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Original

Analysis of silent information regulator 1 (SIRT1) gene polymorphisms in antituberculosis- drug-induced hepatotoxicity in a prospective cohort study

Yu Wang, Xiu-Ying Yan, Jing-Can Wu, Gui-Yi Ji, Shou-Quan Wu, Wei-Wei Huang, Guo Chen, Andrew J. Sandford, and Jian-Qing He

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Volume 54 p. 775 - 781

Abstract

International Journal of Clinical Pharmacology and Therapeutics, Vol. 54 – No. 10/2016 (775-781)

Analysis of silent information regulator 1 (SIRT1) gene polymorphisms in antituberculosis- drug-induced hepatotoxicity in a prospective cohort study

Yu Wang¹*, Xiu-Ying Yan¹*, Jing-Can Wu¹, Gui-Yi Ji¹, Shou-Quan Wu¹, Wei-Wei Huang¹, Guo Chen², Andrew J. Sandford³, and Jian-Qing He¹

¹Department of Respiratory and Critical Care Medicine, West China Hospital, Sichuan University, ²Division of Geriatrics, Sichuan Provincial People’s Hospital, Chengdu, Sichuan, China, and ³Centre for Heart Lung Innovation, University of British Columbia and St. Paul’s Hospital, Vancouver, BC, Canada
Objective: Antituberculosisdrug-induced hepatotoxicity (ATDH) is a common and sometimes serious side effect related to tuberculosis (TB) treatment. A number of risk factors and host genetics contribute to the development of ATDH. However, genetic factors of ATDH remain to be identified. Silent Information Regulator 1 (SIRT1), an essential metabolism gene, was proved to be involved in ATDH in mice. The aim of this investigation was to study the association between ATDH and tag-single nucleotide polymorphisms (tag-SNPs) of the SIRT1 gene in a prospective cohort study in patients with TB. Methods: 280 newly diagnosed TB patients were recruited in this study before starting first line anti-TB treatment and were followed up for 3 months after initiating anti-TB therapy. The tag-SNPs were selected by using Haploview 4.2 based on the HapMap database of Han Chinese Beijing. Genotyping was performed by polymerase chain reaction (PCR) and the Sequenom MassARRAY iPLEX platform. Results: 24 (9.8%) of the 245 patients included in the final analysis developed hepatotoxicity during the following up period. No significant differences in the allele, genotype, or haplotype frequency distributions of the tag- SNPs (rs7069102, rs2273773, rs4746720) of the SIRT1 gene were identified between the ATDH and non-ATDH groups (all p > 0.05). Conclusions: The SIRT1 gene may not contribute to the risk for developing hepatotoxicity during anti-TB treatment in the Han Chinese population.Correspondence to:
Dr. Jian-Qing He
Department of Respiratory and Critical Care Medicine
West China Hospital, Sichuan University
No. 37 Guoxue Xiang, Wuhou Distric,
Chengdu 610041, Sichuan, China
Email: [email protected]

Case Report

Rifampicin-induced antineutrophil cytoplasmic antibody-positive vasculitis: a case report and review of the literature

Guiyi Ji, Xuemei Zeng, Andrew J. Sandford, and Jian-Qing He

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42.00 $

Volume 54 p. 804 - 807

Abstract

International Journal of Clinical Pharmacology and Therapeutics, Vol. 54 – No. 10/2016 (804-807)

Rifampicin-induced antineutrophil cytoplasmic antibody-positive vasculitis: a case report and review of the literature

Guiyi Ji¹*, Xuemei Zeng²*, Andrew J. Sandford³, and Jian-Qing He¹

¹Department of Respiratory and Critical Care Medicine, West China Hospital, Sichuan University, ²Department of Respiratory and Critical Care Medicine, Chengfei Hospital, Chengdu, Sichuan, China, and ³Centre for Heart Lung Innovation, University of British Columbia and St. Paul’s Hospital, Vancouver, BC, Canada
Antineutrophil cytoplasm antibody (ANCA)-associated vasculitis (AAV) is a pauci-immune necrotizing vasculitis that involves small vessels. Herein, we report an extremely rare case of rifampicin (RFP)-induced AAV. A 42-yearold female was transferred to the West China Hospital due to cough with phlegm for 3 months, fever for 1 month, and fatigue for 2 weeks. The patient was diagnosed with pulmonary tuberculosis (TB) and received anti-TB treatment with isoniazid, RFP, ethambutol, and pyrazinamide (PZA) at her local hospital. After 5 days of anti-TB treatment, her creatinine level rose to 420.2 μmol/L from a normal level prior to anti-TB treatment. Serum proteinase 3 (PR3)-ANCA was positive. After discontinuing the anti-TB drugs and administering protective renal treatment, her renal function improved, whereas PR3-ANCA remained positive. With RFP rechallenge after transfer to our hospital, the patient developed oliguria. Her urine volume increased gradually after RFP was discontinued 3 days later. Therefore, RFPinduced AAV was suspected. Eventually, the patient received prednisone and anti-TB therapy, including isoniazid, ethambutol, PZA, and moxifloxacin. After 2 months, PZA was discontinued. During 6 months of normal, and PR3-ANCA became negative at 4 months. This outcome is characteristic of RFP-induced AAV.

*Contributed equally.Correspondence to:
Jian-Qing He, MD
Department of Respiratory and Critical Care Medicine
West China Hospital, Sichuan University
Chengdu 610041, Sichuan, China
Email: [email protected]

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