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The cytoskeleton protein β-actin may mediate T cell apoptosis during acute rejection reaction after liver transplantation in a rat model.

Sat, 12/09/2017 - 13:45
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The cytoskeleton protein β-actin may mediate T cell apoptosis during acute rejection reaction after liver transplantation in a rat model.

Am J Transl Res. 2017;9(11):4888-4901

Authors: Chen X, Zheng J, Cai J, Li H, Li S, Wang L, Cheng D, Chen H, Yang Y, Chen G, Zhang Q, Peng Y, Wang Q, Wang G

Abstract
Cytoskeletal proteins and associated regulatory proteins are essential for maintaining cell structure and growth. β-actin is a major component of the cytoskeleton, and β-actin remodeling is involved in lymphocyte migration, infiltration and apoptosis. However, little is known about whether changes in β-actin expression affect lymphocyte cell fate, particularly during acute rejection after liver transplantation in a rat model. In our studies, grafts were harvested on days 5, 7 or 9 after xenogeneic rat liver transplantation. The acute rejection grade was histopathologically evaluated. Recipient-derived CD8+ T lymphocytes gradually infiltrated into liver allografts in cases of severe acute rejection. The apoptotic rate of CD8+ T lymphocytes peaked on day 7 and then decreased. Moreover, changes in β-actin expression were consistent with the apoptotic rate of CD8+ T lymphocytes in both allografts and peripheral blood based on western blotting and immunohistochemistry results. Additionally, jasplakinolide (an actin-stabilizing drug) evoked CD8+ T lymphocyte apoptosis. In conclusion, our study is the first to describe the fluctuating expression levels and dynamics of the cytoskeletal protein β-actin and its potential roles in the pathogenesis of acute rejection following rat liver transplantion. Our results enhance the understanding of the roles of CD8+ T lymphocytes during acute rejection and suggest that β-actin regulation leads to apoptosis.

PMID: 29218087 [PubMed]

Trimethoprim-Sulfamethoxazole-induced Hepatotoxicity in a Renal Transplant Patient.

Sat, 12/09/2017 - 13:45
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Trimethoprim-Sulfamethoxazole-induced Hepatotoxicity in a Renal Transplant Patient.

Indian J Nephrol. 2017 Nov-Dec;27(6):482-483

Authors: Slim R, Asmar N, Yaghi C, Honein K, Sayegh R, Chelala D

Abstract
Drug-induced liver injury (DILI) represents liver damage from various therapeutic drugs. Antimicrobials are among the most common causes of DILI. We report a case of hepatic toxicity due to Trimethoprim-sulfamethoxazole (TMP-SMX) in a patient who underwent renal transplantation. Diagnosis has been made after a careful history taking, exclusion of competing etiologies and reversal of biochemical abnormalities after withdrawal of the antibiotic. TMP-SMX liver toxicity is well known but remains unpredictable and is rarely reported.

PMID: 29217891 [PubMed]

Post-reperfusion bronchospasm in a deceased donor liver transplant recipient: An enigma.

Sat, 12/09/2017 - 13:45
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Post-reperfusion bronchospasm in a deceased donor liver transplant recipient: An enigma.

Indian J Anaesth. 2017 Nov;61(11):939-940

Authors: Bharath K, Nandhakumar A, Singh H, Shanmugam V

PMID: 29217864 [PubMed]

Accessible Pediatric Liver Transplantation in India: A Long way to go.

Sat, 12/09/2017 - 13:45
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Accessible Pediatric Liver Transplantation in India: A Long way to go.

Indian Pediatr. 2017 Nov 15;54(11):911-912

Authors: Rela M, Shanmugham NP

PMID: 29217801 [PubMed - in process]

Hepatitis delta virus persists during liver regeneration and is amplified through cell division both in vitro and in vivo.

Sat, 12/09/2017 - 13:45
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Hepatitis delta virus persists during liver regeneration and is amplified through cell division both in vitro and in vivo.

