Allopurinol-induced aplastic anemia in a patient with chronic kidney disease

Kim, Y W; Park, B S; Ryu, Chong-Hyon; Park, S J; Kang, Shin-Wook; Kim, Y H; Song, In Sang; Shon, Ji‐Hong

doi:10.5414/cnp71203

Cited by 13 publications

(5 citation statements)

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“…Several cases of aplastic anemia have been reported leading to some fatalities [11] particularly in patients concomitantly using drugs causing bone marrow suppression and/or renal insufficiency [9,12].…”

Section: Discussionmentioning

confidence: 99%

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Agranulocytosis: an adverse effect of allopurinol treatment

Mari¹,

Ricci²,

Imberti³

et al. 2013

Ital J Med

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Introduction: Allopurinol is a xanthine oxidase inhibitor that is primarily used to treat hyperuricemia and its complications. The drug is rarely associated with adverse effects, but those that occur can be significant. Hematologic side effects, including bone marrow suppression, severe anemia, thrombocytopenia, and leukopenia, have been reported in 0.2-0.6% of treated patients. Materials and methods: We report a case of agranulocytosis associated with allopurinol therapy in a patient admitted for fever.

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Section: Discussionmentioning

confidence: 99%

“…Potential inhibition of purine and pyrimidine biosynthesis in genetically-predisposed patients could be responsible for the suppression of the marrow cell line [1,2,12,17,18,20,21].…”

Section: [ ( ) T D $ F I G ]mentioning

confidence: 99%

Agranulocytosis: an adverse effect of allopurinol treatment

Mari¹,

Ricci²,

Imberti³

et al. 2013

Ital J Med

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“…We have demonstrated that repeat‐dose toxicity studies with orally administered febuxostat did not show any evidence of myelotoxic potential for febuxostat in subjects with renal impairment . Whereas serious blood dyscrasias have been reported with the use of allopurinol, no cases of neutropenia have yet to be documented with febuxostat …”

Section: What Is Known and Objectivementioning

confidence: 84%

Acute neutropenia associated with initiation of febuxostat therapy for hyperuricaemia in patients with chronic kidney disease

2013

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“…Allopurinol is known to cause anaemia symptoms, such as macrocytic anaemia and aplastic anaemia, as side effects in humans and rodents (Chao, Yang, & Lee, ; Kim et al, ; Lin et al, ). In particular, aplastic anaemia which is a serious condition and is clinically problematic.…”

Section: Discussionmentioning

confidence: 99%

Perfecting a high hypoxanthine phosphoribosyltransferase activity–uricase KO mice to test the effects of purine‐ and non‐purine‐type xanthine dehydrogenase (XDH) inhibitors

Hosoya

Uchida

Shibata

et al. 2020

British J Pharmacology

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Background and Purpose: Purine metabolism in mice and human differ in terms of uricase (Uox) activity as well as hypoxanthine phosphoribosyltransferase (HPRT) activity. The aim of this study was the establishment of high HPRT activity-Uox knockout (KO) mice as a novel hyperuricaemic model. Then to investigate the effects of purine-type xanthine dehydrogenase (XDH) inhibitor, allopurinol, and non-purinetype XDH inhibitor, topiroxostat, on purine metabolism. Experimental Approach: A novel hyperuricaemic mouse model was established by mating B6-ChrXC MSM mice with uricase KO mice. The pharmacological effects of allopurinol and topiroxostat were explored by evaluating urate, hypoxanthine, xanthine and creatinine in the plasma and urine of these model mice. Furthermore, we analysed the effect of both drugs on erythrocyte hypoxanthine phosphoribosyltransferase activity. Key Results: Plasma urate level and urinary urate/creatinine ratio significantly decreased after administration of allopurinol 30 mgÁkg −1 or topiroxostat 1 mgÁkg −1 for 7 days. The urate-lowering effect was equivalent for allopurinol and topiroxostat.However, the urinary hypoxanthine/creatinine ratio and xanthine/creatinine ratio after treatment with topiroxostat were significantly lower than for allopurinol. In addition, the urinary oxypurine/creatinine ratio was significantly lowered after treatment with topiroxostat, but allopurinol elicited no such effect. Furthermore, allopurinol inhibited mouse erythrocyte hypoxanthine phosphoribosyltransferase, while topiroxostat did not. Conclusions and Implications:High hypoxanthine phosphoribosyltransferase activity-uricase KO mice were established as a novel hyperuricaemic animal model.In addition, topiroxostat, a non-purine-type xanthine dehydrogenase inhibitor, elicited a potent plasma urate-lowering effect. However, unlike allopurinol, topiroxostat did not perturb the salvage pathway, resulting in lowered total oxypurine excretion.Abbreviations: BUN, blood urea nitrogen; CRP, C-reactive protein; FE, fractional excretion; HPRT, hypoxanthine phosphoribosyltransferase; IMP, inosine 5 0 -monophosphate; KO, knockout; PRPP, 5-phosphoribosyl-1-pyrophosphate; ULE, urate-lowering effect; Uox, urate oxidase (uricase); WT, wild-type; XDH, xanthine dehydrogenase.Takuji Hosoya and Makoto Hosoyamada contributed equally to this work.

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Allopurinol-induced aplastic anemia in a patient with chronic kidney disease

Cited by 13 publications

References 0 publications

Agranulocytosis: an adverse effect of allopurinol treatment

Agranulocytosis: an adverse effect of allopurinol treatment

Acute neutropenia associated with initiation of febuxostat therapy for hyperuricaemia in patients with chronic kidney disease

Perfecting a high hypoxanthine phosphoribosyltransferase activity–uricase KO mice to test the effects of purine‐ and non‐purine‐type xanthine dehydrogenase (XDH) inhibitors

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