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Abstract
<p class="first" id="d12437938e67">Lp(a) and diabetes are both known and established
risk factors for the development
of cardiovascular disease. However, studies trying to link both risk factors find
an inverse association between Lp(a) and risk of prevalent and incident diabetes.
It is not yet clear though whether this association is causal and whether this possible
causal link is due to Lp(a) concentration itself, to length of the apo(a) isoforms,
or both. The results of Mendelian Randomisation studies are highly heterogeneous.
This review aims to shed light on the most recent findings of epidemiological and
Mendelian Randomisation studies and disentangle the contradictory results. Only part
of the observed association of Lp(a) with diabetes can likely be explained by causality
and may also be driven by reverse causation, co-morbidities, or medications. Furthermore,
this review also summarizes the role of Lp(a) within patients with diabetes. Several
studies suggest that elevated Lp(a) is a causal independent risk factor for CVD in
patients. Although therapies that specifically target and lower Lp(a) have not been
evaluated in diabetic patients, analysis of the large PCSK9 clinical outcomes trials
suggest they are beneficial on cardiovascular outcomes.
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