The 13C-caffeine breath test detects significant fibrosis in patients with nonalcoholic steatohepatitis.

BACKGROUND: The C-caffeine breath test (CBT) is a noninvasive tool for the evaluation of the cytochrome P450 system, implicated in the development of nonalcoholic steatohepatitis. GOAL: To apply the CBT to assess the extent of hepatic fibrosis in patients with nonalcoholic fatty liver disease (NAFLD). METHODS: Twenty-six consecutive patients (mean age 56.1+/-6.85 y, 69.2% women) with NAFLD underwent the CBT, in addition to the clinical and laboratory evaluations and liver biopsy. Ten healthy individuals matched for age served as controls. RESULTS: Mean delta over baseline values differed significantly between patients and controls (1.51+/-0.9 vs. 2.37+/-0.8 Delta per thousand/mg, respectively) (P=0.01) and were significantly higher in patients with fibrosis stage <2 (Brunt's system) (2.0+/-0.77 vs. 1.3+/-0.9 for stage > or =2, P=0.05). Mean delta over baseline values correlated highly with fibrosis stage (P=0.01), albumin (P=0.007), international normalized ratio (P=0.04), bilirubin (P=0.0008), and platelet count (P=0.0001). On multivariate stepwise logistic regression analysis, CBT was the best predictor of severe fibrosis (stage > or =2) (odds ratio 0.274, 95% confidence interval 0.086-0.872, P=0.028), with an area under the curve of 0.788. CONCLUSIONS: The CBT is safe and easy to perform. It can reliably predict severe hepatic fibrosis in patients with NAFLD. Further large-scale studies are still needed.

The role of enzyme-linked immunosorbent assay D-dimer in patients with acute coronary syndrome presenting with normal cardiac enzymes.

Plasma D-dimer levels, the primary degradation product of cross-linked fibrin, are elevated in acute coronary syndrome (ACS). However, the role of D-dimer in patients presenting to the Emergency Department with ACS and normal cardiac enzymes is unknown. We conducted a prospective, observational study in the Emergency Department of a major tertiary university-affiliated center. The study included 124 patients presented to the Emergency Department with ACS and normal cardiac enzymes. Blood samples were collected and assayed for D-dimer levels with the enzyme-linked immunosorbent assay (ELISA) test. The D-dimer values were correlated with the clinical, laboratory and electrocardiographic findings on admission, as well as with the catheterization findings and with hospital length of stay. ELISA D-dimer levels positively correlated with sex, hypertension and smoking (r = -0.27, P = 0.002; r = 0.33, P = 0.0002; and r = -0.24, P = 0.007, respectively). Significant correlation was also observed between ELISA D-dimer and cardiac medications including beta-blocker (r = 0.22, P = 0.01), aspirin (r = 0.18, P = 0.04), nitrate (r = 0.20, P = 0.002), acute phase reactants fibrinogen (r = 0.45, P = 0.0001) and C-reactive protein (r = 0.29, P = 0.004), ischemic electrocardiographic changes (r = 0.21, P = 0.02) and length of stay (r = 0.29, P = 0.001). The catheterization findings were also correlated with the ELISA D-dimer levels (r = 0.31, P = 0.02). The ELISA D-dimer test may add important clinical data concerning patients with ACS and normal cardiac enzymes.

Insulin and losartan reduce proteinuria and renal hypertrophy in the pregnant diabetic rat.

This study was designed to investigate the effect of hyperglycemia and angiotensin II (AngII) on renal hypertrophy and proteinuria in the pregnant diabetic rat. Secondary objectives were to evaluate changes in components of the renin-angiotensin axis and the effects of administration of losartan on pregnancy outcome. Fifty-three pregnant rats were allocated to 6 groups (1) nondiabetic controls (n = 12), (2) nondiabetic controls administered losartan (70-80 mg/kg/day; n = 10), (3) rats in which intravenous streptozotocin (STZ) was used to induce diabetes (55 mg/kg on day 10 of pregnancy; n = 10), (4) diabetic rats treated with losartan (n = 7), (5) diabetic rats treated with insulin (4 U/day; n = 7), and (6) diabetic rats treated with insulin and losartan (n = 7). Urinary protein excretion measured 4 days after STZ was 4 times greater in the rats with STZ-induced diabetes and significantly less in diabetic rats given losartan, insulin, or both. Postpartum kidney weight was greater in the rats with STZ-induced diabetes (2.04 +/- 0.21 g) than in the controls (1.37 +/- 0.14 g; P <.05) and reduced in the diabetic rats given losartan, insulin, or both (1.57 +/- 0.22, 1.73 +/- 0.13, and 1.51 +/- 0.14 g, respectively; P <.05). Plasma levels of angiotensin II in rats given losartan were more than 3.5 times greater than those in controls (749 +/- 436, 596 +/- 323, 567 +/- 349, and 159 +/- 28 pg/mL; P <.001). Postpartum activity of angiotensin-converting enzyme was increased in the untreated diabetic rats compared with that in control rats (162 +/- 12 vs 117 +/- 16 nmol/mL/min; P <.05). This increase was abolished by treatment with losartan or insulin. The number of newborns and mean weight of each newborn was similar in all groups. In summary, administration of losartan or insulin prevented, in part, kidney hypertrophy and protein excretion in the diabetic pregnant rat. Losartan did not affect the number or weight of newborns. Because angiotensin II receptor-blockers are contraindicated in pregnancy, good control of diabetes through the use of insulin should be advantageous.