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At least 19 recordsLinked to original sources
PubMed1979

Drug effects on the liver: a tabular compilation of drugs and drug-related hepatic diseases.

Geneic and chemical names of drugs and the possible adverse effects of these drugs on the human liver were tabulated. All drugs compiled in these tables have been approved by the Federal Drug Administration. They are currently available in the United States, and they are listed in the 1979 Physicians' Desk Reference. The tables include: (1) names of drugs that have caused a characteristic morphologic change, such as cholestatic lobular hepatitis; (2) morphologic diagnoses that have been documented after administration of each drug; and (3) references that can be matched to each drug and to its effects on the liver.

Chemical and Drug Induced Liver Injury↗
PubMed1983

Drug effects on the liver. An updated tabular compilation of drugs and drug-related hepatic diseases.

Generic and chemical names of drugs and the possible adverse effects of these drugs on the human liver are tabulated. Most drugs compiled in these tables have been approved by the Federal Drug Administration. They are currently available in the United States, and they are listed in the 1983 Physicians' Desk Reference. Some important investigational drugs are listed also. The tables include: (1) generic names of drugs that have caused a characteristic morphologic change, such as granulomatous hepatitis; (2) morphologic diagnoses that have been documented after administration of each drug; and (3) references that can be matched to each drug and to its effects on the liver.

Carcinoma, Hepatocellular↗
PubMed1975

Effect of "drugs for liver disease" on hepatotoxic action of carbon tetrachloride. II. Effect of protoporphyrin and phosphorylcholine on microsomal drug-metabolizing enzyme activities and the components in injuried liver.

The effect of "drugs for liver disease", protoporphyrin (PP) and phosphorylcholine (PC), on CCl4-induced liver injury was studied. Attention was given to the levels of microsomal drug-metabolizing enzyme and lipolytic enzyme activities and of some microsomal components such as phospholipid and peroxides. Administration of PP to CCl4-poisoned rats was found to increase the decreased microsomal drug-metabolizing enzyme activities, aminopyrine N-demethylase, aniline p-hydroxylase, cytochrome P-450 and b5 and lipolytic enzyme activity in CCl4-poisoned liver (12-20% increase as compared with those of the poisoned rats), and returned to control levels earlier than in CCl4-poisoned rats. Furthermore, administration of PP to CCl4-poisoned rats caused a decrease in the lipid peroxidation. A single dose of PP to normal rats was shown to increase these parameters, to a small extent. One of the mechanisms may be attributed to the fact that PP increases the biosynthesis of the hemoproteins by means of the incorporation of PP into the pigments and protects the membranes from lipid peroxides and the free radicals. On the other hand, administration of PC to the poisoned rats did not enhance the levels of the drug-metabolizing enzyme activities except for aminopyrine N-demethylase. Phospholipid phosphorous content, however, increased by 13-14% when PC was given. Thus, it is considered that PC may enhance the reconstitution of phospholipids in the injured membrane.

Aminopyrine N-Demethylase↗
PubMed1985

Organ tolerance of non-steroidal anti-inflammatory drugs: effect on liver cells.

Experimental studies in mice and in rats showed the good tolerance of a new non-steroidal anti-inflammatory drug, flunoxaprofen, by normal and CCl4 damaged liver. The activity of an enzyme-inducing drug, such as phenobarbital, showed a greater increase after pretreatment with indomethacin than with flunoxaprofen or benoxaprofen. High doses of benoxaprofen and indomethacin significantly decreased bromosulphonphthalein excretion in rats with normal or CCl4 damaged liver; the effect was not observed with flunoxaprofen administered at the same dose as benoxaprofen. Moreover, benoxaprofen and indomethacin but not flunoxaprofen induced a significant increase of some serum liver enzymes in CCl4 poisoned rats.

Animals↗
PubMedDate not supplied

Chemosensitivity testing of primary tumor cells from gastric cancer patients with liver metastasis can identify effective antitumor drugs.

The liver metastasis of gastric carcinoma is resistant to conventionally available treatment. Twenty patients with liver metastasis of gastric cancer were treated by arterial drug infusion using a reservoir and seven cases were treated with systemic chemotherapy. The resected primary gastric cancer specimen was used for chemosensitivity assay with 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyl-2H tetrazolium bromide (MTT) endpoint, and the patients were treated without reference to the results of the chemosensitivity assay. The mean survival period was assessed according to the histology of the primary lesion, the grade of liver metastasis and, the presence of peritoneal dissemination. No significant differences were observed in the primary tumor histology and grade of liver metastasis, but the survival period of the patients with liver metastasis and peritoneal dissemination was significantly shorter than that of the patients without peritoneal dissemination. Nine patients were treated with drugs that were effective in the chemosensitivity assay, and their responses included two complete responses and two partial responses; these patients showed a significantly prolonged survival period compared with patients treated with drugs that were not effective in the assay. The chemosensitivity assay is useful for evaluating the effectiveness of antitumor agents against liver metastasis of gastric cancer.

Adult↗
PubMed1975

Effect of "drugs for liver disease" on hepatotoxic action of carbon tetrachloride. I. Changes of lysosomal enzyme levels and effect of protoporphyrin on the levels.

