Phillips, Rupert, Chaudry, Sabah and Chevassut, Timothy (2017) [Correspondence] Clonal hematopoiesis and atherosclerosis. The New England Journal of Medicine. ISSN 0028-4793

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Abstract

Jaiswal et al. report the results of four case–control studies that confirm a near doubling in the risk of coronary heart disease in patients with CHIP,1 a finding that was first reported in the Journal in 2014.2 The authors postulate that two mechanisms may be involved: the promotion of inflammatory responses, as supported in a study involving Tet2 knockout mice, and an increase in the number of myeloid cells, a finding that appears to be more relevant for patients with JAK2 mutations, which confer a much larger risk than the more common DNMT3A, TET2, and ASXL1 mutations, in which blood counts remain normal. However, the authors do not provide data relating to red-cell distribution width, which is the only blood-cell index that has been shown to have a significant association with CHIP2 and which has been associated with an unexplained increase in all-cause mortality in an aging population. 3,4 In understanding how CHIP promotes atherosclerosis, it is important to explore the causal relationship between clonal hematopoiesis and red-cell anisocytosis to determine whether these are independent or associated risk factors for cardiovascular disease.

Item Type:	Article
Schools and Departments:	Brighton and Sussex Medical School > Brighton and Sussex Medical School
Subjects:	R Medicine R Medicine > RC Internal medicine R Medicine > RC Internal medicine > RC0254 Neoplasms. Tumors. Oncology Including cancer and carcinogens
Depositing User:	Timothy Chevassut
Date Deposited:	04 Jun 2018 10:00
Last Modified:	04 Jun 2018 10:03
URI:	http://srodev.sussex.ac.uk/id/eprint/76279

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