[Adenovirus-related acute liver failure treated with intravenous immunoglobulin]. / Insuficiencia hepática aguda por adenovirus tratada con inmunoglobulina intravenos.

BACKGROUND: Acute liver failure in pediatric age is a serious multisystem disease, characterized by a failure of the synthesis and detoxification function of the liver. Among the etiologies, viral infection should be investigated. Treatment is supportive and some cases require liver transplantation. CASE REPORT: A 2-year-old girl was admitted for acute liver failure. The PCR viral panel was positive for Adenovirus 41 and IgG antibodies to SARS-CoV-2 were also found. Supportive treatment was started without improvement, so intravenous immunoglobulin was administered, with resolution of the liver failure. CONCLUSIONS: Immunoglobulin has immunomodulatory mechanisms in children with severe acute hepatitis of infectious etiology, so in some cases, its administration can be considered as adjuvant therapy.

ANTECEDENTES: La insuficiencia hepática aguda en pacientes pediátricos es una enfermedad multisistémica grave, caracterizada por falla de la función de síntesis y detoxificación del hígado. Dentro de su origen debe investigarse alguna infección viral. El tratamiento es de soporte y algunos casos requieren trasplante hepático. REPORTE DE CASO: Paciente pediátrica de 2 años, que ingresó al servicio médico por insuficiencia hepática aguda. El panel viral por PCR fue positivo para adenovirus 41 y anticuerpos IgG para SARS-CoV-2. Se inicio tratamiento de soporte sin reacción satisfactoria, por lo que se administró inmunoglobulina intravenosa, con resultados adecuados y curación de la insuficiencia hepática. CONCLUSIONES: La inmunoglobulina tiene mecanismos inmunomoduladores en pacientes pediátricos con hepatitis aguda grave de origen infeccioso, por lo que en algunos casos puede considerase su administración como terapia adyuvante.

A case report of Stevens-Johnson syndrome caused by omeprazole.

RATIONALE: Stevens-Johnson syndrome (SJS) is a rare but severe skin-mucosal reaction with a high mortality rate. It is characterized by sudden, painful blistering lesions on the skin, often accompanied by high fever and systemic toxicity. Lesions typically appear on the dorsal surfaces of the hands, feet, forearms, legs, and soles of the feet. They can also affect the conjunctiva, oral mucosa, labial mucosa, and vaginal mucosa. Patients may experience complications such as pneumonia, severe comorbidities, and liver and renal failure. PATIENT CONCERNS: A 51-year-old female patient was admitted to the hospital due to "abdominal distention and skin yellowing for 20 days." After using omeprazole, she developed a rash all over her body, and her liver function further deteriorated, ultimately leading to chronic acute liver failure. DIAGNOSES: The diagnosis included fever, rash suspected to be drug-induced, chronic and acute liver failure, and decompensation of post-Hepatitis B cirrhosis. INTERVENTIONS: During hospitalization, suspected adverse drug reactions were discontinued, and symptomatic supportive treatment with methylprednisolone and fluid replacement was promptly provided. OUTCOMES: The patient's symptoms and follow-up showed that the rash disappeared and liver and kidney function improved significantly after treatment. LESSONS: We explored how chronic acute liver failure can cause immune system abnormalities and immune paralysis in patients, manifested as susceptibility to infection. This case report describes a drug-induced allergic reaction - SJS - in patients with chronic acute liver failure, as well as subsequent treatment, including hormone dosage and treatment duration. I hope this report will help enrich the relevant literature on drug-induced SJS combined with chronic and acute liver failure, laying the foundation for improving the survival rate of patients with the disease.

Acute hepatitis A with haemophagocytic lymphohistiocytosis: G-6PD deficiency-induced haemolytic anaemia and bile cast nephropathy.

Hepatitis A virus (HAV) infection typically presents as a self-limiting illness but it can cause debilitating symptoms and rarely fulminant hepatitis (acute liver failure), which is often fatal. WHO estimates that in 2016, 7134 persons died from hepatitis A worldwide (accounting for 0.5% of the mortality due to viral hepatitis). Fulminant hepatic failure is observed in less than 1% of cases of acute viral hepatitis A. Haemophagocytic lymphohistiocytosis (HLH) is a clinical syndrome of excessive inflammation and tissue destruction owing to abnormal immune activation. Acquired HLH due to viral infections (also known as virus-associated haemophagocytic syndrome) is most commonly associated with Epstein-Barr virus and cytomegalovirus (CMV). HAV-associated HLH has been rarely reported. Haemolysis of mild to moderate degree is not unheard of in cases of hepatitis A, which is often immune-mediated. Here, we present the case of a man in his 30s, with G6PD deficiency unmasked by acute viral hepatitis A, which later on progressed to hyperacute liver failure, HLH and renal failure.

