- Email: [email protected]
HCV infection in the HIV patient in oran algeria
21ST ANNUAL CONFERENCE—2013
ABSTRACTS
DILI
industrial applications, on liver carcinogenesis still remain elusive. Aims: To study the role of isocyanate in liver carcinogenesis. Methods: Experiments were performed on the cultured human liver epithelial cell line to ascertain the possible molecular risks associated with isocyanate exposure using Nsuccinimidyl N-methylcarbamate, a chemical entity that mimics the effects of methyl isocyanatein vitro. Qualitative and quantitative assessment of phosphorylation states of ATM, H2AX, ATR and p53, put forth the kinetics of DNA damage. Analyses of apoptosis in treated cells and inflammatory cytokines secreted in culture supernatant were done through annexin-V FITC/PI assay and cytometric bead array respectively. Cytogenetic studies along with inter simple sequence repeat PCR were done in control and treated cells to check for the possible precariousness at the chromosomal and microsatellite levels of the genome. Results: An increasing trend of all the DNA damage responsive parameters along with the apoptotic index were displayed in treated cells. Isocyanate exposed cells secreted an elevated levels of inflammatory cytokines in the culture supernatant. Cytogenetic analysis and inter simple sequence repeat PCR revealed varied chromosomal anomalies with greater instability at the microsatellite level. Conclusion: To conclude, these findings demonstrate that human liver epithelial milieu could confront with molecular risks due to isocyanate exposure attributing to defective DNA repair pathway along with de-regulated cell cycle and genomic instability which may accelerate the development of HCC.
been suspected. Despite drug discontinuation, weakness, skin itching, weight loss intensified. She was hospitalized to our clinic six weeks after disease onset. There were significant jaundice and visible traces after scratching; tachycardia. Liver and spleen were not palpable. Laboratory analyses showed elevation of ALT> AST (5-6 times higher ULN), total bilirubin (36 times higher ULN) due to both fractions, hypoalbuminemia (2.6 g/dl). Tests for autoantibodies were negative. Serum thyroid-stimulating hormone level was less than 0.01 uIU/ml (N: 0.4–4), free thyroxine two times higher ULN. Liver biopsy revealed parenchymatous and canalicularbilirubinostasis, necrosis of some hepatocytes. We diagnosed: Thiamazole-induced hepatitis. Hepatic failure: jaundice, hypoalbuminemia, thyrotoxicosis. In spite of drug withdrawal and administration of Ademethionine, UDCA, plazmapheresis, we observed a very slow regression of jaundice. Prednisolone prescription led to a rapid full patient's recovery with normalization of all biochemical markers during a month. The patient passed later radioactive iodine ablation of the thyroid gland. Discussion: Here we observed a mixed (dose-dependent and idiosyncratic) liver injury. There was an untypical form of hepatotoxicity - hepatocellular damage with jaundice, without increase in laboratory markers of cholestasis, what makes the uniqueness of this clinical case. Conclusion: Severe jaundice is a rare adverse effect of antithyroid drugs’ therapy. The liver injury is usually reversible after drug withdrawal but in some cases can require Prednizolone administration. Physicians should keep in mind such a rare adverse reaction of antithyroid drugs.
