Displaying publications 1 - 20 of 37 in total

Abstract:
Sort:
  1. Maiwall R, Pasupuleti SSR, Choudhury A, Kim DJ, Sood A, Goyal O, et al.
    Hepatol Int, 2023 Jun;17(3):662-675.
    PMID: 36571711 DOI: 10.1007/s12072-022-10463-z
    BACKGROUND AND AIM: Acute-on-chronic liver failure (ACLF) is a severe form of alcoholic hepatitis (SAH). We aimed to study the natural course, response to corticosteroids (CS), and the role of the Asian Pacific Association for the Study of Liver (APASL) research consortium (AARC) score in determining clinical outcomes in AH patients.

    METHODS: Prospectively collected data from the AARC database were analyzed.

    RESULTS: Of the 1249 AH patients, (aged 43.8 ± 10.6 years, 96.9% male, AARC score 9.2 ± 1.9), 38.8% died on a 90 day follow-up. Of these, 150 (12.0%) had mild-moderate AH (MAH), 65 (5.2%) had SAH and 1034 (82.8%) had ACLF. Two hundred and eleven (16.9%) patients received CS, of which 101 (47.87%) were steroid responders by day 7 of Lille's model, which was associated with improved survival [Hazard ratio (HR) 0.15, 95% CI 0.12-0.19]. AARC-ACLF grade 3 [OR 0.28, 0.14-0.55] was an independent predictor of steroid non-response and mortality [HR 3.29, 2.63-4.11]. Complications increased with degree of liver failure [AARC grade III vs. II vs I], bacterial infections [48.6% vs. 37% vs. 34.7%; p liver transplant.

    Matched MeSH terms: Acute-On-Chronic Liver Failure*
  2. Tan SS
    Med J Malaysia, 2005 Jul;60 Suppl B:133-5.
    PMID: 16108194
    Matched MeSH terms: Liver Failure/surgery; Liver Failure/therapy*
  3. Boey CC
    Med J Malaysia, 2005 Jul;60 Suppl B:90-3.
    PMID: 16108184
    Matched MeSH terms: Liver Failure/surgery*
  4. Verma N, Dhiman RK, Singh V, Duseja A, Taneja S, Choudhury A, et al.
    Hepatol Int, 2021 Jun;15(3):753-765.
    PMID: 34173167 DOI: 10.1007/s12072-021-10175-w
    BACKGROUND: Multiple predictive models of mortality exist for acute-on-chronic liver failure (ACLF) patients that often create confusion during decision-making. We studied the natural history and evaluated the performance of prognostic models in ACLF patients.

    METHODS: Prospectively collected data of ACLF patients from APASL-ACLF Research Consortium (AARC) was analyzed for 30-day outcomes. The models evaluated at days 0, 4, and 7 of presentation for 30-day mortality were: AARC (model and score), CLIF-C (ACLF score, and OF score), NACSELD-ACLF (model and binary), SOFA, APACHE-II, MELD, MELD-Lactate, and CTP. Evaluation parameters were discrimination (c-indices), calibration [accuracy, sensitivity, specificity, and positive/negative predictive values (PPV/NPV)], Akaike/Bayesian Information Criteria (AIC/BIC), Nagelkerke-R2, relative prediction errors, and odds ratios.

    RESULTS: Thirty-day survival of the cohort (n = 2864) was 64.9% and was lowest for final-AARC-grade-III (32.8%) ACLF. Performance parameters of all models were best at day 7 than at day 4 or day 0 (p  12 had the lowest 30-day survival (5.7%).

    CONCLUSIONS: APASL-ACLF is often a progressive disease, and models assessed up to day 7 of presentation reliably predict 30-day mortality. Day-7 AARC model is a statistically robust tool for classifying risk of death and accurately predicting 30-day outcomes with relatively lower prediction errors. Day-7 AARC score > 12 may be used as a futility criterion in APASL-ACLF patients.