Role of therapeutic plasmapheresis in acute liver failure in paediatric patients: A case series.

Paediatric acute liver failure (PALF) is a rare yet severe condition that is associated with high mortality. Apart from liver transplant, no specific therapy exists, particularly in developing countries. Evidence suggests that removal of damage-associated molecular patterns, cytokines, toxins, and other metabolites that accumulate due to impaired liver function can enhance natural recovery. Plasmapheresis can be used to remove these products; however, there is limited evidence to support this approach. This case series discusses three critically ill patients with acute liver failure who underwent plasmapheresis. The patients included a seven-year-old boy (Case 1), a 17-year-old boy (Case 2), and a 16-monthold boy (Case 3). Two patients showed significant improvement in bilirubin level, coagulation profile, inotropes requirement, and Glasgow coma scale score. Unfortunately, one patient with PALF, complicated with multi-organ dysfunction, died due to refractory shock on the fourth day of hospitalisation. Our findings illustrate that early use of therapeutic plasmapheresis in PALF can lead to improvement in clinical outcome. It may serve as a bridging therapy for liver transplant and for the spontaneous regeneration of the patient's liver.

Acute Liver Failure as an Index Presentation of Hematolymphoid Malignancy: A Rare Case Report.

Acute liver failure (ALF) is usually due to viral hepatitis and toxins. We have recently seen a patient with diffuse large B-cell lymphoma (DLBCL) presenting with ALF. High clinical suspicion is necessary for making a diagnosis of this rare etiology presenting as ALF. The outcome is better if an early diagnosis is made in such cases and appropriate treatment is initiated.

Association between serum alkaline phosphatase and clinical prognosis in patients with acute liver failure following cardiac arrest: a retrospective cohort study.

BACKGROUND: Acute liver failure (ALF) following cardiac arrest (CA) poses a significant healthcare challenge, characterized by high morbidity and mortality rates. This study aims to assess the correlation between serum alkaline phosphatase (ALP) levels and poor outcomes in patients with ALF following CA. METHODS: A retrospective analysis was conducted utilizing data from the Dryad digital repository. The primary outcomes examined were intensive care unit (ICU) mortality, hospital mortality, and unfavorable neurological outcome. Multivariable logistic regression analysis was employed to assess the relationship between serum ALP levels and clinical prognosis. The predictive value was evaluated using receiver operator characteristic (ROC) curve analysis. Two prediction models were developed, and model comparison was performed using the likelihood ratio test (LRT) and the Akaike Information Criterion (AIC). RESULTS: A total of 194 patients were included in the analysis (72.2% male). Multivariate logistic regression analysis revealed that a one-standard deviation increase of ln-transformed ALP were independently associated with poorer prognosis: ICU mortality (odds ratios (OR) = 2.49, 95% confidence interval (CI) 1.31-4.74, P = 0.005), hospital mortality (OR = 2.21, 95% CI 1.18-4.16, P = 0.014), and unfavorable neurological outcome (OR = 2.40, 95% CI 1.25-4.60, P = 0.009). The area under the ROC curve for clinical prognosis was 0.644, 0.642, and 0.639, respectively. Additionally, LRT analyses indicated that the ALP-combined model exhibited better predictive efficacy than the model without ALP. CONCLUSIONS: Elevated serum ALP levels upon admission were significantly associated with poorer prognosis of ALF following CA, suggesting its potential as a valuable marker for predicting prognosis in this patient population.

Diagnosis, prevention and risk-management of drug-induced liver injury due to medications used to treat mycobacterium tuberculosis.

