Acute Disease ; Cardiomyopathies ; chemically induced ; Chemical and Drug Induced Liver Injury ; Critical Illness ; Ethylene Oxide ; poisoning ; Humans ; Male ; Middle Aged ; Nervous System Diseases ; chemically induced ; Occupational Diseases ; chemically induced ; Respiratory Tract Diseases ; chemically induced

Adult ; Chemical and Drug Induced Liver Injury ; etiology ; Dinitrobenzenes ; poisoning ; Humans ; Male ; Occupational Diseases ; chemically induced

We report a case of 61-yr-old man with stable psoriasis who progressively developed generalized pustular eruption, erythroderma, fever, and hepatic dysfunction following oral terbinafine. Skin biopsy was compatible with pustular psoriasis. After discontinuation of terbinafine and initiating topical corticosteroid and calcipotriol combination with narrow band ultraviolet B therapy, patient's condition slowly improved until complete remission was reached 2 weeks later. The diagnosis of generalized pustular psoriasis (GPP) induced by oral terbinafine was made. To our knowledge, this is the first report of GPP accompanied by hepatic dysfunction associated with oral terbinafine therapy.
Suppuration/chemically induced ; Psoriasis/*chemically induced ; Naphthalenes/*adverse effects ; Middle Aged ; Male ; Liver Diseases/*chemically induced ; Humans ; Antifungal Agents/*adverse effects ; Administration, Oral

To study the mechanism of endotoxin-induced hepatocellular injury in rats, a single dose of endotoxin, 15mg/kg, was injected intraperitoneally with or without dexamethasone pretreatment. Studies included light microscopic, histochemical, and electron microscopic observations with concomitant assay of free acid phosphatase activity of liver homogenateg. The results showed an increase of acid phosphatase activity as early as 30 minutes after the injection of endotoxin, and by light microscopy random focal necrosis of liver cells at 1 hour and fibrin thrombi formation in sinusoids especially within the area of necrosis at 3 hours. However, ultrastructural alteration was noted as early as 5 minutes after the injection of endotoxin characterized by marked dilatation of RER. The degree of necrosis, fibrin thrombus formation, and the elevation of free acid phosphatase activity in the liver homogenates seemed to parallel each other suggesting a possible interrelationship among these phenomena. However, the ultrastructnral changes of the hepatocytes were present far ahead of the appearance of fibrin thrombi formation. Therefore, the causal relationship of the fibrin thrombi to liver cell injury appeared unlikely. Despite the increase of free acid phosphatase activity in liver homogenates, no demonstrable structural disruption of lysosomal membrane was noted. In view of the prominent changes of RER 5 minutes after the endotoxin administration, the primary injurious effect of endotoxin affects the membrane system of all organelles including the lysosomal membrane, leading to the leakage of lysosomal enzymes into the cytoplasmic sap. Dexamethasone pretreatment alleviated necrosis and markedly inhibited fibrin thrombus formation, and the mechanism of this effect is considered to be a stabilizing effect of glucocorticoid upon membrane systems.
Acid Phosphatase/metabolism ; Animal ; Endotoxins* ; Injections, Intraperitoneal ; Liver/enzymology ; Liver/pathology* ; Liver Diseases/chemically induced ; Liver Diseases/metabolism ; Liver Diseases/pathology* ; Male ; Necrosis ; Rats

Recently the use of herbal preparations as remedies for various medical conditions, has been rapidly increasing in Korea. In our previous study, 38.9% of patients with chronic liver disease were found to use some sorts of herbal preparations. They believe herbal preparations are safe although the ingredients has never been rigorously substantiated. Toxicities of certain herbal preparations are caused by their contaminants and adulterated ingredients or concurrently used conventional drugs rather than specific components of the herbal preparations. Furthermore, in most instances, multiple herbal ingredients are used by the prescribers of oriental medicine. All of these conditions frequently impose diagnostic difficulties. There are myriads of plant-derived hepatotoxic substances which may or may not cause liver injury in individuals. The severity of liver injury depends largely on the toxicity of the substance, the amount of exposure and the individual's susceptibility. These toxic substances cause liver injury not only through the mechanism of intrinsic hepatotoxicity but also through the idiosyncrasy as in conventional drug-induced injury. Therefore, theoretically, it is possible to apply pre-existing CAMs (Causality Assessment Methods) to the assessment of causality in cases with diagnostic difficulties.
English Abstract ; Humans ; Liver Diseases/*chemically induced ; Phytotherapy/*adverse effects ; Plant Preparations/*adverse effects

OBJECTIVETo explore the hepatic injury induced by CCl4in SD rat.

METHOD40 SD rats were allocated to male and female group, consisting of 20 animals/sex/group. SD rats were given at 2 mL x kg(-1) of 10% CCl4 through celiac injection per 3 day for 12 days. All rats were killed by anaesthesia of ethyl ether and bleeding through abdominal aorta at 12th day. Liver tissue was fixed in 10% neutral formalin, embedded in paraffin, cut at a nominal thickness of 3 microm, stained with hematoxylin and eosin ( H&E) , evaluated at by microscopic examination.

RESULT19 cases with local necrosis, 8 cases with fatty degeneration, 9 cases with cystic degeneration and 2 cases with fibrosis were seen in group male. 20 cases with local necrosis, 9 cases with fatty cases degeneration, 1 case with cystic degeneration and 1 case with fibrosis were seen in group female. The incidence of cystic degeneration in male group was found significantly higher than that in female group (P < 0. 05) , but the incidence of other lesions was no significant difference between male and female group.

