Measures have been put in place and policies have been drafted to improve this situation and provide the best possible care to persons with haemophilia. “
“Acquired www.selleckchem.com/products/VX-770.html inhibitors directed against coagulation factor VIII:C (FVIII) interfere and/or neutralize its procoagulant function and result in severe and often life-threatening hemorrhagic complications. These inhibitors are autoantibodies, usually arising in individuals with no prior history of clinical bleeding. Auto-FVIII antibodies usually are polyclonal;

they express their neutralizing capacity with type II pharmacokinetics, result in serious clinical bleeding, and require different treatment and immune tolerance strategies, including the frequent use of coagulation factor bypassing agents such as activated prothrombin complex concentrates (aPCCs) or recombinant factor VIIa (rFVIIa), and/or early institution of immunosuppressive therapies. KPT 330 This chapter

reviews the pathophysiology, clinical picture, and management strategies for this relatively rare acquired condition, which arises in previously noncoagulopathic, nonhemophilic individuals. “
“Regular replacement therapy (prophylaxis) for haemophilia has been shown to prevent development of disabling arthropathy and to provide a better quality of life compared to treatment on demand; however, at a substantially higher cost. Calculations based on pharmacokinetic principles have shown that shortening dose intervals may reduce cost. The aim of this prospective, randomized, crossover pilot study was to CYTH4 address whether daily dosing is feasible, if it reduces concentrate consumption and is as effective in preventing bleeding as the standard prophylactic dosing regimen. In a 12 + 12 month crossover study, 13 patients were randomized to start either their own previously prescribed standard dose, or daily dosing adjusted to maintain

at least the same trough levels as obtained with the standard dose. Ten patients completed the study. A 30% reduction in cost of factor concentrates was achieved with daily prophylaxis. However, the number of bleeding events increased in some patients in the daily dosing arm and patients reported decreased quality of life during daily prophylaxis. Daily treatment had a greater impact on daily life, and the patients found it more stressful.Prophylaxis with daily dosing may be feasible and efficacious in some patients. A substantial reduction of factor consumption and costs can be realized, but larger studies are needed before the introduction of daily prophylaxis into clinical routine can be recommended. “
“Summary.  Severe haemophilic arthropathy of the elbow is a significant cause of morbidity among adults with haemophilia. However, previous reports of total elbow arthroplasty (TEA) in the haemophilic population have been based on small numbers of patients with relatively short-term follow-up.

52, p<0.01). 6MWD also showed strong correlation with physical component score on the SF-36 in all

groups (r=0.51, p<0.01). In multivariate analysis, hepatitis C remained an independent predictor of 6MWD improvement (p=0.048). There was a trend towards worse 6MWD in NASH recipients (p=0.06). At 1-month post-LT, only 5/46 (10.9%) of recipients were enrolled in a rehabilitation program and at 1-year none were participating. Conclusions: 6MWD is lower in male patients up to 1 year post-LT as compared to HC and CLD patients. Among LT recipients, male sex and NASH are associated with poorer 6-minute walk performance, which is a simple and inexpensive measure of functional performance that can be easily applied in clinical practice. A minority of LT recipients MK-2206 in vivo are enrolled in a rehabilitation program highlighting the opportunity for early lifestyle intervention to potentially improve functional capacity after LT. Disclosures: see more Josh Levitsky – Consulting: Transplant Genomics Inc; Grant/Research Support: Novartis; Speaking and Teaching: Gilead, Salix The following people have nothing to disclose: Sarah Uttal, Lisa B. VanWagner, Brittany Lapin, Amanda Jichlinkski, Joshua Lee, Madeleine Heldman,