INTRODUCTION: Many of the first line medications for the treatment of active and latent M. tuberculosis are hepatoxic and cause a spectrum of anti-tuberculosis drug induced liver injury (ATLI), including acute liver failure (ALF). Despite advances in recognition of and prevention of ATLI, isoniazid remains one of the leading causes of DILI as well as drug-induced ALF. AREAS COVERED: A literature search of the incidence, risk factors, current societal guidelines, monitoring, and prophylactic medication usage in ATLI was performed using PubMed and institutional websites. Relevant articles from 1972 to 2024 were included in this review. EXPERT OPINION: Current societal guidelines regarding ATLI monitoring are mixed, but many recommend liver enzyme testing of high-risk populations. We recommend liver test monitoring for all patients on multi-drug therapy as well as those on isoniazid therapy. Precision medicine practices, such as N-acetyltransferase-2 polymorphism genotyping, are thought to be beneficial in reducing the incidence of ATLI in high-risk populations. However, broader implementation is currently cost prohibitive. Hepatoprotective drugs are not currently recommended, although we do recognize their potential. In patients who develop ATLI but require ongoing anti-TB treatment, strategies to restart the same or less hepatotoxic regimens are currently being followed.

Stealthy Invader: Clinically Inapparent But Rapidly Progressive Multifocal Metastatic Melanoma Unveiled as Root Cause of Liver Failure.

BACKGROUND: Acute liver failure (ALF) secondary to metastatic melanoma presents a rare and diagnostically challenging clinical scenario. CASE REPORT: We report the case of a 57-year-old male who succumbed to fulminant liver failure attributed to hepatic infiltration by malignant melanoma. Despite extensive diagnostic evaluation, the underlying cause of ALF remained elusive until postmortem examination revealed multifocal metastatic melanoma. Notably, the autopsy disclosed a remarkable finding: a 10 cm lymph node in the right axilla, conspicuously harboring metastatic melanoma cells. Surprisingly, this progressive lymph node was not detected on admission or during comprehensive imaging studies conducted 24 h prior to death. Rigorous cross-referencing of radiological and autopsy findings highlighted the accuracy of prior interventions visible on imaging, further accentuating the dynamic nature of metastatic melanoma progression. CONCLUSION: This case underscores the importance of vigilance in detecting metastatic melanoma, even in atypical sites, and emphasizes the need for multidisciplinary collaboration in complex clinical scenarios.

Clinical significance of transjugular liver biopsy in acute liver failure - a real-world analysis.

BACKGROUND: Histopathological characterization obtained by transjugular liver biopsy (TJLB) may theoretically contribute to clarification of the exact aetiology of acute liver failure (ALF). It's unclear whether the histopathological information from TJLB, due to the small specimen size, significantly contributes to diagnosing ALF causes, guiding therapy decisions, or predicting overall prognosis. This retrospective study aimed to analyse safety and clinical significance of TJLB in patients with ALF. METHODS: This retrospective, monocentric study investigated safety and efficacy of TJLB in patients with ALF over a ten-year period at a tertiary care transplant-center. The predictive value of various clinical and laboratory characteristics as well as histopathological findings obtained by TJLB on 28-day liver-transplant-free survival were evaluated by calculating uni- and multivariate Cox-proportional hazard regression models. Additional univariate logistic regression analyses were performed to explore the influence of degree of intrahepatic necrosis on the secondary endpoints intensive-care-unit (ICU) admission, need for endotracheal intubation, renal replacement therapy and high-urgency listing for LTX. RESULTS: A total of 43 patients with ALF receiving TJLB were included into the study. In most cases (n = 39/43 cases) TJLB confirmed the initially already clinically presumed ALF aetiology and the therapeutic approach was unchanged by additional histological examination in the majority of patients (36/43 cases). However, in patients with a high suspicion for aetiologies potentially treatable by medical immunosuppression (e.g. AIH, GvHD), TJLB significantly influenced further treatment planning and/or adjustment. While the degree of intrahepatic necrosis showed significance in the univariate analysis (p = 0.04), it did not demonstrate a significant predictive effect on liver transplant-free survival in the multivariate analysis (p = 0.1). Only consecutive ICU admission was more likely with higher extent of intrahepatic necrosis (Odds ratio (OR) 1.04 (95% CI 1-1.08), p = 0.046). CONCLUSIONS: Performance of TJLB in ALF led to a change in suspected diagnosis and to a significant change in therapeutic measures only in those patients with a presumed high risk for aetiologies potentially responsive to immunosuppressive therapy. Clinical assessment alone was accurate enough, with additional histopathological examination adding no significant value, to predict overall prognosis of patients with ALF.

