Bone Health in Patients With Hematopoietic Disorders of Bone Marrow Origin: Systematic Review and Meta- Analysis

Oxford University Press (OUP) - Tập 32 Số 4 - Trang 731-742 - 2017
K. Steer1,2, Mariya Stavnichuk3,2, Martin Morris4, Svetlana V. Komarova3,5,6,2
1Department of Pharmacology and Therapeutics, Faculty of Medicine, McGill University, Montreal, Canada
2Shriners Hospital for Children–CanadaMontrealCanada
3Department of Anatomy and Cell Biology, Faculty of Medicine, McGill University, Montreal, Canada
4Schulich Library of Physical Sciences, Life Sciences, and Engineering, McGill University, Montreal, Canada
5Department of Anatomy and Cell BiologyFaculty of MedicineMcGill UniversityMontrealCanada
6Faculty of Dentistry, McGill University, Montreal, Canada

Tóm tắt

ABSTRACT   Blood cell production and bone homeostasis are physically interlinked systems that exhibit active cross-talk. We examined how bone health is affected in patients with hematopoietic disorders due to abnormal proliferation of bone marrow cells. The electronic databases Medline, Embase, PubMed, BIOSIS Previews, Web of Science, and Cochrane were searched for studies presenting numerical values for trabecular bone volume or bone mineral density in control and patients with hematopoietic disorders. We identified 5 studies for beta-thalassemia, 6 for sickle cell anemia, 2 for polycythemia vera and essential thrombocythemia, 3 for chronic myelogenous leukemia, 6 for myelofibrosis, 5 for multiple myeloma, and 4 studies each for systemic mastocytosis, lymphocytic leukemia, and hemochromatosis. The effect of the disease state on bone density was significant and negative for beta-thalassemia (r = –2.00; 95% confidence interval [CI] –3.41, –0.58; p < 0.005), sickle cell anemia (–0.91; –1.36, –0.47; p < 0.00005), chronic myelogenous leukemia (–0.55; –0.88, –0.22; p < 0005), mastocytosis (–0.99; –1.16, –0.82; p < 0.00001), lymphoblastic leukemia (–0.69; –0.98, –0.40; p < 0.00001), multiple myeloma (–0.67; –0.99, –0.35; p < 0.00005), and hemochromatosis (–1.15; –1.64, –0.66; p < 0.00001). The changes were negative but not significant for polycythemia vera (–0.16; –0.38, 0.05; p = 0.069) and essential thrombocythemia (–0.33; –0.92, 0.26; p = 0.14). In myelofibrosis, disease state was associated with increased bone density (0.74; 0.12, 1.36; p < 0.05). Bone density change significantly and negatively correlated with the level of ferritin and bone marrow cellularity but not with hemoglobin or erythropoietin. Thus, independent of hematopoietic lineage, abnormal proliferation of bone marrow cells appears to be associated with bone loss. Iron metabolism may independently contribute to bone homeostasis. © 2016 American Society for Bone and Mineral Research.

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Oxford University Press (OUP)

Tập 32 Số 4

731-742

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