Gut. 2017 Dec 07;:

Authors: Giersch K, Bhadra OD, Volz T, Allweiss L, Riecken K, Fehse B, Lohse AW, Petersen J, Sureau C, Urban S, Dandri M, Lütgehetmann M

Abstract
OBJECTIVE: Hepatitis delta virus (HDV) was shown to persist for weeks in the absence of HBV and for months after liver transplantation, demonstrating the ability of HDV to persevere in quiescent hepatocytes. The aim of the study was to evaluate the impact of cell proliferation on HDV persistence in vitro and in vivo.
DESIGN: Genetically labelled human sodium taurocholate cotransporting polypeptide (hNTCP)-transduced human hepatoma(HepG2) cells were infected with HBV/HDV and passaged every 7 days for 100 days in the presence of the entry inhibitor Myrcludex-B. In vivo, cell proliferation was triggered by transplanting primary human hepatocytes (PHHs) isolated from HBV/HDV-infected humanised mice into naïve recipients. Virological parameters were measured by quantitative real time polymerase chain reaction (qRT-PCR). Hepatitis delta antigen (HDAg), hepatitis B core antigen (HBcAg) and cell proliferation were determined by immunofluorescence.
RESULTS: Despite 15 in vitro cell passages and block of viral spreading by Myrcludex-B, clonal cell expansion permitted amplification of HDV infection. In vivo, expansion of PHHs isolated from HBV/HDV-infected humanised mice was confirmed 3 days, 2, 4 and 8 weeks after transplantation. While HBV markers rapidly dropped in proliferating PHHs, HDAg-positive hepatocytes were observed among dividing cells at all time points. Notably, HDAg-positive cells appeared in clusters, indicating that HDV was transmitted to daughter cells during liver regeneration even in the absence of de novo infection.
CONCLUSION: This study demonstrates that HDV persists during liver regeneration by transmitting HDV RNA to dividing cells even in the absence of HBV coinfection. The strong persistence capacities of HDV may also explain why HDV clearance is difficult to achieve in HBV/HDV chronically infected patients.

PMID: 29217749 [PubMed - as supplied by publisher]

Incidence, clinical findings, and survival of hepatosplenic T-cell lymphoma in the United States.

Sat, 12/09/2017 - 13:45
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Incidence, clinical findings, and survival of hepatosplenic T-cell lymphoma in the United States.

Am J Hematol. 2017 Jun;92(6):E99-E101

Authors: Durani U, Go RS

PMID: 28263402 [PubMed - indexed for MEDLINE]

The Impact of the New Kidney Allocation System on Prior Living Kidney Donors' Access to Deceased Donor Kidney Transplants: An Early Look.

Sat, 12/09/2017 - 13:45
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The Impact of the New Kidney Allocation System on Prior Living Kidney Donors' Access to Deceased Donor Kidney Transplants: An Early Look.

Am J Transplant. 2017 Apr;17(4):1103-1111

Authors: Wainright JL, Kucheryavaya AY, Klassen DK, Stewart DE

Abstract
This study investigated the early effects of the new kidney allocation system (KAS) on the access of prior living kidney donors (PLDs) to deceased donor kidney transplants. Using data from the Organ Procurement and Transplantation Network, we compared prevalent and incident cohorts of PLDs in the 1-year periods before and after KAS implementation (pre-KAS group: December 4, 2013, to December 3, 2014, n = 50 [newly listed PLDs]; post-KAS group: December 4, 2014, to December 3, 2015, n = 39). We assessed transplant rates per active patient-year, waiting times, and Kidney Donor Profile Index (KDPI) of transplanted kidneys. Transplant rates were not statistically different before and after KAS implementation for either prevalent (2.37 vs. 2.29, relative risk [RR] 0.96; 95% confidence interval [CI] 0.62-1.49) or incident (4.76 vs. 4.36, RR 0.92; 95% CI 0.53-1.60) candidates. Median waiting time (MWT) to deceased donor kidney transplant for prevalent PLDs in the post-KAS cohort was 102.6 days compared with 82.3 days in the pre-KAS cohort (p = 0.98). The median KDPI for PLD recipients was 31% with KAS versus 23% before KAS (p = 0.02). Despite a sharp decrease in the MWT for highly prioritized candidates with calculated panel reactive antibodies of 98-100% (from >7000 to 1164 days), PLDs still had much shorter waiting times (MWT 102.6 days). The new system continues to provide quick access to high-quality organs for PLDs.