Corresponding author. Kewal Krishan Maudar. E-mail: [email protected]
Corresponding Author. Maria Sergeevna Zharkova. E-mail: [email protected]
A CASE OF SEVERE JAUNDICE CAUSED BY THIAMAZOLE THERAPY
HCV INFECTION IN THE HIV PATIENT IN ORAN ALGERIA
Maria Sergeevna Zharkova, Marina Trofimovich Maevskaya, Elena Nikolaevna Shirokova, Tatjana Petrovna Nekrasova, Marina Victorovna Ivashkin
Nadjet Allab Mouffok, Fatima Bensadoun, Ahmed Kouiad Belkadi
Hepatology Department, University Clinical Hospital N 2, First Moscow State Medical University, Moscow, Russia
Introduction: Co-infections of HIV and HCV are frequent and became a concern considering the longevity of the HIV patient thanks to the HAART. Objectives: to determine the frequency of Co-infection VIH/VHC, the various implied genotypes, the clinical and biological characteristics, the assumption of responsibility in Oran hospital and the difficulties encountered. Methods: retrospective study on file during the period of 2003 to 2012, the patients included are those which were infected by the HIV and had positive HCV antibodies. The epidemiologic, clinical, biological characteristics (ALAT, prothrombin, albumin, bilirubin, fibrotest-Acti
Objective: Hepatotoxicity is a rare serious adverse reaction to antithyroid agents. It occurs with a frequency of 0.1– 0.2% of treated patients. Here we describe a case of severe jaundice with expected poor prognosis in a Thiamazoletreated patient with thyrotoxicosis. Case report: A 48-year-old woman with thyrotoxicosis developed jaundice after two weeks of Thiamazole therapy (40 mg/day). Viral hepatitis and mechanical biliary obstruction were excluded. Drug-induced liver injury had
S38
CHUOran
© 2013, INASL
JOURNAL OF CLINICAL AND EXPERIMENTAL HEPATOLOGY
Corresponding Author. Nadjet Allab Mouffok. E-mail: [email protected]
ANTINECROINFLAMMATORY EFFECTS OF ATORVASTATIN AGAINST CARBON TETRA CHLORIDE-INDUCED HEPATOTOXICITY IN RATS Yousef Doustar, Daryoush Mohajeri, Ali Rezaii Department of Pathobiology, Tabriz Branch, Islamic Azad University, Tabriz, Iran
Background and Aims: Atorvastatin is widely used in the treatment of hepatic disease. The aim of present study is to determine the necroinflammatory activity of atorvastatin against CCl4 -induced hepatotoxicity in rats. Methods: Thirty adult Wistar male albino rats were divided randomly into 5 groups. Group I served as Control group and received normal saline (1ml.kg-1; i.p), Group II received CCl4 (1 ml/kg, s.c), Group III received Atorvastatin (5 mg/kg, p.o) +CCl4 (1 ml/kg, i.p) ,Group IV received Atorvastatin (10 ml/kg, p.o) +CCl4 (1 ml/kg, i.p), and
Group V received Atorvastatin (15 ml/kg, p.o) +CCl4 (1 ml/kg, i.p) for 28 consecutive day. On 28thday blood samples from all rats of every group were collected and levels of SGPT, SGOT, ALP and bilirubin by standard kits were assayed. The liver tissues were taken for histopathological examination. Results: Rats in group II, III and IV showed different abnormal changes with different degrees consist of fatty change, lymphocytic infiltration, necrosis, congestion and hemorrhage were distinguished and no fatty change were observed and was similar to normal hepatocyte in group V rats. The animals treated with CCl4 exhibited a significant (P<0.001) rise in SGOT, SGPT, ALP and bilirubin levels when compared to the control group. Conclusion:The results of the study clearly demonstrated that the atorvastatin exhibited potent hepatoprotective activity against CCl4-induced hepatic damage in rats. This may be due to their antioxidant and free radical scavenging properties. In this study, an increase in the activities of SGPT, SGOT, ALP and bilirubin in serum evidenced the CCl4-induced hepatocellular damage because these are cytoplasmic in location and are released into the circulation after cellular damage. Corresponding Author: Yousef Doustar. E-mail: [email protected] DILI
Test), virological (HCV PCR, genotype), echographic, therapeutic and outcome are collected on standardized cards. Results: Among the 2150 files of HIV patients, 22 Co-infections HIV/HCV were colliges. They are 14 men and 8 women. The age varies between 29 and 59 (average 43.5). The origin contamination is difficult to determine (dental care 18%, intravenous drug-addiction 11%, others). The PCR positive among 12 patients lay between 4.96 to 7.15 log. The genotypes most met were genotype 1 (15/ 22), the VHC 1a in 9 cases and VHC 1b in 6 cases. Genotype 2a2c is found in 5 cases and genotype 4 in two cases. The Co-infection with the virus of hepatitis B was noted in ttree cases. Like Co-morbidity, four tuberculosis under treatment, a diabetes and arterial high pressure, an important chronic nicotinism. The fibro-test concluded in a fibrosis F0-F1/A0 at 9 cases, F1-F2/A1 in 5 cases and A3 at two another cases, the fibrosis was severe F4/A3 in 5 cases. The treatment was founded among 17 patients. After 5 months of treatment by PEG-IFN and Ribavirin, we note 9 favorable answers with a clear reduction in the fibrosis and negative RNA HCV in 9 cases, a non-response in three cases, a lost case of sight and in the other cases in progress. The treatment was tolerated in the majority but was enameled by the side effects with type of hepatic toxicity in particular among patients under antimycobacteria-therapy in 4 cases. Conclusion: The Co-infection by the viruses of hepatitis and the HIV is obvious public health problems. Hepatitis C at the PVVIH is often active, the therapeutic failure with HAART is more frequent and hepatic toxicity is real among these patients multi-therapy.
