CE is superior to push enteroscopy and small bowel barium radiography for diagnosing clinically significant small bowel pathology in patients with OGIB. In study populations, the IY of CE over push enteroscopy and small bowel barium radiography for clinically significant findings is >or=30% with an NNT of 3, primarily due to visualization of additional vascular and inflammatory lesions by CE.

In study populations, CE is superior to all other modalities for diagnosing non-stricturing small bowel CD, with a number needed to test (NNT) of 3 to yield one additional diagnosis of CD over small bowel barium radiography and NNT = 7 over colonoscopy with ileoscopy. These results are due to a highly significant IY with CE over all other modalities in patients with established non-stricturing CD being evaluated for a small bowel recurrence. While there was no significant difference seen between CE and alternate modalities for diagnosing small bowel CD in patients with a suspected initial presentation of CD, the trend toward significance for a number of modalities suggests the possibility of a type II error. Larger studies are needed to better establish the role of CE for diagnosing small bowel CD in patients with a suspected initial presentation of CD.

The assessment of the severity of acute pancreatitis (AP) is a critical early step in its management, as severity of AP predicts prognosis. A range of options are available for assessment of severity in AP, including clinical evaluation, standardized prognostic criteria, computed tomography (CT), and biochemical markers. Clinical assessment has limited accuracy for predicting severity early in the course of AP. Therefore, additional assessment using biochemical and radiologic criteria in combination with standardized criteria is appropriate to determine severity and prognosis in AP; a strategy emphasizing daily assessment of severity should be used. The APACHE II is the scoring system of choice for evaluating severity in AP, although it remains an imperfect tool. Computed tomographic grading of AP and the development of the CT severity index allow for heightened accuracy in the prediction of severity. C-Reactive protein is the standard for serum marker assessment of severity and prognosis in AP; other markers, including interleukin-6, polymorphonuclear elastase, and trypsinogen activation peptide, hold promise. The focus of this review is to examine the role of diagnostic tests in evaluating severity and predicting prognosis among patients with AP and to provide a diagnostic algorithm for initial management.

Because of the demonstration of a genetic linkage between glucokinase and Type II diabetes, and the central role of glucokinase on glucose metabolism, we studied glucokinase activity in the liver of patients with and without Type II diabetes. Glucokinase activity was decreased by about 50% in obese subjects with diabetes (n = 12) compared with (p < 0.01) lean controls (n = 9) and (p < 0.05) obese controls (n = 10). There was no difference between lean and obese controls. Fifty percent of subjects with diabetes had lower liver glucokinase activity than the lowest value of the controls. These data further support the important role that glucokinase plays in the pathogenesis of Type II diabetes.

We tested the hypothesis that liver protein kinase C (PKC) is increased in non-insulin-dependent diabetes mellitus (NIDDM). To this end we examined the distribution of PKC isozymes in liver biopsies from obese individuals with and without NIDDM and in lean controls. PKC isozymes a, 13, e and g were detected by immunoblotting in both the cytosol and membrane fractions. Isozymes y and 6 were not detected. There was a significant increase in immunodetectable PKC-a (twofold), -E (threefold), and -C (twofold) in the membrane fraction isolated from obese subjects with NIDDM compared with the lean controls. In obese subjects without NIDDM, the amount of membrane PKC isozymes was not different from the other two groups. We next sought an animal model where this observation could be studied further. The Zucker diabetic fatty rat offered such a model system. Immunodetectable membrane PKC-ci, -13, -e, and -t were significantly increased when compared with both the lean and obese controls. The increase in immunodetectable PKC protein correlated with a 40% elevation in the activity of PKC at the membrane. Normalization of circulating glucose in the rat model by either insulin or phlorizin treatment did not result in a reduction in membrane PKC isozyme protein or kinase activity. Further, phlorizin treatment did not improve insulin receptor autophosphorylation nor did the treatment lower liver diacylglycerol. We conclude that liver PKC is increased in NIDDM, a change that is not secondary to hyperglycemia. It is possible that PKCmediated phosphorylation of some component in the insulin signaling cascade contributes to the insulin resistance observed in NIDDM. (J. Clin. Invest. 1995Invest. .95:2938Invest. -2944