PMID: 27805305 [PubMed - indexed for MEDLINE]

How to do liver transplantation using renoportal bypass.

Fri, 12/08/2017 - 13:45

How to do liver transplantation using renoportal bypass.

ANZ J Surg. 2017 Dec 07;:

Authors: Grezzana-Filho TJM, Chedid MF, Chedid AD, Bassani-Filho EL, Pereira PF, Leipnitz I, Backes AN, Kruel CRP

PMID: 29216680 [PubMed - as supplied by publisher]

Gluten peptides drive healthy and celiac monocytes toward an M2-like polarization.

Fri, 12/08/2017 - 13:45

Gluten peptides drive healthy and celiac monocytes toward an M2-like polarization.

J Nutr Biochem. 2017 Nov 05;54:11-17

Authors: Barilli A, Gaiani F, Prandi B, Cirlini M, Ingoglia F, Visigalli R, Rotoli BM, de'Angelis N, Sforza S, de'Angelis GL, Dall'Asta V

Abstract
Celiac disease (CD) is an immune-mediated enteropathy triggered by ingested gluten in genetically susceptible individuals and sustained by both adaptive and innate immune responses. Recent studies in murine macrophages demonstrated that the activation of arginase (ARG) metabolic pathway by gluten peptides contributes to the modulation of intestinal permeability in vitro. Here we characterize the effects of gluten on arginine metabolism and cell polarization in human monocytes from both healthy and CD subjects; both a simplified enzymatic digestion of gliadin and a physiological digestion of whole wheat have been tested. Results indicate that gluten digests induce the onset of an M2-like phenotype in activated macrophages; more precisely, both isoforms of arginase, ARG1 and ARG2, are induced likely due to the inhibition of mTOR and the consequent induction of C/EBPβ transcription factor. These effects are independent from the origin of gluten as well as from the digestive protocol employed; moreover, no statistical difference can be evidenced between healthy and CD patients, excluding a diverse predisposition of CD monocytes to gluten-triggered polarization with respect to healthy immune cells. Overall, the present findings sustain a role for arginase pathway in the immune response elicited by human monocytes toward ingested gluten that, hence, deserves particular attention when addressing the pathogenesis of CD.

PMID: 29216605 [PubMed - as supplied by publisher]

Nigella sativa oil modulates the therapeutic efficacy of mesenchymal stem cells against liver injury in irradiated rats.

Fri, 12/08/2017 - 13:45

Nigella sativa oil modulates the therapeutic efficacy of mesenchymal stem cells against liver injury in irradiated rats.

