scholarly journals Acute Liver Failure with Diffuse Liver Metastasis from Breast Cancer, Not Detected by Computed Tomography: 2 Case Reports

2018 ◽  
Vol 11 (3) ◽  
pp. 699-704 ◽  
Author(s):  
Takatsugu Ogata ◽  
Yuichiro Kikawa ◽  
Misato Ogata ◽  
Hironaga Satake ◽  
Yukimasa Hatachi ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Computed Tomography ◽  
Liver Metastasis ◽  
Liver Failure ◽  
Acute Liver Failure ◽  
Hepatic Failure ◽  
Poor Prognosis ◽  
Alcoholic Hepatitis ◽  
Case Reports ◽  
History Of

Diffuse liver metastasis is a rare pattern of liver metastasis that is associated with hepatic failure and poor prognosis. We experienced 2 cases of acute liver failure due to diffuse metastasis that could not be detected using computed tomography. In case 1, it was difficult to differentiate diffuse metastasis from alcoholic hepatitis. In case 2, it was difficult to diagnose diffuse liver metastasis because the patient had no history of malignancy. When liver enzyme levels are elevated, it is necessary to consider liver metastasis as a potential cause, regardless of computed tomography findings.

Late Increase of Peripheral CD34+ Cells Number during Acute Liver Failure Recovery.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 4223-4223
Author(s):  
Bernard Drénou ◽  
Anne Corlu ◽  
Yoann Desille ◽  
Christèle Sicot ◽  
Olivier Fardel ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Liver Function ◽  
Liver Failure ◽  
Acute Liver Failure ◽  
Acute Hepatitis ◽  
Hepatic Failure ◽  
Alcoholic Hepatitis ◽  
Factor V ◽  
Cd34 Cells ◽  
Over Time

Abstract Human Hematopoietic Stem Cells (HSC) of bone marrow origin are reported to transdifferentiate into various cell types, including cells of hepatic lineage, and to be involved in hepatic repopulation. As it has been previously reported in the course of myocardial infarction, we hypothesized that CD34+ cells would appear early in severe acute liver failure and could predict a favourable outcome. Methods: We quantified circulating CD34+ cells in peripheral blood of 146 patients without and with severe hepatic failure (HF) defined by factor V <50%: 20 acute hepatitis with HF, 26 acute alcoholic hepatitis with HF, 22 major right hepatectomy (6/23 developped HF) and 78 controls (31 healthy subjects, 23 cirrhosis, 24 cirrhosis with chronic HF). CD34+ cells were quantified by flow cytometry, according to ISHAGE guidelines in both one and dual platform approaches. Phenotypic and functional analyses were performed in selected cases. In case of acute HF, quantification was done every day until correction of liver function. One patient underwent liver transplantation. The number of circulating CD34+ cells was correlated with factor V level. Results were presented using median and range. Results : At inclusion, the numbers of CD34+ cells /mm3 were similar in different groups (healthy controls = 1.0 [0.1– 4.0]; cirrhosis = 0.9 [0.1–5.1]; cirrhosis with chronic HF = 1.0 [0.1–3.7]; alcoholic hepatitis with HF = 1.2 [0.1–6.0]; liver resection 24H after surgery = 0.8 [0.2–3.2]; acute hepatitis with HF = 0.7 [0.2–3.1]. For patients with acute hepatitis with HF, the number of CD34+ increased over time, from 0.7 [0.2–3.1] to 1.8 [0.5–9.6] at the 4th day after admission and was significantly (p <10–3) correlated with correction of factor V. There was no correlation between the number of CD34+ and the time between admission and onset of the disease. There was no significant increase over time in the hepatectomy group nor in the alcoholic hepatitis group. CD34+ cells detected during acute hepatitis regeneration presented an immature phenotype and coexpressed CD33, CD90, CD133, CD117, CD135 (FLT3-R), CD38, HLA-DR and not V-Cadherin. Clonogenic progenitor cell assays did not reveal specific features and correlation between number of CD34 and BFU-E colonies were in favour of their hematopoietic potentiality. Conclusion: By contrast with data reported in acute myocardial infarction in which early mobilisation of CD34+ cells was observed, we found that the increase of circulating CD34+ HSC is a late event occurring at the time of the recovery of liver function in acute severe hepatic failure. The hematopoietic potentiality of mobilized CD34+ cells suggests that they do not play a major role in liver repopulation in fulminant acute hepatitis.

