Serum Levels Of Receptor Research Articles

Serum soluble toll-like receptor 2: a novel biomarker for systemic lupus erythematosus disease activity and lupus-related cardiovascular dysfunction.

To assess the serum levels of soluble toll-like receptor (sTLR2) as an endogenous negative regulator of TLR2 signaling in systemic lupus erythematosus (SLE) patients, to investigate the correlation between sTLR2 and SLE disease activity index (SELDAI), SLE-related cardiovascular risk factors and ventricular dysfunction and to evaluate the effect of different therapeutic regimens on serum sTLR2 levels. Ninety-six SLE patients, along with 30 healthy controls, were enrolled in the study. Echocardiography measurements were performed. Serum levels of (sTLR2) were measured using enzyme-linked immunosorbent assay (ELISA). Serum lipid profiles, uric acid and creatinine were also detected. Mean serum levels of sTLR2 in SLE patients was 3.98±4.4ng/mL, which was significantly decreased as compared with that of the control group (11.3±4.9ng/mL; P<0.0001). sTLR2 was negatively correlated with SELDAI, low-density lipoprotein (LDL) and left ventricular diastolic dysfunction. sTLR2 levels were increased in patients receiving hydroxychloroquine, statins and corticosteroids. Serum sTLR2 can attenuate disease activity and negatively impact left ventricular diastolic dysfunction and hypercholersterelemia in SLE patients. Statins, corticosteroids and chloroquine increase sTLR2 levels.

Effect of leptin receptor Q223R polymorphism on breast cancer risk.

Leptin receptor (LEPR) is a member of the class I cytokine receptor super-family that is known implicated in the initiation and progression of breast cancer. We have investigated the effect of Q223R polymorphism on the breast cancer susceptibly in a sample of Iranian subjects. We utilized a polymerase chain reaction (PCR) restriction fragment length polymorphism (RFLP) method to investigate the association of LEPR Q223R polymorphism with breast cancer risk in a case control study consisting of 100 breast cancer cases and 100 controls without breast cancer. Serum levels of leptin and soluble leptin receptor (sOB-R) were measured by ELISA method. The genotype (QQ, QR, and RR) distributions were 25, 56, and 19 % in breast cancer cases and 54, 40, and 6% in controls, respectively. The frequency of 223 RR genotype was significantly elevated in breast cancer cases as compared to controls (χ(2)= 20.072, P<0.001). Similar significance differences were also found in allele frequencies for Q and R between two groups (χ(2)= 19.027, P< 0.001). Additionally, there were significant association between Q223R genotypes and breast cancer risk; homozygotes for RR genotype (OR= 6.840; 95% confidence interval [CI] = 2.434-19.218), heterozygotes for QR (OR=3.024; 95% CI = 1.620-5.644, P = 0.001), and QR+RR genotype (OR= 3.522; 95% CI = 1.934-6.414, P < 0.001), respectively. Our results showed that the LEPR Q223R polymorphism is associated with increased breast cancer risk as well as tumor grade in a sample of Iranian subjects.

Serum Levels of Soluble Urokinase Plasminogen Activator Receptor in Infants with Late-onset Sepsis.

Soluble urokinase plasminogen activator receptor (suPAR) has been studied in a variety of diseases. The aim of the study is to investigate the levels of suPAR in neonates with sepsis. The infants enrolled to this prospective study were classified into four groups. Group 1, 2, and 3 were referred as the patient groups (40 infants), and group 4 was referred as control group (26 infants). Blood samples for whole blood count, C-reactive protein (CRP), suPAR and blood culture were obtained before initiating antimicrobial therapy, and two further samples were obtained on day 3 and at the end of the treatment for CRP and suPAR. The mean gestational ages of patient and control groups was similar. The median level of initial suPAR was 18.8 ng/mL (range 6.8-30.1 ng/mL) in the patient groups, and 6.0 ng/mL (range 3.7-10.8 ng/mL) in the control group (P < 0.001). A significant decrease in suPAR level was observed from the inclusion to the third day and end of the treatment (P < 0.001). The area under the curve (AUC) for suPAR is 0.959 (95% Cl: 0.919-0.999) and for CRP is 0.782 (95% Cl: 0.669-0.895). At a cut-off value of 11.3 ng/mL for suPAR the specificity was 100%, and the sensitivity was 82.5%. There was a positive correlation between laboratory values of CRP and suPAR (r: 0.359, P = 0.003). This is the first study that investigated the levels of suPAR in neonates and our results demonstrate that suPAR is a powerful marker of inflammation in infants with sepsis.