Lactate as an early prognostic indicator in yellow phosphorus rodenticide-induced acute hepatic failure: a retrospective observational study in a tertiary care hospital.

INTRODUCTION: Acute hepatic failure due to yellow phosphorus rodenticide ingestion is often lethal. This study aimed to analyze demographic characteristics and prognostic indicators, focusing on hyperlactataemia as a potential early indicator of mortality in patients poisoned with yellow phosphorus rodenticide. MATERIALS AND METHODS: This was a retrospective study of 96 patients poisoned with a yellow phosphorus-containing rodenticide (Ratol paste, which contains 3% yellow phosphorus). We examined demographic details, clinical symptoms, and biochemical markers to identify prognostic indicators. RESULTS: Demographics were similar among survivors and non-survivors. Mortality (36.5%) correlated with a higher ingested dose and treatment delays, with a mean (±SD) of 5.26 ± 2.2 survival days among those who died. Symptoms, including gastrointestinal and neurological features, typically appeared 48 h after ingestion. Non-survivors developed increased aminotransferase activities (74.3%), prolonged prothrombin time (65.7%), and hyperbilirubinaemia (65.7%) during hospitalization, significantly more commonly compared to survivors (P < 0.0001). Hyperlactataemia (lactate concentration >2 mmol/L) was present in 97.1% of non-survivors, with increased serial lactate concentrations observed in 88.6%. The median (interquartile range) admission lactate concentration among non-survivors was 4.6 mmol/L (3.36-7.53 mmol/L), and their peak median (interquartile range) lactate concentration was 6.1 mmol/L (8.74-10.6 mmol/L). In non-survivors, an increased lactate concentration preceded increased aminotransferase activities and prolonged prothrombin time. Logistic regression and receiver operating characteristic curve analysis confirmed that a 24 h lactate concentration ≥2.67 mmol/L predicted death with 94.3% sensitivity and 91.8% specificity. DISCUSSION: The majority of patients who ingest yellow phosphorus remain asymptomatic initially and typically present to hospital following the onset of gastrointestinal symptoms, usually a day later. As progression to death occurs within a week of yellow phosphorus ingestion in most cases, determining prognosis as early as possible enables swift referral to a liver transplant centre. Based on our study, a 24 h lactate concentration ≥2.67 mmol/L appears to be an early prognostic indicator of death. In another study, a lactate concentration >5.8 mmol/L was found to be a poor prognostic indicator. CONCLUSIONS: Hyperlactataemia on admission and increased serial lactate concentrations appear to be early poor prognostic signs in patients with yellow phosphorus-induced liver failure.

Current Status and Outcomes of Living Donor Liver Transplantation for Pediatric Acute Liver Failure: Results From a Multicenter Retrospective Study Over Two Decades.

BACKGROUND: Although the outcomes of living donor liver transplantation (LDLT) for pediatric acute liver failure (PALF) have improved, patient survival remains lower than in patients with chronic liver disease. We investigated whether the poor outcomes of LDLT for PALF persisted in the contemporary transplant era. METHODS: We analyzed 193 patients who underwent LDLT between December 2000 and December 2020. The outcomes of patients managed in 2000-2010 (era 1) and 2011-2020 (era 2) were compared. RESULTS: The median age at the time of LDLT was 1.2 years both eras. An unknown etiology was the major cause in both groups. Patients in era 1 were more likely to have surgical complications, including hepatic artery and biliary complications (p = 0.001 and p = 0.013, respectively). The era had no impact on the infection rate after LDLT (cytomegalovirus, Epstein-Barr virus, and sepsis). The mortality rates of patients and grafts in era one were significantly higher (p = 0.03 and p = 0.047, respectively). The 1- and 5-year survival rates were 76.4% and 70.9%, respectively, in era 1, while they were 88.3% and 81.9% in era 2 (p = 0.042). Rejection was the most common cause of graft loss in both groups. In the multivariate analysis, sepsis during the 30 days after LDLT was independently associated with graft loss (p = 0.002). CONCLUSIONS: The survival of patients with PALF has improved in the contemporary transplant era. The early detection and proper management of rejection in patients, while being cautious of sepsis, should be recommended to improve outcomes further.

Acute liver failure.

