scholarly journals Spontaneous life-threatening hemobilia during acute liver failure successfully treated with transarterial embolization

2014 ◽  
Vol 97 (6) ◽  
pp. 361
Author(s):  
V Boecxstaens ◽  
S Heye ◽  
G Maleux ◽  
Ph Roelandt ◽  
D Cassiman ◽  
...  
Keyword(s):  
Liver Failure ◽  
Acute Liver Failure ◽  
Transarterial Embolization ◽  
Life Threatening

scholarly journals A Case of Exertional Heat Stroke Complicated by Hypoxic Hepatitis

2020 ◽  
Vol 2020 ◽  
pp. 1-4
Author(s):  
Bertram K. Woitok ◽  
Shawki Bahmad ◽  
Gregor Lindner
Keyword(s):  
Supportive Care ◽  
Liver Failure ◽  
Acute Liver Failure ◽  
Multiorgan Failure ◽  
Heat Stroke ◽  
Exertional Heat Stroke ◽  
Hypoxic Hepatitis ◽  
Threatening Condition ◽  
Life Threatening ◽  
Delayed Referral

Background.Exertional heat stroke is a life-threatening condition often complicated by multiorgan failure. We hereby present a case of a 25-year-old male presenting with syncope after a 10  km run in 28°C outside temperature who developed acute liver failure. Case Presentation. Initial temperature was found to be 41.1°C, and cooling measures were rapidly applied. He suffered from acute renal failure and rhabdomyolysis and proceeded to acute liver failure (ASAT 6100 U/l and ALAT 6561 U/l) due to hypoxic hepatitis on day 3. He did not meet criteria for emergency liver transplantation and recovered on supportive care. Conclusions. Acute liver failure due to heat stroke is a life-threatening condition with often delayed onset, which nevertheless resolves on supportive care in the majority of cases; thus, a delayed referral to transplant seems to be reasonable.

scholarly journals ACTION OF VITAMIN E ON EXPERIMENTAL SEVERE ACUTE LIVER FAILURE

2017 ◽  
Vol 54 (2) ◽  
pp. 123-129 ◽  
Author(s):  
Fabiano Moraes MIGUEL ◽  
Elizângela Gonçalves SCHEMITT ◽  
Josieli Raskopf COLARES ◽  
Renata Minuzzo HARTMANN ◽  
Maria Isabel MORGAN-MARTINS ◽  
...  
Keyword(s):  
Vitamin E ◽  
Liver Failure ◽  
Acute Liver Failure ◽  
Clinical Syndrome ◽  
Control Group ◽  
Activity Levels ◽  
Liver Functions ◽  
Life Threatening ◽  
Hepatocyte Necrosis ◽  
The One