DRUG-NDUCED HEPATOTOXICITY 2011–2012 Hasmik Ghazinyan, Aregnazan Mkhitaryan, Ara Asoyan, Stepan Atoyan Nork Clinical Hospital
Background: Drug-induced liver injury can mimic acute or chronic liver disease.>1000 drugs cause hepatotoxicity, including 20-40% of all instances of fulminant hepatic failure. The manifestations of drug- induced hepatotoxicity are highly variable, ranging from asymptomatic elevation of liver enzymes to fulminant hepatic failure and death. Aim: To present description and predictors of drug-induced hepatotoxicity according to our clinic data. Methods: Out of 325 patients with acute hepatitis in 42 (7.8%) were diagnosed drug-induced hepatitis. The mean age of them was 32(4-60), 34 (80%) were women, 8(20%) were children. In 29 (70%) patients body mass index (BMI) ranged 25-35 kg/m2. The diagnosis of drug-induced liver injury is exclusion with initial suspicion based on circumstation evidence (markers of viral: antiHAVIgM, HBsAg, anti-HBcor IgM,anti HCV, antiHEV and autoimmune hepatitis as well as other reasons). Serum chemical indications included ALT, AST, alkaline phosphates (ALP), total bilirubin, GGT, pt % and albumin. Results: Out of 42 patients 22 were with jaundice and elevated serum bilirubin levels ranged 35-530 mcmol/l
Journal of Clinical and Experimental Hepatology | March 2013 | Vol. 3 | No. 1S | S37–S40
S39
ABSTRACTS
DILI
industrial applications, on liver carcinogenesis still remain elusive. Aims: To study the role of isocyanate in liver carcinogenesis. Methods: Experiments were performed on the cultured human liver epithelial cell line to ascertain the possible molecular risks associated with isocyanate exposure using Nsuccinimidyl N-methylcarbamate, a chemical entity that mimics the effects of methyl isocyanatein vitro. Qualitative and quantitative assessment of phosphorylation states of ATM, H2AX, ATR and p53, put forth the kinetics of DNA damage. Analyses of apoptosis in treated cells and inflammatory cytokines secreted in culture supernatant were done through annexin-V FITC/PI assay and cytometric bead array respectively. Cytogenetic studies along with inter simple sequence repeat PCR were done in control and treated cells to check for the possible precariousness at the chromosomal and microsatellite levels of the genome. Results: An increasing trend of all the DNA damage responsive parameters along with the apoptotic index were displayed in treated cells. Isocyanate exposed cells secreted an elevated levels of inflammatory cytokines in the culture supernatant. Cytogenetic analysis and inter simple sequence repeat PCR revealed varied chromosomal anomalies with greater instability at the microsatellite level. Conclusion: To conclude, these findings demonstrate that human liver epithelial milieu could confront with molecular risks due to isocyanate exposure attributing to defective DNA repair pathway along with de-regulated cell cycle and genomic instability which may accelerate the development of HCC.