Relationship between interleukin-1 type 1 and 2 receptor gene polymorphisms and the expression level of membrane-bound receptors.

The biological activity of the multifunctional cytokine interleukin-1 (IL-1) is mediated by its receptors. The aim of this study was to determine if an association exists between single nucleotide polymorphisms (SNPs) in the IL-1 type 1 and 2 receptor genes (IL1R1 and IL1R2) and the expression level of membrane-bound IL1Rs on subpopulations of mononuclear cells or serum levels of soluble IL-1 receptors. It was observed that healthy individuals with the genotype TT in SNP rs2234650:C>T had a lower percentage of intact CD14(+) monocytes expressing IL1R1 on their surface. The SNP rs4141134:T>C in IL1R2 has also been associated with the percentage of intact CD3(+) T cells expressing IL1R2. Furthermore, individuals carrying the CC allele of SNP rs4141134:T>C and the TT allele of SNP rs2071008:T>G in IL1R2 had a lower density of IL1R2s on the surface of CD14(+) monocytes in lipopolysaccharide (LPS)-stimulated PBMC cultures. In summary, this study demonstrated that IL-1 receptor gene polymorphisms could be one of the factors influencing the expression of membrane-bound IL-1 receptors (IL1R) on immunocompetent cells.

Serum levels of soluble receptor for advanced glycation end-products and metabolic syndrome: The Northern Manhattan Study

ObjectiveRecent studies have shown a strong link between serum soluble receptor for advanced glycation end-products (sRAGE) levels and cardiovascular risk factors and disease. What is less clear is the relationship between metabolic risk factors and sRAGE levels. Here, we tested the hypothesis that lower sRAGE levels may be associated with the metabolic syndrome (MetS) in an urban multi ethnic population. Materials/methodsFrom the Northern Manhattan Study (NOMAS), we included 1101 stroke-free participants (mean age: 71±9years, 60% women, 64% Hispanic, 18% black, 16% white). Serum sRAGE was measured by ELISA. Quantile regression analysis was performed to evaluate the association between sRAGE and MetS components and MetS, after adjusting for sociodemographics, smoking status and kidney function. ResultsThe median (interquartile) sRAGE was 899pg/ml (647–1248pg/ml), 42% had metabolic syndrome. The prevalence of unfavorable metabolic factors was 50% for waist circumference (WC), 81% for blood pressure, 39% for fasting glucose, 35% for reduced high density lipoproteins (HDL), and 23% for triglycerides. After adjustment, the median sRAGE levels were at least 120pg/ml lower in those who had elevated WC (p<0.0001), blood pressure (p=0.0014), and fasting glucose (p<0.0001), and those who had 2 or more unfavorable metabolic factors. No relationship was seen between sRAGE levels and elevated triglycerides or reduced HDL levels. Interaction and stratified analyses revealed that the association of sRAGE with MetS was more prominent in Hispanics compared to whites, and displaying no association with components of MetS in blacks. ConclusionssRAGE levels were mainly associated with MetS factors related to obesity, diabetes and hypertension, and displayed variation with ethnicity in a multi-ethnic population. Further studies of sRAGE, MetS and their relationship to cardiovascular disease are warranted.

AB0080 In Both SLE and Seropositive RA, the Interleukin-6 (IL-6) System is Active, and Shifted towards Trans-Signalling

BackgroundIL-6 signals via a receptor consisting of gp130 (CD130) and either membrane-bound IL-6 receptor α (CD126) present on leukocytes and hepatocytes or soluble (sIL-6Rα) on all other cells, the latter...

Acculturative stress and inflammation among Chinese immigrant women.

Among Chinese immigrant populations, increasing duration of US residence is associated with elevated risk for various chronic diseases. Although life-style changes after migration have been extensively studied in immigrant populations, the psychosocial impact of acculturative stress on biological markers of health is less understood. Thus, the purpose of the present study is to examine associations between acculturative stress and inflammatory markers in a Chinese immigrant population. Study participants (n = 407 foreign-born Chinese American women) completed questionnaires assessing levels of stress, including acculturative stress and positive and negative life events in the previous year. Participant height and weight were measured using standard protocols, and blood samples were drawn for assessment of circulating serum levels of C-reactive protein (CRP) and soluble tumor necrosis factor receptor 2 (sTNFR2). Higher levels of acculturative stress were significantly associated with higher levels of CRP (B = 0.07, 95% confidence interval = 0.01-0.13, p = .031) and sTNFR2 (B = 0.02, 95% confidence interval = 0.004-0.03, p = .012), adjusting for age and body mass index. The latter association was no longer statistically significant when overall acculturation (i.e., identification with American culture) was included in the model. Life events were not associated with CRP or sTNFR2. This is one of the first studies to demonstrate that acculturative stress is associated with inflammatory markers in a Chinese immigrant population. Replication in other immigrant samples is needed to fully establish the biological correlates and clinical consequences of acculturative stress.

