Hyperuricemia and bone marrow transplantation

Giorgio Lambertenghi Deliliers, Claudio Annaloro

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Blood uric acid levels and purine metabolism are affected in many ways after bone marrow transplantation (BMT). Although BMT is usually performed when patients have a low residual disease burden, a proportion of them are still at risk of tumor lysis syndrome, even with limited disease or after nonmyeloablative conditioning regimens; moreover, an alteration in uric acid turnover can also be observed in patients with persistently normal uric acid blood levels. Apart from this obvious complication, multiple physiopathological events occurring after transplantation may derange uric acid homeostasis. Although there is only indirect evidence (derived from obstetric eclampsia and experimental gout arthritis), a transplant-related increase in cytokine production (particularly TNF, IL-1 and IL-6) may activate xanthine oxidase which, in turn, may be responsible for a further cytokine bout: deranged cytokine homeostasis is involved in the pathogenesis of some of the main acute post-BMT complications, such as hepatic veno-occlusive disease (VOD) and acute graft-versus-host disease (aGVHD). Hyperuricemia is also a well-known side effect of cyclosporine A, the reference drug for the prevention of post-BMT GVHD, which may affect uric acid turnover by reducing glomerular filtration and/or affecting tubular handling; the available evidence favors the former explanation. Hyperuricemia is found in long-term transplanted patients as part of a metabolic pattern reminiscent of the so-called 'X' or 'metabolic' syndrome related to insulin resistance: there is still no precise interpretation of this post-transplant complication nor any definite data concerning its real incidence and outcome. Hyperuricemia is frequently regarded as a marginal finding in the context of X syndrome, but it is pathogenetically linked to the other component of the syndrome and has proved to be autonomously responsible for tissue and vessel damage. Finally, BMT is a possible therapeutic strategy for some inherited forms of hyperuricemia, particularly Lesch-Nyhan disease, although there is still some perplexity concerning the possibility of preventing the development of neurological impairment.

Original languageEnglish
Pages (from-to)105-114
Number of pages10
JournalContributions to Nephrology
Volume147
Publication statusPublished - 2005

Fingerprint

Hyperuricemia
Uric Acid
Bone Marrow Transplantation
Cytokines
Homeostasis
Hepatic Veno-Occlusive Disease
Metabolic Syndrome X
Tumor Lysis Syndrome
Lesch-Nyhan Syndrome
Transplants
Eclampsia
Experimental Arthritis
Xanthine Oxidase
Gout
Graft vs Host Disease
Interleukin-1
Cyclosporine
Obstetrics
Insulin Resistance
Interleukin-6

ASJC Scopus subject areas

  • Nephrology

Cite this

Deliliers, G. L., & Annaloro, C. (2005). Hyperuricemia and bone marrow transplantation. Contributions to Nephrology, 147, 105-114.

Hyperuricemia and bone marrow transplantation. / Deliliers, Giorgio Lambertenghi; Annaloro, Claudio.

In: Contributions to Nephrology, Vol. 147, 2005, p. 105-114.

Research output: Contribution to journalArticle

Deliliers, GL & Annaloro, C 2005, 'Hyperuricemia and bone marrow transplantation', Contributions to Nephrology, vol. 147, pp. 105-114.
Deliliers, Giorgio Lambertenghi ; Annaloro, Claudio. / Hyperuricemia and bone marrow transplantation. In: Contributions to Nephrology. 2005 ; Vol. 147. pp. 105-114.
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