Alopecia areata (AA) is a non-scarring, inflammatory hair loss disease that is believed to involve an autoimmune mechanism. In other chronic autoimmune skin conditions, such as psoriasis, there is evidence that affected individuals have an increased risk of coronary heart disease and heart failure. We investigated the potential for a relationship between AA and heart disease using tissues from the C3H/HeJ mouse model.
The mortality rate in 18 month old C3H/HeJ mice grafted induced AA of 12+ months duration was 28.6% (n=14) in contrast to controls with 15.4% (n=18), a statistically insignificant difference. However, we observed that the heart sizes/wet weights in surviving AA mice (n=10) were statistically significantly greater than age and sex matched normal littermates (n=11).
We conducted quantitative PCR (qPCR) analysis of AA mouse heart and skin tissues for selected genes involved in apoptosis and inflammation. We observed IL18, IL18 receptor-1 (IL18r1) and IL18 binding protein (IL18bp) increased significantly by 4.6, 2.8 and 5.2 fold respectively in the heart (respectively 2.4, 3.1 and 5.2 fold in skin) compared to controls.
It has been shown by others that IL18 levels, in both circulation and resident myocardial tissues are increased in patients with heart diseases. Experimentally, administration of IL18 increases heart mass and wall thickness which leads to cardiac dysfunction. In humans, peripheral blood ELISA analysis of cardiac troponin I (cTnI) levels, a marker of cardiac tissue damage, revealed highest cTnI levels in patients with advancing AA and lowest in patients with stable or regressing AA, however, this result failed to achieve statistical significance.
Based on our observations, the development of AA may be associated with a somewhat increased risk of heart disease with increased IL18 mediated activity in cardiac tissues.