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Results for “HEPATITIS, TOXIC”

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PubMed2004

Pulmonary and hepatic toxicity due to nitrofurantoin and fluconazole treatment.

OBJECTIVE: To reemphasize potential risks associated with chronic nitrofurantoin use and to report a case of combined pulmonary and hepatic toxicity precipitated from acute use of fluconazole concomitantly with chronic nitrofurantoin. CASE SUMMARY: A 73-year-old white man taking nitrofurantoin 50 mg/day for 5 years developed combined hepatic and pulmonary toxicity after taking fluconazole acutely for onychomycosis. Two months after starting fluconazole, the patient's hepatic enzymes showed elevation 5 times the upper limits of normal. In addition, the patient reported fatigue, dyspnea on exertion, pleuritic pain, burning trachea pain, and a cough. Chest X-rays showed bilateral pulmonary disease consistent with nitrofurantoin toxicity. Both drugs were determined to be the cause of the patient's pulmonary and hepatic toxicity, so they were discontinued. Pulmonary function tests measured after discontinuation were abnormal and also consistent with nitrofurantoin toxicity. The patient's hepatic and pulmonary toxicity resolved upon discontinuation of both drugs and use of inhaled corticosteroids. DISCUSSION: Changes in hepatic enzyme measurement, pulmonary function measurements, and chest X-rays indicate that our patient developed hepatic and pulmonary toxicity due to his drug therapy. An objective causality assessment revealed that these adverse events were probably due to fluconazole given with nitrofurantoin. Either drug may have caused the hepatic toxicity. However, it is possible that pharmacokinetic changes induced by an interaction with fluconazole precipitated the nitrofurantoin-induced pulmonary toxicity. CONCLUSIONS: Our patient developed pulmonary and hepatic toxicity after starting fluconazole in combination with chronic nitrofurantoin. A potential drug interaction of unknown mechanism may have been the cause of the toxicities.

Aged↗

PubMed1993

Hepatic toxicity associated with fluorouracil plus levamisole adjuvant therapy.

PURPOSE: To determine the frequency and nature of hepatic toxicity associated with fluorouracil (5-FU) plus levamisole adjuvant therapy. PATIENTS AND METHODS: All patients had resection of stage II or stage III colon cancer and were randomized to receive observation only, levamisole alone, or 5-FU plus levamisole. Serial liver function studies were documented in 1,025 patients who did not develop recurrence during the year of therapy. RESULTS: One hundred forty-nine (39.6%) of 376 patients treated with 5-FU plus levamisole showed laboratory abnormalities consistent with hepatic toxicity, compared with 16.3% of 251 patients treated with levamisole alone and 16.1% of 398 untreated controls. Most common was elevation of alkaline phosphatase, frequently accompanied by elevations of transaminase or serum bilirubin. Characteristically, these changes were mild, not associated with symptoms, and resolved when therapy was stopped. In some instances, they were associated with elevated carcinoembryonic antigen (CEA) tests or with fatty liver seen on computed tomographic (CT) scan or liver biopsy. CONCLUSION: Mild and reversible hepatotoxicity is a common consequence of 5-FU plus levamisole adjuvant therapy, but this is only rarely symptomatic. However, the oncologist should be alert to this phenomenon, since the associated laboratory and imaging findings may simulate those associated with hepatic metastasis.

Antineoplastic Combined Chemotherapy Protocols↗

PubMed2001

Severe toxic hepatitis associated with amoxycillin and clavulanic acid.

Toxic hepatitis secondary to amoxycillin-clavulanic acid is an infrequent clinical picture. Most of the cases are reported to have a benign course. We report two cases of severe hepatic failure following amoxycillin-clavulanic acid use. One of the cases had cholestatic features primarily, and the other had hepatocellular injury prominently. The first case had also findings of trombotic trombositic purpura and had a fatal course.

Adult↗

PubMed2001

[Clozapine-induced toxic hepatitis].