Brian Poole, Tanvi Subramanian, Eduardo A. Bustamante, Suvai Gunasekaran, Christopher S. Tapia, Annapoorani Veerappan, She-Yan Wong Background/Aim: Among HCV LT recipients, older recipient age has been associated with graft loss, but the natural history of HCV among young (age <40y) adults undergoing LT is unknown. Using MELD-era UNOS data, we evaluated young HCV LT recipients and compared their outcomes to older age cohorts. Methods: All US adult HIV(-), HCV-positive LT recipients from 2002-2013 were included (N=25,968). Graft loss (re-LT or death) was estimated using the Kaplan-Meier method and the association between

recipient age and survival assessed with Cox regression. Results: Overall, recipients were 25% female, 70% White, with mean age of 54.5y. Recipients <40y (n=105, 0.4% 18-29y; n=459, 1.8% 30-39y) vs >40yrs, had higher % female (31 vs 24), mean MELD at LT (24 vs 20), % rejection (18 vs 10), and lower mean donor risk index clonidine (1.3 vs 1.4), and % HCC (11 vs 44). Overall, the 1-, 3-, and 5-yr graft loss rates were 23%, 32%, and 40%. Using 40+y cohort as reference (40% 5-y graft loss), 5-y graft loss was higher at 63% and 42% for recipient age cohorts 18-29 and 30-39y respectively (p<0.001) (Fig). In adjusted analysis, recipient age 19-29y had 81%(HR 1.81, CI 1.39-2.37, p<0.001) and 30-39 had 17%(1.17, 1.01-1.36, p=0.04) higher rate of graft loss. In recipients 18-29, 30-39 and 40+y, re-LT occurred in 10% 10% and 5%; HCV-related death in 22%, 21% and 13% (p<0.001 for both). Among patients <40y, recipient age/y (HR 0.95, CI: 0.94-0.98), donor age/y (1.02, 1.02-1.03), recipient female (1.39; 1.06-1.83), MELD at LT per point (1.02, 1.00-1.

Bioengineered liver organoids were generated by seeding freshly isolated hFLC through the vena cava and portal vein of the intact liver scaffold. These seeded scaffolds remained in a perfusion bioreactor up to two weeks. In parallel, hFLCs were seeded on decellularized liver ECM discs (300 μm thick, 8 mm diameter) and were cultured for 3 weeks in hepatic differentiation medium. Confocal microscopy

was used to determine the extent of progenitor cell differentiation into hepatocytes and cholangiocyies in disk organoids and whole liver scaffold. Urea, albumin and drug metabolism AZD3965 were guantified as paramaters of liver function. hFLCs seeded on liver ECM discs differentiated into hepatocytes and cholangiocytes. The cells showed predominant albumin expression along with loss of AFP expression at 3 weeks. The cells also expressed other mature hepatocyte markers like HNF-4α, α-1AT and CYP450 1A2, 2A and 3A. The cells in the ductular structures expressed bile duct specific markers like CK19, SOX9, EpCAM, ASBT, β-catenin and the presence of primary cilia, thus demonstrating differentiation check details towards cholangiocyte lineage along with maintaining apicobasal polarity. Similarly, hFLC seeded in whole liver scaffolds showed progressive tissue formation and organization with clusters of hepatocytes expressing albumin, AFP, CYP450 3A and 2A, E-cad, Hep-1

and EpCAM, and several long ductular structures staining positive for biliary markers CK19, EpCAM, Interleukin-3 receptor ASBT spawning for 200-400μm in length. Urea and albumin secretion was higher in the whole bioengineered liver and liver disc organoids compared to control hFLCs cultured in petri dishes. Several metabolites of diazepam and 7-ethoxycoumarin were also detected by LC-MS/MS, showing broad

CYP450 activity in both culture systems. Our results demonstrate the efficient generation of bioengineered human liver tissue with hFLC that recapitulates stepwise development of hepatocyte and bile duct formation. Altogether, this study demonstrates the potential of this technology to study and mimic human liver development. These models provide novel approaches for liver bioengineering, drug discovery and toxicology, and ultimately for the treatment of liver disease. Disclosures: The following people have nothing to disclose: Pedro M. Baptista, Dipen Vyas, Emma Moran, Anthony Atala, Shay Soker There is considerable interest in the use of bone marrow(BM) cells in liver cirrhosis, however the role of purified haematopoietic stem cells(HSC) and use of repeated infusions have not been studied. We also set out to determine whether increased retention of HSC within the injured liver by modulating their response to Sphingosine 1-phosphate(S1P) would augment their anti-fibrotic effect. Liver injury was induced in BoyJ(CD45.

