Abstract
BackgroundThis study aimed to measure the serum soluble tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) and interleukin-17A (IL-17A) levels in hypertensive patients with/without asymptomatic organ damage (AOD), as well as to determine the relationship between the serum sTWEAK and IL17-A levels, and carotid intima media thickness (CIMT), proteinuria, retinopathy, and the left ventricle mass index (LVMI).MethodsThe study included 159 patients diagnosed with and followed-up for primary hypertension (HT); 79 of the patients had AOD (61 female and 18 male) and 80 did not (52 female and 28 male). sTWEAK and IL-17A levels were measured in all patients.ResultsThe sTWEAK level was significantly lower in the patients with AOD than in those without AOD (858.4 pg/mL vs. 1151.58 pg/mL, P = 0.001). The sTWEAK level was negatively correlated with the mean microalbuminuria level and LVMI. The median IL-17A level was significantly higher in the patients with AOD than in those without AOD (2.34 pg/mL vs. 1.80 pg/mL, P = 0.001). There was a positive correlation between mean IL-17A level, and mean microalbuminuria level, CIMT, and LVMI. Multivariate logistic regression analysis showed that patient age, sTWEAK level, and mean 24-h systolic blood pressure were predictors of AOD.ConclusionsThe sTWEAK level was lower and IL-17A level was higher in the patients with AOD. It remains unknown if sTWEAK and IL-17A play a role in the pathophysiology of AOD. Prospective observational studies are needed to determine the precise role of sTWEAK and IL-17A in the development of target organ damage.
Highlights
This study aimed to measure the serum soluble tumor necrosis factor-like weak inducer of apoptosis and interleukin-17A (IL-17A) levels in hypertensive patients with/without asymptomatic organ damage (AOD), as well as to determine the relationship between the serum sTWEAK and IL17-A levels, and carotid intima media thickness (CIMT), proteinuria, retinopathy, and the left ventricle mass index (LVMI)
Both of these forms are biologically active [9]. sTWEAK binds to fibroblast growth factor-inducible molecule 14 (Fn14) receptors, and plays a role in cellular proliferation, migration, apoptosis, differentiation, angiogenesis, and inflammation via the nuclear factor κB (NFκB) pathway [10]
Mean 24-h systolic blood pressure (SBP) and 24-h diastolic blood pressure (DBP) were significantly higher in the AOD group, there weren’t any significant differences between groups according to the type of antihypertensive drugs used (P > 0.05)
Summary
This study aimed to measure the serum soluble tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) and interleukin-17A (IL-17A) levels in hypertensive patients with/without asymptomatic organ damage (AOD), as well as to determine the relationship between the serum sTWEAK and IL17-A levels, and carotid intima media thickness (CIMT), proteinuria, retinopathy, and the left ventricle mass index (LVMI). As other members of the TNF superfamily, TWEAK has multiple forms: mTWEAK, which is bonded to the membrane, and sTWEAK, which is a soluble variant produced following proteolytic cleavage by endoprotease furin. Both of these forms are biologically active [9]. The literature does include studies on sTWEAK and IL-17A in patients with HT [4,5,7], but does not include any studies on the relationship between sTWEAK and IL-17A, and asymptomatic organ damage (AOD) in HT patient
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