J Photochem Photobiol B. 2017 Dec 02;178:447-456

Authors: Radwan RR, Mohamed HA

Abstract
Stem cell transplantation is a novel strategy for regenerative medicine in liver disease. This study was conducted to explore the modulatory effect of Nigella sativa oil (NSO) on the therapeutic potential of mesenchymal stem cells (MSCs) against irradiation-induced liver damage in rats. Liver damage was induced by a total body exposure to a single dose of 7Gy. NSO (2mg/kg/day) was then given orally for 4 consecutive weeks starting 24h after irradiation with or without a single intravenous MSCs administration, then rats were sacrificed four weeks after exposure to γ radiation. Data revealed that irradiation elevated aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities in serum, increased hepatic malondialdehyde (MDA) content and reduced hepatic superoxide dismutase (SOD) activity. Furthermore, it caused elevation in pro-inflammatory mediators such as interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) associated with reduction in anti-inflammatory cytokine interleukin-10 (IL-10) and it increased fibrogenic marker transforming growth factor-β (TGF-β) in liver tissues. It was observed that combined NSO/MSCs therapy provided more beneficial tissue repair comparable to MSCs alone as demonstrated by modulating the tested parameters. Finally, these results were confirmed by histopathological examination. In conclusion, dual therapy with NSO and MSCs could serve as a promising approach for alleviating radiation-induced liver injury in patients with radiotherapy.

PMID: 29216568 [PubMed - as supplied by publisher]

Living donor liver transplantation for adult Budd Chiari syndrome - Resection without replacement of retrohepatic IVC: A case report.

Fri, 12/08/2017 - 13:45

Living donor liver transplantation for adult Budd Chiari syndrome - Resection without replacement of retrohepatic IVC: A case report.

Int J Surg Case Rep. 2017 Dec 01;42:50-54

Authors: Sabra TA, Okajima H, Tajima T, Fukumitsu K, Hata K, Yasuchika K, Masui T, Taura K, Kaido T, Uemoto S

Abstract
INTRODUCTION: Suprahepatic caval resection and replacement of inferior vena cava (IVC) is standard procedure in deceased donor liver transplantation for patients with Budd-Chiari syndrome (BCS). However, replacement of IVC in living donor liver transplantation (LDLT) is difficult. We report a case of BCS successfully treated by LDLT without replacement of IVC.
PRESENTATION OF CASE: A 52-years-old female with a primary BCS due to IVC thrombosis. A vena cava (VC) stent placed after angioplasty without improvement of the hepatic, portal venous flow and liver functions, Transjugular intrahepatic portosystemic shunt was considered and the patient had a rapid deterioration and increased ascites. The patient was scheduled for living donor liver transplantation (LDLT). Her Child-Paugh and MELD scores were 11, 18, respectively at time of transplantation. Left lobe was obtained from her son. Preservation of the native suprarenal IVC was impossible due to massive fibrosis and thrombosed. The suprahepatic IVC was also fibrotic and unsuitable for anastomosis with hepatic vein. The retrohepatic IVC resected include suprahepatic IVC together with the liver. The supradiaphragmatic IVC was reached and encircled through opening the diaphragm around the IVC and a vascular clamp applied on the right atrium with subsequent anastomosis with hepatic vein of the graft. The hemodynamic stability of the patient was maintained throughout the operation without IVC replacement due to developed collateral vessels.
CONCLUSION: Patients with Budd-Chiari syndrome with obstructive IVC are successfully treated with living donor liver transplantation without replacement of IVC.

PMID: 29216531 [PubMed - as supplied by publisher]

Sessile serrated adenoma/polyp leading to acute appendicitis with multiple pyogenic liver abscesses: A case report.

Fri, 12/08/2017 - 13:45

Sessile serrated adenoma/polyp leading to acute appendicitis with multiple pyogenic liver abscesses: A case report.

Int J Surg Case Rep. 2017 Dec 02;42:38-43

Authors: Sato K, Banshodani M, Nishihara M, Nambu J, Kawaguchi Y, Shimamoto F, Dohi K, Sugino K, Ohdan H

