A previous study has found an association between chronic inflammatory disorders e.g. psoriasis, rheumatoid arthritis, and inflammatory bowel disease and increased vascular stiffness(1). Psoriasis and hidradenitis suppurativa (HS) are believed to have shared comorbidities and pathophysiology despite their morphologically different manifestations in the skin. In order to evaluate a putative association between the chronic inflammatory skin disease HS and arterial stiffness, an observational cross-sectional retrospective study was carried out as part of the Danish General Suburban Population Study (GESUS) (1), in which 430 patients with HS from the general population (representing mild HS; Table 1), 32 patients with HS from a hospital-based out-patient clinic (representing severe HS, Table 1), and 20,780 controls underwent measurements of arterial vascular tone and stiffness using photoplethysmography (Pulse Trace PCA2®; Micro Medical Ltd, Kent, UK). The method of Pulse Trace has been validated by correlation with intra-arterial sensing techniques, and is a simple cost-effective screening method[2]. All analyses were performed using SAS 9.3. This study was accepted by the ethics committee of Region Zealand (project number SJ-191, SJ-113, SJ-114) in Denmark (2,3). RESULTS Reflection index (RI) is an expression of arterial vascular tone and stiffness of small arteries. The raw data showed a significantly lower RI for both HS groups groups, compared to controls. The results remained significant when adjusting for confounders (age, sex, smoking and metabolic syndrome) in the out-patient clinic HS group (-11.26 (-17.75- -4.76), P=0.0002*), but not in the population HS group (Table 2). Stiffness index (SI) expresses arterial stiffness in large arteries. Both HS groups showed no significant difference in either SI or vascular age in multivariate analysis, when compared with controls (Table 2). DISCUSSION This study suggests that decreased vascular tone and stiffness of small arteries may be associated with severe HS, and at the same time found no difference in arterial stiffness in large arteries. The significance for the out-patient clinic HS group, but not the population HS group may reflect a dose-response relationship. Vascular tone in vascular smooth muscle cells of small arteries depends on competing vasodilators and vasoconstrictors. We speculate that the inflammation of HS may induce a dysfunctional balance e.g. through increased TNF-alpha with subsequent increase of the vasodilator nitric oxide resulting in the lower arterial vascular tone observed. Additionally, mast cells are increased in HS [4], possibly increasing levels of the vasodilator histamine. HS patients often suffer from stress which could increase sympathetic activity, thereby adrenalin/cortisol and subsequent vasodilation in e.g. muscles. The more peripheral an artery is, the more collagen it contains and the stiffer it is. The finding of lower vascular tone may also be suggestive of a different elastin:collagen ratio in small arteries in HS. The healing process of HS lesions is known to involve scarring formation of sinus tracts [5], which may suggest a hypothesis of altered connective tissue. This study found no difference in SI expressing arterial stiffness of large arteries between HS and controls. Our previous study found an association between HS and myocardial infarction, but no association with stroke, nor peripheral arterial stiffness of lower extremities in medium/large arteries [6], suggesting regional differences in vascular beds in HS. The major limitation of the study is the missing values of pulse trace measurement (Table 1) creating possible selection bias. Although unable to draw any clinical conclusions, we believe these results may contribute to the future research of the complexity of HS and cardiovascular risk profiling. This study suggests that decreased vascular tone and stiffness of small arteries may be associated with severe HS, and at the same time found no difference in arterial stiffness in large arteries. The significance for the out-patient clinic HS group, but not the population HS group may reflect a dose-response relationship. Vascular tone in vascular smooth muscle cells of small arteries depends on competing vasodilators and vasoconstrictors. We speculate that the inflammation of HS may induce a dysfunctional balance e.g. through increased TNF-alpha with subsequent increase of the vasodilator nitric oxide resulting in the lower arterial vascular tone observed. Additionally, mast cells are increased in HS [4], possibly increasing levels of the vasodilator histamine. HS patients often suffer from stress which could increase sympathetic activity, thereby adrenalin/cortisol and subsequent vasodilation in e.g. muscles. The more peripheral an artery is, the more collagen it contains and the stiffer it is. The finding of lower vascular tone may also be suggestive of a different elastin:collagen ratio in small arteries in HS. The healing process of HS lesions is known to involve scarring formation of sinus tracts [5], which may suggest a hypothesis of altered connective tissue. This study found no difference in SI expressing arterial stiffness of large arteries between HS and controls. Our previous study found an association between HS and myocardial infarction, but no association with stroke, nor peripheral arterial stiffness of lower extremities in medium/large arteries [6], suggesting regional differences in vascular beds in HS. The major limitation of the study is the missing values of pulse trace measurement (Table 1) creating possible selection bias. Although unable to draw any clinical conclusions, we believe these results may contribute to the future research of the complexity of HS and cardiovascular risk profiling.