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991.
Candidates with fulminant hepatic failure (Status-1A) receive the highest priority for liver transplantation (LT) in the United States. However, no studies have compared wait-list mortality risk among end-stage liver disease (ESLD) candidates with high Model for End-Stage Liver Disease (MELD) scores to those listed as Status-1A. We aimed to determine if there are MELD scores for ESLD candidates at which their wait-list mortality risk is higher than that of Status-1A, and to identify the factors predicting wait-list mortality among those who are Status-1A. Data were obtained from the Scientific Registry of Transplant Recipients for adult LT candidates (n = 52,459) listed between September 1, 2001, and December 31, 2007. Candidates listed for repeat LT as Status-1 A were excluded. Starting from the date of wait listing, candidates were followed for 14 days or until the earliest occurrence of death, transplant, or granting of an exception MELD score. ESLD candidates were categorized by MELD score, with a separate category for those with calculated MELD > 40. We compared wait-list mortality between each MELD category and Status-1A (reference) using time-dependent Cox regression. ESLD candidates with MELD > 40 had almost twice the wait-list mortality risk of Status-1A candidates, with a covariate-adjusted hazard ratio of HR = 1.96 (P = 0.004). There was no difference in wait-list mortality risk for candidates with MELD 36-40 and Status-1A, whereas candidates with MELD < 36 had significantly lower mortality risk than Status-1A candidates. MELD score did not significantly predict wait-list mortality among Status-1A candidates (P = 0.18). Among Status-1A candidates with acetaminophen toxicity, MELD was a significant predictor of wait-list mortality (P < 0.0009). Posttransplant survival was similar for Status-1A and ESLD candidates with MELD > 20 (P = 0.6). CONCLUSION: Candidates with MELD > 40 have significantly higher wait-list mortality and similar posttransplant survival as candidates who are Status-1A, and therefore, should be assigned higher priority than Status-1A for allocation. Because ESLD candidates with MELD 36-40 and Status-1A have similar wait-list mortality risk and posttransplant survival, these candidates should be assigned similar rather than sequential priority for deceased donor LT.  相似文献   
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A 59-year-old man with human immunodeficiency virus (HIV) was referred for persistently elevated liver enzyme activities. His HIV was well controlled on antiretroviral therapy and his viral load was undetectable. He had no history of chronic liver disease and had minimal alcohol intake. He was asymptomatic and his physical exam was unremarkable without any stigmata of liver disease. Beyond the elevations in alkaline phosphatase and gamma-glutamyl transferase, the rest of his laboratory work, including viral hepatitis serologies and serum α-fetoprotein, was within normal limits. A computed tomography (CT) scan revealed a mildly nodular liver but hepatic mass or ascites was not seen. He was subsequently followed every 3 to 6 months without any change in his clinical symptoms, laboratory values, or imaging tests. Two years after the original visit, the patient presented with acute onset of abdominal pain, an AFP of 15.8 ng/mL, and a 9-cm hepatic mass on imaging. Given his preserved liver function, he underwent right hepatic lobectomy. Histologic examination of the resected tissue was consistent with hepatocellular carcinoma (HCC). The uninvolved liver was noncirrhotic and unremarkable except for mild portal inflammation. As the vast majority of HIV patients who develop HCC have established chronic liver diseases such as hepatitis B and/or C along with cirrhosis, this case of HCC in an HIV patient without cirrhosis or viral hepatitis is rare. Although current screening guidelines recommend imaging only for patients with HIV and hepatitis B/C cirrhosis, closer monitoring may be important in HIV patients with even subtle liver dysfunction.  相似文献   
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Anemia is the primary hematological manifestation of both Plasmodium falciparum malaria and HIV‐1 in pediatric populations in sub‐Saharan Africa. We have previously shown that HIV‐1 positive and exposed children have greater risk of developing severe anemia (hemoglobin, Hb <6.0 g dL?1) during acute malaria. However, enhanced severity of anemia was unrelated to either erythropoietic suppression or parasite‐driven red blood cell hemolysis. To further explore mechanisms of anemia, circulating inflammatory mediators (IMs) were determined using a 25‐plex bead array in P. falciparum‐infected (Pf[+]) children (3–36 month, n = 194) stratified into three groups: HIV‐1 negative (HIV‐1[?]/Pf[+]); HIV‐1 exposed (HIV‐1[exp]/Pf[+]); and HIV‐1 infected (HIV‐1[+]/Pf[+]). IL‐12, MIG/CXCL9, eotaxin/CCL11, and GM‐CSF differed significantly and progressively increased across the groups (HIV‐1[?]→HIV‐1[exp]→HIV‐1[+]). To further explore the relationship between the inflammatory milieu (i.e., cytokines, chemokines, and growth factors) and HIV‐1 status, the large panel of IMs was reduced into discrete groups by principal component factor analysis. Of the six principal components that emerged, three components were significantly higher in the HIV‐1 [+]/pf[+] and HIV[exp]/Pf[+] groups, demonstrating that inflammatory profiles differ according to HIV‐1 status. Additional analyses exploring the relationship between the components and anemia revealed significant positive correlations between Hb and Component 3 (IL‐1Ra, IL‐7, IL‐17, IFN‐α, IFN‐γ, MIG/CXCL9) in the HIV‐1[?]/Pf[+] group, and Component 4 (IL‐4, IL‐5, IL‐12, Eotaxin/CCL11) in HIV‐1[+]/Pf[+] children. Further analyses of the HIV‐1[+]/Pf[+] group revealed that IL‐12 had the strongest association with anemia. Results presented here demonstrate that there are unique relationships between the inflammatory environment and anemia in HIV‐1 positive and exposed children with malaria. Am. J. Hematol. 87:652–658, 2012. © 2012 Wiley Periodicals, Inc.  相似文献   
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Board certification is intended to protect the public by identifying practitioners that have met minimum standards for education and training in their specialty or discipline. For varied reasons, clinical neuropsychology, like professional psychology as a whole, has struggled to achieve levels of board certification comparable to the medical profession. Rohling, Lees-Haley, Langhinrichsen-Rohling, & Williamson (2003) Rohling, M. L., Lees-Haley, P. R., Langhinrichsen-Rohling, J. and Williamson, D. J. 2003. A statistical analysis of board certification in clinical neuropsychology. Archives of Clinical Neuropsychology, 18: 331352.  [Google Scholar] have recently published a critique of the board certification process in clinical neuropsychology as it is conducted by American Board of Clinical Neuropsychology (ABCN), arguing that one reason for this failure is the overly restrictive nature of the process. In their paper, Rohling et al. provide a signal detection analysis that makes several assumptions about the process and conclude with recommendations for improving the process to better identify “competent” neuropsychologists in practice. While we agree in principle with many of their recommendations, and ABCN had, in fact, implemented several prior to publication of their article, the article contains many faulty assumptions and logical inconsistencies that we believe are harmful to constructive review of the certification process. In this article, we provide a critical review of their analysis and present new and additional data that demonstrate the procedure is not overly restrictive. A primary consideration is the low incidence of seeking board certification among professionals who identify themselves as neuropsychologists (i.e., a low application rate), rather than an overly restrictive process. We describe steps taken to improve the process and conclude that there are numerous areas of agreement with Rohling et al., including the need for ongoing review and continued improvement in the board certification process in all psychological specialties.  相似文献   
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