35 Bcl-2 was the first gene identified as a regulator of apoptosis,36 and subsequently, several bcl-2 homologues were discovered that act as either proapoptotic or antiapoptotic effectors. The present data are in agreement with previous Epigenetics inhibitor observations demonstrating that the overexpression of bcl-2, mcl-1, and bcl-xL37, 38 prevents cells from undergoing apoptosis,

whereas bax, apaf-1, caspase-6, and p53 function to promote cell death.39 Ca buffering also shifted the Bax/Bcl-2 ratio toward the antiapoptotic profile, and this resulted in the accelerated restoration of liver mass after PH. This agrees with recent proteomic data showing that apoptosis pathways are inhibited during liver regeneration.40 Additionally, hepatocyte growth factor, an essential stimulus for liver regeneration, is known to have antiapoptotic activity in injured tissue.41 Similarly, TNF, another initiator of liver regeneration, also

modulates apoptosis in addition to stimulating hepatocyte proliferation.42 Although our results suggest that Ca buffering accelerates liver regeneration by inhibiting apoptosis, an effect on cell proliferation cannot be entirely excluded because Bax/Bcl-2 family proteins regulate liver regeneration independently of their role in modulating apoptosis in the liver.43, 44 Moreover, Ca buffering Selleck BGB324 might also accelerate liver regeneration by modulating ATP production in the mitochondrial matrix because the activity of enzymes of the tricarboxylic acid cycle is regulated by Ca2+.13 Heterologous expression of the Ca2+ binding protein PV has been widely used to study the role of Ca2+ many signaling in the regulation of the cell cycle. PV was targeted to the nucleus or cytoplasm, and with this approach, the role of nuclear Ca2+ in regulating the cell cycle was established in a liver cell

line.9 More recently, PV expression in the cytosol of hepatocytes in vivo demonstrated that cytosolic Ca2+ affects progression through the cell cycle after PH.32 Using PV targeted to the mitochondria, we have now shown that Ca also regulates liver regeneration. Future advances in this field should lead to a better understanding of the ways in which these various Ca2+ compartments act in an integrated manner to regulate liver regeneration. The authors thank Gilson Nogueira for his technical support and Soraya Smaili for antibodies against Bax and Bcl-2 and useful discussions. The authors also thank Dawidson A. Gomes for assistance in the design of the parvalbumin construct. Confocal imaging was supported by CEMEL (Centro de Microscopia Eletrônica, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, Brazil). Additional Supporting Information may be found in the online version of this article. “
“Purpose: Allograft hepatitis C is accelerated following liver transplantation (LT). Factors associated with disease progression include viral, demographic, and genetic characteristics of recipients and donors.

CX3CR1 activation was the dominant pertussis-sensitive Tofacitinib cell line mechanism controlling transendothelial migration under flow, and expression of the CX3CR1 ligand CX3CL1 is increased on hepatic sinusoids in chronic inflammatory liver disease. Exposure of CD16+ monocytes to immobilized purified CX3CL1 triggered β1-integrin-mediated adhesion to vascular cell adhesion molecule-1 and induced the development of a migratory phenotype. Following

transmigration or exposure to soluble CX3CL1, CD16+ monocytes rapidly but transiently lost expression of CX3CR1. Adhesion and transmigration across HSECs under flow was also dependent on vascular adhesion protein-1 (VAP-1) on the HSECs. Conclusion: Our data suggest that

