N-acetyl cysteine therapy in acute viral hepatitis

Gündüz, Hüseyin; Karabay, Oğuz; Tamer, Ali; Özaras, Reşat; Mert, Ali

doi:10.3748/wjg.v9.i12.2698

Cited by 24 publications

(15 citation statements)

References 24 publications

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“…N‐Acetylcystein (NAC): NAC was found to inhibit HBV replication in a cell culture model , and whereas NAC might be beneficial in the setting of acute liver failure , no significant benefit was found in acute viral hepatitis .…”

Section: Do Other Therapies Work Too?mentioning

confidence: 99%

Management of severe acute to fulminant hepatitis B: to treat or not to treat or when to treat?

Tillmann

Zachou

Dalekos

2011

Liver International

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Despite a decline in cases of acute hepatitis B and the low hepatitis B virus (HBV) chronicity rates in adults, still some patients progress to HBV‐related fulminant liver failure. In this review, we discuss treatment options that may prevent the progression of severe acute hepatitis B to fulminant liver failure and death. In severe acute HBV with prolonged prothrombin time and increased bilirubin, interferon failed to be effective while antiviral treatment, particularly with lamivudine, appears to improve survival (mean survival almost 80%). Outcome without antiviral therapy has remained considerably poor, whereas there is no convincing evidence of amelioration of HBV‐targeted immunity. Of note, most patients who died or required transplantation despite lamivudine therapy, were started on lamivudine at advanced stages compared with those survived. This suggests that prompt and timely antiviral therapy is crucial. Owing to the abovementioned results the design of randomized placebo‐control trials in the setting of severe acute hepatitis B seems unethical. On the contrary, the design of multicentre double‐blind randomized trials to compare the efficacy between lamivudine and entecavir or even tenofovir in acute severe HBV cases is ideally needed, but these studies appear to be very difficult to perform considering that these cases are not frequent and therefore, it is almost impossible to have two arms adequately numerous and homogenous for statistical evaluation. Thus, in the absence of solid evidence based data, the hepatologists could treat their patients with severe acute hepatitis B with lamivudine or the most potent antivirals entecavir or tenofovir.

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Section: Do Other Therapies Work Too?mentioning

confidence: 99%

Management of severe acute to fulminant hepatitis B: to treat or not to treat or when to treat?

Tillmann

Zachou

Dalekos

2011

Liver International

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“…NAC is a comparatively safe drug for APAP-induced liver injury (AILI) and is currently being used to treat acute viral hepatitis and other acute hepatic failures (10). However, some studies show that a prolonged treatment with a high dose of NAC (600 to 1200 mg/kg per day) interferes with the normal hepatic mitochondrial metabolic processes and impairs liver regeneration after AILI by interrupting nuclear factor (NF)-jB signal pathways (22,34,37).…”

Section: Introductionmentioning

confidence: 99%

An Indole Derivative Protects Against Acetaminophen-Induced Liver Injury by Directly Binding to N-Acetyl-p-Benzoquinone Imine in Mice

