• Title/Summary/Keyword: hepatotoxic hepatitis

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A Case Report of Facial Nerve Palsy in Herpes Zoster Oticus with Chronic Hepatitis B (만성 간염환자의 이성(耳性) 대상포진 치험 1례)

  • Kim, Min-Hi;Kim, Ja-Hye;Yoon, Hwa-Jung;Ko, Woo-Shin
    • The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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    • v.18 no.2
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    • pp.80-85
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    • 2005
  • A female visited the Dept. of Oriental Ophthamology & Otolaryngology & Dermatology, Dong-eui University with Facial Nerve Palsy in Herpes Zoster Oticus. She had been taking ill with chronic hepatitis B and taking western medicine. We treated a patient with only Oriental Medicine.(the herbal medication and acupuncture etc). Because she was afraid of herbal medicine -induced hepatitis, went through an examination about LFT profile regularly. The symptom of Herpes Zoster Oticus was improved and there was no abnormality in LFT profile. Through this case, we thought that it is possible to treat the other disease of the patient with chronic hepatitis using herbal medication without hepatotoxic hepatitis. But for the safety of patient and doctor in several case, we need to accumulate objective data about the side effect of herbal medications inducing hepatotoxic hepatitis.

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RECENT ADVANCES IN HEPATOTOXICITY STUDIES

  • Satoh, Tetsuo
    • Toxicological Research
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    • v.7 no.2
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    • pp.113-128
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    • 1991
  • Hepatotoxicity has many facets. Those to be discussed in this review include the mechanism for the hepatotoxic effects, nature of the injury, and animal models of hepatotoxicity suitable for the detection of chemical injury. Some therapeutic drugs used for treatment of hepatitis are also presented. In addition, as an important and serious problem in future, alternative toxicity testing is discussed.

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In vitro hepatocyte inflammation by chaparral extract (Chaparral 추출물에 의한 in vitro 간세포 염증반응)

  • Kim, Ilrang
    • Korean Journal of Food Science and Technology
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    • v.53 no.3
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    • pp.344-347
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    • 2021
  • In this study, the hepatotoxic mechanism of chaparral (Larrea tridentata) was investigated through in vitro experiments that measured cell death, inflammatory cytokine secretion, and intracellular fat accumulation by treating HepG2 hepatocytes with a 70% ethanol extract of chaparral at concentrations ranging from 0.001 to 100 ㎍/mL. Cell death was observed after treatment with chaparral extract at concentrations of 1-100 ㎍/mL (p<0.05). The secretion of the inflammatory cytokines, interleukin-8 and macrophage-colony stimulating factor, and fat accumulation were significantly increased even at a concentration of 0.1 ㎍/mL, which was 10 times lower than the observed concentration resulting in cell death (p<0.05). Hepatitis caused by inflammatory cytokine secretion and fat accumulation was shown to be a form of hepatotoxicity induced by chaparral extract. Hepatitis was expressed at a concentration lower than that causing serious toxicity such as cell death, suggesting that hepatotoxicity, including hepatitis, may be caused by ingestion of low concentrations of chaparral.

Prediction of the Hepatotoxicity Risk Factor Induced by Antituberculosis Agents in Koreans (한국인의 항결핵제에 의한 간독성 위험인자 예측)