CD16+ monocytes are recruited by a combination of adhesive signals involving VAP-1 and CX3CR1 mediated integrin-activation. PD-1/PD-L1 cancer Thus a novel combination of surface molecules, including VAP-1 and CX3CL1 promotes the recruitment of CD16+ monocytes to the liver, allowing them to localize at sites of chronic inflammation and fibrosis. (Hepatology 2010) The liver contains bone marrow-derived myeloid dendritic cells (mDCs) and macrophages (Kupffer cells) that are recruited from blood via the hepatic sinusoids. They act as immune sentinels to detect and coordinate responses to invading pathogens and antigens entering the liver through the portal vein.1-3 Under basal conditions, these cells are replenished by recruitment of precursors from

blood, which increases with inflammation. The exact nature of the precursor cells is unclear, but they likely reside within the circulating CD16+ monocyte population.4-7 mDCs arise from bone marrow-derived progenitors within the monocyte pool.8-10 Several populations 2-hydroxyphytanoyl-CoA lyase of precursors have been proposed, including lineage-negative CD11c+ monocytes, CD34+ progenitors,11 and human CD16+ monocytes.12 Human monocytes display heterogeneity defined by expression of chemokine receptors, adhesion molecules, CD14, and CD16.13-15 The CD14+CD16++ subset expresses high levels of the chemokine receptor CX3CR1 and is believed to give rise to DCs with potent antigen-presenting capabilities16 and inflammatory tissue macrophages.15, 17 Furthermore, transendothelial migration of CD16+ monocytes in vitro induces differentiation into functional DCs, suggesting that recruitment itself may shape their subsequent differentiation.18 Integral to mDC function is the capacity to traffic from one anatomical compartment to another. In the liver, this involves a pathway that traverses the space of Disse and takes the cells along the hepatic sinusoids to the portal tract lymphatics.19-21 The recruitment of precursor mDCs from the blood into tissues across endothelium is poorly understood.

CX3CR1 activation was the dominant pertussis-sensitive 5-Fluoracil price mechanism controlling transendothelial migration under flow, and expression of the CX3CR1 ligand CX3CL1 is increased on hepatic sinusoids in chronic inflammatory liver disease. Exposure of CD16+ monocytes to immobilized purified CX3CL1 triggered β1-integrin-mediated adhesion to vascular cell adhesion molecule-1 and induced the development of a migratory phenotype. Following

transmigration or exposure to soluble CX3CL1, CD16+ monocytes rapidly but transiently lost expression of CX3CR1. Adhesion and transmigration across HSECs under flow was also dependent on vascular adhesion protein-1 (VAP-1) on the HSECs. Conclusion: Our data suggest that

CD16+ monocytes are recruited by a combination of adhesive signals involving VAP-1 and CX3CR1 mediated integrin-activation. U0126 molecular weight Thus a novel combination of surface molecules, including VAP-1 and CX3CL1 promotes the recruitment of CD16+ monocytes to the liver, allowing them to localize at sites of chronic inflammation and fibrosis. (Hepatology 2010) The liver contains bone marrow-derived myeloid dendritic cells (mDCs) and macrophages (Kupffer cells) that are recruited from blood via the hepatic sinusoids. They act as immune sentinels to detect and coordinate responses to invading pathogens and antigens entering the liver through the portal vein.1-3 Under basal conditions, these cells are replenished by recruitment of precursors from