scholarly journals Fulminant Hepatic Failure Due to Dengue

2012 ◽  
Vol 9 (2) ◽  
pp. 73-75 ◽  
Author(s):  
A Sedhain ◽  
S Adhikari ◽  
S Regmi ◽  
S K Chaudhari ◽  
M Shah ◽  
...  
Keyword(s):  
Platelet Count ◽  
Liver Failure ◽  
Acute Liver Failure ◽  
Hepatic Failure ◽  
Case Reports ◽  
Acute Hepatic Failure ◽  
Reye's Syndrome ◽  
Medical College ◽  
Healthy Female ◽  
Major Outbreak

Dengue Fever (DF) is only rarely considered as a cause of acute liver failure even globally and only a few case reports of acute hepatic failure and encephalopathy occurring in DF in adults are available. We report a case of Acute Liver Failure due to Dengue during a major outbreak in 2010 in Chitwan. A 20 year old previously healthy female presented to the emergency department of Chitwan Medical College with fever, jaundice and altered sensorium. She was tested positive for Dengue IgM. Her biochemical and clinical parameters were suggestive of acute liver failure with total billirubin of 10.1 mg/dL, direct billirubin of 5.2 mg/dL, ALT 5760 IU, AST 14100 IU, alkaline phosphatase of 1250 IU, PT INR of 1.76 and platelet count of 30,000 /mm3. Other causes for acute hepatic failure like acute viral hepatitis, leptospirosis, malaria, Reye’s syndrome were ruled out. The patient was admitted and managed in the ICU with supportive care and platelet transfusion. With treatment she made a significant clinical and biochemical improvement with AST of 105 IU, ALT of 120 IU and platelet count of 150,000/mm3. She was discharged after 11 days of hospital stay.DOI: http://dx.doi.org/10.3126/kumj.v9i2.6293 Kathmandu Univ Med J 2011;9(2):73-5

scholarly journals Analysis of the safety of pretransplant corticosteroid therapy in patients with acute liver failure and late‐onset hepatic failure in Japan

JGH Open ◽  
2021 ◽  
Vol 5 (4) ◽  
pp. 428-433
Author(s):  
Takuro Hisanaga ◽  
Isao Hidaka ◽  
Isao Sakaida ◽  
Nobuaki Nakayama ◽  
Akio Ido ◽  
...  
Keyword(s):  
Liver Failure ◽  
Acute Liver Failure ◽  
Corticosteroid Therapy ◽  
Hepatic Failure ◽  
Late Onset ◽  
Late Onset Hepatic Failure

scholarly journals Acute Liver Failure due to Miliary Liver Metastasis

2020 ◽  
Vol 7 (3) ◽  
pp. e00294
Author(s):  
Charles A. Lavender ◽  
Jessica Stout ◽  
Hui-Yong Chung ◽  
Michael Johnson ◽  
Ragesh B. Thandassery
Keyword(s):  
Liver Metastasis ◽  
Liver Failure ◽  
Acute Liver Failure

Acute Fulminant Hepatic Failure in a Woman Treated With Phenytoin and Trimethoprim-Sulfamethoxazole

2000 ◽  
Vol 124 (12) ◽  
pp. 1800-1803 ◽  
Author(s):  
Marius J-M. Ilario ◽  
Jose E. Ruiz ◽  
Constantine A. Axiotis
Keyword(s):  
Liver Injury ◽  
Liver Failure ◽  
Acute Liver Failure ◽  
Fulminant Hepatic Failure ◽  
Hepatic Failure ◽  
Acute Hepatic Failure ◽  
Hepatic Necrosis ◽  
Rare Occurrence ◽  
Autopsy Findings ◽  
Massive Hepatic Necrosis