Erratum to: The correlation of serum levels of leptin, leptin receptor and NO x (NO2 − and NO3 −) in patients with obstructive sleep apnea syndrome

Erratum to: The correlation of serum levels of leptin, leptin receptor and NO x (NO2 − and NO3 −) in patients with obstructive sleep apnea syndrome

The correlation of serum levels of leptin, leptin receptor and NO x (NO2 − and NO3 −) in patients with obstructive sleep apnea syndrome

The aim of this study was to investigate the relations between nitric oxide (NO) and leptin levels in a cohort of untreated adult Obstructive sleep apnea syndrome (OSAS) patients. Between June 1, 2012, and January 1, 2013, we evaluated a total of 58 subjects including 36 OSAS patients and 22 healthy controls, both polysomnographically confirmed. Following the completion of polysomnographic evaluation, serum samples were taken at 08:00. Leptin, leptin receptor, NO2 (-) and NO3 (-) levels were analyzed by commercial ELISA kits. Data analysis was performed using the Statistical Package for the Social Sciences (SPSS) version 16.0 (SPSS Inc., Chicago, IL, USA). There was no statistically significant difference between the OSAS patients and control groups with relation to the demographic parameters and body mass index (p > 0.05). Significantly higher serum leptin and plasma NO levels were found in OSAS patients compared to the controls (p < 0.001). In this study, higher leptin levels which were positively correlated with NO levels in OSAS group may indicate a possible link with increased incidence of airway pathologies in these patients.

Serum-soluble urokinase receptor levels do not distinguish focal segmental glomerulosclerosis from other causes of nephrotic syndrome in children

In this prospective study, we measured serum levels of the soluble urokinase receptor (suPAR) in pediatric patients with nephrotic syndrome of various etiologies. Mean levels of suPAR were 3316 pg/ml in 99 patients with steroid-resistant focal segmental glomerulosclerosis and 3253 pg/ml in 117 patients with biopsy-proven minimal change disease, which were similar to that of 138 patients with steroid-sensitive nephrotic syndrome (3150 pg/ml) and 83 healthy controls (3021 pg/ml). Similar proportions of patients in each group had suPAR over 3000 pg/ml. Compared with controls, suPAR levels were significantly higher in patients with focal segmental glomerulosclerosis (FSGS) and estimated glomerular filtration rate (eGFR) under 30 ml/min per 1.73 m(2) (6365 pg/ml), congenital nephrotic syndrome (4398 pg/ml), and other proteinuric diseases with or without eGFR under 30 ml/min per 1.73 m(2) (5052 and 3875 pg/ml, respectively; both significant). There were no changes following therapy and during remission. Levels of suPAR significantly correlated in an inverse manner with eGFR (r=-0.36) and directly with C-reactive protein (r=0.20). The urinary suPAR-to-creatinine ratio significantly correlated with proteinuria (r=0.25) in 151 patients and controls. Using generalized estimating equations approach, serum suPAR significantly correlated with eGFR (coefficient=-13.75), age at sampling (2.72), and C-reactive protein (39.85). Thus, serum suPAR levels in nephrotic syndrome are similar to controls, and do not discriminate between FSGS, minimal change disease, or steroid-responsive illness.

Evation of High-Mobility Group Box 1 after Clinical Autologous Islet Transplantation and Its Inverse Correlation with Outcomes

A major problem after clinical autologous islet transplantation (AIT) is the difficulty in achieving insulin independence. To follow up on our demonstration in a murine model that high-mobility group box 1 (HMGB1) was released from islets and involved in early loss of transplanted islets, we tested the role of HMGB1 in clinical AIT. Serum HMGB1 levels from 15 AIT patients were significantly elevated during islet infusion (7.6 ± 1.2 ng/ml) and 24 h after infusion (8.0 ± 1.4 ng/ml) compared to admission levels (2.4 ± 0.6 ng/ml). The first elevation of HMGB1 was associated with islet damage, but the later elevation was not. The change in the HMGB1 level from admission to first peak (ΔHMGB1) was significantly higher in the AIT group (8.1 ± 1.1 ng/ml) than in the pancreatectomy-only control (2.2 ± 0.5 ng/ml) (p < 0.05). Circulating serum levels of soluble receptor for advanced glycation end products (sRAGE) were also elevated during islet infusion. In vitro studies demonstrated that damaged human islets released HMGB1 but not sRAGE. In terms of outcomes, the insulin-free group showed significantly lower ΔHMGB1 (5.2 ± 0.6 ng/ml) and higher ΔsRAGE (2.3 ± 0.6 ng/ml) than the insulin-dependent group (10.6 ± 1.9 ng/ml and 0.7 ± 0.2 ng/ml, respectively). The ΔHMGB1 correlated with the number of white blood cell, IP-10, EGF, and eotaxin. In conclusion, serum HMGB1 was elevated in AIT and could be associated with inflammatory reactions that deteriorate islet engraftment. Therefore, anti-HMGB1 therapy might be a candidate for further improving the outcomes of clinical AIT.