blood, which increases with inflammation. The exact nature of the precursor cells is unclear, but they likely reside within the circulating CD16+ monocyte population.4-7 mDCs arise from bone marrow-derived progenitors within the monocyte pool.8-10 Several populations Cediranib (AZD2171) of precursors have been proposed, including lineage-negative CD11c+ monocytes, CD34+ progenitors,11 and human CD16+ monocytes.12 Human monocytes display heterogeneity defined by expression of chemokine receptors, adhesion molecules, CD14, and CD16.13-15 The CD14+CD16++ subset expresses high levels of the chemokine receptor CX3CR1 and is believed to give rise to DCs with potent antigen-presenting capabilities16 and inflammatory tissue macrophages.15, 17 Furthermore, transendothelial migration of CD16+ monocytes in vitro induces differentiation into functional DCs, suggesting that recruitment itself may shape their subsequent differentiation.18 Integral to mDC function is the capacity to traffic from one anatomical compartment to another. In the liver, this involves a pathway that traverses the space of Disse and takes the cells along the hepatic sinusoids to the portal tract lymphatics.19-21 The recruitment of precursor mDCs from the blood into tissues across endothelium is poorly understood.

In case 2, esophageal

varices with active bleeding were ligated, and injected tissue glue at the bleeding spots of gastric varices. We succeeded to stop the bleeding in both case 1 and 2. In case 3, the stomach was filled with a lot of blood clots and dark red blood. The patient was urgently transferred to artery embolism treatment, but still died after the operation because of pulmonary selleck inhibitor infection, hemorrhagic shock and cardiac insufficiency. Emergency endoscopy associated mortality was zero. Conclusion: Emergency endoscopic hemostatic for liver transplantation patients with massive UGB was safe and effective. And the doctors and nurses should make well preparation and cooperation, pay close attention to the patients and keep clear of the endoscopic view, chose the most appropriate hemostatic method in order to reduce the fatality rate. Key Word(s): 1. liver transplantation; 2. gastrointestinal

hemorrhage; 3. gastroscopy; 4. perioperative Presenting Author: TADATERU MAEHATA Additional Authors: OSAMU GOTO, RYO MORITA, MIDORI SUZUKI, YOSHINORI SATO, SHINYA ISHIGOOKA, SHUN ICHIRO OZAWA, KOSUKE HOSOYA, YASUMASA MATSUO, MASAKI YAMASHITA, HIROYUKI YAMAMOTO, HIROSHI YASUDA, FUMIO ITOH Corresponding Author: TADATERU MAEHATA Affiliations: Keio University, St. Marianna University School of Medicine, St. Marianna IWR-1 manufacturer University School of Medicine,

St. Marianna University School of Medicine, St. Marianna University School of Medicine, St. Marianna University School of Medicine, St. Marianna University School of Medicine, St. Marianna University School of Medicine, St. Marianna University School of Medicine, St. Marianna University School of Medicine, St. Marianna University School of Medicine, St. Marianna University School of Medicine Objective: Recently, ESD has been widely accepted as a curative, less-invasive treatment for early gastric cancer and contributes greatly to the preservation of gastric function. In clinical practice, however, for cases not indicated for filipin ESD, we occasionally encounter treatments such as diagnostic ESD that are considered overindications. Some cases result in incomplete resection because of positive vertical margins. In this study, we examined the limitations of ESD (conditions of lesions worthy of full-thickness resection) by identifying the clinicopathological factors involved in positive vertical margins (pVM1) among cases of early gastric cancer resected using ESD. Methods: The therapeutic outcomes of ESD were retrospectively assessed for 478 patients with 490 EGC lesions resected en bloc with ESD at the St. Marianna University Hospital, Kanagawa, from June 2005 to December 2013. All cases were categorized into the pVM1 and pVM0 groups.

3C). These results were further confirmed

in the partial hepatectomy model. CB2 mRNA expression was induced 48 and 72 hours after partial hepatectomy (Fig. 3D), and CB2−/− mice also showed a retarded regenerative response, as shown by western blot analysis and immunohistochemistry of PCNA expression (Fig. 3E) or bromodeoxyuridine staining (not shown). Altogether, these data indicate that CB2 receptors accelerate liver regeneration. Further experiments aimed at delineating the molecular mechanisms underlying the beneficial effect of CB2 receptors on hepatocyte survival and regeneration.24, 25 We first investigated the impact of CB2 receptor deficiency on hepatic expression of factors with known effects on hepatocyte survival and/or regeneration.24, 25 The induction of inducible nitric oxide synthase (iNOS), TNF-α, and IL-6 mRNA was attenuated in CCl4-treated CB2−/− Selleck Selinexor mice as compared to WT counterparts (Fig. 4A) whereas the induction profile