Abstract
INTRODUCTION: Although appendicitis is a common disease, appendicitis concurrent with liver abscesses and sessile serrated adenoma/polyp (SSA/P) is rare.
PRESENTATION OF CASE: A 69-year-old man presented with symptoms of abdominal pain and fever. Computed tomography (CT) revealed multiple liver abscesses and an enlarged appendix with a pseudotumoral appearance, which suggested acute appendicitis. In the emergency operation, ileocecal resection was performed for the perforated appendicitis with an inflammatory mass in the ileocecum. On macroscopic examination, the torose lesion was localized at next to the appendiceal orifice. The tumor was diagnosed as SSA/P based on the microscopic finding. The postoperative course was uneventful, and the liver abscesses were cured by antibiotic therapy. The patient was discharged 17days after the surgery.
DISCUSSION: In this case, SSA/P localization at next to the appendiceal orifice was suggested as the cause of the perforated appendicitis with multiple liver abscesses. The patient was successfully treated with a combination of surgery and antibiotic therapy.
CONCLUSION: This is the first reported case of a patient with SSA/P that led to acute appendicitis with multiple pyogenic liver abscesses.

PMID: 29216529 [PubMed - as supplied by publisher]

Systematic integrative analysis of gene expression identifies HNF4A as the central gene in pathogenesis of non-alcoholic steatohepatitis.

Fri, 12/08/2017 - 13:45

Systematic integrative analysis of gene expression identifies HNF4A as the central gene in pathogenesis of non-alcoholic steatohepatitis.

PLoS One. 2017;12(12):e0189223

Authors: Baciu C, Pasini E, Angeli M, Schwenger K, Afrin J, Humar A, Fischer S, Patel K, Allard J, Bhat M

Abstract
Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in the Western world, and encompasses a spectrum from simple steatosis to steatohepatitis (NASH). There is currently no approved pharmacologic therapy against NASH, partly due to an incomplete understanding of its molecular basis. The goal of this study was to determine the key differentially expressed genes (DEGs), as well as those genes and pathways central to its pathogenesis. We performed an integrative computational analysis of publicly available gene expression data in NASH from GEO (GSE17470, GSE24807, GSE37031, GSE89632). The DEGs were identified using GEOquery, and only the genes present in at least three of the studies, to a total of 190 DEGs, were considered for further analyses. The pathways, networks, molecular interactions, functional analyses were generated through the use of Ingenuity Pathway Analysis (IPA). For selected networks, we computed the centrality using igraph package in R. Among the statistically significant predicted networks (p-val < 0.05), three were of most biological interest: the first is involved in antimicrobial response, inflammatory response and immunological disease, the second in cancer, organismal injury and development and the third in metabolic diseases. We discovered that HNF4A is the central gene in the network of NASH connected to metabolic diseases and that it regulates HNF1A, an additional transcription regulator also involved in lipid metabolism. Therefore, we show, for the first time to our knowledge, that HNF4A is central to the pathogenesis of NASH. This adds to previous literature demonstrating that HNF4A regulates the transcription of genes involved in the progression of NAFLD, and that HNF4A genetic variants play a potential role in NASH progression.

PMID: 29216278 [PubMed - in process]

A multi-scale spatial model of hepatitis-B viral dynamics.

Fri, 12/08/2017 - 13:45

A multi-scale spatial model of hepatitis-B viral dynamics.

PLoS One. 2017;12(12):e0188209

Authors: Cangelosi Q, Means SA, Ho H

Abstract
Chronic hepatitis B viral infection (HBV) afflicts around 250 million individuals globally and few options for treatment exist. Once infected, the virus entrenches itself in the liver with a notoriously resilient colonisation of viral DNA (covalently-closed circular DNA, cccDNA). The majority of infections are cleared, yet we do not understand why 5% of adult immune responses fail leading to the chronic state with its collateral morbid effects such as cirrhosis and eventual hepatic carcinoma. The liver environment exhibits particularly complex spatial structures for metabolic processing and corresponding distributions of nutrients and transporters that may influence successful HBV entrenchment. We assembled a multi-scaled mathematical model of the fundamental hepatic processing unit, the sinusoid, into a whole-liver representation to investigate the impact of this intrinsic spatial heterogeneity on the HBV dynamic. Our results suggest HBV may be exploiting spatial aspects of the liver environment. We distributed increased HBV replication rates coincident with elevated levels of nutrients in the sinusoid entry point (the periportal region) in tandem with similar distributions of hepatocyte transporters key to HBV invasion (e.g., the sodium-taurocholate cotransporting polypeptide or NTCP), or immune system activity. According to our results, such co-alignment of spatial distributions may contribute to persistence of HBV infections, depending on spatial distributions and intensity of immune response as well. Moreover, inspired by previous HBV models and experimentalist suggestions of extra-hepatic HBV replication, we tested in our model influence of HBV blood replication and observe an overall nominal effect on persistent liver infection. Regardless, we confirm prior results showing a solo cccDNA is sufficient to re-infect an entire liver, with corresponding concerns for transplantation and treatment.