A case of clozapine-induced toxic hepatitis in a 49-year old woman with schizophrenia is described. The daily clozapine dose was clinically titrated to 300 mg. Subsequently, the patient experienced lethargy and anorexia, and fever, eosinophilia, leucocytosis and abnormal liver parameters were found. The serum concentration of clozapine was 8595 nmol/l, and treatment was discontinued. After eight days, the condition stabilised, and low-dose clozapine treatment was successfully reinstituted with serum monitoring (TDM).

Chemical and Drug Induced Liver Injury↗

PubMed1979

[Characteristics of the development of acute toxic hepatitis in rats stimulated with prodigiozan].

Acute toxic hepatitis was induced in Wistar rats by means of a single injection of 40% CCl4 on a peach-kernell oil base (0.2 ml/100 g body weight). Under conditions of stimulation with the bacterial polysaccharide prodigiosan, the resistance of hepatocytes to CCl4 sharply increased, which was shown by diminished severity of hepatic parenchyma destruction.

Acute Disease↗

PubMed1989

[A morphological evaluation of the preventive and therapeutic action of low-intensity laser radiation on the course of acute toxic hepatitis].

The optimal schedule of the preventive and therapeutical effect of helium-neon laser on the acute toxic hepatitis induced in rats by CCl4 is established. The laser dose of 5-10 mVt/cm2 for 5-10 min prevents the toxic hepatitis while therapeutical use of 7 to 10 such schedules reduces the intensity of the protein and fat degeneration, parenchymal necrosis and inflammatory infiltration.

Acute Disease↗

PubMed1978

[Structuro-functional changes in dog liver and regional lymph node lysosomes in toxic hepatitis].

Structural and functional changes in the dog liver and regional lymph nodes lysosomes were studied during toxic hepatitis induced by CCl4 administration (single and repeated). Total activity of lysosomal enzymes (acid RNA-ase and beta-galactosidase) was higher in the regional lymph nodes than in the liver, reflecting the barrier, protective function of the organ. During acute toxic hepatitis the specific activities of acid RNA-ase and cathepsin D displayed a sharp rise. No normalization of the indices under study occurred during the observation period (from 8 to 30 days). At the same time there was a rise of the regional lymph node weight and an elevation of the relative macrophage and neutrophil content in the sinuses. The increased activity of the lysosome enzymes in the regional lymph nodes in injury of the liver was connected with greater functional load on the lymph nodes effecting hydrolysis of biopolymeres which penetrated into the regional lymphatic node with the lymph.

Animals↗

PubMedDate not supplied

[A comparative evaluation of the effect of different types of sapropel on dynamic liver function in intact rats and in the modelling of toxic hepatitis].

A course of silicic sapropel applications compared to calcareous sapropel induced a reversible fall of total lipid concentration in blood serum of intact rats. Sapropels of different kinds and of the same kind but obtained from different depths of the same deposit varied by their ability to correct hepatic function in rats with toxic hepatitis. The highest benefit was registered in application of carbonate sapropels taken from the depth of 1.5-2.5 m.

Animals↗

PubMed1982

Plasma lipoprotein pattern in relation to liver histology after toxic hepatitis and experimental biliary obstruction in rabbits.

Plasma lipoproteins were studied in relation to liver histology in rabbits in the course of toxic hepatitis and compared to those after experimental biliary obstruction. The lipoprotein electrophoretic pattern became deeply abnormal during the acute phase of toxic hepatitis and correlated with the degree of liver injury, improving during recovery. Liver damage was more severe after carbon tetrachloride than after alcohol and milder after allylo-isopropyl-acetamide, a porphyrinogenic substance. Lipoprotein abnormalities were not followed by significantly reduced levels of cholesterol esters in the plasma. In comparison, animals with biliary obstruction developed milder liver damage presented gross abnormalities of plasma lipids and lipoproteins, followed by relative deficiency of cholesterol esterification. It is concluded that lipoprotein changes in acute liver injury, although non-specific, are a sensitive index of liver damage and recovery. Serious acute liver injury can exist without significant fall in cholesterol esters.

Alanine Transaminase↗

PubMedDate not supplied

Hepatic toxicity of nonsteroidal anti-inflammatory drugs.

