Portopulmonary hypertension (PPHTN) is a recognized complication of end-stage liver disease that adversely affects the outcome of orthotopic liver transplantation (OLT). There are limited data on the role of Doppler echocardiography in assessing pulmonary artery systolic pressure (PASP) in this population. The purpose of our study was to examine the accuracy of Doppler echocardiography in evaluating pulmonary artery pressures in liver transplant candidates. Clinical and demographic data were gathered retrospectively for 78 liver transplant candidates (48 men and 30 women, mean age 51 ؎ 9.6 yr) who had PASP determined both by right heart catheterization (RHC) and echocardiography. Paired sample t-test was used to compare mean PASP by echocardiography and RHC. Correlation of PASP between echocardiography and RHC was determined using Pearson's linear correlation. P ortopulmonary hypertension (PPHTN) is a recognized complication of end-stage liver disease that adversely affects the outcome of orthotopic liver transplant (OLT). The prevalence of PPHTN varies from 0.61% to 4% 1,2 in patients with cirrhosis; however, the prevalence in patients referred for OLT may be as high as 8.5%. 3,4 The wide variability in prevalence is partly attributable to varying definitions of PPHTN.Direct measurement of pulmonary artery pressure by right-heart catheterization (RHC) remains the gold standard for detecting pulmonary hypertension. However, Doppler echocardiography using transtricuspid valve gradient allows noninvasive estimation of pulmonary artery systolic pressure (PASP). [5][6][7][8][9] Although small studies have been conducted previously regarding echocardiography and the noninvasive estimation of PASP, the question of accuracy of this test in estimating pulmonary artery pressures still remains unanswered. In the setting of liver transplant patients, there is limited data comparing the usefulness of echocardiography in the assessment of PPHTN. The purpose of our study was to examine the accuracy of Doppler echocardiography in evaluating pulmonary artery pressures in liver transplant candidates. MethodsWe retrospectively reviewed the medical records of all patients enrolled in the Liver Center who were undergoing evaluation for OLT at the University of Illinois at Chicago Medical Center between 1995 and 2002. One hundred eighty-seven patients were referred for cardiac workup before liver transplantation. Of these, 15 patients did not have any workup done because of failure to show up for the appointment. The remaining 172 patients underwent echocardiograms; however, PASP could not be determined in 32 of these patients because of suboptimal windows. Twenty-two of the remaining 140 patients had a normal PASP (PASP Ͻ 30 mm Hg with no right ventricle [RV] enlargement or failure) and did not undergo RHC. Thus, these patients were excluded from analysis. Forty patients did not undergo RHC despite meeting criteria for abnormal PASP (PASP Ͼ 30 mm Hg or RV failure or enlargement) because of the following reasons: 29 patients were no...

Infection with the enteric pathogen enterohemorrhagic Escherichia coli (EHEC) causes a variety of symptoms ranging from nonbloody diarrhea to more severe sequelae including hemorrhagic colitis, altered sensorium and seizures, and even life-threatening complications, such as hemolytic uremic syndrome and thrombotic thrombocytopenic purpura. The more severe consequences of EHEC infection are attributable to the production of Shiga toxin (Stx) and its subsequent effects on the vasculature, which expresses high levels of the Stx receptor, Gb3. Interestingly, the intestinal epithelium does not express Gb3. Despite the lack of Gb3 receptor expression, intestinal epithelial cells translocate Stx. The effect of Stx on intestinal epithelial cells is controversial with some studies demonstrating induction of inflammation and others not. This may be difficult to resolve because EHEC expresses both proinflammatory molecules, such as flagellin, and factor(s) that dampen the inflammatory response of epithelial cells. The goal of our study was to define the effect of Stx on the inflammatory response of intestinal epithelial cells and to determine whether infection by EHEC modulates this response. Here we show that Stx is a potent inducer of the inflammatory response in intestinal epithelial cells and confirm that EHEC attenuates the induction of IL-8 by host-derived proinflammatory cytokines. More importantly, however, we show that infection with EHEC attenuates the inflammatory response by intestinal epithelial cells to its own toxin. We speculate that the ability of EHEC to dampen epithelial cell inflammatory responses to Stx and cytokines facilitates intestinal colonization.

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