PMID: 29216213 [PubMed - in process]

Long-term Results and Quality of Life Assessment in Biliary Atresia Patients: A 35-Year Experience in a Tertiary Hospital.

Fri, 12/08/2017 - 13:45

Long-term Results and Quality of Life Assessment in Biliary Atresia Patients: A 35-Year Experience in a Tertiary Hospital.

J Pediatr Gastroenterol Nutr. 2017 Dec 05;:

Authors: Wong CWY, Chung PHY, Tam PKH, Wong KKY

Abstract
OBJECTIVES: To review long-term transplant-free survival and quality of life of patients with biliary atresia.
METHODS: A retrospective study reviewing all patients with Kasai operation between 1 January 1980 and 31 December 2015 was performed to evaluate the transplant-free survival. Subgroup analysis of patients over 20 years old was carried out to assess the quality of life using the Short Form-36 Health Survey and incidences of disease-related complications. Comparison between patients with native and transplanted liver was performed using two-tailed independent samples t-test (p-value < 0.05=significant).
RESULTS: The 20-year Kaplan-Meier transplant-free survival of the 141 patients in our study was 51%. The subgroup analysis of long-term survivors revealed a trend of increased prevalence of complications like esophageal varices, portal hypertension and recurrent admissions in the patient groups with raised serum bilirubin.Thirty-one patients were successfully contacted for quality of life assessment, 26 (16 with native liver and 10 with transplanted liver) responded (76.5%). BA patients who were documented to have active complications have a significantly lower vitality score (50.7 versus 57.5, p = 0.015). There was no statistically significant difference in the scores between the transplanted group and the disease-free control group. However, the native liver group achieved a lower score in both the general health section (42.9 versus 49.6, p = 0.029) and the overall physical component (49.6 versus 54.4, p = 0.037).
CONCLUSIONS: A significant proportion of our patients survive with their native liver for over 20 years. These long-term survivors may suffer from complications that impair their quality of life. They require continuous life-long care.

PMID: 29216021 [PubMed - as supplied by publisher]

[Study of migration and distribution of bone marrow cells transplanted animals with B16 melanoma ].

Fri, 12/08/2017 - 13:45

[Study of migration and distribution of bone marrow cells transplanted animals with B16 melanoma ].

Patol Fiziol Eksp Ter. 2017 Apr-Jun;61(2):10-21

Authors: Poveshchenko AF, Solovieva AO, Zubareva KE, Strunkin DN, Gricyk OB, Poveshchenko OV, Shurlygina AV, Konenkov VI