    Matched MeSH terms: Acute-On-Chronic Liver Failure*
  5. Rosmawati M
    Med J Malaysia, 2005 Jul;60 Suppl B:125-6.
    PMID: 16108192
    Matched MeSH terms: Liver Failure, Acute/classification*; Liver Failure, Acute/etiology*; Liver Failure, Acute/pathology
  6. Ganesalam K
    Med J Malaysia, 2005 Jul;60 Suppl B:127-32.
    PMID: 16108193
    Matched MeSH terms: Liver Failure, Acute/complications; Liver Failure, Acute/etiology; Liver Failure, Acute/physiopathology*
  7. Ansari RM, Omar NS
    Malays J Med Sci, 2017 May;24(3):1-4.
    PMID: 28814927 DOI: 10.21315/mjms2017.24.3.1
    Dietary health supplements for weight loss seem to be the future nowadays. However, this industry is plagued by lack of regulations and ignorance regarding the constituents of the supplements. Of all the supplements consumed, the ones for weight loss are most commonly found in the market. Reports of liver failure, kidney impairment and worsening of chronic ailments in patients who consume these supplements are surfacing recently which make us question the credibility of these products. The safety of these products lie in the clear stating of the ingredients by the manufacturer, well informed patient, knowledgeable physician and tight regulations from the regulatory board.
    Matched MeSH terms: Liver Failure
  8. Ooi ET, Ganesananthan S, Anil R, Kwok FY, Sinniah M
    Med J Malaysia, 2008 Dec;63(5):401-5.
    PMID: 19803300
    This is a retrospective study of the gastrointestinal symptoms, signs and laboratory parameters in adult dengue patients admitted to Kuala Lumpur Hospital from 1st December 2004 to 31st December 2004. Clinical and laboratory parameters that may predict the need for intensive care were investigated. Six hundred sixty-six patients with clinical and biochemical features consistent with dengue infection were identified. Patients were stratified into those who required intensive care and those who were managed in non high dependency wards. Serum alanine aminotransaminase (ALT) levels were normal in 22.8% of patients and 5.9% of patients had acute fulminant hepatitis. More patients with dengue haemorrhagic fever (DHF) had elevated ALT levels as compared to patients with classic dengue fever (DF) (p = 0.012). Patients with DF had a statistically significant lower mean ALT level as compared to patients with DHF. Abdominal pain (p = 0.01) and tenderness (p<0.001), gastrointestinal bleed (p<0.001), jaundice (p<0.001), hepatomegaly (p<0.001) and ascites (p<0.001) were predictors of need for intensive care. We conclude that gastrointestinal manifestations are very common in dengue patients. Presence of abdominal pain and tenderness, gastrointestinal bleed, jaundice, hepatomegaly and ascites can be used to triage patients requiring intensive care.
    Matched MeSH terms: Liver Failure, Acute/blood; Liver Failure, Acute/diagnosis; Liver Failure, Acute/therapy; Liver Failure, Acute/virology*
  9. Pham TS, Reda A, Ngan Nguyen TT, Ng SJ, Huan VT, Viet DC, et al.
    Transfus Apher Sci, 2020 Dec;59(6):102907.
    PMID: 32883595 DOI: 10.1016/j.transci.2020.102907
    We report a case of blood exchange transfusion to treat acute liver failure following hepatitis B infection at the Infectious Disease Department of Children's Hospital No.2 in Ho Chi Minh City, Vietnam. A 3.5-month old baby boy was admitted to the hospital with a presentation of progressively worsening jaundice for the past one month. The patient was diagnosed with hepatitis B infection with a positive HBV DNA quantitative assay. Plasma exchange was indicated in view of progressive liver failure and gradually increasing hepatic coma. However, it was impossible to perform plasmapheresis in this case because the patient was small (in terms of age and weight) and there was no suitable plasma exchange filter. Accordingly, the patient was treated with 3 times of blood exchange transfusion in combination with an antiviral drug, lamivudine. After each blood exchange transfusion, the biochemical values (bilirubin, liver enzymes, and coagulation profile) gradually improved and he was discharged after 1 month of treatment. Blood exchange transfusion is an effective procedure for managing acute liver failure, where plasma exchange is not possible while waiting for the recovery of liver functions or liver transplantation.
    Matched MeSH terms: Liver Failure, Acute/therapy*
  10. Choudhury A, Jindal A, Maiwall R, Sharma MK, Sharma BC, Pamecha V, et al.
    Hepatol Int, 2017 Sep;11(5):461-471.
    PMID: 28856540 DOI: 10.1007/s12072-017-9816-z
    BACKGROUND AND AIMS: Acute-on-chronic liver failure (ACLF) is a progressive disease associated with rapid clinical worsening and high mortality. Early prediction of mortality and intervention can improve patient outcomes. We aimed to develop a dynamic prognostic model and compare it with the existing models.

