Medical Biochemistry

Background: Ankylosing spondylitis (AS) is a chronic inflammatory disease of spine and sacroiliac joints; it is characterized by new bone formation, and the disease processes can be accompanied by osteoporosis. In the present study, we investigated changes in bone mineral density (BMD) and in the levels of various bone turnover-related biomarkers and cytokines in a cohort of AS patients, with regard to clinical parameters, disease activity, and treatment regimen. Methods: 55 AS patients and 33 healthy controls included in the study. Spinal mobility was assessed by the Bath Ankylosing Spondylitis Metrology Index (BASMI), and radiologic changes were scored by the Bath Ankylosing Spondylitis Radiologic Index (BASRI). Patients were also evaluated with the Bath Ankylosing Spondylitis Functional Index (BASFI) and the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI). Bone mineral density (BMD) assessed by dual energy X-ray absorptiometry. Various biomarkers and cytokines of bone turnover including osteoprotegerin (OPG), serum band 5 tartrate-resistant acid phosphatase (TRAP-5), soluble receptor activator of nuclear factor kappa-B ligand (sRANKL), secreted frizzled-related protein 1 (sFRP-1), Dickkopf-related protein 1 (DKK-1), and sclerostin were studied. The levels of TRAP-5, NTX, sRANKL, sclerostin, sFRP-1, DKK-1, and IFNγ, were similar between the patients and controls (p > 0.05), while BMD of femoral neck, and OPG levels were significantly lower in AS patients (p < 0.05). In a subgroup analysis, patients with active disease had significantly higher concentrations of OPG compared with the inactive group. Rest of the biomarkers and cytokines of bone turnover were similar between the active and inactive disease groups. Subgroup analysis of patients receiving anti-TNFα agents and conventional therapy revealed that OPG concentrations were significantly lower in the patients receiving biological drugs, while BAP and DKK-1 were significantly higher in the patients treated with conventional agents. Conclusions: In this cross-sectional study we showed that OPG levels were significantly lower in AS patients compared to healthy subjects. On the other hand, the levels of wingless (Wnt) signal pathway inhibitors seem not altered. Ectopic bone formation in AS may be related to dysfunction of these molecules at the cellular level.

The aim of this study was to compare the effect of chronic inflammation on insulin resistance, serum leptin levels, and body composition (BC) in patients with ankylosing spondylitis (AS) and healthy controls. Twentyeight AS patients and 17 healthy controls were included in this study. Subjects with hypertension, diabetes, hyperlipidemia, and obesity were excluded. Acute phase reactants and serum levels of glucose, insulin, lipids, and leptin were studied. BC was determined anthropometrically and by foot-to-foot body fat analyzer (BIA, bioelectrical impedance analysis). Quantitative insulin-sensitivity check index, homeostasis model assessment for insulin resistance, and McAuley indices were calculated. Spinal mobility was assessed by the Bath Ankylosing Spondylitis Metrology Index (BASMI). Patients were also evaluated with the Bath Ankylosing Spondylitis Functional Index and the Bath Ankylosing Spondylitis Disease Activity Index. Age, sex distribution, smoking status, serum lipids, insulin concentrations, and insulin resistance indices were comparable between AS patients and controls (p>0.05). However, acute phase reactants were significantly higher and leptin levels were significantly lower in the AS patients than in controls (p<0.05). Fat percent assessed by both BIA and anthropometrical methods was lower in the male and female AS patients than in controls, and this reduced fat level reached statistical significance for men (p<0.05). There were significant correlations between percent body fat, body mass index, leptin, age, and BASMI (p<0.05; r=0.6, 0.75, 0.35, −0.41, respectively). On the other hand, body fat percent, waist-to-hip ratio, C-reactive protein, and BASMI were significantly correlated with serum leptin levels (p< 0.05; r=0.75, −0.42, −0.52, −0.47, respectively). Chronic inflammatory condition in AS may be responsible for the reduced body fat content and lower circulating leptin concentrations. Insulin levels and insulin resistance indices seem similar in patients and controls in the absence of classic vascular risk factors.

We aimed to evaluate some of the vascular biomarkers in newly diagnosed, colchicine naive familial Mediterranean fever (FMF) patients. Our primary aim was to investigate the effect of regular colchicine treatment on these variables. Twenty-four (12 males [M] and 12 females [F], 33.3±13.4 years) newly diagnosed FMF patients were included in the study. These patients were started on colchicine treatment following the initial assessment and were studied again no earlier than 2 months. Five patients were lost to follow-up, and assessment of the on-treatment patients was performed on the remaining 19 patients (8 M and 11 F, 33.6±11.8 years). There were 19 healthy subjects (11 M and 8 F, 32.2±7.2 years) who served as a control group. Cellular adhesion molecules (CAMs; soluble intercellular adhesion molecule-1 [sICAM-1] and soluble CD146 [sCD146]), plasminogen activator inhibitor-1 (PAI-1), fetuin-A and hs-CRP were studied. Examinations were performed on attack-free periods. The levels of hs-CRP, fetuin-A, sICAM-1, and PAI-1 were significantly higher in newly diagnosed patients compared to those of controls (P<0.05). All studied parameters were significantly downregulated after regular colchicine therapy (P<0.05). Comparison of on-treatment data with controls showed that the levels of the vascular biomarkers, except sC-D146, were similar between the groups (P>0.05). On-treatment sCD146 was found significantly lower than the controls (P<0.05). In regression analysis, none of the independent variables in the model significantly predicted the vascular biomarkers (P>0.05). Administration of therapeutic doses of colchicine markedly reduces vascular injury parameters and normalizes the values in FMF.

KARADAG F , CILDAG O , ALTINISIK M , KOZACI LD , KITER G , ALTUN C . Respirology 2004; 9 : 33-37 Objective: The purpose of this study was to assess the serum concentrations of those trace elements that act as a component of oxidative stress in COPD patients. Clinically stable COPD outpatients ( n = 26) and healthy controls ( n = 24) were studied. Methodology: Serum concentrations of copper (Cu) and zinc (Zn) were determined using a Varian Spectra AA220 flame atomic absorption spectrophotometer. Serum concentration of iron (Fe) was measured by the ferene assay, using a commercially available kit (IL Test TM Iron) with the ILAb TM 900 autoanalyser. The lipid peroxidation product malondialdehyde (MDA) in serum samples was measured spectrophotometrically in terms of TBARS (thiobarbituric acid reactive substances). Results: The serum MDA concentration in COPD patients was found to be similar to the control group (0.68 ± 0.15 nmol/mL vs 0.62 ± 0.13 nmol/mL, respectively; P = 0.163). The serum concentrations of the trace elements in both study groups were in the normal reference range. There was no difference in Fe concentration between COPD patients and the control group (0.81 ± 0.38 m g/mL vs 0.92 ± 0.41 m g/mL; P = 0.360). Copper concentrations were higher (1.06 ± 0.26 m g/mL vs 0.92 ± 0.19 m g/mL; P < 0.040); while zinc was lower in the COPD group compared to the controls (0.83 ± 0.25 m g/mL vs 1.03 ± 0.23 m g/mL; P = 0.006). Serum Zn concentrations were lower in the severe COPD patients compared to mild-moderate COPD patients ( P = 0.038).