ブックタイトル第43回日本集中治療医学会学術集会プログラム・抄録集

概要

第43回日本集中治療医学会学術集会プログラム・抄録集

－279－　Many studies analyzed the role of NGAL as an early diagnostic marker for AKI in AHF. Plasma NGAL levels do notadequately predict AKI in some studies but in other admission NGAL measurement appears a sensible tool for worsening renalfunction during hospitalization and prognosis. A cut off of 134 ng/ml has been related to worsening renal function withsensibility and specificity at 92% and 71% respectively.　To variation between studies could be link to the fact that studies did not use identical definitions for AKI, and this definitionis critical in biomarker research. Further clinical trials are needed to determine the diagnostic utility of sCyC and NGAL as abiomarker of AKI. In most cases patients with AHF are admitted with clinical signs and symptoms of congestion and fluidoverload. These biomarkers cannot be yet recommended because of a lack of evidence of cost effectiveness. In addition,creatinine is still the preferred marker for serial monitoring of renal function in individuals.2. Assessment of liver function　Abnormal liver function tests（LFTs）in HF patients occur from different mechanisms lack of perfusion and congestion. Adecreased cardiac output state leading to impaired organ perfusion is associated with acute centrilobular hepatocellular damage,ischemic hepatic then necrosis are mainly related to aspartate transaminase（AST）, alanine transaminase（ALT）, and bilirubin.Whereas, elevated right atrial filling pressures with increased central venous pressure and systemic congestion lead tocongestive hepatic injury and are related to all liver function tests, especially gamma-glutamyltranspeptidase（GGT）, alkalinephosphatase（ALP）, and bilirubin.　Threes larges cohorts studied the abnormal LFTs in AHF: A post hoc analysis of 1134 patients of SURVIVE trial（TheSurvival of Patients With Acute Heart Failure in Need of Intravenous Inotropic Support）, the AHEAD trial（Acute HeartFailure Database）with 8818 patients, and a post hoc analysis of the trial EVEREST（Efficacy of Vasopressin Antagonism inHeart Failure Outcome Study with Tolvaptan）with 2061 patients. The prevalence of abnormal LFTs was between 46-76% atadmission.　Abnormal alkaline phosphatase was associated with marked signs of systemic congestion and elevated right-sided fillingpressure and associated with worse 180-day mortality. Abnormal transaminases were associated with clinical signs ofhypoperfusion and with greater 31-day and 180-day mortality compared with normal transaminase profiles. LFTs abnormalitieswere strongly associated with AHF severity（left ventricular ejection fraction and NYHA functional class）and clinicalmanifestation. Two other studies showed prognostic value of total bilirubin levels. Low albumin levels also have been found tohave prognostic value in patients with acute decompensated HF.　After elimination of potential biliary tract obstruction and/or primary hepatic pathology abnormal LFTs signify the presenceof cardiohepatic syndromes and, give indication on the the mechanism of liver injury and heart dysfunction: liver congestion incase of elevated AP and/ or liver ischaemia in case of elevated transaminases. More studies are necessary to evaluate thekinetic of the abnormal LFTs but abnormal LFTs may therefore offer a guide to manage the AHF patients: reducing congestionin cases of increased AP and/or towards improving perfusion in cases of increased transaminases. Alterations in liver functionalso lead to changes in liver drug metabolism and reductions in the synthesis of plasma protein binding with impact on drugeffects（like anticoagulant agents）.References1. 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