    METHODS: A total of 1402 ACLF patients, enrolled in the APASL-ACLF Research Consortium (AARC) with 90-day follow-up, were analyzed. An ACLF score was developed in a derivation cohort (n = 480) and was validated (n = 922).

    RESULTS: The overall survival of ACLF patients at 28 days was 51.7%, with a median of 26.3 days. Five baseline variables, total bilirubin, creatinine, serum lactate, INR and hepatic encephalopathy, were found to be independent predictors of mortality, with AUROC in derivation and validation cohorts being 0.80 and 0.78, respectively. AARC-ACLF score (range 5-15) was found to be superior to MELD and CLIF SOFA scores in predicting mortality with an AUROC of 0.80. The point scores were categorized into grades of liver failure (Gr I: 5-7; II: 8-10; and III: 11-15 points) with 28-day cumulative mortalities of 12.7, 44.5 and 85.9%, respectively. The mortality risk could be dynamically calculated as, with each unit increase in AARC-ACLF score above 10, the risk increased by 20%. A score of ≥11 at baseline or persisting in the first week was often seen among nonsurvivors (p = 0.001).

    CONCLUSIONS: The AARC-ACLF score is easy to use, dynamic and reliable, and superior to the existing prediction models. It can reliably predict the need for interventions, such as liver transplant, within the first week.

    Matched MeSH terms: Acute-On-Chronic Liver Failure/mortality*
  11. Lee WS, Sokol RJ
    J Pediatr, 2013 Oct;163(4):942-8.
    PMID: 23810725 DOI: 10.1016/j.jpeds.2013.05.036
    Matched MeSH terms: Liver Failure, Acute/diagnosis; Liver Failure, Acute/genetics*; Liver Failure, Acute/therapy*
  12. Sarin SK, Choudhury A, Sharma MK, Maiwall R, Al Mahtab M, Rahman S, et al.
    Hepatol Int, 2019 11;13(6):826-828.
    PMID: 31595462 DOI: 10.1007/s12072-019-09980-1
    The article Acute-on-chronic liver failure: consensus recommendations of the Asian Pacific association for the study of the liver (APASL): an update, written by [Shiv Sarin], was originally published electronically on the publisher's internet portal (currently SpringerLink) on June 06, 2019 without open access.
    Matched MeSH terms: Acute-On-Chronic Liver Failure
  13. Devarbhavi H, Aithal G, Treeprasertsuk S, Takikawa H, Mao Y, Shasthry SM, et al.
    Hepatol Int, 2021 Apr;15(2):258-282.
    PMID: 33641080 DOI: 10.1007/s12072-021-10144-3
    Idiosyncratic drug-induced liver injury mimics acute and chronic liver disease. It is under recognized and underrecognised because of the lack of pathognomonic diagnostic serological markers. Its consequences may vary from being asymptomatic to self-limiting illness to severe liver injury leading to acute liver failure. Its incidence is likely to be more common in Asia than other parts of the world, mainly because of hepatotoxicity resulting from the treatment of tuberculosis disease and the ubiquitous use of traditional and complimentary medicines in Asian countries. This APASL consensus guidelines on DILI is a concise account of the various aspects including current evidence-based information on DILI with special emphasis on DILI due to antituberculosis agents and traditional and complementary medicine use in Asia.
    Matched MeSH terms: Liver Failure, Acute
  14. Anand L, Choudhury A, Bihari C, Sharma BC, Kumar M, Maiwall R, et al.
    Hepatology, 2019 08;70(2):587-596.
    PMID: 30113706 DOI: 10.1002/hep.30205
    Autoimmune hepatitis (AIH) is considered less common in the Asia Pacific region. Due to this, AIH flare as a cause of acute on chronic liver failure (ACLF) is often overlooked and treatment delayed. We aimed at the defining clinical and histopathological spectrum and role of steroid therapy in AIH-ACLF. Patients with AIH-ACLF, prospectively recruited and followed between 2012 and 2017, were analyzed from the Asian Pacific Association for the Study of the Liver ACLF Research Consortium (AARC) data base. Diagnosis of AIH was confirmed using International Autoimmune Hepatitis Group score or simplified AIH score with histopathological evidence. Of 2,825 ACLF patients, 82 (2.9%) fulfilled criteria of AIH (age 42.1 ± 18.1 years, 70% female). At baseline, mean bilirubin was 18.6 ± 8.2 mg/dL, Child-Turcotte-Pugh score was 11.7 ± 1.4, and Model for End-Stage Liver Disease (MELD) score was 27.6 ± 6.5. Mean immunoglobulin G was 21.61 ± 7.32 g/dL, and this was elevated ≥1.1 times in 97% of cases; 49% were seronegative. Liver histology was available in 90%, with median histological activity index of 10 (interquartile range, 7-12); 90% with moderate to severe interface activity; 56% showing significant parenchymal necrosis (bridging and confluent necrosis); and cirrhosis in 42%. Twenty-eight (34%) patients received steroid therapy and showed shorter intensive care unit (ICU) stay (median 1.5 versus 4 days, P < 0.001) and improved 90-day survival (75% versus 48.1%, P = 0.02) with comparable incidence of sepsis (P = 0.32) compared to those who did not. Patients of advanced age, more severe liver disease (MELD >27; 83.3% sensitivity, 78.9% specificity, area under the receiver operating characteristic curve 0.86), presence of hepatic encephalopathy, and fibrosis grade ≥F3 had an unfavorable response to corticosteroid therapy. Conclusion: AIH presenting as ACLF is not uncommon in Asian patients; a low threshold for liver biopsy is needed to confirm the diagnosis as nearly half the patients are seronegative; early stratification to steroid therapy or liver transplantation (MELD >27, hepatic encephalopathy in ≥F3) would reduce ICU stay and improve outcomes.
    Matched MeSH terms: Acute-On-Chronic Liver Failure/diagnosis*; Acute-On-Chronic Liver Failure/drug therapy*; Acute-On-Chronic Liver Failure/etiology
  15. Choudhury A, Kumar M, Sharma BC, Maiwall R, Pamecha V, Moreau R, et al.
    J Gastroenterol Hepatol, 2017 Dec;32(12):1989-1997.
    PMID: 28374414 DOI: 10.1111/jgh.13799
    BACKGROUND AND AIM: Systemic inflammatory response syndrome (SIRS) is an early marker of sepsis and ongoing inflammation and has been reported in large proportion of acute-on-chronic liver failure (ACLF) patients. Whether sepsis is the cause or the result of liver failure is unclear and is vital to know. To address this, the study investigated the course and outcome of ACLF patients without SIRS/sepsis.