Tandem triplication of the BCL2 gene in CD5-positive intravascular large B cell lymphoma with bone marrow involvement

Dear Editor, Intravascular large B cell lymphoma (IVLBCL) is a rare subtype of diffuse large B cell lymphoma (DLBCL) characterized by the selective growth of lymphoma cells within the lumina of vessels [1]. Cytogenetically, the majority of IVLBCL cases demonstrated complex karyotypes with multiple numerical and structural changes, and the most frequent duplicated regions were shown to be the 11q13→qter region and all of chromosome 18 [2, 3]. On the other hand, triplications of chromosome segments other than 1q have been rarely found in hematological malignancies [4–8]. Here, we describe an unusual case of IVLBCL with a tandem triplication of the BCL2 gene at 18q21. An 82 year-old female was admitted because of fever. Computed tomography scans revealed hepatosplenomegaly without lymphadenopathy. Peripheral blood (PB) examination showed hemoglobin 105 g/L, platelets 52×10/L, and leukocytes 10.1× 10/Lwith 15% abnormal lymphocytes. Serum levels of lactate dehydrogenase (LDH) and soluble interleukin-2 receptor were 6,382 IU/L (normal range, 115~217) and 8,429 U/mL (124~ 466), respectively. Bone marrow (BM) was normocellular with 42.4 % abnormal lymphocytes positive for CD5, CD19, CD20, and HLA-DR (Fig. 1a). Pathological examination of the BM revealed a focal and sinusoidal growth pattern of large lymphoid cells, indicating a diagnosis of IVLBCL (Fig. 1b). Immunohistochemistry demonstrated that they were positive for CD5, CD20, BCL2, and MUM1, but negative for CD10 and BCL6 (Fig. 1c, d). The patient received R-CHOP therapy and achieved hematological complete remission. However, 12 months later, she relapsed and died of progressive disease. G banding and spectral karyotyping of BM cells showed 47,XX,del (2)(q?),+del(3)(p?),der(10)t(10;20)(q24;?), dup(17)(q21q23),dup(18)(q11.2q23) [20] (Fig. 1e). Unexpectedly, fluorescence in situ hybridization (FISH) detected three BCL2 signals on the dup(18)(q11.2q23), indicating a tandem triplication of BCL2 (Fig. 1f). Namely, the short 18q fragment containing BCL2 attached to the dup(18). FISH on interphase nuclei confirmed four BCL2 signals. According to the Mitelman Database, nine cases of hematological malignancies with duplication/triplication of 18q (duplication, eight; triplication, one) in the stem-lines have been described [4, 9, 10]. All cases were diagnosed with B lymphoid malignancies. The duplicated regions in two cases of acute lymphoblastic leukemia did not contain 18q21, whereas those in seven cases of B cell lymphomas (DLBCL, four; IVLBCL, one; Burkitt lymphoma, one; mantle cell lymphoma, one) retained 18q21. Thus, duplication/triplication of 18q including 18q21 seems to be specifically associated with B cell lymphomas and suggests the significance of BCL2 in their pathogenesis. Among these, one case with trp(18)(?q21q23) exhibited a tandem triplication of BCL2 [2]. This 62-year-old male was diagnosed as having IVLBCL with BM/PB involvement, thrombocytopenia (34×10/L), and high LDH (2,266 U/L). Lymphoma cells were positive for K. Yamamoto (*) :A. Okamura :K. Yakushijin :H. Matsuoka : H. Minami Division of Medical Oncology/Hematology, Department of Medicine, Graduate School of Medicine, Kobe University, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan e-mail: kyamamo@med.kobe-u.ac.jp

Vitamin D Increases Serum Levels of the Soluble Receptor for Advanced Glycation End Products in Women With PCOS

