Elevated serum levels of soluble ICAM-1 in non-Hodgkin's lymphomas correlate with tumour burden, disease activity and other prognostic markers

The serum levels of soluble ICAM-1 (CD54) were significantly elevated in patients with non-Hodgkin's lymphomas (NHL, n  = 127) and hairy cell leukaemia (HCL, n  = 15) compared with healthy controls ( n  = 31). In high-grade malignant NHL ( n  = 79) the sICAM-1 levels correlated with the tumour mass as reflected in the Ann Arbor staging system but not with bulky disease. Further, the sICAM-1 levels correlated with disease activity as reflected by the presence of B symptoms and with other known prognostic markers, in particular serum thymidine kinase (sTK). In patients with low-grade malignant NHL ( n  = 48) a trend towards higher serum levels of sICAM-1 was found in patients with advanced stage and B symptoms. In both low- and high-grade malignant NHL, elevated levels of sICAM-1 were associated with poorer overall and disease-free survival. The present results indicate that sICAM-1 levels have a prognostic power equal to that of other serum markers claimed to be of prognostic value in NHL, namely serum lactate dehydrogenase (LDH), erythrocyte sedimentation rate (ESR), beta-2-microglobulin (β₂m), serum thymidine kinase (sTK), albumin and orosomucoid. The cellular origin and the possible interactions between soluble and surface ICAM-1 and its ligands needs further exploration.     

The tumor necrosis factor family and and correlation with disease activity and response to treatment in hairy cell leukemia

Hairy cell leukemia (HCL) is a well recognized indolent B-cell lymphoproliferative disorder. HCL cell proliferation is regulated by growth factors and cytokines, of which tumor necrosis factor-alpha (TNF-alpha) may be one of the most important. The mechanism of TNF-alpha-induced HCL cell growth is mediated via 2 receptors, which are present in both cellular and soluble forms. In this study we determined the serum levels of TNF-alpha and their soluble receptors - sTNF-R60 and sTNF-R80 - in 23 HCL patients and correlated them with clinical parameters before and after therapy. Patients were classified according to their clinical status as either "active" at diagnosis or during relapse and "non-active" (responding to therapy with partial and complete remission). Most patients were treated with 2-CDA, following which serum levels of TNF-alpha, sTNF-R60 and sTNF-R80 were significantly decreased, particularly in CR. Significant differences in paired observation values were noted for TNF-alpha and sTNF-R80, indicating a good correlation with the clinical status of disease, but this was not the case for sTNF-R60 (coefficients of correlation between levels of TNF-alpha and sTNF-R80 and of TNF-alpha and sTNF-R60 were r = 0.85 and r= 0.64, respectively). These results suggest that decreases in both TNF-alpha and sTNF-R80 are indicative of response to treatment, while increased levels accompany active disease. Accordingly, we conclude that serum levels of the TNF family, as for the sIL-2R and IL-1 family, may also be used as sensitive markers for monitoring HCL status. Levels may be indicative of the clinical efficacy of therapy and can be used as an indicator of the presence of residual disease.     

Serum levels of interleukin-1b,tumour necrosis factor-a and interleukin-2 in rheumatoid arthritis. Correlation with disease activity

Summary Cytokines are potent immunoregulatory factors and may be directly involved in the disordered immunoregulation found in chronic rheumatic diseases. Interleukin-1b (IL-1b), Interleukin-2 (IL-2) and Tumour Necrosis Factor-a (TNF-a) have been implicated in the pathogenesis of rheumatoid arthritis (RA) as mediators of chronic inflammation. Serum levels of IL-1b and TNF-a measured by radioimmunoassay were significantly higher in patients with RA than in healthy controls of similar sex and age while serum levels of IL-2 were significantly lower in the same patients. Further IL-1b and TNF-a were significantly elevated in RA patients with active disease and IL-2 was significantly reduced when compared with patients with low active disease. Serum IL-1b and TNF-a appear to correlate with systemic inflammation, and systemic features of RA may result from dissemination of cytokines produced in the synovium. The role of IL-2 in RA remains controversial. Reduced levels of IL-2 may be an expression of a deficiency of T-cells to produce IL-2 in the active phases of RA or may be due to a possible absorption of IL-2 by lymphocyte receptors.     