Acute liver failure (ALF) is a life-threatening disorder characterised by rapid deterioration of liver function, coagulopathy, and hepatic encephalopathy in the absence of pre-existing liver disease. The cause of ALF varies across the world. Common causes of ALF in adults include drug toxicity, hepatotropic and non-hepatotropic viruses, herbal and dietary supplements, antituberculosis drugs, and autoimmune hepatitis. The cause of liver failure affects the management and prognosis, and therefore extensive investigation for cause is strongly suggested. Sepsis with multiorgan failure and cerebral oedema remain the leading causes of death in patients with ALF and early identification and appropriate management can alter the course of ALF. Liver transplantation is the best current therapy, although the role of artificial liver support systems, particularly therapeutic plasma exchange, can be useful for patients with ALF, especially in non-transplant centres. In this Seminar, we discuss the cause, prognostic models, and management of ALF.

KHSRP ameliorates acute liver failure by regulating pre-mRNA splicing through its interaction with SF3B1.

Acute liver failure (ALF) is characterized by the rapidly progressive deterioration of hepatic function, which, without effective medical intervention, results in high mortality and morbidity. Here, using proteomic and transcriptomic analyses in murine ALF models, we found that the expression of multiple splicing factors was downregulated in ALF. Notably, we found that KH-type splicing regulatory protein (KHSRP) has a protective effect in ALF. Knockdown of KHSRP resulted in dramatic splicing defects, such as intron retention, and led to the exacerbation of liver injury in ALF. Moreover, we demonstrated that KHSRP directly interacts with splicing factor 3b subunit 1 (SF3B1) and enhances the binding of SF3B1 to the intronic branch sites, thereby promoting pre-mRNA splicing. Using splicing inhibitors, we found that Khsrp protects against ALF by regulating pre-mRNA splicing in vivo. Overall, our findings demonstrate that KHSRP is an important splicing activator and promotes the expression of genes associated with ALF progression by interacting with SF3B1; thus, KHSRP could be a possible target for therapeutic intervention in ALF.

Novel insights into autophagy in gastrointestinal pathologies, mechanisms in metabolic dysfunction-associated fatty liver disease and acute liver failure.

In this editorial, we comment on three articles published in a recent issue of World Journal of Gastroenterology. There is a pressing need for new research on autophagy's role in gastrointestinal (GI) disorders, and also novel insights into some liver conditions, such as metabolic dysfunction-associated fatty liver disease (MAFLD) and acute liver failure (ALF). Despite advancements, understanding autophagy's intricate mechanisms and implications in these diseases remains incomplete. Moreover, MAFLD's pathogenesis, encompassing hepatic steatosis and metabolic dysregulation, require further elucidation. Similarly, the mechanisms underlying ALF, a severe hepatic dysfunction, are poorly understood. Innovative studies exploring the interplay between autophagy and GI disorders, as well as defined mechanisms of MAFLD and ALF, are crucial for identifying therapeutic targets and enhancing diagnostic and treatment strategies to mitigate the global burden of these diseases.

Case Report: Dengue Fever Progressing to Acute Liver Failure and Hepatic Encephalopathy.

Dengue fever is an important arboviral disease that significantly impacts the disease burden among populations residing in tropical regions. Dengue infection is known to have a broad spectrum of clinical manifestations, which range from fatal, life-threatening shock, encephalitis, and myocarditis to asymptomatic illness. Mild hepatic dysfunction with deranged hepatic laboratory parameters is a known entity with dengue fever. However, dengue presenting as acute liver failure associated with hepatic encephalopathy without shock or signs of plasma leakage is rare. Therefore, we are reporting the case of a young male with dengue fever presented as acute liver failure from a tertiary care center in central India to spread awareness among healthcare professionals worldwide regarding unusual presentations of dengue fever and consideration of dengue fever as a differential diagnosis in patients presenting with acute liver failure, especially in endemic regions.

[Liver transplantation in acute and acute-on-chronic liver failure]. / Lebertransplantation bei akutem und akut-auf-chronischem Leberversagen.

Acute liver failure (ALF) and acute-on-chronic liver failure (ACLF) are diseases with a rapidly progressive course and high mortality. Apart from treating the underlying triggers and intensive care measures, there are very limited therapeutic options for either condition. Liver transplantation is often the only life-saving treatment, but it cannot always be employed due to contraindications and severe disease progression. ACLF is characterized by underlying liver cirrhosis and typical triggers such as bacterial infections, bleeding, or alcohol binges. ALF occurs in previously healthy livers, usually as a result of purely hepatotoxic events. Disease differences are also reflected in the course and regulations of liver transplantation. Newer prognostic parameters and prioritization programs for ACLF can help improve both waiting list mortality and outcomes after transplantation.

