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接受硫唑嘌呤治疗的患者中嘌呤核苷磷酸化酶和腺苷脱氨酶缺乏抑制作用。

Lack of inhibition of purine nucleoside phosphorylase and adenosine deaminase in patients treated with azathioprine.

作者信息

Maddocks J L, Al-Safi S A

出版信息

Br J Clin Pharmacol. 1985 Jan;19(1):108-11. doi: 10.1111/j.1365-2125.1985.tb02623.x.

Abstract

Deficiency of the purine salvage enzymes purine nucleoside phosphorylase (PNP) and adenosine deaminase (ADA) are known causes of immunodeficiency. Evidence for inhibition of these enzymes was sought in 16 patients on azathioprine therapy by testing for deoxyguanosine (PNP deficiency) and deoxyadenosine (ADA deficiency) in urine using a novel phosphorescence method. These abnormal nucleosides were not found in urine of azathioprine treated patients or in 30 normal controls but were easily detected in urine from proven cases of PNP and ADA deficiency suggesting lack of in vivo inhibition of PNP and ADA by azathioprine.

摘要

嘌呤补救酶嘌呤核苷磷酸化酶(PNP)和腺苷脱氨酶(ADA)缺乏是已知的免疫缺陷病因。通过一种新型磷光法检测尿液中的脱氧鸟苷(PNP缺乏)和脱氧腺苷(ADA缺乏),在16例接受硫唑嘌呤治疗的患者中寻找这些酶受到抑制的证据。在硫唑嘌呤治疗患者的尿液中以及30名正常对照中均未发现这些异常核苷,但在经证实的PNP和ADA缺乏病例的尿液中很容易检测到,这表明硫唑嘌呤在体内不会抑制PNP和ADA。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/36c4/1463784/8177fba76486/brjclinpharm00150-0109-a.jpg

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