    METHODS: Consecutive ACLF patients were monitored for the development of SIRS/sepsis and associated complications and followed till 90 days, liver transplant or death.

    RESULTS: Of 561 patients, 201 (35.8%) had no SIRS and 360 (64.2%) had SIRS with or without infection. New onset SIRS and sepsis developed in 74.6% and 8% respectively in a median of 7 (range 4-15) days, at a rate of 11% per day. The cumulative incidence of new SIRS was 29%, 92.8%, and 100% by days 4, 7, and 15. Liver failure, that is, bilirubin > 12 mg/dL (odds ratio [OR] = 2.5 [95% confidence interval {CI} = 1.05-6.19], P = 0.04) at days 0 and 4, and renal failure at day 4 (OR = 6.74 [95%CI = 1.50-13.29], P = 0.01), independently predicted new onset SIRS. Absence of SIRS in the first week was associated with reduced incidence of organ failure (20% vs 39.4%, P = 0.003), as was the 28-day (17.6% vs 36%, P = 0.02) and 90-day (27.5% vs 51%,P = 0.002) mortality. The 90-day mortality was 61.6% in the total cohort and that for those having no SIRS and SIRS at presentation were 42.8% and 65%, respectively (P Liver failure predicts the development of SIRS. New onset SIRS in the first week is an important determinant of early sepsis, organ failure, and survival. Prompt interventions in this 'golden window' before development of sepsis may improve the outcome of ACLF.