Abstract
Purpose. Reveal features migration and distribution of syngeneic bone marrow cells (BMC) and subpopulations (MSC) after transplantation into the recipient carrier B16 melanoma bodies. Methods. We used mouse male and female C57BL/6 mice. Induction of Tumor Growth: B16 melanoma cells implanted subcutaneously into right hind paw of female C57BL/6 mice at a dose of 2.5 x 105 cells / mouse. migration study in vivo distribution and BMC and MSC was performed using genetic markers - Y-chromosome specific sequence line male C57Bl/6 syngeneic intravenous transplantation in females using the polymerase chain reaction (PCR) in real time on Authorized Termal Cycler - Light Cycler 480 II / 96 (Roche). Introduction suspension of unseparated bone marrow cells, mesenchymal stem cells from donor to recipient male mice (syngeneic recipient female C57BL/6), followed by isolation of recipients of organs was performed at regular intervals, then of organ recipients isolated DNA. Results. It was shown that bone marrow cells positive for Y-chromosome in migrate lymphoid (lymph nodes, spleen, bone marrow) or in non-lymphoid organs (liver, heart, brain, skin) syngeneic recipients. In addition to the migration of cells from the bone marrow to other organs, there is a way back migration of cells from the circulation to the bone marrow. B16 melanoma stimulates the migration of transplanted MSCs and BMC in bone marrow. It is found that tumor growth enhanced migration of transplanted bone marrow cells, including populations of MSCs in the bone marrow. In the early stages of tumor formation MSC migration activity higher than the BMC. In the later stages of tumor formation undivided population of bone marrow cells migrate to the intense swelling compared with a population of MSCs. Conclusion. The possibility of using bone marrow MSCs for targeted therapy of tumor diseases, because migration of MSCs in tumor tissue can be used to effectively deliver anticancer drugs.

PMID: 29215830 [PubMed - as supplied by publisher]

Plasma MicroRNA-21, 26a, and 29a-3p as Predictive Markers for Treatment Response Following Transarterial Chemoembolization in Patients with Hepatocellular Carcinoma.

Fri, 12/08/2017 - 13:45

Plasma MicroRNA-21, 26a, and 29a-3p as Predictive Markers for Treatment Response Following Transarterial Chemoembolization in Patients with Hepatocellular Carcinoma.

J Korean Med Sci. 2018 Jan 01;33(1):e6

Authors: Kim SS, Cho HJ, Nam JS, Kim HJ, Kang DR, Won JH, Kim J, Kim JK, Lee JH, Kim BH, Lee MY, Cho SW, Cheong JY

Abstract
BACKGROUND: We investigated an association between the levels of plasma microRNA (miRNA)-21, -26a, and -29a-3p and treatment outcomes following transarterial chemoembolization (TACE) in patients with hepatocellular carcinoma (HCC).
METHODS: A total of 198 patients with TACE-treated HCC were followed up for TACE refractoriness and liver transplantation (LT)-free survival. Pretreatment plasma miRNA-21, -26a, and -29a-3p levels were measured using quantitative real-time polymerase chain reaction.
RESULTS: During the mean follow-up of 22.3 (range, 0.7-79) months, 118 (59.6%) patients exhibited TACE refractoriness. Multivariate analyses showed that expression of a specific combination of miRNAs (miRNA-21 ≥ 2.5, miRNA-26a ≥ 1.5, and miRNA-29a-3p < 0.4) was associated with early TACE refractoriness (within 1 year; hazard ratio [HR], 2.32; 95% confidence interval [CI], 1.08-4.99; P = 0.031) together with tumor size (HR, 4.62; 95% CI, 1.50-14.21; P = 0.008), and macrovascular invasion (HR, 3.80; 95% CI, 1.19-12.20; P = 0.025). However, miRNA-21, -26a, and -29a-3p levels were not significantly associated with overall TACE refractoriness or LT-free survival. Additionally, large tumor size and macrovascular invasion were common predictive factor of overall TACE refractoriness and survival.
CONCLUSION: Combination of plasma miRNA-21, -26a, and -29a-3p expression could predict early TACE refractoriness in patients with TACE-treated HCC.

PMID: 29215815 [PubMed - in process]

Kidney Transplantation in Patients with Atypical Hemolytic Uremic Syndrome due to Complement Factor H Deficiency: Impact of Liver Transplantation.

Fri, 12/08/2017 - 13:45

Kidney Transplantation in Patients with Atypical Hemolytic Uremic Syndrome due to Complement Factor H Deficiency: Impact of Liver Transplantation.