Reversal of IFN-gamma, oxLDL and prolactin serum levels correlate with clinical improvement in patients with peripartum cardiomyopathy

AIM: Peripartum cardiomyopathy (PPCM) is characterized by acute onset of heart failure of unknown aetiology. We aimed to identify mechanisms involved in initiation and progression of the disease. METHODS AND RESULTS: Serum markers related to cardiac function, apoptosis, oxidative stress, remodelling, inflammation and the nursing hormone prolactin were analyzed in PPCM patients and healthy controls. The kinetics of these markers were compared between patients who improved cardiac function (IMP) and those patients who did not improve (NIMP), over 6 months follow-up. All patients received ACE-inhibitors, beta-blockers and diuretics. Baseline levels of TGF-beta-1 were significantly lower, MMP-9 and VEGF were not different; all other markers were significantly higher in PPCM compared with controls. Only baseline NT-proBNP levels were higher in NIMP compared with IMP. After 6 months, NT-proBNP, oxLDL and IFN-gamma were significantly lower in IMP and the decrease in oxLDL, IFN-gamma and prolactin was significant in IMP but not in NIMP. Significant correlations were observed between the kinetics of NT-proBNP, oxLDL, prolactin and IFN-gamma in PPCM patients. CONCLUSION: Baseline NT-proBNP and the failure to decrease oxLDL, IFN-gamma and prolactin are associated with poor outcome in PPCM, suggesting a potential role of these factors in the pathophysiology of PPCM and for risk stratification of PPCM patients.     

Serum levels of matrix metalloproteinase 3 and macrophage colony‐stimulating factor 1 correlate with disease activity in ankylosing spondylitis

Objective

To assess the usefulness of measuring serum matrix metalloproteinase 3 (MMP‐3) and macrophage colony‐stimulating factor (M‐CSF) in patients with ankylosing spondylitis (AS).

Methods

Serum levels of MMP‐3 and M‐CSF were measured in AS patients who did and did not receive infliximab treatment. These were compared with those of 28 healthy subjects.

Results

In the group of AS patients not treated with biologics, both M‐CSF and MMP‐3 correlated with the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) values, but not with each other. Logistic regression analysis showed that MMP‐3 values were high in those with severely active disease. Infusions of infliximab in AS patients led to a significant decrease in the values of the BASDAI as well as the serum MMP‐3, but no change in the serum M‐CSF values.

Conclusion

MMP‐3 and M‐CSF are potentially useful markers of AS disease activity.

     

Serum leptin levels correlate with interleukin-6 levels and disease activity in patients with ankylosing spondylitis

OBJECTIVE: To determine whether serum leptin levels are elevated in men with ankylosing spondylitis (AS) and whether the levels correlate with serum cytokine profiles and disease activity of AS. METHODS: Forty-two male patients with newly diagnosed AS were enrolled. Their Bath AS Disease Activity Index (BASDAI), body mass index (BMI), and acute phase reactants, such as erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levels, were assessed. Serum leptin levels were determined using radioimmunoassay (RIA) and serum cytokine profiles, including tumour necrosis factor (TNF)-alpha, interleukin (IL)-6, and interferon (IFN)-gamma, were determined using enzyme-linked immunosorbent assay (ELISA). These results were compared with those from 42 age-matched healthy men. After a follow-up period of 31.0+/-20.1 months, clinical and biochemical variables were reassessed in the men with AS. RESULTS: At baseline, patients with AS had significantly elevated serum levels of leptin, leptin adjusted for BMI (leptin/BMI), TNFalpha, and IL-6, but not IFN-gamma, as compared to the controls. Serum leptin/BMI levels correlated well with IL-6 levels, and both leptin/BMI and IL-6 levels correlated well with BASDAI and CRP levels in patients with AS. The changes in leptin/BMI and IL-6 levels between the baseline and follow-up measurements correlated well with one another (p<0.05) and both correlated well with the changes in BASDAI (p<0.05). CONCLUSION: Serum leptin/BMI levels were increased and significantly associated with IL-6 levels and disease activity in men with AS, suggesting a possible role for leptin in the inflammatory reactions of AS.     