  • Lee, Ji-Sun;Kim, Hyun-Ah;Cho, Eun;Lee, Ok-Sang;Lim, Sung-Cil
    • YAKHAK HOEJI
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    • v.55 no.4
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    • pp.352-360
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    • 2011
  • Standard combination chemotherapy including isoniazid, rifampin, pyrazinamide, and ethambutol is very effective against tuberculosis. But, these medicines can cause hepatotoxicity which is the main reason for treatment interruption or change in drug regimen. In order to identify risk factors associated with hepatotoxcity in Koreans and assess elevated baseline LFTs' contributions to hepatotoxicity, a retrospective case control study was performed. The medical records of 277 patients who diagnosed with tuberculosis at a community hospital from January 1st, 2007 to June 30th, 2010 were reviewed. Patients were categorized into 3 groups (non toxic group, patients without increase in LFT levels; mild to moderate hepatotoxic group and severe hepatotoxic group). And the correlation between risk factors and hepatotoxicity was analyzed by using SPSS program. The overall incidence of hepatotoxicity was 18% and 8.7% of patients developed severe toxicity. Patients in the severe toxic group had the longest treatment period among the three groups. In 75% of severe toxic group, hepatotoxicity occurred within 18.3 days after starting medication. Hypoalbuminemia (serum albumin <3 g/dl) was a significant risk factor for development of severe toxicity. Elevated baseline transaminase (except ALT), total bilirubin, and preexisting hepatitis were also risk factors which were more than twice as likely to increase risk of severe hepatotoxicity (p>0.05). In conclusion, hypoalbuminemia (serum albumin level <3 g/dl) was a significant risk factor for anti-tuberculosis druginduced severe toxicity. Therefore, before starting antituberculosis chemotherapy, serum albumin level should be assessed at baseline. In high-risk patients (hypoalbuminemia, elevated LFTs) for hepatotoxicty, liver function should be closely monitored up to at least 21 days after taking medication.

A Study on the Prevalence and Risk Factors of Liver Dysfunction among the Workers in Chemical Factories (화학공장 근로자들의 간기능 이상 유병률 및 위험인자에 관한 연구)

  • Cheong, Hae-Kwan;Kim, Joung-Soon
    • Journal of Preventive Medicine and Public Health
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    • v.30 no.1 s.56
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    • pp.103-128
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    • 1997
  • The object of this study is to evaluate the possibility of chemical-induced liver disorder among workers exposed to various chemicals and to classify the the liver function abnormalities by causes and to analyse the risk factors for each liver disorders. A cross-sectional study including questionnaire survey, physical examination, laboratory tests and ultrasonography of liver was conducted on 1,126 workers, 459 workers in a coal chemical plant(company A) and 667 workers in an insulation material manufacturing factory(company B). An industrial hygienist reviewed the chemicals used in both companies and evaluated the work environments to classify the workers by chemical exposure semiquantitatively. The results are as follows: 1. Of 459 workers in company A, 83 workers(18.1%) are classified as nonexposed, group 163(35,5%) as short-term exposure group, 155(33.8%) as intermediately exposed group and 58(12.6%) as long-term exposed group bared on the mean daily exposure to hepatotoxic chemicals evaluated by an industrial hygienist. Of 667 workers in company B, 484(72.6%) workers were classified as nonexposed and 183(35.5%) as exposed group. 2. Workers with SGOT level higher than 40 IU/l were (10.0%) in company A and 77(11.5%) in company 3, and those with SGPT level higher than 35 IU/l were 118(25.7%) in company A and 198(29.7%) in company B. The differences were not significant between companies and between exposure groups(p>0.05). Workers with $\gamma-GT$ level higher than 62 IU/l were 29(6.3%) in company A and 77(11.5%) in company B (p<0.01). The difference between exposure groups was not significant(p>0.05) within companies. Workers with liver function abnormalities(defined as SGOT higher than 40 IU/l or SGPT higher than 35 IU/l) were 338(30.0%) among 1,126 workers. Of 338 workers with live. function abnormalities 139(12.3%) had fatty liver by ultrasonography, 79(7.0%) had alcoholic liver(defined as workers with liver function abnormalities with weekly alcohol consumption greater than 280 g for more than 5 years), 54(4.8%) had hepatitis B, 12(1.1%) had hepatitis C and the other 114(33.7%) was not otherwise classified. Prevalences of alcoholic liver and fatty liver were significantly lower in company A(prevalence ratio 0.24 for alcoholic liver, p<0.001, prevalence ratio 0.76 for fatty liver, p<0.05) but prevalences of liver disorders between exposure groups within companies were not significant(p>0.05). 3. Summary prevalence ratios(SPR) of live. function abnormalities, fatty live. and other liver disorders, adjusted by age and company were not significantly higher in exposed group in any chemicals(p>0.05) but in some chemicals, SPRs were significantly lower. 4. On simple analysis of risk factors for liver function abnormalities, prevalence odds ratio(POR) of those with age between 30 and 39 was 1.54(p<0.01) and those with age ever 40 was 1.51(p<0.01). POR of those with histories of liver disorders and general anesthesia was 1.77(p<0.001) and 4.02 for those with overweight and 6.23 for those with obesity, defined by body mass index(p<0.001). 5. On logistic regression analysis, risk factors of liver function abnormality were fatty liver(POR 2.92 for grade 1, 12.15 for grade 2), presence of hepatitis B surface antigen(POR 3.62) and obesity(POR 5.38 for overweight and 16.52 for obesity). Presence of hepatitis B surface antigen(POR 0.18) was the only preventive facto. of fatty live. Company(POR 0.30) and obesity(POR 2.49 for overweight, 4.52 for obesity) were related to the alcoholic live. Obesity(POR 2.94 for overweight) was the only significant risk factor of hepatitis B and there was no significant risk factor for liver function abnormality not otherwise classified. It is concluded that the evidence of liver disorder related with chemical exposure is not evident in these factories. It is also postulated that fatty liver and alcoholic liver is most common causes of liver function abnormalities among workers and effort for weight control and improvement of life style should be done.