been suspected. Despite drug discontinuation, weakness, skin itching, weight loss intensified. She was hospitalized to our clinic six weeks after disease onset. There were significant jaundice and visible traces after scratching; tachycardia. Liver and spleen were not palpable. Laboratory analyses showed elevation of ALT> AST (5-6 times higher ULN), total bilirubin (36 times higher ULN) due to both fractions, hypoalbuminemia (2.6 g/dl). Tests for autoantibodies were negative. Serum thyroid-stimulating hormone level was less than 0.01 uIU/ml (N: 0.4–4), free thyroxine two times higher ULN. Liver biopsy revealed parenchymatous and canalicularbilirubinostasis, necrosis of some hepatocytes. We diagnosed: Thiamazole-induced hepatitis. Hepatic failure: jaundice, hypoalbuminemia, thyrotoxicosis. In spite of drug withdrawal and administration of Ademethionine, UDCA, plazmapheresis, we observed a very slow regression of jaundice. Prednisolone prescription led to a rapid full patient's recovery with normalization of all biochemical markers during a month. The patient passed later radioactive iodine ablation of the thyroid gland. Discussion: Here we observed a mixed (dose-dependent and idiosyncratic) liver injury. There was an untypical form of hepatotoxicity - hepatocellular damage with jaundice, without increase in laboratory markers of cholestasis, what makes the uniqueness of this clinical case. Conclusion: Severe jaundice is a rare adverse effect of antithyroid drugs’ therapy. The liver injury is usually reversible after drug withdrawal but in some cases can require Prednizolone administration. Physicians should keep in mind such a rare adverse reaction of antithyroid drugs.
Corresponding author. Kewal Krishan Maudar. E-mail: [email protected]
Corresponding Author. Maria Sergeevna Zharkova. E-mail: [email protected]
A CASE OF SEVERE JAUNDICE CAUSED BY THIAMAZOLE THERAPY
HCV INFECTION IN THE HIV PATIENT IN ORAN ALGERIA
Maria Sergeevna Zharkova, Marina Trofimovich Maevskaya, Elena Nikolaevna Shirokova, Tatjana Petrovna Nekrasova, Marina Victorovna Ivashkin
Nadjet Allab Mouffok, Fatima Bensadoun, Ahmed Kouiad Belkadi
Hepatology Department, University Clinical Hospital N 2, First Moscow State Medical University, Moscow, Russia
Introduction: Co-infections of HIV and HCV are frequent and became a concern considering the longevity of the HIV patient thanks to the HAART. Objectives: to determine the frequency of Co-infection VIH/VHC, the various implied genotypes, the clinical and biological characteristics, the assumption of responsibility in Oran hospital and the difficulties encountered. Methods: retrospective study on file during the period of 2003 to 2012, the patients included are those which were infected by the HIV and had positive HCV antibodies. The epidemiologic, clinical, biological characteristics (ALAT, prothrombin, albumin, bilirubin, fibrotest-Acti
Objective: Hepatotoxicity is a rare serious adverse reaction to antithyroid agents. It occurs with a frequency of 0.1– 0.2% of treated patients. Here we describe a case of severe jaundice with expected poor prognosis in a Thiamazoletreated patient with thyrotoxicosis. Case report: A 48-year-old woman with thyrotoxicosis developed jaundice after two weeks of Thiamazole therapy (40 mg/day). Viral hepatitis and mechanical biliary obstruction were excluded. Drug-induced liver injury had
S38
CHUOran
© 2013, INASL
JOURNAL OF CLINICAL AND EXPERIMENTAL HEPATOLOGY
Corresponding Author. Nadjet Allab Mouffok. E-mail: [email protected]
ANTINECROINFLAMMATORY EFFECTS OF ATORVASTATIN AGAINST CARBON TETRA CHLORIDE-INDUCED HEPATOTOXICITY IN RATS Yousef Doustar, Daryoush Mohajeri, Ali Rezaii Department of Pathobiology, Tabriz Branch, Islamic Azad University, Tabriz, Iran
Background and Aims: Atorvastatin is widely used in the treatment of hepatic disease. The aim of present study is to determine the necroinflammatory activity of atorvastatin against CCl4 -induced hepatotoxicity in rats. Methods: Thirty adult Wistar male albino rats were divided randomly into 5 groups. Group I served as Control group and received normal saline (1ml.kg-1; i.p), Group II received CCl4 (1 ml/kg, s.c), Group III received Atorvastatin (5 mg/kg, p.o) +CCl4 (1 ml/kg, i.p) ,Group IV received Atorvastatin (10 ml/kg, p.o) +CCl4 (1 ml/kg, i.p), and
