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At least 109 records · Page 6Linked to original sources
PubMed1998

Mechanisms of hepatic toxicity. IV. Pathogenetic mechanisms involved in hepatitis C virus-inducedliver diseases.

The pathogenetic mechanisms for liver damage in acute hepatitis C are not clear, but a host immune cellular response may be involved. In chronic hepatitis C, there is strong evidence that host cellular immune response is involved in the control of viral replication and contributes to hepatocellular damage. As hepatitis C virus infection persists, continuous liver damage and regeneration, together with enhanced fibrogenesis, may eventually lead to cirrhosis in a proportion of patients. Transplant patients on high-dose immunosuppression may have high-level intrahepatic hepatitis C viral expression, and, in this setting, the virus may induce direct cytopathic liver damage.

Acute Disease↗
PubMedDate not supplied

[Effect of qualitatively varying nutrition on the histological structure of the liver of pregnant rats in experimental toxic hepatitis].

The effect of rations with differing proportions of protein, 20, 25, 30 and 40 per cent in calorific value, and group B vitamins on the structure of the liver was studied in 40 pregnant rats with experimental affection of the liver and in 10 control animals. Histological and electron microscopic investigations were conducted. Diets containing 25 and 30 per cent protein and a double amount of group B vitamins were noted to help restore the structure of the hepatic tissue in pregnant rats with toxic hepatitis. The diet containing 30 per cent of protein produces the optimal normalizing effect.

Animal Nutritional Physiological Phenomena↗
PubMed1979

[Role of vacuolar apparatus overload in lysosomal changes in liver cells in acute toxic hepatitis].

Physical and chemical properties of the rat liver lysosomes with single Triton WR 1339 overloading were studied during the administration of a detergent to intact rats and those with acute toxic hepatitis. Administration of the latter to intact animals was accompanied by a reduction of the floating density of the particles, solubilization of the lysosome enzymes and by increased fragility of the particles in the hypotonic medium. Lysosomes of the hepatocytes in rats with toxic hepatitis also displayed signs of overloading of the vacuolar apparatus with the preparation administered. The most pronounced solubilization of the lysosomal enzymes beta-galactosidase, acid RNA-ase, cathepsin D--was noted in case of combined action of CCl4 and Triton WR 1339 24, 48, 72 hours and 7 days after the CCl4 poisoning. Possible consequences of overloading of the vacuolar apparatus of the rat hepatocytes are discussed.

Acute Disease↗
PubMed1989

[Severe toxic hepatitis during flutamide (Eulexin) treatment].

A case of severe toxic hepatitis in a patient with metastatic prostatic cancer treated for three months with flutamide (Eulexin) combined with an LHRH analogue, goserelin (Zoladex) is described. The patient developed severe liver failure with jaundice, ascites and severe encephalopathy. The condition reversed after discontinuation of flutamide. Less severe, but otherwise similar, adverse reactions have been reported in the literature, and the importance of considering the drug as a potential hepatotoxin is stressed.

Anilides↗
PubMed2006

[Alcohol abuse case of severe liver dysfunction induced by acetaminophen poisoning which was diagnosed as non-hepatic toxicity on admission].

A 41-year-old female attempted suicide by taking 7.8g acetaminophen and was transferred to our hospital four hours after ingestion. The patient was diagnosed as non-hepatic toxicity (below the line set by the Rumack Matthew nomogram). Laboratory data showed an elevation in serum liver enzymes and coagulation defects at 3 days after ingestion, therefore, the patient was treated with plasma exchange and an oral administration of N-acetylcysteine (NAC). The elevation of liver enzymes was maximal at 4 days after ingestion, and the laboratory data became normalized at approximately 9 days after ingestion. In this case, habitual alcohol intake may have exacerbated the severe liver injury. We should consider an exacerbation of hepatotoxicity and administer NAC in any case having a history of habitual alcohol intake, even if the case was diagnosed as non-hepatic toxicity by the nomogram.

Acetaminophen↗
PubMed2004

Toxic hepatitis in a case of Angelman syndrome associated with Lennox-Gastaut syndrome.

We report a 26-month-old boy with Angelman syndrome associated with Lennox-Gastaut syndrome, who developed a rash and a persistent toxic hepatitis after lamotrigine was added to valproate therapy. The patient had typical findings of both Angelman and Lennox-Gastaut syndromes. Chromosome analysis performing by FISH analysis showed a deletion in chromosome 15 (q11.2 q11.2). Although some cases of Angelman syndrome associated with Lennox-Gastaut syndrome were reported in the literature, valproate and/or lamotrigine induced toxic hepatitis in Angelman syndrome has hitherto never been described. We conclude that VPA and LTG combination should be given with great caution or avoided in patients with Angelman syndrome.

