Author Affiliations: Institute of Human Genetics (Drs Razvi and Pearce), Newcastle University, and Endocrine Unit, Royal Victoria Infirmary (Dr Pearce), Newcastle upon Tyne, England; and Department of Endocrinology, Gateshead Health National Health Service (NHS) Foundation Trust, Gateshead, England (Dr Razvi).
We agree with Marfella et al that innate immune overactivity may explain the increased cardiovascular (CV) risk seen in subclinical hypothyroidism (SCH). However, several other possible mechanisms may also be responsible.1 An atherogenic lipid profile is seen in SCH that is improved with levothyroxine treatment.2 In addition, abnormal rheology,3 diastolic dysfunction,4 and impaired endothelial function2 are also seen in SCH, most of which are reversed with treatment. The mechanistic processes that underlie the high CV risk in SCH as well their effect on “hard” vascular outcomes need to be studied in a future randomized controlled trial. Furthermore, as noted in our recent analysis,5 the reasons for differences in outcomes of treatment in younger and older individuals with SCH also require study.
Razvi S, Pearce SHS. Subclinical Hypothyroidism and Cardiovascular Disease—Reply. Arch Intern Med. 2012;172(19):1523–1524. doi:10.1001/2013.jamainternmed.597
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