Human herpes viruses as cause of liver injury and acute liver failure

2020 ◽  
Vol 65 (4) ◽  
Author(s):  
Barbara Imperatrice ◽  
Gabriele Giudici ◽  
Alfredo Marzano
Keyword(s):  
Liver Injury ◽  
Liver Failure ◽  
Acute Liver Failure ◽  
Herpes Viruses ◽  
Human Herpes ◽  
Human Herpes Viruses

scholarly journals Tc-99m GSA scintigraphy within the first 3 days after admission as an early predictor of outcome in severe acute liver injury

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yuji Suzuki ◽  
Keisuke Kakisaka ◽  
Takuro Sato ◽  
Ryouichi Mikami ◽  
Hiroaki Abe ◽  
...  
Keyword(s):  
Liver Transplantation ◽  
Liver Injury ◽  
Liver Failure ◽  
Acute Liver Failure ◽  
Acute Liver Injury ◽  
Area Under The Curve ◽  
Region Of Interest ◽  
Free Survival ◽  
Risk Of Death ◽  
Poor Outcome

AbstractPatients with severe acute liver injury (SLI) usually recover spontaneously. However, some SLI patients progress to acute liver failure with varying degrees of hepatic encephalopathy. Acute liver failure is associated with high mortality and can be substantially reduced by liver transplantation. Therefore, distinguishing SLI patients who might progress to acute liver failure and are at a risk of death is important when evaluating patients needing liver transplantation. The present study aimed to determine whether technetium-99m-diethylenetriaminepentaacetic acid galactosyl human serum albumin (Tc-99m GSA) scintigraphy can predict the prognosis of patients with SLI. This prospective observational study included 69 SLI patients. The accuracy of Tc-99m GSA for predicting death or liver transplantation for 6 months was assessed. Between the two groups of patients stratified based on the cut-off values from the receiver operating characteristic curves, 6-month transplant-free survival was compared. Sixteen (23.2%) patients died or underwent liver transplantation from admission (poor outcome). The hepatic accumulation index was calculated by dividing the radioactivity of the liver region of interest by that of the liver-plus-heart region of interest at 15 min (i.e., LHL15). The LHL15 in the 16 patients (0.686) was significantly lower than that in survivors (0.836; P < 0.0001). The optimal LHL15 cut-off for distinguishing poor outcome and survival was 0.737 with a sensitivity of 81.3%, specificity of 88.7%, and area under the curve of 0.907 (95% CI, 0.832–0.981). When patients were divided into two groups based on the LHL15 cut-off value, the 6-month transplant-free survival was significantly lower in patients with an LHL15 level ≤ 0.737. Tc-99m GSA scintigraphy may help predict the prognosis of patients with SLI.

Hepatoprotective effects of ginsenoside Rk3 in acetaminophen-induced liver injury in mice by activation of autophagy

2021 ◽  
Author(s):  
Linlin Qu ◽  
Rongzhan Fu ◽  
xiaoxuan Ma ◽  
Daidi Fan
Keyword(s):  
Liver Injury ◽  
Liver Failure ◽  
Acute Liver Failure ◽  
Acute Liver Injury ◽  
Common Causes ◽  
Hepatoprotective Effects

Acetaminophen (APAP)-induced acute liver injury (AIALI) is one of the most common causes of acute liver failure. Owing to the limitations of N-acetylcysteine (NAC), which is the only antidote currently...

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.

Antiviral activity of Colombian Labiatae and Verbenaceae family essential oils and monoterpenes on Human Herpes viruses

2015 ◽  
Vol 28 (2) ◽  
pp. 130-137 ◽  
Author(s):  
Yaneth Miranda Brand ◽  
Vicky Constanza Roa-Linares ◽  
Liliana Amparo Betancur-Galvis ◽  
Diego Camilo Durán-García ◽  
Elena Stashenko
Keyword(s):  
Antiviral Activity ◽  
Essential Oils ◽  
Herpes Viruses ◽  
Human Herpes ◽  
Human Herpes Viruses

Molecular Detection of Human Herpes Viruses in Suspected Measles Serum Samples from Senegal, 2014 to 2017