ABSTRACT BACKGROUND Severe Acute Liver Failure (ALF) is a life-threatening clinical syndrome characterized by hepatocyte necrosis, loss of hepatic architecture, and impairment of liver functions. One of the main causes of ALF is hepatotoxicity from chemical agents, which damage hepatocytes and result in increase of reactive oxygen species. The vitamin E isoform is the one with the strongest biological antioxidant activity. OBJECTIVE To evaluate the antioxidant effect of vitamin E in this ALF model. METHODS We used 56 rats (mean weight of 300 g) divided into eight groups, four groups assessed at 24 hours and 4 assessed at 48 hours after induction: control group (CO); Vitamin E (Vit. E); Thioacetamide (TAA) and Thioacetamide + Vitamina E (TAA+Vit.E). Rats were submitted to injections of thioacetamide (400 mg/kg i.p.) at baseline and 8 hours later. Vitamin E (100 mg/kg ip) was administered 30 minutes after the second dose of thioacetamide. The 48-hour group rats received two additional doses of vitamin E (24h and 36h). At 24h or 48 hours after the administration of the first dose of TAA, rats were weighed and anesthetized and their blood sampled for evaluation of liver integrity through enzymes aspartate aminotransferase (AST) and alanine aminotransferase (ALT). Liver tissue was sampled for assessment of lipid peroxidation (LPO) by the technique TBARS, antioxidant enzymes SOD, CAT, GPx and GST activity, levels of the NO 2 /NO 3 and histology by H&E in two times. The results were expressed as mean ± standard deviation and statistically analyzed by ANOVA followed by Student-Newman-Keuls, with P <0.05 considered as significant. RESULTS After treatment with vitamin E, we observed a reduction in liver enzymes AST (U/L) (101.32±19.45 in 24 hours and 97.85±29.65 in 48 hours) related to the TAA group (469.56± 0.69 in 24 hours and 598.23±55.45 in 48 hours) and ALT (U/L) (76.59±8.56 in 24 hours and 68.47±6.49 in 48 hours) compared to the TAA group (312.21±10.23 in 24 hours and 359.15±17.58 in 48 hours). There was a reduction of LPO (nmol/mg Prot) in the TAA+Vit.E group (0.77±0.07 in 24 hours and 0.95±0.08 in 48 hours) compared to the TAA group (1.50±0.07 in 24 hours e 1.65±0.16 in 48 hours). SOD decreased in the TAA+Vit.E group (49.48±9.47 in 24 hours and 62.45±18, 47 in 48 hours), related to the TAA group (98.46±15.48 in 24 hours and 154.13±21.46 in 48 hours), as well as GST (nmol/min/mg Prot) in the TAA+Vit.E group (350.57±36.93 in 24 hours and 453.29±13.84 in 48 hours) compared to the TAA group (561.57±64.56 in 24 hours and 673.43±38.13 in 48 hours). There was an increase in CAT (pmol/min/mg Prot) in the TAA+Vit.E group (3.40±0.44 in 24 hours and 3.0±0.35 in 48 hours) compared to the TAA group (1.65±0.21 in 24 hours and 1.86±0.42 in 48 hours). The GPx (nmol/min/mg Prot) increased in 24 hours in the TAA+Vit.E group (1.01±0.16) compared to the TAA group (0.41±0.04) and decreased in 48 hours (1.19±0.17) compared to the TAA group (1.76±0.21). There was a reduction in NO2/NO3 (mmol/L) levels in the TAA+Vit.E group (31.47±4.26 in 24 hours and 38.93±5.20 in 48 hours) compared to the TAA group (49.37±5.12 in 24 hours and 53.53±5.97 in 48 hours). The histopathological evaluation showed a decrease in liver injury (necrosis and inflammation) in both studied times. CONCLUSION These results suggest that vitamin E was able to protect the liver from lesions caused by thioacetamide.

scholarly journals Plasma Exchange as a Rescue Therapy for Acute Liver Failure

2021 ◽  
Author(s):  
Nupur B Patel ◽  
Anand Sharma ◽  
Itish Patnaik ◽  
Ashok Kumar
Keyword(s):  
Liver Failure ◽  
Acute Liver Failure ◽  
Plasma Exchange ◽  
Resource Constraints ◽  
Rescue Therapy ◽  
Therapeutic Option ◽  
Liver Function Tests ◽  
Threatening Condition ◽  
Life Threatening

Acute Liver Failure (ALF) is a life-threatening condition and often necessitates Liver Transplantation (LT). However, LT is not available to most patients in developing countries due to resource constraints. Here, authors presents a case of 30-year-old female with ALF and fulfilled the criteria for LT. The aetiology of ALF could not be diagnosed in her. Due to the lack of LT facilities, she was offered plasma exchange as a therapeutic option, which resulted in improvement in sensorium and Liver Function Tests (LFT) {bilirubin, International Normalised Ratio (INR), Aspartate Aminotransferase (AST), Alanine Aminotransferase (ALT)} over a period of two weeks. She was discharged and was doing well during follow-up. Plasma exchange is a less studied but potential treatment option for ALF when LT is not feasible.

Clinical and Biochemical Profile of Acute Liver Failure with Hepatic Encephalopathy in Children from Eastern Nepal

1970 ◽  
Vol 31 (2) ◽  
pp. 89-92
Author(s):  
Gauri Shankar Shah ◽  
Manoj Kumar Singh ◽  
Dheeraj Shah
Keyword(s):  
Hepatic Encephalopathy ◽  
Liver Failure ◽  
Acute Liver Failure ◽  
Preventive Measures ◽  
Community Education ◽  
Mortality Rates ◽  
Mushroom Poisoning ◽  
Factors Influencing ◽  
Study Results ◽  
Life Threatening

