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We report that one 18-year-old female patient with no epilepsia history developed severe epileptiform seizures while she was receiving "ciclosporin A (CsA)-mycophenolate-methylprednisolone" antirejection therapy after combining one week's voriconazole administration following allogeneic hematopoietic stem cell transplantation (allo-HSCT) for myelodysplastic syndromes (MDS). Her blood concentration of CsA was 378 ng/ml (elevated ↑64%, contrasted with the level before the addition of voriconazole) on the second day of admission, and the MRI of head showed leukoencephalopathy in bilateral occipital and left frontal lobe on the 4(th) day of admission. The most likely mechanism is that because of voriconazole's enzyme inhibition and CsA as the substrate of hepatic enzymes, voriconazole elevated the blood concentration of CsA and enhanced its toxicity. This case highlights the importance of clinical pharmacists joining the medical team and optimizing the patients' treatment protocols by performing a systematic literature research, accumulating the knowledge of the potential drug interaction and examining prescriptions.

Qibao Meiran Wan is a Chinese herbal product sold as a therapy for tonifying the liver and kidney, dizziness, premature graying of hair, backache, constipation, and night sweats. It is widely available in Chinese pharmacies and drugstores and is sold without prescription. We describe a case of acute liver injury in a 26-year-old Chinese man who developed symptomatic hepatitis 1 month after starting Qibao Meiran Wan. There was no evidence of viral hepatitis, Epstein-Barr virus, cytomegalovirus, autoimmune hepatitis, or Budd-Chiari syndrome. The liver injury slowly resolved over 20 days after discontinuing the herbal product. Herbal toxicity was later confirmed by a liver biopsy. Qibao Meiran Wan contains a mixture of several plants including Polygonum multiflorum, which was previously associated with hepatotoxicity. To our knowledge, this is the first report of hepatotoxicity by Qibao Meiran Wan. Clinicians treating patients with acute hepatitis of unclear etiology should pay attention to the consumption of Qibao Meiran Wan.

A 9-year-old boy received a rifampicin-isoniazid-ethambutol regimen for suspected extra-pulmonary tuberculosis, and glucurolactone and vitamin B6 to provide liver protection and decrease neurotoxicity associated with isoniazid. Baseline serum aminotransferase and total bilirubin levels were within normal limits before anti-tubercular treatment. After 4 days of treatment, the patient’s body temperature increased (from 38.0°C to 40.1°C) and on the 11th day of treatment, serum chemistry results showed 400 U/L aspartate transaminase, 535 U/L alanine aminotransferase and 76.8 μmol/L total bile acid, which likely indicated drug-induced hepatic injury. After discontinuing isoniazid or administering anti-tubercular therapy without isoniazid, hyperpyrexia gradually resolved; hyperpyrexia reappeared following rechallenge with isoniazid. The patient’s liver function returned to normal after symptomatic treatment. Thus, hyperpyrexia that accompanied hepatic injury was considered to be related to isoniazid. This case indicated that hyperpyrexia could also appear during anti-tubercular treatment owing to its hepatotoxicity.

Objectives To explore the effects of simvastatin on NF-κB activation in cholesterol diet rabbit artery and the underlying mechanisms of the beneficial effects of simvastatin on atherosclerosis (AS). Methods Twenty-four male rabbits were randomly divided into three groups: normal diet groups, cholesterol diet groups and the simvastatin groups which received both cholesterol diet and simvastatin 5 mg/kg/days intragastrically, After 16 weeks rabbits were executed and the aortas were harvested for the pathologic and morphologic observations. Western blot was used to determine cytoplasmic p-I-κB α, I-κB α protein expression and cytoplasmic and nuclear NF-κB p65 protein expression of rabbit aortas. Results Compared with normal diet groups, cholesterol diet groups demonstrated remarkably atherosclerosis in the arteries. And the expression of cytoplasmic p-I-κBа and nuclear NF-κB p65 expression was obviously increased, but I-κB α was markedly decreased in cholesterol diet groups (n=6; p Conclusions NF-κB activation might be involved in the process of atherosclerosis in high cholesterol diet rabbits. Simvastatin could ameliorates atherosclerosis (AS) through interfering NF-κB activation and translocation