    Matched MeSH terms: Acute-On-Chronic Liver Failure/complications*; Acute-On-Chronic Liver Failure/diagnosis; Acute-On-Chronic Liver Failure/mortality; Acute-On-Chronic Liver Failure/therapy*
  16. Balasubramaniam S, Choy YS, Talib A, Norsiah MD, van den Heuvel LP, Rodenburg RJ
    JIMD Rep, 2012;5:113-22.
    PMID: 23430926 DOI: 10.1007/8904_2011_107
    Mitochondrial disorders are a heterogeneous group of often multisystemic and early fatal diseases caused by defects in the oxidative phosphorylation (OXPHOS) system. Given the complexity and intricacy of the OXPHOS system, it is not surprising that the underlying molecular defect remains unidentified in many patients with a mitochondrial disorder. Here, we report the clinical features and diagnostic workup leading to the elucidation of the genetic basis for a combined complex I and IV OXPHOS deficiency secondary to a mitochondrial translational defect in an infant who presented with rapidly progressive liver failure, encephalomyopathy, and severe refractory lactic acidemia. Sequencing of the GFM1 gene revealed two inherited novel, heterozygous mutations: a.539delG (p.Gly180AlafsX11) in exon 4 which resulted in a frameshift mutation, and a second c.688G > A (p.Gly230Ser) mutation in exon 5. This missense mutation is likely to be pathogenic since it affects an amino acid residue that is highly conserved across species and is absent from the dbSNP and 1,000 genomes databases. Review of literature and comparison were made with previously reported cases of this recently identified mitochondrial disorder encoded by a nuclear gene. Although limited in number, nuclear gene defects causing mitochondrial translation abnormalities represent a new, rapidly expanding field of mitochondrial medicine and should potentially be considered in the diagnostic investigation of infants with progressive hepatoencephalomyopathy and combined OXPHOS disorders.
    Matched MeSH terms: Liver Failure
  17. Balasubramaniam S, Wamelink MM, Ngu LH, Talib A, Salomons GS, Jakobs C, et al.
    J Pediatr Gastroenterol Nutr, 2011 Jan;52(1):113-6.
    PMID: 21119539 DOI: 10.1097/MPG.0b013e3181f50388
    Matched MeSH terms: Liver Failure, Acute/diagnosis; Liver Failure, Acute/etiology*; Liver Failure, Acute/metabolism
  18. Lee WS, McKiernan P, Kelly DA
    J Pediatr Gastroenterol Nutr, 2005 May;40(5):575-81.
    PMID: 15861019
    OBJECTIVE: To study the etiology, outcome and prognostic indicators in children with fulminant hepatic failure in the United Kingdom.
    DESIGN: Retrospective review of all patients <17 years with fulminant hepatic failure from 1991 to 2000. Fulminant hepatic failure was defined as presence of coagulopathy (prothrombin time >24 seconds or International Normalized Ratio >2.0) with or without hepatic encephalopathy within 8 weeks of the onset of symptoms.
    SETTING: Liver Unit, Birmingham Children's Hospital, United Kingdom.
    RESULTS: Ninety-seven children (48 male, 49 female; median age, 27 months; range, 1 day-192.0 months) were identified with fulminant hepatic failure. The etiologies were: 22 metabolic, 53 infectious, 19 drug-induced, and 3 autoimmune hepatitis. The overall survival rate was 61%. 33% (32/97) recovered spontaneously with supportive management. Fifty-five children were assessed for liver transplantation. Four were unstable and were not listed for liver transplantation; 11 died while awaiting liver transplantation. Liver transplantation was contraindicated in 10 children. Of the 40 children who underwent liver transplantation, 27 survived. Children with autoimmune hepatitis, paracetamol overdose or hepatitis A were more likely to survive without liver transplantation. Children who had a delay between the first symptom of liver disease and the onset of hepatic encephalopathy (median, 10.5 days versus 3.5 days), higher plasma bilirubin (299 micromol/L versus 80 micromol/L), higher prothrombin time (62 seconds versus 40 seconds) or lower alanine aminotransferase (1288 IU/L versus 2929 IU/L) levels on admission were more likely to die of fulminant hepatic failure or require liver transplantation (P < 0.05). On multivariate analysis, the significant independent predictors for the eventual failure of conservative therapy were time to onset of hepatic encephalopathy >7 days, prothrombin time >55 seconds and alanine aminotransferase =2384 IU/L on admission.
    CONCLUSIONS: Children with fulminant hepatic failure with severe coagulopathy, lower alanine aminotransferase on admission and prolonged duration of illness before the onset of hepatic encephalopathy are more likely to require liver transplantation. Early referral to a specialized center for consideration of liver transplantation is vital.
    Matched MeSH terms: Liver Failure, Acute/etiology*; Liver Failure, Acute/mortality; Liver Failure, Acute/therapy*
  19. Devarbhavi H, Choudhury AK, Sharma MK, Maiwall R, Al Mahtab M, Rahman S, et al.
    Am J Gastroenterol, 2019 06;114(6):929-937.
    PMID: 31021832 DOI: 10.14309/ajg.0000000000000201
    OBJECTIVES: Acute insults from viruses, infections, or alcohol are established causes of decompensation leading to acute-on-chronic liver failure (ACLF). Information regarding drugs as triggers of ACLF is lacking. We examined data regarding drugs producing ACLF and analyzed clinical features, laboratory characteristics, outcome, and predictors of mortality in patients with drug-induced ACLF.