Park

Seo

Tadi

et al. 2013

Antioxidants & Redox Signaling

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Aims: Acetaminophen (APAP)-induced liver injury is mainly due to the excessive formation of reactive oxygen species (ROS) and reactive nitrogen species (RNS) through the formation of a reactive intermediate, N-acetyl-pbenzoquinone imine (NAPQI), in both humans and rodents. Here, we show that the indole-derived synthetic compound has a protective effect against APAP-induced liver injury in C57Bl/6 mice model. Results: NecroX-7 decreased tert-butylhydroperoxide (t-BHP)-and APAP-induced cell death and ROS/RNS formation in HepG2 human hepatocarcinoma and primary mouse hepatocytes. In mice, NecroX-7 decreased APAP-induced phosphorylation of c-Jun N-terminal kinase ( JNK) and 3-nitrotyrosine (3-NT) formation, and also protected mice from APAP-induced liver injury and lethality by binding directly to NAPQI. The binding of NecroX-7 to NAPQI did not require any of cofactors or proteins. NecroX-7 could only scavenge NAPQI when hepatocellular GSH levels were very low. Innovation: NecroX-7 is an indole-derived potent antioxidant molecule, which can be bound to some types of radicals and especially NAPQI. It is well known that the NAPQI is a major intermediate of APAP, which causes necrosis of hepatocytes in rodents and humans. Thus, blocking NAPQI formation or eliminating NAPQI are novel strategies for the treatment or prevention of APAP-induced liver injury instead of GSH replenishment. Conclusion: Our data suggest that the indole-derivative, NecroX-7, directly binds to NAPQI when hepatic GSH levels are very low and the NAPQI-NecroX-7 complex is secreted to the blood from the liver. NecroX-7 shows more preventive and similar therapeutic effects against APAP-induced liver injury when compared to the effect of N-acetylcysteine in C57Bl/6 mice.

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“…This is in line with Huseyin et al The data about using of oral NAC in the treatment of AHA are restricted. To our knowledge, there is no any study assessed the effects of NAC on AHA except one published study evaluating the effect of NAC on AVH (A & B), this article has shown that NAC did not have effect on the length of hospital stay of AVH infection and, on the period in which the ALT value came back to normal and also the prognosis of biochemical parameters [9].…”

Section: Resultsmentioning

confidence: 83%

“…N-acetyl cysteine (NAC) can be used as an antidote in paracetamol intoxication and also can be used as a mucolytic [7,8]. N-acetyl cysteine can increase the amount of glutathione within the cell and maintain cell integrity [9]. The necessity for a medicine to decrease the duration of acute viral hepatitis is obvious, but it has not been found yet.…”

Section: Introductionmentioning

confidence: 99%

N-acetyl Cysteine Therapy as Adjunctive Therapy for Treatment of Acute Hepatitis A

Al-Fadhli

Saraya

Qasem

2017

Afro-Egyptian Journal of Infectious and Endemic Diseases

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Background and study aim: Hepatitis A is an acute, usually mild and self-limiting disease affecting the liver. We aim to assess the effect of oral N-acetyl cysteine compared with placebo on length of hospital stay in adult patients who were admitted to the hospital with acute hepatitis A which might cause earlier resolution of hepatitis. Subjects and Methods: 40 patients were diagnosed as acute hepatitis A and classified into two groups, the first one involved 20 patients who received oral Nacetyl cysteine and supportive treatment, and the second one involved also 20 patients but they received placebo and supportive treatment. We measured complete blood count (CBC), kidney profile (KP), liver function test (LFT), blood glucose, C-reactive protein (CRP) and coagulation profiles on the day of presentation, and every other day till the day of discharge from the hospital. Serological tests were done for HAV Immunoglobulin M (IgM), HEV IgM, HBsAg, HBcIgM, antibody to Hepatitis C virus. Results: The mean length of hospital stay in the NAC group was 13.2 days compared with 14.3 days in the placebo group. Length of hospital stay differed significantly between groups. The mean time of reliving symptoms at presentation was 3.6 days in the NAC group and 4.4 days in the placebo group. The mean time of reliving symptoms at presentation was significantly lower in NAC group than in placebo group. Conclusion: use of oral NAC as adjunctive therapy for treatment of acute hepatitis A was safe in these patients and was associated with a shorter length of patient stay in the hospital.

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N-acetyl cysteine therapy in acute viral hepatitis

Cited by 24 publications

References 24 publications

Management of severe acute to fulminant hepatitis B: to treat or not to treat or when to treat?

Management of severe acute to fulminant hepatitis B: to treat or not to treat or when to treat?

An Indole Derivative Protects Against Acetaminophen-Induced Liver Injury by Directly Binding to N-Acetyl-p-Benzoquinone Imine in Mice

N-acetyl Cysteine Therapy as Adjunctive Therapy for Treatment of Acute Hepatitis A

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