J Korean Med Sci. 2018 Jan 01;33(1):e4

Authors: Kim S, Park E, Min SI, Yi NJ, Ha J, Ha IS, Cheong HI, Kang HG

Abstract
BACKGROUND: Atypical hemolytic uremic syndrome (aHUS) is a rare disease that is often associated with genetic defects. Mutations of complement factor H (CFH) are the most common genetic defects that cause aHUS and often result in end-stage renal disease. Since CFH is mainly produced in the liver, liver transplantation (LT) has been performed in patients with defective CFH.
METHODS: The clinical courses of four kidney allograft recipients who lost their native kidney functions due to aHUS associated with a CFH mutation were reviewed.
RESULTS: Subject A underwent kidney transplantation (KT) twice, aHUS recurred and the allograft kidney failed within a few years. Subject B received a KT and soon experienced a recurrence of aHUS coinciding with infection. Her allograft kidney function has worsened, and she remains on plasma infusion therapy. Subject C underwent LT followed by KT. She is doing well without plasma infusion therapy after combined LT-KT for 3 years. Subject D received KT following LT and is now recurrence-free from aHUS.
CONCLUSION: In patients with aHUS associated with a CFH mutation, KT without LT was complicated with a recurrence of aHUS, which might lead to allograft loss. Conversely, LT was successful in preventing the recurrence of aHUS and thus might be another option for a recurrence-free life for aHUS patients associated with CFH mutation.

PMID: 29215813 [PubMed - in process]

Preserved Liver Transplant After PD-1 Pathway Inhibitor for Hepatocellular Carcinoma.

Fri, 12/08/2017 - 13:45

Preserved Liver Transplant After PD-1 Pathway Inhibitor for Hepatocellular Carcinoma.

Am J Gastroenterol. 2017 Dec;112(12):1895-1896

Authors: Varkaris A, Lewis DW, Nugent FW

PMID: 29215617 [PubMed - in process]

Liver Transplantation in Cryptogenic Cirrhosis: Outcome comparisons between NASH, Alcoholic and AIH cirrhosis.

Fri, 12/08/2017 - 13:45

Liver Transplantation in Cryptogenic Cirrhosis: Outcome comparisons between NASH, Alcoholic and AIH cirrhosis.

Transplantation. 2017 Dec 05;:

Authors: Thuluvath PJ, Hanish S, Savva Y

Abstract
BACKGROUND: The outcomes of liver transplantation (LT) in patients with cryptogenic cirrhosis (CC) have not been adequately examined except for small case series. We believe that patients currently listed as CC have truly cryptogenic liver disease and may have different post-LT outcomes compared to nonalcoholic steatohepatitis (NASH).
METHODS: We compared the post-LT outcomes of adults with CC (n=3241) and compared them with cirrhosis from NASH (n=4089), alcohol (AC, n=7837) and autoimmune hepatitis (AIH, n=1435) using the UNOS database from 2002-16. We excluded those who had multi-organ transplantation and hepatocellular carcinoma. In addition to the well-known predictors of liver transplant outcomes, we analyzed the impact of Karnofsky Performance Status (KPS) score at LT on immediate and late outcomes.
RESULTS: There were significant differences in clinical characteristics between the groups. Despite these differences in clinical characteristics and risk factors, CC had similar graft and patient survival to NASH, AC and AIH when assessed by Kaplan-Meier survival. Multivariate Cox regression analysis showed that graft and patient survival was similar in all 4 groups after adjusting for other confounders. Hispanics had a 24% lower risk of death (Hazard Ratio {HR} 0.76) compared to Whites in these combined cohorts after adjusting for all risk factors. In addition to other known risk factors, KPS score of 30% or less was associated with a 33% increase in risk of death (HR 1.33) on multivariate analysis.
CONCLUSION: Patients with CC had similar graft and patient survival when compared to NASH, AC and AIH cirrhosis.

PMID: 29215462 [PubMed - as supplied by publisher]

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