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A Case of Hepatotoxicity by Salvia Plebeia R. Br.

  • Son, Chang-gue
    • The Journal of Internal Korean Medicine
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    • v.40 no.6
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    • pp.1219-1224
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    • 2019
  • Objective: To investigate the possibility of hepatotoxicity by supplemental foods or folk herbs such as Salvia Plebeia R. Br. Methods: A hospitalized male patient with alcoholic liver disease and electrolyte imbalance had recovered, and then followed by rapid hepatic serum enzymes after taking S. Plebeia. This study monitored the clinical outcome and biochemical parameters. Result: A 58-year male had drunk frequently, which led to alcoholic steatohepatitis and hospitalization. Two weeks after his discharge from hospital, he felt nausea, dizziness, and mild difficulties in speech and walking, resulting in re-hospitalization at the Korean Medical Hospital. The symptoms disappeared on correction of the electrolyte imbalance suspected to have been caused by severe sweating while working in the outdoors, and the patient was discharged. During treatment and monitoring of his health as an outpatient, the serum hepatic enzyme rapidly elevated approximately 10-fold in hepatic enzymes; the enzyme levels fluctuated according to whether or not he was taking the boiled water of S. Plebeia. The RUCAM score was 12, which met the criteria for toxic hepatitis by S. Plebeia. His general condition and abnormal hepatic enzymes recovered with cessation of S. Plebeia and administration of Chungganplus syrup (CGX). Conclusion: This study reports the hepatotoxic risk of Salvia Plebeia, which is commonly used as a folk remedy in Korea.

In vitro hepatocyte inflammation by Ephedra sinica extracts (마황 추출물의 in vitro 간세포 염증반응 유도)

  • Kim, Ilrang
    • Korean Journal of Food Science and Technology
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    • v.51 no.1
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    • pp.24-28
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    • 2019
  • In this study, the in vitro hepatotoxic mechanism of Ephedra sinica (ma-huang) was investigated by measuring the degree of cell death, secretion of cytokine, and fat accumulation by treating HepG2 cells with 70% ethanolic extracts of ma-huang. Cell death was observed at concentrations of around $5-100{\mu}g/mL$ by treatment with ma-huang extracts (p<0.05). The secretion of interleukin 8 (IL-8) and macrophage colony-stimulating factor (M-CSF), which are inflammatory cytokines, were significantly promoted at concentrations of around 0.05-100 and $0.5-100{\mu}g/mL$, respectively (p<0.05). In this experiment, it was shown that the extracts of ma-huang stimulate the secretion of inflammatory cytokines, such as IL-8 and M-CSF, and lead to fat accumulation in the hepatocytes, thereby causing inflammation of the hepatocytes. Hepatotoxicity was observed at around 10-500 times lower concentration than the concentration required to cause serious toxicity, such as cell death, suggesting that hepatic toxicity (hepatitis) may be induced at a low dose.