Incidence of acute liver failure and its associated mortality in patients with dengue infection: A systematic review and meta-analysis.

Acute liver failure (ALF) is a devastating consequence of dengue infection. This systematic review and meta-analysis assessed the incidence of ALF in dengue infection and its associated mortality. We systematically searched the EMBASE and MEDLINE databases from inception to December 2023 for observational studies reporting ALF incidence and mortality in dengue patients. Twenty-one studies encompassing 26,839 dengue-infected patients were included. Meta-analysis revealed a pooled incidence of ALF in cases of general dengue infection of 2.0 % (95 % CI, 1.2-3.0 %), with 1.2 % (95 % CI, 0.6-2.1 %) in adults and 5.0 % (95 % CI, 1.5-10.2 %) in children. ALF incidence was 17.3 % (95 % CI, 6.5 %-31.5 %) in severe dengue and 7.4 % (95 % CI, 0.8-18.5 %) in dengue shock syndrome. The pooled mortality rate of dengue-associated ALF was 47.0 % (95 % CI, 32.9-61.2 %). These findings underscore the detrimental impact of dengue infection on the development of the relatively uncommon, albeit life-threatening, condition of ALF.

Understanding the molecular crossroads in acute liver failure: A pathway to new therapies.

In this editorial we comment on the article published in a recent issue of the World Journal of Gastroenterology. Acute liver failure (ALF) is a critical condition characterized by rapid hepatocellular injury and organ dysfunction, and it often necessitates liver transplant to ensure patient survival. Recent research has elucidated the involvement of distinct cell death pathways, namely ferroptosis and pyroptosis, in the pathogenesis of ALF. Ferroptosis is driven by iron-dependent lipid peroxidation, whereas pyroptosis is an inflammatory form of cell death; both pathways contribute to hepatocyte death and exacerbate tissue damage. This comprehensive review explores the interplay between ferroptosis and pyroptosis in ALF, highlighting the role of key regulators such as silent information regulator sirtuin 1. Insights from clinical and preclinical studies provide valuable perspectives on the dysregulation of cell death pathways in ALF and the therapeutic potential of targeting these pathways. Collaboration across multiple disciplines is essential for translating the experimental insights into effective treatments for this life-threatening condition.

Acute liver failure with a massive upper GI bleed meeting the criteria of MIS-C.

Multisystem inflammatory syndrome in children (MIS-C) is a known complication of COVID-19. There is still limited knowledge about this condition. Here, we report the case of a previously healthy toddler boy, who presented with acute liver failure and duodenal lesions resulting in severe haematemesis and haemorrhagic shock, requiring intensive care unit care. The patient had persistent transaminitis, a deranged coagulation profile, inflammatory markers were elevated, and laboratory tests were negative for common infectious hepatitis aetiologies as well as COVID-19 Reverse transcription polymerase chain reaction. His COVID-19 antibody was reactive. Upper gastrointestinal endoscopy revealed a Forrest grade III duodenal ulcer. Looking into the constellation of symptoms and laboratory findings a confirmed diagnosis of acute viral hepatitis caused by MIS-C was made. Hence, he was given intravenous methylprednisolone along with intravenous immunoglobulins, after which he improved clinically and transaminitis resolved. The patient was discharged on clinical improvement and was doing fine on follow-up up to 6 months.

[Fulminant acute liver failure secondary to severe dengue in a child: case report]. / Falla hepática aguda fulminante secundaria a dengue severo en un niño: reporte de un caso.

Dengue is a common infectious disease in tropical areas such as Peru. This virus can cause underreported and potentially fatal complications such as acute liver failure. We report the case of a 7-year-old boy who presented with fever, headache, and abdominal pain. On ultrasound, we found hepatomegaly and labs severe thrombocytopenia and elevated transaminases. During hospitalization he was diagnosed with severe dengue and developed acute liver failure, kidney injury, and encephalopathy. Although intensive care management and assisted ventilation, he developed multiple organ dysfunctions with fluid refractoriness and capillary leak. Acute liver failure secondary to severe dengue is a rare complication with an unfavorable outcome.