We read with interest the letter from Skinner, Nader and Connes and their comments on our recently published study on the burden of type 2 diabetes (T2D) in patients with sickle cell disease (SCD). The authors call attention to variation in T2D risk across patients with different SCD genotypes. Despite the fact that SCD is caused by single gene disorders, patients with SCD demonstrate a complex spectrum of complications and phenotypic heterogeneity that can be partially explained by the variability of fetal haemoglobin levels and co‐inheritance of alpha thalassaemia. It is plausible to speculate that SCD patients of different genetic foundation could present distinct pathophysiology features, including lipid profile and anthropometrics, which in turn could influence the likelihood of being diagnosed with T2D.
To answer the questions raised by Dr. Skinner and colleagues, we must acknowledge the inherent limitations of administrative health databases in performing studies of disease burden. Herein we describe the challenges of further exploration of these currently available data and the necessary methodological considerations for such epidemiological studies, particularly possible information and selection biases.
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