Ben Ari Z, Mehta A, Lennard L, Burroughs A K
Liver Transplantation Unit, Royal Free Hospital, Hampstead, London, UK.
J Hepatol. 1995 Sep;23(3):351-4. doi: 10.1016/0168-8278(95)80481-1.
Azathioprine can cause severe myelosuppression. The inherited activity of the enzyme thiopurine methyltransferase has been recently recognised as a major factor in the susceptibility to myelosuppression. Thiopurine methyltransferase deficiency occurs at a frequency of one in 300 and is associated with profound myelosuppression after a short course of azathioprine. Very low thiopurine methyltransferase activity represents the TPMTL/TPMTL genotype, and can be detected before therapy with azathioprine is started. We describe the first documented case of azathioprine-induced severe myelosuppression due to thiopurine methyltransferase deficiency in autoimmune liver disease. The azathioprine dose was low (1 mg/kg) and pancytopenia occurred after 56 days therapy. It would be advisable to measure thiopurine methyltransferase activity before patients with autoimmune hepatitis are exposed to azathioprine.
硫唑嘌呤可导致严重的骨髓抑制。硫嘌呤甲基转移酶的遗传活性最近被认为是骨髓抑制易感性的一个主要因素。硫嘌呤甲基转移酶缺乏症的发生率为300分之一,与短期使用硫唑嘌呤后发生的严重骨髓抑制有关。极低的硫嘌呤甲基转移酶活性代表TPMTL/TPMTL基因型,可在开始使用硫唑嘌呤治疗前检测到。我们描述了自身免疫性肝病中首例因硫嘌呤甲基转移酶缺乏导致硫唑嘌呤诱导严重骨髓抑制的记录病例。硫唑嘌呤剂量较低(1mg/kg),治疗56天后出现全血细胞减少。在自身免疫性肝炎患者接触硫唑嘌呤之前,建议检测硫嘌呤甲基转移酶活性。