2021 ◽  
Author(s):  
Mamadou Malado Jallow ◽  
Amary Fall ◽  
Serigne Fallou Wade ◽  
Ndeye Sophie Fall ◽  
Davy Kiori ◽  
...  
Keyword(s):  
Molecular Detection ◽  
Seasonal Pattern ◽  
Clinical Specimen ◽  
Human Herpesvirus ◽  
Case Definition ◽  
Herpes Viruses ◽  
Human Herpes ◽  
Serum Samples ◽  
Cutaneous Lesions ◽  
Human Herpes Viruses

Herpesviruses are known to cause a diversity of clinical syndromes, ranging from minor cutaneous lesions to life-threatening illnesses, especially in immunocompromised hosts. Here, we investigate retrospectively the contribution of five human herpesviruses, including herpes simplex virus Cytomegalovirus (CMV), the Epstein–Barr virus (EBV), human herpesvirus 6, and varicella zoster virus (VZV) in serum samples collected from measles suspected patients with at least fever and rash. Sera specimens were first tested for serological evidence of measles and rubella virus infection by ELISA, and DNA extracted from an aliquot of each clinical specimen for molecular detection of human herpes viruses by RT-qPCR. A total of 3,358 specimens have been collected and tested for herpes viruses. Nearly half of the overall suspected cases were children younger than 5 years (49.4%). Of the 3,358 sera tested by ELISA, 227 (6.7%) were measles laboratory confirmed and 152 (4.5%) rubella laboratory confirmed. Herpes viruses were detected in 1763 (52.5%), and VZV was the most common with 44.3%, followed by EBV with 10.7%. Coinfections were found in 352 (20%) cases, and the most common co-detections were VZV/EBV or VZV/CMV (169 and 81 cases, respectively). A clear seasonal pattern of VZV, EBV, and CMV identification was observed, with the highest incidence between February and April each year. Results of this investigation provide more insights into cutaneous rash syndrome etiologies in patients sampled in the framework of measles/rubella surveillance in Senegal, which is useful for the guidance of both case definition revision and clinical practice as well as for public health policy.

Liver failure

2020 ◽  
pp. 3089-3100
Author(s):  
Jane Macnaughtan ◽  
Rajiv Jalan
Keyword(s):  
Liver Transplantation ◽  
Liver Disease ◽  
Hepatic Encephalopathy ◽  
Liver Injury ◽  
Liver Failure ◽  
Acute Liver Failure ◽  
Organ Failure ◽  
Clinical Manifestations ◽  
Chronic Liver ◽  
Chronic Liver Failure

Liver failure occurs when loss of hepatic parenchymal function exceeds the capacity of hepatocytes to regenerate or repair liver injury. Acute liver failure is characterized by jaundice and prolongation of the prothrombin time in the context of recent acute liver injury, with hepatic encephalopathy occurring within 8 weeks of the first onset of liver disease. Acute-on-chronic liver failure is characterized by hepatic and/or extrahepatic organ failure in patients with cirrhosis associated with an identified or unidentified precipitating event. The commonest causes of acute liver failure are acute viral hepatitis and drugs. Acute-on-chronic liver failure is most commonly precipitated by infection, alcohol abuse, and superimposed viral infection. The main clinical manifestations are hepatic encephalopathy, coagulopathy, jaundice, renal dysfunction, and haemodynamic instability. Infection and systemic inflammation contribute to pathogenesis and critically contribute to prognosis. Specific therapy for the underlying liver disease is administered when available, but this is not possible for most causes of liver failure. Treatment is predominantly supportive, with particular emphasis on (1) correction or removal of precipitating factors; (2) if encephalopathy is present, using phosphate enemata, nonhydrolysed disaccharide laxatives, and/or rifaximin; (3) early detection and prompt treatment of complications such as hypoglycaemia, hypokalaemia, cerebral oedema, infection, and bleeding. The onset of organ failure should prompt discussion with a liver transplantation centre. The mortality of acute liver failure (without liver transplantation) is about 40%. Patients with acute liver failure who do not develop encephalopathy can be expected to recover completely. Those who recover from an episode of acute-on-chronic liver failure should be considered for liver transplantation because otherwise their subsequent mortality remains high.

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