Introduction: Hepatic encephalopathy is a potentially reversible neurophyschiatric abnormality in the setting of liver failure. Acute liver failure (ALF) is a potentially life-threatening disorder in children. Objectives: The present study evaluated the clinical profile, outcome and factors influencing the outcome of children presenting with acute liver failure and hepatic encephalopathy presenting to a referral hospital of Eastern Nepal. Methodology: Thirty children (17 males and 13 females) were admitted with this diagnosis during two year period.Prospective study. Results: The most common cause of acute liver failure was mushroom poisoning seen in 30% of cases. Only 37% (11 out of 30) children survived, most of them in early stages (Stage I and II) of encephalopathy. Bleeding manifestations were significantly more common (P=0.002) in deaths as compared to survivors. Conclusion: As liver failure is associated with high mortality rates especially in absence of facilities for liver transplantation, efforts should be directed in favor of implementing preventive measures such as vaccination and community education to prevent toxin ingestion. Key Words: Acute liver failure; Hepatic encephalopathy; Mushroom poisoning DOI: 10.3126/jnps.v31i2.4639 J Nep Paedtr Soc 2010;31(2):89-92

Acute Liver Failure

2016 ◽  
Vol 27 (4) ◽  
pp. 420-429 ◽  
Author(s):  
Ami Grek ◽  
Lisa Arasi
Keyword(s):  
Renal Failure ◽  
Critical Care ◽  
Respiratory Failure ◽  
Mortality Rate ◽  
Liver Failure ◽  
Acute Liver Failure ◽  
Mortality Rates ◽  
The Past ◽  
Organ Systems ◽  
Life Threatening

Acute liver failure, also known as fulminant hepatic failure, is a rare life-threatening disease that has a high mortality rate and affects many organ systems. Causes of acute liver failure vary—it can be attributed to drugs, viruses, and other uncommon sources. Complications of liver failure can include encephalopathy, cerebral edema, sepsis, renal failure, gastrointestinal bleeding, and respiratory failure. Fortunately, with advances in critical care medicine and emergent liver transplant, mortality rates have decreased in the past decade. This article reviews acute liver failure, its manifestations in different organ systems, and its treatment.

scholarly journals A rare cause of acute liver failure due to haemophagocytic lymphohistiocytosis secondary to diffuse large B-cell lymphoma

JRSM Open ◽  
2021 ◽  
Vol 12 (3) ◽  
pp. 205427042098362
Author(s):  
Andrew Coppola ◽  
Chia Chey ◽  
Emma O’Donovan ◽  
Monira Rahman
Keyword(s):  
Liver Failure ◽  
Acute Liver Failure ◽  
B Cell ◽  
Immune Cell ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Haemophagocytic Lymphohistiocytosis ◽  
Large B Cell Lymphoma ◽  
Life Threatening ◽  
Large B Cell

Acute liver failure is a life-threatening condition commonly caused by drug-induced hepatotoxicity or viral hepatitides. However, there are a number of rarer causes such as haemophagocytic lymphohistiocytosis. Haemophagocytic lymphohistiocytosis is a syndrome of uncontrolled immune cell activation, triggered by infection or malignancy, which carries a high mortality. Whilst mild to moderate liver injury is commonly seen with haemophagocytic lymphohistiocytosis, acute liver failure has rarely been reported in adults. We present a case of a 74-year-old man with acute liver failure secondary to haemophagocytic lymphohistiocytosis triggered by undiagnosed large B-cell lymphoma. Initially treated for biliary sepsis, there was a delay in the diagnosis of haemophagocytic lymphohistiocytosis and despite initiating chemotherapy, he died soon after. This case highlights the importance of considering haemophagocytic lymphohistiocytosis as a rare cause of acute liver failure, as given the life-threatening potential of haemophagocytic lymphohistiocytosis, a prompt diagnosis may allow early initiation of chemotherapy for any chance of survival.

scholarly journals Case Report: Pediatric Recurrent Acute Liver Failure Caused by Neuroblastoma Amplified Sequence (NBAS) Gene Mutations

2021 ◽  
Vol 8 ◽  
Author(s):  
Bingxin Jiang ◽  
Fangfei Xiao ◽  
Xiaolu Li ◽  
Yongmei Xiao ◽  
Yizhong Wang ◽  
...  
Keyword(s):  
Liver Failure ◽  
Acute Liver Failure ◽  
Gene Mutations ◽  
Kidney Injury ◽  
Compound Heterozygote ◽  
Healthy Children ◽  
Whole Exome ◽  
Threatening Condition ◽  
Chinese Girl ◽  
Life Threatening