of monocyte chemoattractant protein-1 (MCP-1), IL-10, and Toll-like receptor 4 (TLR4) was similar in both groups (Fig. 4B). Following CCl4 administration, up-regulation of iNOS in hepatocytes is a compensatory protective pathway with respect to hepatocyte apoptosis.26-29 Given the impairment of iNOS induction in the liver of CB2−/− mice exposed to CCl4, we investigated whether an NO donor would attenuate the exacerbation of liver injury in these mice. Treatment with SIN-1 reduced the rate of TUNEL-positive hepatocytes in CCl4-exposed CB2−/− mice, whereas liver high throughput screening compounds injury was unchanged in CCl4-injected WT animals (Fig. 5A). However, SIN-1

did not significantly improved liver regeneration in WT mice (not shown) or in CB2−/− animals, although a trend to increase was noted in the latter group (P = 0.13; Fig. 5B). These results suggest that CB2 inactivation leads to defective induction of hepatic iNOS, thereby enhancing hepatocyte death following acute liver injury. In contrast, the impairment of liver regeneration found in CCl4-treated CB2−/− mice may result from additional mechanisms. IL-6 plays a major role in hepatocyte survival and regeneration.24, 25, 30 Given the impairment of IL-6 induction in the Selleck Rapamycin liver of CCl4-treated CB2−/− mice, we explored whether defective liver regeneration would be restored by IL-6 administration. IL-6 did not affect TUNEL staining in CCl4-treated WT or CB2−/− mice at 24 hours (Fig. 6A). In contrast, IL-6 restored PCNA expression in CCl4-treated CB2−/− animals to 75% of its level in CCl4-treated WT animals (Fig. 6B). These findings suggest that IL-6 deficiency is a key event in the impairment of liver regeneration observed in CB2−/− animals. MMPs contribute to liver injury and regeneration. IL-6 has been shown to down-regulate hepatic MMP-2 activity following acute CCl4 administration.31 We therefore investigated whether CB2 receptors modulate hepatic MMP activity via an IL-6–dependent mechanism.

8, 9 The real cause is not clear; it is postulated that there exists a selection pressure between the HCV viral genotype and host immune responses during evolution that might determine HCV genotype–specific treatment responses.10 Whether the driving force of selection applies to viral replication as well as the preference of the viral genotype distribution in terms of host genetic diversities warrants further molecular-based studies in the future. Chung-Feng Huang M.D* †, Chia-Yen Dai M.D., Ph.D* § ¶, Jee-Fu Huang M.D.* ¶ **, Wan-Long Chuang M.D., Ph.D.* ¶, Ming-Lung Yu M.D., Ph.D.* ‡ ¶,

* Hepatobiliary Division, Department of Internal Medicine, Kaohsiung Medical University Hospital, Casein Kinase inhibitor Kaohsiung, Taiwan, † Departments of Occupational Medicine, ‡ Internal Medicine, Kaohsiung Municipal Ta- Tung Hospital, Kaohsiung, Taiwan, § LY2109761 price Graduate Institute of Medicine, ¶ Faculty of Internal Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan, ** Department of Internal Medicine, Kaohsiung Municipal Hsiao-Kang Hospital, Kaohsiung, Taiwan. “
“Patients with underlying acute and chronic liver disease are at risk of morbidity and mortality after surgery. The magnitude of the risk is related to the severity of liver disease, the type of surgery

and the urgency of the surgery. The severity of liver disease as measured by the model for end-stage liver disease (MELD) score and the Child-Turcotte-Pugh (CTP) score can be used to risk stratify patients with liver disease undergoing surgery. Even in patients with well-preserved liver synthetic function, the presence of significant portal hypertension can lead to adverse outcomes after surgery, particularly