CONCLUSIONCCl4 induces local necrosis , fatty degeneration, fibrosis and cystic degeneration in SD rat. The incidences of local necrosis , fatty degeneration and fibrosis were no significantly difference between male and female rat, but the incidence of cystic degeneration in male rats was significant higher than that in female rats.

Animals ; Carbon Tetrachloride ; Chemical and Drug Induced Liver Injury ; Cysts ; chemically induced ; pathology ; Disease Models, Animal ; Female ; Liver ; pathology ; Liver Cirrhosis ; chemically induced ; pathology ; Liver Diseases ; pathology ; Liver Neoplasms ; chemically induced ; pathology ; Male ; Precancerous Conditions ; chemically induced ; pathology ; Rats ; Rats, Sprague-Dawley ; Sex Factors

A 3-year-old Thoroughbred filly was referred to the Equine Hospital, Korea Racing Association for evaluation of hematuria, inappetite, weight loss and depression. From 25 days prior to admission, the horse was treated for right carpal lameness with 20 mg intramuscular administration of triamcinolone acetonide per day for consecutive 10 days by a local veterinarian. Clinical and laboratory findings included vaginal hyperemia, flare in bladder wall, neutrophilia, lymphopenia, polyuria, polydipsia and laminitis in the end. High activities of aspartate transaminase and gamma glutamyltransferase and high concentration of total bilirubin indicated hepatopathy. Further hematology, serum biochemistry and urinalysis did not reveal any abnormalities. Medical history, physical and clinicopathologic findings suggest that the laminitis and hepatopathy in this horse were most likely induced by repeated administration of exogenous corticosteroid. However, guarded prognosis of treating laminitis undermined the benefit of improvement of hematuria following electroacupuncture stimulation. The combined stimulation of kidney related acupoints (Shen Peng, Shen Shu), lumber related acupoints (Yao Qian, Yao Zhong) and associate acupoints (Guan Yuan Shu, Bai Hui) at 5Hz, 1-2V, for 40 minutes was of value in the treatment of hematuria. This case shows that horses under steroids may exhibit laminitis and steroid hepatopathy. Early recognition and good management of laminitis are important in the limitation of complications.
Animals ; Electroacupuncture/veterinary ; Female ; Foot Diseases/chemically induced/pathology/*veterinary ; Forelimb/pathology ; Glucocorticoids/*adverse effects/therapeutic use ; Hoof and Claw/pathology ; Horse Diseases/*chemically induced/pathology ; Horses ; Lameness, Animal/*chemically induced/drug therapy ; Liver Diseases/chemically induced/*veterinary ; Triamcinolone Acetonide/*adverse effects/therapeutic use

OBJECTIVE: To assess the risk of aristolochic acid (AA)-associated cancer in patients with AA nephropathy (AAN). METHODS: A retrospective study was conducted on patients diagnosed with AAN at Peking University First Hospital from January 1997 to December 2014. Long-term surveillance and follow-up data were analyzed to investigate the influence of different factors on the prevalence of cancer. The primary endpoint was the incidence of liver cancer, and the secondary endpoint was the incidence of urinary cancer during 1 year after taking AA-containing medication to 2014. RESULTS: A total of 337 patients diagnosed with AAN were included in this study. From the initiation of taking AA to the termination of follow-up, 39 patients were diagnosed with cancer. No cases of liver cancer were observed throughout the entire follow-up period, with urinary cancer being the predominant type (34/39, 87.17%). Logistic regression analysis showed that age, follow-up period, and diabetes were potential risk factors, however, the dosage of the drug was not significantly associated with urinary cancer. CONCLUSIONS No cases of liver cancer were observed at the end of follow-up. However, a high prevalence of urinary cancer was observed in AAN patients. Establishing a direct causality between AA and HCC is challenging.
Humans ; Retrospective Studies ; Incidence ; Carcinoma, Hepatocellular ; Liver Neoplasms/epidemiology* ; Kidney Diseases/chemically induced* ; Aristolochic Acids/adverse effects*

Adult ; Chemical and Drug Induced Liver Injury ; Dimethylformamide ; adverse effects ; Formamides ; analysis ; Humans ; Kidney ; physiopathology ; Kidney Diseases ; chemically induced ; physiopathology ; urine ; Kidney Function Tests ; Liver ; physiopathology ; Liver Diseases ; physiopathology ; urine ; Liver Function Tests ; Male ; Middle Aged ; Occupational Exposure

This article made a brief analysis of clinical adverse effects of cinnabar. Except for allergic reaction, almost all the adverse events of cinnabar were caused by unreasonable application. The majority of the poisoning cases were associated with excessive and/or long-term dosage, and improper preparation methods, such as decocting, heating or fumigating. Children showed to be prone to poisoning. The poisoning caused by unreasonable use of cinnabar should be considered to be drug alert, but not advert effect. And the toxicity of cinnabar could be avoided by normalizing the preparation method, controlling the dosage and duration.
Chemical and Drug Induced Liver Injury ; etiology ; Coma ; chemically induced ; Drug Compounding ; adverse effects ; Drug Incompatibility ; Drug Overdose ; Gastrointestinal Diseases ; chemically induced ; Humans ; Hypersensitivity ; etiology ; Mercury Compounds ; adverse effects ; poisoning ; Mercury Poisoning ; prevention & control ; therapy