Circulating endothelin-1 levels in type 2 diabetic patients with ischaemic heart disease

To investigate whether circulating endothelin-1 (Et-1) may be related to the increased incidence and severity of ischaemic heart disease in type 2 diabetes mellitus, we compared the concentrations in type 2 diabetic patients and in non-diabetic patients with coronary artery disease (CAD) angiographically documented. Plasma levels of Et-1 were determined in 34 type 2 diabetic patients with CAD (16 with stable angina, 6 with unstable angina, 12 with previous myocardial infarction) and in 19 non-diabetic patients with CAD (4 with stable angina, 5 with unstable angina, 10 with previous myocardial infarction). Fifteen diabetic patients without CAD and 9 healthy volunteers served as control subjects. In the type 2 diabetic patients, the mean Et-1 levels were 3.19±1.61 pmol/l in those with stable angina, 3.58±1.92 pmol/l in those with unstable angina, 4.24±2.53 pmol/l in those with myocardial infarction. These values were not significantly different one another, nor from the values obtained from type 2 diabetic controls (3.64±2.13 pmol/l). In the non-diabetic patients, the mean Et-1 levels were 3.92±0.73 pmol/l in those with stable angina, 4.35±1.67 pmol/l in those with unstable angina, 4.33±1.66 pmol/l in those with myocardial infarction. These values were not significantly different one another, but significantly higher than those obtained from healthy controls (2.07±0.67 pmol/l;P<0.001). No significant differences were found in Et-1 levels between diabetic and non-diabetic patients with stable, unstable angina and previous myocardial infarction. In contrast, a statistically significant difference was found in Et-1 levels between diabetic and non-diabetic control subjects (P<0.05). In conclusion, similar raised concentrations of Et-1 in diabetic and non-diabetic patients with stable, unstable angina and previous myocardial infarction do not support the hypothesis that higher levels of Et-1 in diabetic patients are responsible for the increased incidence of CAD in diabetes mellitus. However, the raised Et-1 levels found in diabetic patients in the absence of CAD strongly suggest that a generalised endothelial dysfunction, documented in our study by increased levels of Et-1, most probably precedes subsequent cardiovascular diseases.     

Serum levels of matrix metalloproteinase 3 and macrophage colony-stimulating factor 1 correlate with disease activity in ankylosing spondylitis

OBJECTIVE: To assess the usefulness of measuring serum matrix metalloproteinase 3 (MMP-3) and macrophage colony-stimulating factor (M-CSF) in patients with ankylosing spondylitis (AS). METHODS: Serum levels of MMP-3 and M-CSF were measured in AS patients who did and did not receive infliximab treatment. These were compared with those of 28 healthy subjects. RESULTS: In the group of AS patients not treated with biologics, both M-CSF and MMP-3 correlated with the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) values, but not with each other. Logistic regression analysis showed that MMP-3 values were high in those with severely active disease. Infusions of infliximab in AS patients led to a significant decrease in the values of the BASDAI as well as the serum MMP-3, but no change in the serum M-CSF values. CONCLUSION: MMP-3 and M-CSF are potentially useful markers of AS disease activity.     

老年男性糖尿病脑梗死患者血MMP-9和TIMP-1水平变化

用酶联免疫吸附方法(ELISA)检测糖尿病脑梗死组、非糖尿病脑梗死组、糖尿病非脑梗死组、健康对照组的基质金属蛋白酶9(MMP-9)、组织基质金属蛋白酶抑制物1(TIMP-1)的水平.结果 显示糖尿病脑梗死组MMP-9、TIMP-1水平明显明显高于其他3组(P＜0.05),提示其可能在糖尿病脑梗死发病过程中有重要作用.     

Serum soluble TNF receptor I and II levels correlate with disease activity in IBD patients

BACKGROUND: Tumor necrosis factor alpha (TNFalpha) is a proinflammatory cytokine and an important mediator in the pathophysiology of inflammatory bowel disease (IBD). The effects of TNFalpha are mediated by 2 specific receptors, a 55-kDa protein (TNF-RI) and a 75-kDa receptor (TNF-RII), which are usually bound to the cell surface. Soluble TNF receptors I and II (sTNF-RI + II) are released by proteolytic cleavage of the extracellular domains of these receptors. Soluble TNF-Rs act as TNF antagonists and can inhibit TNFalpha-mediated proinflammatory effects. METHODS: Levels of sTNF-RI + II were measured using commercially available enzyme-linked immunosorbent assays (ELISAs). Serum levels of sTNF-RI + II of 76 healthy volunteers were compared to serum levels of 373 clinically well-characterized patients with Crohn's disease (CD) and 118 patients with ulcerative colitis (UC) with different disease activity from the German IBD competence network serum bank. CD patient subgroups were defined according to the Vienna Classification. RESULTS: The serum levels of sTNF-RI were significantly increased in all groups (active, chronic active, and remission) of CD and UC patients compared to healthy controls. sTNF-RII levels were significantly higher in active CD patients compared to UC patients with no overlap of the 95% confidence interval. Significantly higher values of sTNF-RII compared to controls were also observed in CD patients and UC patients in remission. There was no statistically significant difference in sTNF-RI or sTNF-RII levels when patient subgroups were analyzed according to disease behavior or disease localization. CONCLUSION: sTNF-RI is upregulated in the serum of IBD patients compared to healthy controls and could be used as a marker for disease activity. sTNF-RII levels are significantly more elevated in serum of active CD patients as compared to UC and could be used as an additional parameter to discriminate both diseases.     