Abstract Massive hepatic necrosis following exposure to phenytoin and trimethoprim-sulfamethoxazole is a rare occurrence and to the best of our knowledge has not been reported previously. Acute hepatic failure following administration of trimethoprim-sulfamethoxazole has rarely been seen, and only 4 cases have been well documented pathologically. We report a case of acute liver failure in a 60-year-old woman following ingestion of phenytoin and trimethoprim-sulfamethoxazole concomitantly over a 9-day period. Autopsy findings revealed acute fulminant hepatic failure. This case demonstrates the effects of chemical-chemical interactions in the potentiation of hepatotoxicity of single agents and specifically illustrates the need for discontinuing trimethoprim-sulfamethoxazole in the presence of early liver injury.

scholarly journals The Role of Acetyl Cysteine in Cocaethylene (Non-Acetaminophen) Acute Liver Failure

2018 ◽  
Vol 2018 ◽  
pp. 1-4
Author(s):  
Getaw Worku Hassen ◽  
Amaninder Dhaliwal ◽  
Catherine Ann Jenninigs ◽  
Hossein Kalantari
Keyword(s):  
Emergency Department ◽  
Substance Abuse ◽  
Liver Failure ◽  
Liver Transplant ◽  
Acute Liver Failure ◽  
Active Substance ◽  
Vital Signs ◽  
Normal Limits ◽  
History Of ◽  
Acetyl Cysteine

Background.Acute liver failure can result from acetaminophen overdose, viral infection, toxins, and other disease conditions. Liver transplant is available in limited fashion and the criteria are strict as to who should get an available liver. N- Acetyl Cysteine (NAC) has been used in non-acetaminophen induced liver failure with success. Here we report a case of acute liver failure from cocaethylene that was reversed with NAC along with other medical therapy.Case Presentation.A 50-year-old female patient presented to the Emergency Department (ED) with a two-day history of coffee ground vomiting and hematemesis. She reported occasional substance abuse and heavy alcoholism. She reported shortness of breath and chest pain from the recurrent forceful vomiting. The rest of the review of systems was unremarkable except a fall from intoxication. Physical examination revealed anicteric conjunctiva and nontender abdomen and her vital signs were within normal limits. Initial blood work revealed acute liver and renal failure. The patient was started with general medical management and liver transplant service rejected the case due to active substance abuse. She underwent brief hemodialysis and was started on NAC. Over the course of her hospital stay her liver function and kidney function improved significantly and patient was discharged to home.Conclusion.In cases where liver transplant is not an option for various reasons including active substance abuse, a trial of N-Acetyl Cysteine may be beneficial and should be considered in the Emergency Department.

scholarly journals Effect of the Hepatocyte-Specific Deletion of SND1 in Mice on the Liver Insulin Resistance and Acute Liver Failure

2020 ◽  
Author(s):  
Chunyan Zhao ◽  
Xiaoteng Cui ◽  
Baoxin Qian ◽  
Nan Zhang ◽  
Lingbiao Xin ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Liver Failure ◽  
Acute Liver Failure ◽  
Cholesterol Level ◽  
Hepatic Steatosis ◽  
Glucose Homeostasis ◽  
Hepatic Failure ◽  
High Fat Diet ◽  
High Fat ◽  
Specific Deletion

Abstract Background: The multifunctional protein SND1 was reported to be involved in a variety of biological processes, such as cell cycle, proliferation or lipogenesis. We previously proposed that global-expressed SND1 in vivo is likely to be a key regulator for ameliorating HFD-induced hepatic steatosis and systemic insulin resistance. Herein, we are very interested in investigating further whether the hepatocyte-specific deletion of SND1 affects the insulin resistance or acute liver failure (ALF) of mice.Methods: By using Cre-loxP technique, we constructed conditional knockout (LKO) mice of SND1 driven by albumin in hepatocytes and analyze the changes of glucose homeostasis, cholesterol level, hepatic steatosis and hepatic failure under the treatment of high-fat diet (HFD) or upon the simulation of Lipopolysaccharide/galactosamine (LPS/GalN).Results: No difference for the body weight, liver weight, and cholesterol level was detected. Furthermore, we did not observe the alteration of glucose homeostasis in SND1 hepatic knockout mice on either chow diet or high-fat diet. Besides, hepatocyte-specific deletion of SND1 failed to influence the hepatic failure of mice induced by LPS/GalN.Conclusions: These findings suggest that hepatic SND1, independently, is insufficient for changing glucose homeostasis, hepatic lipid accumulation and inflammation. The synergistic action of multiple organs may contribute to the role of SND1 in insulin sensitivity or inflammatory response.