Angelman Syndrome↗
PubMed1975

[Subcellular distribution of acid hydrolases in rat liver during toxic hepatitis].

Changes occurring in the lysosome population were assessed by the results of studies of intracellular distribution of the marker lysosome enzymes--acid phosphatase and acid RNAase. An acute (pure CCl4-0.15 ml per 100 g of weight into the stomach) and chronic (inhalation poisoning after Rabinovici and Wiener) toxic hepatitis was accompanied by an increase in the specific activity of the enzymes in the fraction of heavy mitochondria, this pointing to the change in the sedimentation properties of the lysosomes. An increase in "nonprecipitable" activity of the acid RNA-ase in chronic toxic hepatitis served as the sign of injury of the lysosome membranes.

Acid Phosphatase↗
PubMedDate not supplied

Toxic hepatitis induced by antithyroid drugs: four cases including one with cross-reactivity between carbimazole and benzylthiouracil.

OBJECTIVE: This study was conducted to assess the occurrence of hepatic adverse effects encountered with antithyroid drugs. METHODS: Retrospective review of medical records of 236 patients with hyperthyroidism admitted in our department (in- or out-patients) from 1986 to 1992. RESULTS: Four patients (1.7%) were identified with toxic hepatitis which could reasonably be attributed to the use of antithyroid agent. Two patients had a cholestatic hepatitis induced by carbimazole (Néomercazole). Two others had a mixed (cholestatic and cytolytic) hepatitis following carbimazole. One of the latter two patients further experienced a cytolytic hepatitis which appeared after Benzylthiouracil (Basdène) had replaced carbimazole. Biological features of hepatitis disappeared in all cases after cessation of the incriminated drug, while biliary, viral and immunological searches were negative. Only 2 patients of our retrospective study experienced a mild or severe neutropenia. CONCLUSION: Toxic hepatitis is a potential adverse effect of antithyroid drugs which warrants, as for haematological disturbances, a pre-therapeutic determination and a careful follow-up of relevant biological markers. Moreover, hepatotoxicity may not be restricted to one class of antithyroid agents.

Adult↗
PubMedDate not supplied

Hepatic toxicity of antirheumatic drugs.

BACKGROUND: Many of the diverse group of pharmacologic agents available for the treatment of rheumatic diseases have the potential to cause serious hepatotoxicity. OBJECTIVE: To identify factors associated with drug-induced hepatotoxicity in rheumatic disease. SUMMARY: While mild elevations in plasma transaminase concentrations are associated with almost all nonsteroidal anti-inflammatory drugs (NSAIDs), clinically significant hepatic toxicity is very rare. NSAID-induced liver injury probably has an immunologic basis, but neither a detailed mechanism nor precise incidence rates are known. Methotrexate can cause hepatic fibrosis during chronic use, but the liver injury is poorly reflected by plasma transaminase concentrations; it is difficult to formulate monitoring recommendations when this agent is used in rheumatic disease. Gold and penicillamine have been associated with rare cases of hepatic toxicity as well. CONCLUSIONS: Drug treatment of rheumatic diseases is associated with a small but well-documented risk of hepatotoxicity. Recognizing the clinical syndromes associated with liver injury by these agents facilitates the minimization of morbidity from this complication.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMedDate not supplied

[A comparative study of the effect of hepatoprotectors and inducers on cardiogreen pharmacokinetics in acute toxic hepatitis in the prepuberty period].

CCl4 given to Chinchilla rabbits aged 1 month caused impaired pharmacokinetics of cardiogrin, indicating suppression of absorptive and excretory functions of the liver in prepuberty. Silibor was found to produce no substantial restorative effects on hepatic absorptive and excretory functions in acute toxic hepatitis in the growing body. Phytin was shown to be not inferior to zyxorin and benzonal was superior to all the agents under study in activity.

Acute Disease↗
PubMed2005

Effects of theanine on alcohol metabolism and hepatic toxicity.