Increased urinary levels of CXCL5, CXCL8 and CXCL9 in patients with Type 2 diabetic nephropathy

CXC chemokines are particularly significant for leukocyte infiltration in inflammatory diseases. Recent reports have shown that inflammation is one of potential pathogenic mechanisms for diabetic nephropathy. However, information on inflammation related with CXC chemokines in human Type 2 diabetic nephropathy still remains scarce. We measured urinary and serum levels of three CXC chemokines, CXCL5, CXCL8 and CXCL9, in 45 Type 2 diabetic patients (DM), 42 primary renal disease (PRD) patients and 22 healthy controls by enzyme-linked immunosorbent assay. Urinary levels of CXCL5, CXCL8 and CXCL9 in DM were significantly elevated compared to those in controls (P<.0001, P<.01, P<.001; respectively). They increased consistent with urinary albumin excretion rate (UAER) and correlated with UAER in partial correlation analyses (r=0.41, P<.01; r=0.40, P<.01; r=0.45, P<.01; respectively). Urinary levels of CXCL5 in DM were significantly interrelated to HbA(1c) (r=0.42, P<.01). On the other hand, PRD showed significant increased levels of urinary CXCL8 and CXCL9 compared to controls (P<.001, P<.01; respectively), and so did PRD as UAER increased. However, there were no significant elevations of urinary levels of CXCL5 in PRD in spite of the increased UAER. We found significant associations of UAER in DM with diabetes duration, 1/serum creatinine, urinary CXCL5 (adjusted R(2)=0.67, P<.0001) or CXCL9 (adjusted R(2)=0.69, P<.0001) in a stepwise multiple regression analysis. These results suggest that these three CXC chemokines may be involved in the progression of human Type 2 diabetic nephropathy and that CXCL5 may be of use for telling diabetic nephropathy from primary renal diseases.     

Serum concentrations of sICAM-1, sE-, sP- and sL-selectins in patients with Schistosoma mansoni infection and association with disease severity

Increased serum concentrations of soluble intercellular adhesion molecule-1 (sICAM-1, CD54) and of soluble E- (CD62E), but not soluble P- (CD62P) and L- (CD62 L) selectins, were detected in Malagasy patients living in an hyperendemic focus of Schistosoma mansoni . Levels of sICAM-1 remained elevated for several months after treatment with praziquantel. Serum levels of ICAM-1, but not of other markers, were significantly correlated with the disease severity, as indicated by ultrasonographical data, and with some circulating fibrosis markers (at least hyaluronic acid). sICAM-1 level may reflect endothelial inflammatory reactions, probably harmful, in the liver and may be useful for monitoring morbidity evolution in schistosomiasis mansoni .     

Anti-Jo-1 antibody levels correlate with disease activity in idiopathic inflammatory myopathy

