Objective: Hyperlactatemia has been suggested as a prognostic marker in acetaminophen-induced fulminant hepatic failure, and a modification of the King's College Hospital criteria to incorporate arterial lactate measurements has recently been proposed. The aims of the present study were to further evaluate arterial lactate as a prognostic marker in acetaminophen-induced fulminant hepatic failure and to analyze its relationship to known causes of hyperlactatemia such as multiple organ failure and inflammation.
Design: Data were collected early after admission and again at the time of onset of grade 3-4 hepatic encephalopathy from acetaminophen-induced fulminant hepatic failure. Multiple organ failure and inflammatory response were assessed by the sequential organ failure assessment (SOFA) score and manifestation of the severe inflammatory response syndrome (SIRS), respectively.
Setting: A specialized liver intensive care unit at a tertiary liver center.
Patients: One hundred and one consecutive patients with acetaminophen-induced fulminant hepatic failure and grade 3-4 hepatic encephalopathy.
Interventions: None.
Measurements And Main Results: Arterial lactate was higher in nonsurvivors than in survivors both early after admission (9.8 +/- 6.5 mmol/L vs. 5.2 +/- 4.2 mmol/L, p = .00004) and at the time of onset of hepatic encephalopathy (6.9 +/- 5.6 mmol/L vs. 3.2 +/- 2.0 mmol/L, p < .00001). At both time points, arterial lactate significantly correlated with SOFA score and the number of SIRS components fulfilled. Applying the lactate modification of the King's College Hospital criteria increased their sensitivity but reduced their specificity to <50%.
Conclusions: The study confirmed arterial lactate as a prognostic marker in acetaminophen-induced fulminant hepatic failure. Arterial lactate correlated with SOFA score and with the number of SIRS components fulfilled. The lactate modification of the King's College Hospital criteria showed no obvious advantages over the existing selection criteria.
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http://dx.doi.org/10.1097/01.ccm.0000194724.70031.b6 | DOI Listing |
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Total hepatectomy and liver transplantation has emerged as a game-changing strategy in the treatment of several liver-confined primary or metastatic tumors, opening the new era of transplant oncology. However, the expansion of indications is going to worsen the chronic scarcity of organs, and new strategies are needed to enlarge the donor pool. A possible source of organs could be developing split liver transplantation (SLT) programs.
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Division of Cardiology, Department of Medicine, Columbia University College of Physicians and Surgeons and NewYork-Presbyterian Hospital, New York, New York, USA.
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Arch Insect Biochem Physiol
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College of Marine Life Sciences, Ocean University of China, Qingdao, China.
Zinc homeostasis contributes significantly to numerous physiological processes. Drosophila ZnT35C protein, a zinc transporter encoded by CG3994, is chiefly located on the cell membrane and facilitates the transport of zinc from the cytoplasm to the extracellular space to sustain zinc homeostasis within the organism. Previous studies about ZnT35C have involved diverse structures such as the Malpighian tubules, adult brain, and sensory nervous system.
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Pneumocystis jirovecii pneumonia (PJP) is an opportunistic fungal infection that often occurs secondary to human immunodeficiency virus (HIV) infection. However, for non-HIV immunocompromised patients, such as those undergoing novel immunosuppressive treatments to manage malignancies, organ transplants, or connective tissue diseases, PJP is emerging as an increasing threat. The clinical manifestations of PJP in HIV-infected and non-HIV-infected patients differ significantly.
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