We previously showed that theanine, is a major amino acid in green tea, enhanced doxorubicin (DOX) induced antitumor activity. Besides, theanine induced the elevation of glutathione (GSH) level attributable to the increase of glutamate in the liver of mice, namely theanine would reduce the adverse reaction of DOX. Consequently, theanine was thought to be effective against the tissue changes with GSH level reduction. On the other hand, it is suggested excessive uptake of alcohol causes a production of free radicals, a decrease of GSH level, and an increase in the amount of lipid peroxide (LPO) in liver, and shifting to an alcoholic liver injury. Then, aiming at the prevention and medical treatment of a hepatic toxicity by the food components with little toxicity, we have studied the effect of theanine (i.p.) on ethanol metabolism and hepatic toxicity using ethanol (p.o.) single-administered mice. On the 1st hour after ethanol administration, the ethanol concentrations in blood of the theanine combined groups decreased compared with the ethanol-alone group. The alcohol dehydrogenase and aldehyde dehydrogenase activities in the liver increased by combined theanine. Since the elevation of cytochrome P450 (CYP) 2E1 activity was controlled in the theanine-combined groups, it was considered that these disorders attributable to CYP2E1 in ethanol long-term uptake might be avoidable by theanine. Although LPO increased in 3 h after by single-administration of ethanol, the increase was controlled by theanine-administration and was improved until the normal level. In conclusion, it was indicated that theanine was effective against alcoholic liver injury.

Aldehyde Dehydrogenase↗
PubMed1992

Hepatic toxicity of unmodified and time-release preparations of niacin.

Niacin (nicotinic acid) is used frequently in the treatment of hypercholesteremia. It is available in both unmodified and time-release preparations. The latter were developed in attempts to minimize the skin-flushing reaction that affects virtually all users and may limit acceptance. Adverse effects on the liver from both unmodified and time-release preparations have been recognized for many years. We reviewed the literature on the hepatic toxicity of both types of niacin preparations. Adverse reactions in six patients resulted from the exclusive use of unmodified niacin and in two patients from the exclusive use of time-release preparations. In 10 additional patients, adverse reactions developed after an abrupt change from unmodified to time-release preparations. Many of these patients were ingesting time-release niacin at doses well above the usual therapeutic doses currently recommended. Signs of liver toxicity developed in less than 7 days in four of these 10 patients. In doses that achieve equivalent reductions in serum lipids, hepatic toxicity occurred more frequently with time-release preparations than with unmodified preparations. An awareness of toxicity associated with ingestion of high doses of time-release niacin preparations is important because of their widespread availability and the potential for self-prescribed, unmonitored use.

Chemical and Drug Induced Liver Injury↗
PubMed1979

Hepatic toxicity of adjuvant chemotherapy for carcinoma of the breast.

Four patients developed abnormal liver function tests and focal defects on liver scan while receiving cyclophosphamide, methotrexate and 5-fluorouracil as adjuvant chemotherapy following mastectomy for breast cancer. Liver biopsies showed severe focal inflammation. The biopsy findings and the subsequent clinical course of the patients strongly suggest that these abnormalities were due to hepatic toxicity of the chemotherapy and not metastic breast cancer. A review of serial liver function tests performed on 24 patients in that chemotherapy program revealed that four out of eight patients with elevated alkaline phosphatase prior to therapy developed early metastatic cancer. Elevated alkaline phosphatase occurring during chemotherapy on the other hand was quite common but more likely due to hepatic toxicity of the drugs. The development of abnormal liver function tests even in association with focal defects on liver scan is not sufficient to diagnose metastatic breast cancer in patients receiving adjuvant chemotherapy.

Adult↗
PubMed2004

Nevirapine-induced toxic epidermal necrolysis and toxic hepatitis treated successfully with a combination of intravenous immunoglobulins and N-acetylcysteine.

We describe a case of an HIV-seropositive patient presenting with a severe stomatitis that initially improved with anti-infective agents. Only 13 days after the onset of the stomatitis, the patient developed rapidly progressive constitutional symptoms and a cutaneous eruption. He was diagnosed with a Stevens-Johnson syndrome (SJS) caused by the antiretroviral drug nevirapine (NVP). Despite meticulous supportive care and withdrawal of all drugs, his situation worsened and developed into a toxic epidermal necrolysis (TEN), or Lyell's syndrome, complicated by a toxic hepatitis. Treatment with a novel combination of intravenous immunoglobulins (IVIG) and N-acetylcysteine (NAC) resulted in an exceptionally fast recovery. A literature research revealed no other cases of patients treated with both NAC and IVIG for the combination of TEN and toxic hepatitis. Because of the rapid clinical recovery, this approach merits further investigation. This case report also illustrates the importance of early suspicion of SJS when an HIV-infected patient treated with nevirapine presents with stomatitis.

Journal Article↗
PubMed1976

Hepatic toxicity of antituberculous drugs in children.

Three cases of children who developed hepatic toxicity of different degree while on antituberculous treatment with isoniazid and rifampicin are reported. The clinical picture is presented and the pathogenesis of the hepatic damage is discussed. The pathological findings in the liver are those of a drug induced hepatitis. The combined treatment of tuberculosis in children with isoniazid and rifampicin is potentially dangerous and should be reserved for cases in which resistance to other drugs has been demonstrated.

Adult↗