In order to clarify the action of drugs for liver disease, the effect of protoporphyrin (PP) on CCl4-induced liver injury was studied. Attention was given to the levels of lysosomal enzymes, some components of the liver, and inhibition of enzymes and lysis of lysosomal membranes by lipid peroxides. Administration of PP to CCl4-poisoned rats was found to prevent the decrease in lysosomal lipolytic enzyme level in the liver, but not in other enzyme levels tested. The inhibition of lipolytic enzyme by CCl4 administered may be partially involved in lipid accumulation in the liver. A dose of PP administered to CCl4-poisoned rats for 8 days depressed the neutral lipid content in the liver nearly to the control value. Methyl linoleate hydroperoxide (hydroperoxide) at a lower concentration of 10(-6)% inhibited the lipolytic enzyme acitivity by 30% and in concentrations ranging from 10(-4) to 10(-3)% inhibited beta-glucuronidase activity. Addition of PP to the medium containing 10(-6) to 10(-5)% hydroperoxide and alpha-tocopherol reduced the enzyme inhibition further than in the absence of PP. The hydroperoxide in concentrations varying from 10(-6) to 10(-3)% caused a partial lysis of liver lysosomal membranes, but addition of PP slightly reduced the damage by the hydroperoxide in concentration lower than 10(-5)%.

Acid Phosphatase↗
PubMed2000

Ticlopidine-induced severe cholestatic hepatitis.

We report a case study of an 86-year-old female patient with severe cholestatic hepatitis who was undergoing treatment with oral ticlopidine 250 mg daily for coronary artery disease. The patient had nausea and vomiting and was jaundiced after taking ticlopidine for 6 weeks. She was admitted to the hospital for further evaluation. Ultrasound and endoscopic retrograde cholangiopancreatography eliminated the presence of biliary obstruction. Results from a liver biopsy showed a histopathologic picture consistent with cholestatic hepatitis. Ticlopidine-induced cholestatic hepatitis has been reported 32 times in the foreign literature. This is the first reported severe cholestatic hepatitis (total bilirubin up to 43 mg/dl) case in Taiwan. Ticlopidine-related blood dyscrasia is a renowned adverse drug effect; liver function should be monitored in patients receiving ticlopidine therapy.

Aged↗
PubMed1993

[Protective effects of Taiwan crude drugs on experimental liver injuries].

Protective effects of 41 Taiwan crude drugs on rat hepatic injuries caused by carbon tetrachloride (CCl4) and alpha-naphthylisothiocyanate (ANIT) were investigated. The methanol extracts of Elephantopi Herba and Lonicerae Flos inhibited the release of intrahepatic enzymes and histological changes by CCl4. The methanol extracts of Canarii Radix, Arecae Pericarpium, Cynomorii Caulis, Polygoni Cuspidati Radix, Phyllodii Herba, Junci Caulis Medulla, Rubiae Herba and Rhinacanthi Herba protected the hepatic injury by ANIT. Among them, the water extracts of Cymorii Caulis and Junci Caulis Medulla showed higher protective potency than the methanol extracts. And them this two crude drugs also protected the cholestasis by ANIT.

1-Naphthylisothiocyanate↗
PubMed1995

[The protective effects of drugs H and X on liver cold ischemic injury].

Using isolated perfusion rat liver model (IPRL), we studied the protective effects of drugs H and X on rat's liver cold ischemic injury. After the rat's liver was preserved for 12 hours in Collins II solution with the addition of drugs H and X, the necrotic rate of sinusoidal lining cells was significantly lower than that of control group. Within certain range of the dosage of drugs H and X, the necrotic rate of sinusoidal lining cells was in the inverse ratio of the dosage in the Collins II solution. We also found that drugs H and X had obvious protective effect on liver cell redox function. But these drugs could not inhibit tissue from swelling after Collins II solution preservation. The protective mechanisms of the drugs maybe relate to the remoral of free radicals and suppression of Kupffer's cells activity.

Animals↗
PubMed2004

Clinical experience with molecular adsorbent recirculating system (MARS) in patients with drug-induced liver failure.

The molecular adsorbent recirculating system (MARS) is a novel extracorporeal technique for liver support. We report the clinical results in a group of fourteen patients with drug-induced liver failure. Fourteen patients, aged 22-83 years, with acute or subacute liver failure [mean Child-Turcotte-Pugh (CTP) score 11 (range 8-15)] due to the intake of various drugs (diet pill overdose-2; Chinese traditional medicine (CTM)-4; antibiotic, paracetamol, tuberculostatic, or vasodilator abuse-8) were treated with one to seven sessions of MARS. Beneficial effects such as the improvement of encephalopathy and prothrombin activity, as well as a reduction of bilirubin and ammonia were recorded during MARS treatments. Thirteen out of fourteen patients survived the hospitalization (93%), and two of the discharged patients died during the follow-up of 6-12 months. The overall survival rate was about 79%. MARS therapy can contribute to the improved treatment of drug-induced liver failure patients.

Adult↗