We thank Balta et al for their interest in our recent article exploring the relationship of metabolic syndrome and CIMT measures in patients with psoriasis and psoriatic arthritis. We agree that patients with psoriatic diseases are at higher risk of cardiovascular morbidity and mortality. We also acknowledge that there are multiple cardiovascular risk factors that can be associated with these patients, such as those mentioned by Balta et al.

In our analysis, we did not find any differences between the psoriatic arthritis and psoriasis populations in terms of prior cardiovascular events (i.e., stroke, coronary heart disease, peripheral arterial disease, or vascular intervention), family history of cardiovascular events, diabetes mellitus, and Framingham Risk Scores. All baseline characteristics and medication data available at the time of the analysis were considered for multivariable adjustment. If a variable was not statistically significant, it was not kept in the final multivariable model. Because of the large amount of missing medication data, statin use was not included in the analysis.

We used the definition of metabolic syndrome as defined by National Cholesterol Education Program Adult Treatment Panel III ([1]), which is a well-known and highly referenced algorithm used in clinical settings. The definition does not include lack of physical activity, nonalcoholic fatty liver disease, and other increased inflammatory state in the criteria.

Our study aim was to focus on the risk of subclinical atherosclerosis and metabolic syndrome in psoriatic diseases, and as such, we excluded subjects with coexisting chronic inflammatory conditions prior to enrollment. Other comorbidities that occur in psoriatic diseases, such as obstructive sleep apnea and nonalcoholic fatty liver disease, have on their own been associated with increased CIMT values. Regarding sleep apnea and nonalcoholic fatty liver disease, we reviewed studies in the literature on psoriasis and these comorbidities. We found articles exploring the association of psoriasis and metabolic syndrome and obstructive sleep apnea; however, there was no correlation between psoriasis characteristics and obstructive sleep apnea ([2]). There was also no direct evidence to date of causality established regarding cardiovascular outcomes (such as myocardial infarction or death) or changes in IMT in psoriasis patients with nonalcoholic fatty liver disease. There were no published studies that determined whether psoriasis or nonalcoholic fatty liver disease (among others) was driving increased CIMT, and it may be that the chronic inflammation associated with psoriatic disease drives premature atherosclerosis. It is likely a complex, multifactorial process and it would be valuable to address this in a different study.

We also acknowledge there is an increased prevalence of nonalcoholic fatty liver disease in patients with psoriatic diseases (particularly in psoriasis). In addition, nonalcoholic fatty liver disease is independently associated with carotid atherosclerosis, particularly in people who have multiple metabolic abnormalities ([3]). Unfortunately, nonalcoholic fatty liver disease was not routinely evaluated in our enrolled subjects. To our knowledge, there are little data to support any association between increased CIMT and drug addiction or weight loss.

We appreciate the interest in our study by Balta et al and their thoughtful comments. Because our study was cross-sectional, the temporality of the association and causality of multiple risk factors could not be completely established. Despite the limitations of our study, our findings highlight the need to aggressively address cardiovascular risk in patients with psoriatic disease. We agree that future well-designed prospective studies are required to further validate these additional observations found in psoriatic diseases.