Key result
T4 replacement increases endothelial progenitor cell counts ~3.5-fold from baseline in subclinical hypothyroidism.
Why the study?
Subclinical hypothyroidism is associated with cardiovascular risk factors and possibly disease, but its management and impact on endothelial progenitor cells remain controversial.
Does T(4) replacement therapy improve endothelial progenitor cell count in patients with subclinical hypothyroidism?
Does T(4) replacement therapy improve endothelial progenitor cell count in patients with subclinical hypothyroidism?
Absolute Event Rate: 0.32% vs 0.09%
p-value: p=<0.001
Thyroid hormone replacement therapy in subclinical hypothyroidism improves endothelial progenitor cell counts, suggesting a potential mechanism for cardiovascular risk reduction.
May improve endothelial repair markers in subclinical hypothyroidism; hypothesis-generating for CV benefit, needs RCT confirmation.
CONTEXT: Subclinical hypothyroidism (SCH) is associated with cardiovascular (CV) risk factors, and possibly CV disease. However, its management remains controversial. Endothelial progenitor cells (EPC), expressing both endothelial and stem cell markers, are known to offer a novel CV risk marker. OBJECTIVE: The aim of the study was to ascertain whether EPC count or function is reduced in SCH and whether it improves with T(4) therapy. DESIGN AND INTERVENTION: EPC were studied in peripheral blood by fluorescence-activated cell sorter and following in vitro cultures before and after T(4) together with CV risk factors in 20 SCH and healthy controls (HC). MAIN OUTCOME MEASURE: EPC count was measured at baseline and after T(4) replacement in SCH. RESULTS: EPC count was significantly reduced in SCH compared to HC: median (range)-CD133+/VEGFR-2+, 0.09 (0.02-0.44) vs. 0.47 (0.17-2.12), P < 0.001; CD34+/VEGFR-2+, 0.10 (0.04-0.46) vs. 0.39 (0.11-2.13), P < 0.001; whereas EPC function was similar. There was a significant positive correlation between CD133+/VEGFR-2+ with free T(4) levels (r = 0.38; P = 0.02); high-density lipoprotein cholesterol levels (r = 0.51; P = 0.001); and negative correlation with TSH concentrations (r = -0.64; P < 0.001). After adjustment for conventional CV risk factors, SCH predicted lower EPC count, beta coefficient/P value: CD133+/VEGFR-2+ (-0.77/<0.001), and CD34+/VEGFR-2+ (-0.71/<0.001). In SCH participants, EPC count increased and was similar to HC after T(4); CD133+/VEGFR-2+, 0.32 (0.03-0.94) vs. 0.09 (0.02-0.44), P < 0.001; and CD34+/VEGFR-2+, 0.26 (0.06-0.88) vs. 0.10 (0.04-0.46), P < 0.001. CONCLUSION: SCH predicted lower EPC count, which improved with T(4) treatment, independent of other CV risk factors, providing additional evidence that T(4) replacement may improve CV risk in SCH.
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Shakoor et al. (2009) studied Subclinical hypothyroidism (n=20). T(4) replacement therapy vs. Baseline (pre-treatment) and healthy controls was evaluated on EPC count (CD133+/VEGFR-2+) (p=<0.001). T4 replacement therapy significantly increased endothelial progenitor cell counts in patients with subclinical hypothyroidism (median CD133+/VEGFR-2+ 0.32 vs 0.09 at baseline, P<0.001).
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