Acute liver failure (ALF) in childhood is a rapidly progressive, potentially life-threatening condition that occurs in previously healthy children of all ages. However, the etiology of ~50% of cases with pediatric ALF remains unknown. We herein report a 4-year-old Chinese girl with recurrent ALF (RALF) due to a mutation in the neuroblastoma amplified sequence (NBAS) gene. The patient had suffered from multiple episodes of fever-related ALF since early childhood. She had also suffered from acute kidney injury, hypertension, mild pulmonary hypertension, pleural effusion, and hypothyroidism. A novel compound heterozygote mutation, c.3596G&gt; A (p.C1199Y)/ex.9del (p.216-248del), in the NBAS gene was identified by whole-exome sequencing (WES). The missense mutation c.3596G&gt; A (p. C1199Y) was inherited from her father, and ex.9del (p.216-248del) was inherited from her mother. The patient was managed with intensive treatments, such as renal replacement therapy (CRRT), intravenous antibiotics, and glucose infusion, and was discharged after full recovery. We identified a novel compound heterozygote mutation in the NBAS gene that caused fever-related RALF in a Chinese child, which further expands the mutational spectrum of NBAS.

scholarly journals PTPN14 aggravates inflammation through promoting proteasomal degradation of SOCS7 in acute liver failure

2020 ◽  
Vol 11 (9) ◽  
Author(s):  
Beibei Fu ◽  
Songna Yin ◽  
Xiaoyuan Lin ◽  
Lei Shi ◽  
Yu Wang ◽  
...  
Keyword(s):  
Mouse Model ◽  
Liver Failure ◽  
Acute Liver Failure ◽  
Inhibitory Effect ◽  
Inflammatory Factors ◽  
Control Group ◽  
Inhibitory Effects ◽  
Ikk Complex ◽  
Systemic Disorder ◽  
Life Threatening

Abstract Acute liver failure (ALF) is a rare but life-threatening systemic disorder. The innate immune regulation has an important role in this process; however, the specific mechanisms are not completely clear. Using the LPS + D-GalN-induced ALF mouse model, we found that the survival rate of PTPN14-deficient mice was higher than that of the control group, while the release of inflammatory factors was significantly lower. We further showed that PTPN14 interacted with SOCS7, and promoted the degradation of SOCS7 through ubiquitination at K11 and K48, thereby reducing the protein level of SOCS7 and weakening the inhibitory effects on inflammatory factors. More importantly, SOCS7 blocked the NF-κB signaling pathway by preventing the activity of the IKK complex, and then reduced the expression of downstream inflammatory factors. In this study, we firstly reported the inhibitory effect of SOCS7 on the NF-κB pathway in the ALF mouse model and elucidated the mechanism of PTPN14–SOCS7–NF-κB axis in the regulation of inflammation. These results provide new insights into the clinical treatment of ALF.

scholarly journals Sunitinib-Induced Acute Liver Failure

2021 ◽  
pp. 17-21
Author(s):  
Anum Aqsa ◽  
Sami Droubi ◽  
Shivantha Amarnath ◽  
Hassan Al-Moussawi ◽  
Jeffrey Abergel
Keyword(s):  
Liver Injury ◽  
Liver Failure ◽  
Acute Liver Failure ◽  
Kinase Inhibitor ◽  
Drug Induced ◽  
Drug Induced Liver Injury ◽  
Therapy Initiation ◽  
Pancreatic Neuroendocrine Carcinoma ◽  
Life Threatening ◽  
Transient Elevation

Drug-induced liver injury is an uncommon but life-threatening entity. Sunitinib is a tyrosine kinase inhibitor used for advanced and imatinib-refractory gastrointestinal stromal tumors. It causes transient elevation in liver enzymes. The incidence of fatal acute liver failure is rare. Five cases of sunitinib-induced acute liver injury have been reported in the literature thus far. We present a case of fatal acute liver failure and cardiomyopathy within 2 weeks of sunitinib therapy initiation for advanced pancreatic neuroendocrine carcinoma. We believe our case is unique due to the rarity of its presentation. It highlights hepatotoxicity as a potentially fatal side effect of sunitinib therapy.

Sign in / Sign up

Export Citation Format

Share Document