The hepatic toxicity associated with the use of nonsteroidal anti-inflammatory drugs (NSAIDs) is reviewed. NSAIDs include agents in more than 10 classes of compounds, many of which are capable of producing hepatic injury. When NSAIDs are used to treat rheumatic disease, the hepatic effects of the disease itself may complicate the diagnosis of NSAID-induced hepatic injury. Hepatotoxicity caused by drugs may be either intrinsic or idiosyncratic in nature and may be manifested by hepatocellular injury, cholestasis, or a combination of both types of injury. Intrinsic hepatotoxins, such as salicylates, produce injury in a large percentage of exposed individuals that is often dose related and occurs after a short, fixed latent period. Idiosyncratic injury, such as that caused by sulindac, occurs in unusually susceptible persons, usually after a variable latent period. Injury is not dose related. In most cases of hepatocellular injury, the prognosis of those patients who survive the acute phase of injury is good. Fatalities rarely result from cholestatic injury. Monitoring of serum hepatic-enzyme concentrations is recommended for patients receiving NSAIDs from the indole, pyrazolone, and propionic acid classes since these agents have been associated with the greatest incidence of adverse hepatic reactions. Enzyme monitoring is advisable for high-risk individuals receiving NSAIDs from other classes. Enhance vigilance on the part of clinicians, patients, and pharmaceutical manufacturers is needed to reduce the incidence of hepatotoxicity associated with the use of NSAIDs.

Anti-Inflammatory Agents↗

PubMed1975

Serum cobalt-activated acylase and gamma-glutamyl transpeptidase activities in toxic hepatitis.

Marked activity of cobalt-activated acylase was found in the sera of 33 of 37 patients with acute toxic hepatitis due to poisoning with either amanita mushrooms or chemicals. The activity of the enzyme showed a positive correlation with that of serum transaminases, reached the highest levels on the patient's admission to hospital and within a few days fell rapidly to undetectable levels. Slight acylase activity was observed in the majority of patients intoxicated with drugs or carbon monoxide but was not seen in sera of those poisoned with non-amanita mushrooms who showed no signs of liver injury. Unlike acylase, the serum activity of gamma-glutamyl transpeptidase remained unchanged over the first days of acute toxic hepatitis. The determination of serum cobalt-activated acylase might be of value in the diagnosis of acute liver injury.

Acute Disease↗

PubMed1984

Hepatic toxicity of low doses of mithramycin in hypercalcemia.

The medical records of patients receiving mithramycin for the treatment of hypercalcemia at The Johns Hopkins Oncology Center were reviewed. Of 67 evaluable patients, 11 (16%) developed hepatic toxicity when graded using standard criteria. The pattern of laboratory abnormalities noted suggested mild hepatocellular damage that was reversible within 2 weeks. Review of these patients did not identify factors which predispose to hepatic toxicity, although failure to do so may reflect the limited number of toxic patients evaluated. Mild, reversible hepatic dysfunction appears to be a more common sequela of mithramycin administration than has previously been recognized.

Chemical and Drug Induced Liver Injury↗

PubMed1992

Chaparral-induced toxic hepatitis--California and Texas, 1992.

Cases of acute toxic hepatitis in two patients--one in California and one in Texas--have been attributed to ingestion of an herbal nutritional supplement product derived from the leaves of the creosote bush known commonly as chaparral. This report summarizes the investigations of these cases.

Acute Disease↗

PubMedDate not supplied

[Hepatoprotectors containing phospholipids decrease the immunosuppressive effect of prednisolone in rats with experimental toxic hepatitis].

The experiments on rats with a model toxic hepatitis induced by tetrachloromethane showed that hepatoprotectors containing phospholipids (eplir and essentiale) introduced in combination with prednisolone decrease the immunodepressant effect of this glucocorticoid, as manifested by a decrease in the atrophy of thymus and an increase in the amount of blood lymphocytes, the number of splenic blasts, and the functional activity of mononuclear cells in C3b and Fc(gamma) receptors in peritoneal exudate.

Animals↗

PubMed2003

[A case of toxic hepatitis induced by habitual glue sniffing].

