Investigation of the Levels of Serum Amyloid A, YKL-40, and Pentraxin-3 in Patients with Familial Mediterranean Fever.

BACKGROUND: Familial Mediterranean Fever (FMF) is an autosomal recessive form of recurrent episodes of fever and an autoinflammatory disease characterized by inflammation of the serous membranes. The clinical diagnosis is supported by the laboratory findings. This study investigated the relationship of Serum Amyloid A (SAA), YKL-40, and Pentraxin-3 (PTX-3) with the FMF disease. METHODS: About 50 patients with FMF were enrolled in this study. Patients were divided into three groups according to disease severity score (mild, moderate, and severe). Thirty-seven healthy individuals were included as the control group. Serum SAA, YKL-40, and PTX-3 concentrations were measured using an ELISA kit. RESULTS: Serum SAA and YKL-40 levels of FMF patients were significantly higher than in the control (P < 0.001). PTX-3 levels were found to be higher in patients even though there was no significant difference (P = 0.113). Whereas the positive predictive value was 71.9% for cut-off point of SAA, the positive predictive value was 83.3% for cut-off point of YKL-40. Whereas a significant correlation was detected in SAA and PTX-3 with YKL-40 (respectively; P = 0.036, P < 0.001), there was no correlation between the PTX-3 with SAA (P = 0.219). CONCLUSIONS: YKL-40 can be used together with SAA to support the diagnosis of FMF and to monitor the severity of the disease. In this study, YKL-40 levels were examined for the first time in FMF patients and further studies are necessary using larger patient samples.

One more health benefit of blood donation: reduces acute-phase reactants, oxidants and increases antioxidant capacity.

BACKGROUND: One of the most important problems in finding blood donors is the inadequacy of volunteer number. To overcome this problem, one of the solutions we suggest is innovating new health benefits of blood donation. The aim of the present study is to investigate the effects of blood donation on oxidative status markers and acute-phase reactants. METHODS: A total of 96 healthy volunteers were recruited into the study. Blood samples were withdrawn 5 min before and 24 h after the blood donation. Serum nitric oxide, malondialdehyde levels, and activity of superoxide dismutase and myeloperoxidase were measured spectrophotometrically. Serum levels of high-sensitive C-reactive protein and pentraxin-3 as acute-phase reactants were measured by enzyme-linked immunosorbent assay kits. RESULTS: We found statistically significant lower pentraxin-3 and high-sensitive C-reactive protein levels and higher superoxide dismutase activity and nitric oxide level 24 h after blood donation in serum of blood donor when compared with before blood donation. CONCLUSIONS: These findings suggest that blood donation affected oxidative status and acute-phase reactants in donors. Blood donation removes oxidants and decreases oxidative stress by elevating antioxidant enzyme such as superoxide dismutase. This is one more health benefit or reason why we should donate blood. Further large-scale studies should evaluate this mechanism and compare the same effect of wet cupping therapy.

Evaluation of ADAMTS12, ADAMTS16, ADAMTS18 and IL-33 serum levels in pre-eclampsia.

OBJECTIVE: Pre-eclampsia is the result of impaired trophoblast invasion and spiral artery remodeling managed by inflammatory response in its etiology and physiopathology. The aim of this study was to compare serum molecules including IL-33, ADAMTS12, ADAMTS16 and ADAMTS18 levels between pre-eclampsia and control groups and to investigate the role of these molecules in pre-eclampsia. METHODS: Forty-one women diagnosed as pre-eclampsia between 30 and 40 weeks of gestation and 41 non-complicated pregnant women were enrolled in this cross-sectional, case-control prospective study. ELISA method was used to determine IL-33, ADAMTS12, ADAMTS16 and ADAMTS18 levels within serums in two groups. RESULTS: Serum ADAMTS12 and IL-33 levels were significantly lower in pre-eclampsia group (p < 0.001 and p: 0.028, respectively), however, in sub-group analysis, no significant difference was observed (p > 0.05). The cut-off value of ADAMTS12 levels to discriminate pre-eclampsia with %73.17 sensitivity and %92.68 specificity was 8.27 ng/ml while the cut-off value for IL-33 was 0.23 pg/ml with 82.93% sensitivity and 53.66% specificity. CONCLUSION: Pre-eclampsia is associated with lower serum IL-33 and ADAMTS12 levels.

The Effects of Valsartan and Amlodipine on the Levels of Irisin, Adropin, and Perilipin.

BACKGROUND: Hypertension and obesity are two major threats for public health. Up to the present, antihypertensive medications have been used to lower blood pressure, which seem to provide a better life with lower morbidity and mortality rates. Their effect on etiopathogenesis of hypertension is now an area of developing research. The association between hypertension and obesity also suggests the link between antihypertensive agents and energy hemostasis. We aimed to investigate the effects of antihypertensive treatment on the irisin, adropin, and perilipin levels in patients with essential hypertension and to compare them with healthy volunteers in terms of their effect on energy hemostasis. METHODS: In total, 85 newly diagnosed patients with untreated essential hypertension were admitted to the outpatient clinic. Patients were randomized to one of the following treatment protocols: amlodipine or valsartan for a 12 week period. 42 patients were randomized into the valsartan group and 43 patients into the amlodipine group. Serum perilipin, irisin, and adropin levels were measured before and after drug treatment by ELISA kits. RESULTS: We discovered that the hypertensive patients have lower levels of perilipin and higher levels of adropin compared with the control group. Both amlodipine and valsartan increased the levels of perilipin, irisin, and adropin after 12 weeks of treatment. CONCLUSIONS: In conclusion, in regulating energy balance, perilipin, irisin, and adropin, could be of pathogenic importance in obesity-induced hypertension. Hence, ongoing trials need to elucidate this mechanism.