if it involves hepatic resection. Cardiac and abdominal surgery carry the greatest risk, particularly in emergent situations, and acute liver failure and acute alcoholic hepatitis are generally contraindications for any type of surgery. “
“We read with interest the recent analysis by Remien et al.1 of the prognostic accuracy of the Model for Acetaminophen-induced Liver Damage (MALD). By combining serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), creatinine, Coproporphyrinogen III oxidase and international normalized ratio INR, the authors demonstrate a negative predictive value (NPV) of 100% for predicting death when applied to a mixed cohort of 53 acetaminophen overdoses. This complex model has several limitations to its use at present, including the difficulty in calculating the formula at the patients’ bedside, and in the use of serum AST, which may not always be routinely available in some centers. However, the study does highlight the importance of accurate triage when considering the potential need for liver transplantation following acetaminophen overdose. We similarly demonstrated an extremely high NPV following acetaminophen overdose by utilizing the Sequential Organ Failure Assessment (SOFA) score, where a SOFA score <7 by 96 hours following single timepoint overdose had a NPV of 98.2%.

8, 9 The real cause is not clear; it is postulated that there exists a selection pressure between the HCV viral genotype and host immune responses during evolution that might determine HCV genotype–specific treatment responses.10 Whether the driving force of selection applies to viral replication as well as the preference of the viral genotype distribution in terms of host genetic diversities warrants further molecular-based studies in the future. Chung-Feng Huang M.D* †, Chia-Yen Dai M.D., Ph.D* § ¶, Jee-Fu Huang M.D.* ¶ **, Wan-Long Chuang M.D., Ph.D.* ¶, Ming-Lung Yu M.D., Ph.D.* ‡ ¶,

* Hepatobiliary Division, Department of Internal Medicine, Kaohsiung Medical University Hospital, learn more Kaohsiung, Taiwan, † Departments of Occupational Medicine, ‡ Internal Medicine, Kaohsiung Municipal Ta- Tung Hospital, Kaohsiung, Taiwan, § Caspase inhibitor Graduate Institute of Medicine, ¶ Faculty of Internal Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan, ** Department of Internal Medicine, Kaohsiung Municipal Hsiao-Kang Hospital, Kaohsiung, Taiwan. “
“Patients with underlying acute and chronic liver disease are at risk of morbidity and mortality after surgery. The magnitude of the risk is related to the severity of liver disease, the type of surgery

and the urgency of the surgery. The severity of liver disease as measured by the model for end-stage liver disease (MELD) score and the Child-Turcotte-Pugh (CTP) score can be used to risk stratify patients with liver disease undergoing surgery. Even in patients with well-preserved liver synthetic function, the presence of significant portal hypertension can lead to adverse outcomes after surgery, particularly

if it involves hepatic resection. Cardiac and abdominal surgery carry the greatest risk, particularly in emergent situations, and acute liver failure and acute alcoholic hepatitis are generally contraindications for any type of surgery. “
“We read with interest the recent analysis by Remien et al.1 of the prognostic accuracy of the Model for Acetaminophen-induced Liver Damage (MALD). By combining serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), creatinine, N-acetylglucosamine-1-phosphate transferase and international normalized ratio INR, the authors demonstrate a negative predictive value (NPV) of 100% for predicting death when applied to a mixed cohort of 53 acetaminophen overdoses. This complex model has several limitations to its use at present, including the difficulty in calculating the formula at the patients’ bedside, and in the use of serum AST, which may not always be routinely available in some centers. However, the study does highlight the importance of accurate triage when considering the potential need for liver transplantation following acetaminophen overdose. We similarly demonstrated an extremely high NPV following acetaminophen overdose by utilizing the Sequential Organ Failure Assessment (SOFA) score, where a SOFA score <7 by 96 hours following single timepoint overdose had a NPV of 98.2%.