) includes steatosis and nonalcoholic steatohepatitis (NASH), which can be complicated by cirrhosis and hepatocellular carcinoma [1]. NAFLD affects over 30 % of the general population and is associated with type 2 diabetes mellitus (T2DM), obesity and metabolic syndrome [2, 3]. NAFLD prevalence in T2DM patients is about 70 % using ultrasonography (US) [4]. NAFLD and T2DM share insulinresistance, which in the liver increases gluconeogenesis and glycogenolysis, resulting in hyperglycemia. The pancreatic beta islet cells adapt to hyperglycemia by increasing insulin secretion. Hyperinsulinemia upregulates several lipogenic transcription factors, promoting hepatic lipid synthesis [5]. The association between NAFLD and T2DM seems to be the result of a “common soil” [3]. Several studies showed that NAFLD predicts T2DM and vice versa, and that each condition may act as a progression factor for the other [4]. There is evidence of a high risk of NASH and its progression to hepatocellular carcinoma in T2DM patients [6]. Conversely, recent studies showed that NAFLD not only predicts diabetes [7], but also contributes to poor glycemic control and chronic complications [8]. Despite its clear link with T2DM, the association of NAFLD with family history of diabetes has been poorly investigated. A recent cross-sectional study in nondiabetic individuals with NAFLD demonstrated that family history of diabetes increased the risk of NASH and fibrosis [9]. The aim of this study was to evaluate the prevalence of NAFLD in healthy first degree relatives of T2DM patients (T2DM-rel) and in healthy subjects without family history of T2DM and to assess the risk factors associated with NAFLD development.