The link between toxic hepatitis and exposure to organic solvents is relatively well-documented, but there are no specific laboratory or histologic findings diagnostic of chemical-induced hepatitis. Clinical history, therefore, is very important in making a diagnosis. A history of glue sniffing is sometimes overlooked and glue sniffing has not received much attention as a cause of hepatitis. Toluene, a main organic solvent in glue, is known to cause disturbances in various organs such as the heart, nervous system, liver and kidneys. We present a case of hepatitis in an individual who has sniffed glue for euphoria for 3 years. There is an increasing tendency towards glue sniffing among young adolescents today, so toxicity caused by exposure to organic solvents should be considered as one possible cause of hepatitis in young adolescents.

Adhesives↗

PubMed2004

Free radical oxidation and catalytic activity of aconitate hydratase in rat liver under normal conditions and during toxic hepatitis.

We observed intensification of free radical oxidation, decrease in activity, and changes in catalytic properties of aconitate hydratase in the liver of rats with toxic hepatitis. The total yield and maximum flash intensity of biochemiluminescence increased by 2.2 and 1.7 times, respectively. Differences were revealed in the regulation of aconitate hydratase activity with Fe(2+), Ca(2+), H(2)O(2), and oxidized and reduced glutathione in the liver of rats with toxic hepatitis and control animals.

Aconitate Hydratase↗

PubMedDate not supplied

[The intensity of free radical oxidation and catalytic properties of the rat liver NADP-isocitrate dehydrogenase in the norm and in toxic hepatitis].

Parameters of hepatic free radical oxidation and catalytic properties of NADP-isocitrate dehydrogenase (EC 1.1.1.42; NADP-IDH) have been investigated in normal rats and under conditions of toxic hepatitis. Development of hepatitis was accompanied by the increase of conjugated dienes, malondialdehyde and some chemiluminescence parameters. Toxic hepatitis was also accompanied by the increase of liver NADP-IDH. Homogenous preparations of liver NADP-IDH from normal and toxic rats exhibited different sensitivity to effectors studied (Fe2+, Ca2+, H2O2, reduced glutatione).

Animals↗

PubMed2003

Protective effect of low molecular weight heparin on oxidative injury and cellular abnormalities in adriamycin-induced cardiac and hepatic toxicity.

The aim of the present work is to evaluate the effect of a heparin derivative, low molecular weight heparin (LMWH) on the biochemical changes, tissue peroxidative damage and abnormal antioxidant levels in adriamycin (ADR) induced cardiac and hepatic toxicity. Male Wistar rats (140 +/- 10 g) were divided into four groups: untreated control (group I), ADR group (a single dose intravenous injection of 7.5 mg/kg ADR--group II), LMWH control (300 microg/day per rat s.c. for 1 week--group III) and ADR plus LMWH group (7.5 mg/kg ADR on day 1 of study period followed by LMWH treatment, 300 microg/day per rat commencing on day 8 and continued for a week. At the end of the 2-week experimental period, all animals were terminated. Cellular damage was assessed in terms of serum and tissue lactate dehydrogenase (LDH), aminotransferases and alkaline phosphatase (ALP) activities. Creatine phosphokinase (CPK) was assessed in the serum and heart tissue. The role of LMWH in altering the oxidative stress in ADR-induced toxicity was evaluated on the basis of its influence on cardiac and hepatic lipid peroxidation and antioxidant status (enzymatic and non-enzymatic)--superoxide dismutase (SOD), catalase and glutathione peroxidase (GPx), reduced glutathione (GSH), alpha-tocopherol (Vitamin E) and ascorbate (Vitamin C). LMWH administration to ADR-induced rats prevented the rise in serum and tissue levels of LDH, aminotransferases and ALP, while these parameters were significantly elevated in the ADR group in comparison with the control group. Cardiotoxicity indicated by rise in serum CPK in the ADR group was attenuated by LMWH treatment in group IV. LMWH decreased the cardiac and hepatic lipid peroxidation induced by ADR. Histologic examination revealed that the ADR-induced deleterious changes in the heart and liver tissues were offset by LMWH treatment. Restoration of cellular normalcy accredits LMWH with cytoprotective role in adriamycin-induced cardiac and hepatic toxicity.

Animals↗