Group V received Atorvastatin (15 ml/kg, p.o) +CCl4 (1 ml/kg, i.p) for 28 consecutive day. On 28thday blood samples from all rats of every group were collected and levels of SGPT, SGOT, ALP and bilirubin by standard kits were assayed. The liver tissues were taken for histopathological examination. Results: Rats in group II, III and IV showed different abnormal changes with different degrees consist of fatty change, lymphocytic infiltration, necrosis, congestion and hemorrhage were distinguished and no fatty change were observed and was similar to normal hepatocyte in group V rats. The animals treated with CCl4 exhibited a significant (P<0.001) rise in SGOT, SGPT, ALP and bilirubin levels when compared to the control group. Conclusion:The results of the study clearly demonstrated that the atorvastatin exhibited potent hepatoprotective activity against CCl4-induced hepatic damage in rats. This may be due to their antioxidant and free radical scavenging properties. In this study, an increase in the activities of SGPT, SGOT, ALP and bilirubin in serum evidenced the CCl4-induced hepatocellular damage because these are cytoplasmic in location and are released into the circulation after cellular damage. Corresponding Author: Yousef Doustar. E-mail: [email protected] DILI
Test), virological (HCV PCR, genotype), echographic, therapeutic and outcome are collected on standardized cards. Results: Among the 2150 files of HIV patients, 22 Co-infections HIV/HCV were colliges. They are 14 men and 8 women. The age varies between 29 and 59 (average 43.5). The origin contamination is difficult to determine (dental care 18%, intravenous drug-addiction 11%, others). The PCR positive among 12 patients lay between 4.96 to 7.15 log. The genotypes most met were genotype 1 (15/ 22), the VHC 1a in 9 cases and VHC 1b in 6 cases. Genotype 2a2c is found in 5 cases and genotype 4 in two cases. The Co-infection with the virus of hepatitis B was noted in ttree cases. Like Co-morbidity, four tuberculosis under treatment, a diabetes and arterial high pressure, an important chronic nicotinism. The fibro-test concluded in a fibrosis F0-F1/A0 at 9 cases, F1-F2/A1 in 5 cases and A3 at two another cases, the fibrosis was severe F4/A3 in 5 cases. The treatment was founded among 17 patients. After 5 months of treatment by PEG-IFN and Ribavirin, we note 9 favorable answers with a clear reduction in the fibrosis and negative RNA HCV in 9 cases, a non-response in three cases, a lost case of sight and in the other cases in progress. The treatment was tolerated in the majority but was enameled by the side effects with type of hepatic toxicity in particular among patients under antimycobacteria-therapy in 4 cases. Conclusion: The Co-infection by the viruses of hepatitis and the HIV is obvious public health problems. Hepatitis C at the PVVIH is often active, the therapeutic failure with HAART is more frequent and hepatic toxicity is real among these patients multi-therapy.
DRUG-NDUCED HEPATOTOXICITY 2011–2012 Hasmik Ghazinyan, Aregnazan Mkhitaryan, Ara Asoyan, Stepan Atoyan Nork Clinical Hospital
Background: Drug-induced liver injury can mimic acute or chronic liver disease.>1000 drugs cause hepatotoxicity, including 20-40% of all instances of fulminant hepatic failure. The manifestations of drug- induced hepatotoxicity are highly variable, ranging from asymptomatic elevation of liver enzymes to fulminant hepatic failure and death. Aim: To present description and predictors of drug-induced hepatotoxicity according to our clinic data. Methods: Out of 325 patients with acute hepatitis in 42 (7.8%) were diagnosed drug-induced hepatitis. The mean age of them was 32(4-60), 34 (80%) were women, 8(20%) were children. In 29 (70%) patients body mass index (BMI) ranged 25-35 kg/m2. The diagnosis of drug-induced liver injury is exclusion with initial suspicion based on circumstation evidence (markers of viral: antiHAVIgM, HBsAg, anti-HBcor IgM,anti HCV, antiHEV and autoimmune hepatitis as well as other reasons). Serum chemical indications included ALT, AST, alkaline phosphates (ALP), total bilirubin, GGT, pt % and albumin. Results: Out of 42 patients 22 were with jaundice and elevated serum bilirubin levels ranged 35-530 mcmol/l
Journal of Clinical and Experimental Hepatology | March 2013 | Vol. 3 | No. 1S | S37–S40
S39