Acute Hepatic Failure

2019 ◽  
Author(s):  
Derek J Erstad ◽  
Motaz Qadan
Keyword(s):  
Intensive Care ◽  
Respiratory Distress Syndrome ◽  
Liver Failure ◽  
Respiratory Distress ◽  
Acute Liver Failure ◽  
Fulminant Hepatic Failure ◽  
Cerebral Edema ◽  
Hepatic Failure ◽  
Distress Syndrome ◽  
Diagnosis And Management

Acute liver failure (ALF) is a rare but highly morbid condition that is optimally managed by a multidisciplinary team of surgeons, hepatologists, and intensivists at a tertiary care center that specializes in liver disorders. ALF is caused by four primary mechanisms, including viral infections (most commonly Hepatitis A and B); toxicity from acetaminophen overdose or other substances; postoperative hepatic failure ; and miscellaneous causes such as autoimmune hepatitis, genetic disorders, or idiopathic etiologies. Unlike chronic liver failure in which the body develops compensatory, protective mechanisms, ALF may be associated with severe multisystem organ involvement, including respiratory distress syndrome, renal failure, and cerebral edema. Fulminant hepatic failure represents a rapidly progressive form of ALF that portends worse prognosis. Prompt diagnosis and management of multisystem organ dysfunction in an intensive care setting is paramount to survival. However, a subset of patients will fail to improve with medical management alone. Early identification of these individuals for emergent transplant listing has been shown to improve outcomes. Multiple predictive models for ALF survival have been developed, which are based on weighted evaluation of clinical and laboratory parameters. These models may be used to facilitate treatment, predict prognosis, and guide transplant listing. In this chapter, we provide an in-depth review these concepts, focusing on the classification, epidemiology, diagnosis, and management of ALF. This review contains 5 tables and 69 references. Key Words: acute liver failure, acute respiratory distress syndrome, coagulopathy, cerebral edema, fulminant hepatic failure, hepatic necrosis, liver transplantation, metabolic disarray, multidisciplinary intensive care, prognostication

scholarly journals A case of cryptogenic pseudocirrhosis causing acute liver failure: when clinic and radiology work together

2019 ◽  
Vol 13 (2) ◽  
pp. 121-123
Author(s):  
Martina Finocchi ◽  
Ombretta Para ◽  
Giacomo Zaccagnini ◽  
Lorenzo Corbo ◽  
Lucia Maddaluni ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Liver Failure ◽  
Acute Liver Failure ◽  
Systemic Chemotherapy ◽  
Acute Liver Injury ◽  
Metastatic Breast ◽  
International Normalized Ratio ◽  
Caudate Lobe ◽  
Oncologic Patients ◽  
Liver Changes

It is known that a wild spectrum of hepatic manifestations can be common presentations of metastatic breast cancer. Pseudocirrhosis pattern has been often described as almost always secondary to systemic chemotherapy and it is defined by morphological liver changes that mimic cirrhosis including capsular retraction, nodularity, parenchyma atrophy and caudate lobe, radiologically identifiable. Acute liver injury is an occasional complication in oncologic patients, and it outlines an organ failure when there is evidence of encephalopathy and coagulopathy (international normalized ratio >1.5) in the absence of pre-existing liver disease, with an illness of <26 weeks duration. The two most common etiologies are leukemia/lymphoma followed by breast cancer but also in this case, liver is involved almost always after chemotherapy, hormonotherapy or radiotherapy. Here we present a case of rapid evolving acute liver failure presented as cryptogenic pseudocirrhosis without any evidence of primitive breast cancer but an incidental demonstration.

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