Azathioprine-induced pure red cell aplasia: Case report and review

Agrawal, Amit; Parrott, N. R.; Riad, Hany; Augustine, Titus

doi:10.1016/j.transproceed.2004.09.047

Cited by 27 publications

(19 citation statements)

References 17 publications

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“…2c, right panel). These results are consistent with the anemia and dramatically reduced erythrocytes observed in patients experiencing thiopurine toxicity (20). This demonstrates that the 6-MP sensitivity of erythroid progenitors (designated Terll9, see Fig.…”

Section: Resultssupporting

confidence: 89%

Transporter-Mediated Protection against Thiopurine-Induced Hematopoietic Toxicity

et al. 2008

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Thiopurines are effective immunosuppressants and anticancer agents, but intracellular accumulation of their active metabolites (6-thioguanine nucleotides, 6-TGNs) causes dose-limiting hematopoietic toxicity. Thiopurine S-methyltransferase (TPMT) deficiency is known to exacerbate thiopurine toxicity. However, many patients are highly sensitive to thiopurines for unknown reasons. We show that Mrp4 is abundant in myeloid progenitors and tested the role of the multidrug-resistance protein 4 (Mrp4), an ATP binding cassette (ATP) transporter of monophosphorylated nucleosides, in this unexplained thiopurine sensitivity. Mrp4-deficient mice experienced Mrp4 gene dosage–dependent toxicity caused by accumulation of 6-TGNs in their myelopoietic cells. Therefore, Mrp4 protects against thiopurine-induced hematopoietic toxicity by actively exporting thiopurine nucleotides. We then identified a single-nucleotide polymorphism (SNP) in human MRP4 (rs3765534) that dramatically reduces MRP4 function by impairing its cell membrane localization. This SNP is common (>18%) in the Japanese population and indicates that the increased sensitivity of some Japanese patients to thiopurines may reflect the greater frequency of this MRP4 SNP.

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Section: Resultssupporting

confidence: 89%

Transporter-Mediated Protection against Thiopurine-Induced Hematopoietic Toxicity

et al. 2008

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“…Severe, life-threatening, pancytopenic crises have been reported with these mutations. Very rare cases of pure red cell aplasia are reported with azathioprine [21]. …”

Section: Immunosuppressive Drugsmentioning

confidence: 99%

Anaemia after Renal Transplantation – Role of Immunosuppressive Drugs and a Pathophysiological Appraisal

et al. 2006

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Improvements in patient care and longevity on dialysis programmes together with the increased numbers of patients referred for renal replacement therapy will inevitably result in enlarging numbers of subjects with functioning renal transplants. While this translates to a boon for the patients in terms of survival and quality of life, a very real problem has begun to emerge, that of post-transplantation anaemia (PTA). The prevalence of this condition has been estimated by several studies as varying somewhere between one third and two thirds of all patients, with the same attendant problems as anaemia in the context of chronic kidney disease. PTA is multifactorial in origin and involves interplay between a number of risk factors, not least of all the immunosuppressive protocol. It is the purpose of this article to briefly review the contribution from transplant immunosuppression to PTA and to assess its likely effects on and treatment options for patients.

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“…Acquired PRCA associated with solid organ transplantation rarely occurs and may be caused by immunosuppressants and PVB19 infection. Such immunosuppressants include azathioprine [3] , MMF [4] and tacrolimus [5] , except for CsA. Such a diagnosis was not considered because this patient did not respond to discontinuation of MMF and replacement of tacrolimus by CsA.…”

Section: Discussionmentioning

confidence: 99%

Pure red cell aplasia due to parvovirus B19 infection after liver transplantation: A case report and review of the literature

Liang

Li²,

Yu³

et al. 2007

WJG

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Pure red cell aplasia (PRCA) due to parvovirus B19 (PVB19) infection after solid organ transplantation has been rarely reported and most of the cases were renal transplant recipients. Few have been described after liver transplantation. Moreover, little information on the management of this easily recurring disease is available at present. We describe the first case of a Chinese liver transplant recipient with PVB19-induced PRCA during immunosuppressive therapy. The patient suffered from progressive anemia with the lowest hemoglobin level of 21 g/L. Bone marrow biopsy showed selectively inhibited erythropoiesis with giant pronormoblasts. Detection of PVB19-DNA in serum with quantitative polymerase chain reaction (PCR) revealed a high level of viral load. After 2 courses of intravenous immunoglobulin (IVIG) therapy, bone marrow erythropoiesis recovered with his hemoglobin level increased to 123 g/L. He had a lowlevel PVB19 load for a 5-mo follow-up period without recurrence of PRCA, and finally the virus was cleared. Our case indicates that clearance of PVB19 by IVIG in transplant recipients might be delayed after recovery of anemia.

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Azathioprine-induced pure red cell aplasia: Case report and review

Cited by 27 publications

References 17 publications

Transporter-Mediated Protection against Thiopurine-Induced Hematopoietic Toxicity

Transporter-Mediated Protection against Thiopurine-Induced Hematopoietic Toxicity

Anaemia after Renal Transplantation – Role of Immunosuppressive Drugs and a Pathophysiological Appraisal

Pure red cell aplasia due to parvovirus B19 infection after liver transplantation: A case report and review of the literature

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