OBJECTIVE: Previous case series have examined the relationship between anti-Jo-1 antibody levels and myositis disease activity, demonstrating equivocal results. Using enzyme-linked immunosorbent assays (ELISAs) and novel measures of myositis disease activity, the current study was undertaken to systematically reexamine the association between anti-Jo-1 antibody levels and various disease manifestations of myositis. METHODS: Serum anti-Jo-1 antibody levels were quantified using 2 independent ELISA methods, while disease activity was retrospectively graded using the Myositis Disease Activity Assessment Tool, which measures disease activity in 7 different organ systems via the Myositis Disease Activity Assessment Visual Analog Scale (VAS) and the Myositis Intention-to-Treat Index (MITAX) components. Spearman's rank correlation coefficients and mixed linear regression analysis were used to identify associations between anti-Jo-1 antibody levels and organ-specific disease activity in cross-sectional and longitudinal analyses, respectively. RESULTS: Cross-sectional assessment of 81 patients with anti-Jo-1 antibody revealed a modest correlation between the anti-Jo-1 antibody level and the serum creatine kinase (CK) level, as well as muscle and joint disease activity. Correlation coefficients were similar for CK levels (r(s) = 0.38, P = 0.002), myositis VAS (r(s) = 0.36, P = 0.002), and arthritis VAS (r(s) = 0.40, P = 0.001). In multiple regression analyses of 11 patients with serial samples, anti-Jo-1 antibody levels correlated significantly with CK levels (R(2) = 0.65, P = 0.0002), myositis VAS (R(2) = 0.53, P = 0.0008), arthritis VAS (R(2) = 0.53, P = 0.006), pulmonary VAS (R(2) = 0.69, P = 0.005), global VAS (R(2) = 0.63, P = 0.002), and global MITAX (R(2) = 0.64, P = 0.0003). CONCLUSION: In this large series of patients with idiopathic inflammatory myopathy, anti-Jo-1 antibody levels correlated modestly with muscle and joint disease, an association confirmed by a custom ELISA using recombinant human Jo-1. More striking associations emerged in a smaller longitudinal subset of patients that link anti-Jo-1 antibody levels to muscle, joint, lung, and global disease activity.     

Serum Th1 (CXCL10) and Th2 (CCL2) chemokine levels in children with newly diagnosed Type 1 diabetes: a longitudinal study

Aims Cell‐mediated immunity and pro‐inflammatory cytokines are implicated in the pathogenesis of Type 1 diabetes. The aim of this study was to investigate whether circulating chemokines involved in T‐helper 1 (CXCL10) and T‐helper 2 (CCL2) autoimmunity are increased in children with Type 1 diabetes at onset and follow‐up. Methods Serum CXCL10 and CCL2 were measured in 96 children with newly diagnosed Type 1 diabetes, 59 age‐matched first‐degree relatives of diabetic children and 40 age‐matched non‐diabetic children with no family history of diabetes. In the diabetic children, an additional serum sample was obtained a median of 16 months after diagnosis. Results Serum CXCL10 levels were significantly higher in Type 1 children than in relatives or control children (P < 0.001); 44.7% of patients had a serum CXCL10 level ≥ 2 standard deviation above the mean value of the control group vs. 3.4% of relatives (P < 0.0001). In contrast, serum CCL2 levels were similar in patients, relatives and control subjects. In the Type 1 diabetic patients at follow‐up, CXCL10 was significantly reduced vs. baseline (P = 0.01), while CCL2 did not change. Conclusions In children with newly diagnosed Type 1 diabetes, raised serum CXCL10 and normal CCL2 concentrations signal a predominant T‐helper 1‐driven autoimmune process, which shifts toward T‐helper 2 immunity over the first 1–2 years from diagnosis.     

Serum leptin and ghrelin correlate with disease activity in ANCA-associated vasculitis

OBJECTIVES: To study serum levels of leptin and ghrelin in ANCA-associated vasculitis (AAV). METHODS: Thirty-seven patients with AAV (21 patients with active AAV at initial presentation and during follow-up, 16 patients with AAV in long-term remission) and 21 matched healthy controls were included. Serum levels of leptin and ghrelin were measured at 0, 6 and 12 months by radioimmunoassay. Disease activity was gauged by Birmingham Vasculitis Activity Score (BVAS), CRP and circulating endothelial cells (CECs). RESULTS: Leptin levels were significantly lower in patients than in healthy controls (9.1 +/- 6.1 vs 22.3 +/- 22.4 ng/ml; P < 0.05). The difference persisted when corrected for BMI. Leptin levels increased significantly after 6 (27.8 +/- 21.9 ng/ml; P < 0.001) and 12 months (24.6 +/- 21.0 ng/ml; P < 0.001). Ghrelin levels were significantly elevated in patients compared with controls (402.6 +/- 112.9 vs 294.8 +/- 70.9 pmol/l; P < 0.005) and declined to normal values at 12 months (306.4 +/- 36.2 pmol/l). There was a significant positive correlation between ghrelin levels and disease activity, whereas leptin levels were negatively correlated with disease activity (CRP, BVAS and CECs). Accordingly, correlations between the ghrelin/leptin ratio and markers of disease activity reached the highest level of significance (all P < 0.001). CONCLUSIONS: Active AAV is characterized by decreased serum leptin and increased serum ghrelin, both of which return to normal with successful therapy. The role of leptin and ghrelin during the pathogenesis of AAV and the effects of these peptides on endothelial cells warrant further study.     