    METHODS: We identified drugs as precipitants of ACLF among prospective cohort of patients with ACLF from the Asian Pacific Association of Study of Liver (APASL) ACLF Research Consortium (AARC) database. Drugs were considered precipitants after exclusion of known causes together with a temporal association between exposure and decompensation. Outcome was defined as death from decompensation.

    RESULTS: Of the 3,132 patients with ACLF, drugs were implicated as a cause in 329 (10.5%, mean age 47 years, 65% men) and other nondrug causes in 2,803 (89.5%) (group B). Complementary and alternative medications (71.7%) were the commonest insult, followed by combination antituberculosis therapy drugs (27.3%). Alcoholic liver disease (28.6%), cryptogenic liver disease (25.5%), and non-alcoholic steatohepatitis (NASH) (16.7%) were common causes of underlying liver diseases. Patients with drug-induced ACLF had jaundice (100%), ascites (88%), encephalopathy (46.5%), high Model for End-Stage Liver Disease (MELD) (30.2), and Child-Turcotte-Pugh score (12.1). The overall 90-day mortality was higher in drug-induced (46.5%) than in non-drug-induced ACLF (38.8%) (P = 0.007). The Cox regression model identified arterial lactate (P < 0.001) and total bilirubin (P = 0.008) as predictors of mortality.

    DISCUSSION: Drugs are important identifiable causes of ACLF in Asia-Pacific countries, predominantly from complementary and alternative medications, followed by antituberculosis drugs. Encephalopathy, bilirubin, blood urea, lactate, and international normalized ratio (INR) predict mortality in drug-induced ACLF.

    Matched MeSH terms: Acute-On-Chronic Liver Failure/chemically induced*; Acute-On-Chronic Liver Failure/diagnosis; Acute-On-Chronic Liver Failure/epidemiology
  20. Tan SS, Bujang MA
    Braz J Infect Dis, 2013 Mar-Apr;17(2):164-9.
    PMID: 23453417 DOI: 10.1016/j.bjid.2012.09.007
    OBJECTIVE: To describe the clinical manifestations and outcome of acute liver failure (ALF) associated with dengue viral infection, a rare but severe complication.
    METHODS: One hundred and fifty five consecutive patients with ALF admitted to the national liver centre from 2001 to 2009 were reviewed retrospectively. Eight cases due to dengue infection were identified and their clinical characteristics are described.
    RESULTS: All patients had severe dengue with one dengue shock syndrome. The median (minimum, maximum) age was 33.5 (17, 47) years with 50% female. The median (minimum, maximum) duration from the onset of fever to development of ALF was 7.5 (5, 13) days and the maximum hepatic encephalopathy (HE) grade were III in five patients and II in three patients. Three patients had systemic inflammatory responses (SIRS) on admission and were in grade III HE. The presence of SIRS on admission was associated with higher grade of HE and its development during the course of hospitalization was associated with worsening HE grade. The hepatitis was characterized by marked elevations in: alanine transaminase [median admission 1140.5 u/L (639, 4161); median peak 2487 u/L (998, 5181)], serum bilirubin [median admission 29 μmol/L (23, 291); median peak 127 μmol/L (72, 592)], and prothrombin time [median admission 16.8s (15.3, 26.2); median peak 22s (15.3, 40.7)]. The survival rate with standard medical therapy alone was 100%.
    CONCLUSIONS: Dengue associated ALF manifest about one week after the onset of fever with severe hepatitis and encephalopathy. In our experience, the outcome with standard medical therapy alone is excellent.
    Matched MeSH terms: Liver Failure, Acute/virology*
Filters
Contact Us

Please provide feedback to Administrator (afdal@afpm.org.my)

External Links