Correlation analysis of IGF-1, ZAG,nesfatin-1, HbA1c levels,and type 2 diabetes mellitus complicated with hypothyroidism

To analyze the correlation between IGF-1, ZAG, nesfatin-1, HbA1c levels, and type 2 diabetes mellitus (T2DM) complicated with hypothyroidism.Fifty-five patients with type-2 diabetes who were admitted to our hospital from August 2018 to February 2020 were selected as the control group, and 55 patients with type 2 diabetes combined with hypothyroidism who were admitted to the hospital at the same period were selected as the combined group, and 56 patients who came to our hospital for physical examination at the same period were selected as the healthy group. The general clinical data and relevant laboratory indexes of all patients in the three groups were collected and statistically analyzed. Besides, the correlation between IGF-1, ZAG, nesfatin-1, HbA1c levels, and T2DM complicated with hypothyroidism was analyzed.Levels of FPG, FINS, TC, TG, LDL, 2hPBG, TPOAb, TgAb, and HOMA-IR in the diabetes group and combined group were all significantly higher than those in the healthy group, while HDL and T4 levels in the diabetes group and combined group were lower than those in the healthy group (P < .05). The levels of FPG, FINS, TC, TG, LDL, 2hPBG, TPOAb, and TgAb in the combined group were significantly higher than those in the diabetes group (P < .05), and the levels of HDL and T4 were lower than those in the diabetes group. In addition, the IGF-1 level was positively correlated with ZAG, nesfatin-1, and HbA1c levels in the combined group (P < .05), and IGF-1 (OR: 0.964, 95% CI: 0.943–0.983, P = .001), ZAG (OR: 1.298, 95% CI: 1.121–1.401, P = .005), nesfatin-1 (OR: 0.876, 95% CI: 0.751–0.901, P = .002), and HbA1c (OR: 1.321, 95% CI: 1.121–1.401, P = .012) were independent risk factors for T2DM complicated with hypothyroidism.Regular detection of IGF-1, ZAG, nesfatin-1, and HbA1c levels are of great value for the diagnosis and treatment of patients with T2DM complicated with hypothyroidism.     

急性ST段抬高型心梗患者血清HMGB1检测及其临床意义

目的:探讨血清高迁移率族蛋白1(HMGB1)水平和急性ST段抬高型心肌梗死(STEMI)的关系。方法:正常对照组312例、STEMI组429例,采用酶联免疫吸附法(ELISA)检测血清HMGB1、高敏C反应蛋白(hs-CRP)和α-肿瘤坏死因子(TNF-α)水平。结果:STEMI组血清HMGB1水平明显高于正常对照组,为(10.4±9.3)ng/ml对(2.3±2.3)ng/ml(P<0.001),血清HMGB1水平与hs-CRP,TNF-α水平呈正相关。结论:HMGB1可能参与急性心肌梗死的病理生理过程。     

Circulating levels of the chemokine CCL18 but not CXCL16 are elevated and correlate with disease activity in rheumatoid arthritis

BACKGROUND: Antigen-presenting cells (APC) and T cells are considered to play a significant role in the pathogenesis of rheumatoid arthritis (RA). CCL18 and CXCL16 are two chemokines that facilitate T cell attraction by APC, of which a role in the pathogenesis of RA has been suggested. OBJECTIVE: To compare the circulating levels of CXCL16 and CCL18 in RA with controls and to investigate the relation of CXCL16 and CCL18 with RA disease activity and joint damage. METHODS: Circulating CCL18 and CXCL16 levels were determined in 61 RA patients with a follow-up of 6 years and a group of 41 healthy controls with ELISA. Chemokine levels were correlated with demographic data, disease activity (DAS28) and joint damage (modified Sharp score). In addition, serum CCL18 and CXCL16 levels from a cohort of 44 RA patients treated with anti-TNF-alpha were correlated with disease activity. RESULTS: CCL18 levels in serum were significantly elevated in RA patients compared with controls, while serum CXCL16 levels were not. In contrast to CXCL16, serum CCL18 was positively correlated with disease activity. Both CCL18 and CXCL16 levels decreased upon treatment with anti-TNF-alpha. Neither CCL18 nor CXCL16 correlated with joint damage and progression. CONCLUSION: Here, we show, for the first time, that circulating CCL18 and not CXCL16 levels are elevated in RA patients as compared with controls and correlate with disease activity in RA. More knowledge regarding the regulation and function of both CCL18 and CXCL16 is essential to value their role in RA.