Elevation of serum proinflammatory advanced glycation end products (AGEs) is involved in the pathogenesis of polycystic ovary syndrome (PCOS). The soluble receptor for AGEs (sRAGE) acts as a decoy by binding circulating AGEs. Vitamin D supplementation attenuates the deposition of AGEs in the vascular system of diabetic animals and improves some metabolic aspects of vitamin D-deficient women with PCOS. Additionally, serum anti-Mullerian hormone (AMH) is elevated in women with PCOS, reflecting abnormal ovarian folliculogenesis. The objective of the study was to evaluate the effect of 1,25 dihydroxyvitamin D3 (vit D3) supplementation on serum sRAGE and AMH in vitamin D-deficient women with PCOS. DESIGN, SETTINGS, PARTICIPANTS, AND INTERVENTION: Sixty-seven women with (n = 22) or without (control; n = 45) PCOS who were diagnosed with vitamin D deficiency were enrolled. Fifty-one women were replaced with oral vit D3 for 8 weeks (16 with PCOS and 35 controls) and 16 women were not treated (six with PCOS and 10 controls). Serum 25-hydroxyvitamin D (25 OH-D), sRAGE, and AMH concentrations were measured at baseline and after vit D3 supplementation in the treated group and 8 weeks apart in the nontreated group. Changes in serum sRAGE and AMH concentrations after vit D3 replacement were measured. In all participants, there was a negative correlation between body mass index and serum sRAGE levels (r = -0.3, P = .01). In women with PCOS, but not in controls, vit D3 increased serum sRAGE (P = .03) and decreased serum AMH levels (P < .001). The increase in serum sRAGE positively correlated with the increase in serum 25 OH-D after supplementation in women with PCOS (r = 0.6, P = .01). In women with PCOS, vit D3 might exert a protective effect against the inflammatory action of AGEs by increasing circulating sRAGE. The normalization in serum AMH induced by vit D3 replacement suggests an improvement in folliculogenesis.

Should we try antiviral therapy for hepatitis C virus infection with pyoderma gangrenosum‐like lesions?

Should we try antiviral therapy for hepatitis <scp>C</scp> virus infection with pyoderma gangrenosum‐like lesions?

A3.14 Lymphocyte surface interleukin-6 (IL-6) receptor chains are similarly decreased in SLE and seropositive RA, but not in seronegative RA

Background and ObjectivesIL-6 plays a definite role in RA and has been found increased in SLE. However, differences in serum CRP suggest differences in signalling. We therefore analysed serum IL-6,...

Markers of and Risk Factors for the Development and Progression of Diabetic Kidney Disease

Diabetic kidney disease (DKD) occurs in 25%-40% of patients with diabetes. Given the dual problems of a significant risk of progression from DKD to end-stage renal disease (ESRD) and increased cardiovascular morbidity and mortality, it is important to identify patients at risk of DKD and ESRD and initiate protective renal and cardiovascular therapies. The importance of preventive therapy is emphasized further by worldwide increases in the incidence of diabetes. This review summarizes the evidence regarding the prognostic value and benefits of targeting established and novel risk markers for DKD development and progression. Family history of DKD, smoking history, and glycemic, blood pressure, and plasma lipid level control are established factors for identifying people at greatest risk of DKD development and progression. Absolute albumin excretion rate (AER) and glomerular filtration rate (GFR) measurements also are important, although AER categorization generally lacks the necessary specificity and sensitivity, and estimates of declining GFR are compromised by methodological limitations for GFRs in the normal-to-high range. Emerging risk markers for progressive loss of kidney function include markers of oxidation and inflammation, profibrotic cytokines, uric acid, advanced glycation end products, functional and structural markers of vascular dysfunction, kidney structural changes, and tubular biomarkers. Among these, the most promising are serum uric acid and soluble tumor necrosis factor receptor (type 1 and type 2) levels, especially in relation to GFR changes. At present, these can only be considered as risk markers because they only identify an individual at increased risk of progressive DKD and not necessarily related to the causal pathway promoting kidney damage. Further work is needed to establish whether modulating these factors improves the prognosis in DKD. Although change in urinary peptidome levels also is a promising marker, there currently is neither a clinical assay nor adequate studies defining its prognostic value. Until these or other novel markers become available for clinical use, predictive accuracy often may be increased with greater attention to established markers.

Effects of Janus kinase inhibitor tofacitinib on circulating serum amyloid A and interleukin-6 during treatment for rheumatoid arthritis

The Janus kinase inhibitor tofacitinib is currently being investigated as a disease-modifying agent in rheumatoid arthritis (RA). We investigated the in-vivo effects of tofacitinib treatment for 4 weeks on elevated circulating acute-phase serum amyloid (SAA) levels in 14 Japanese patients with RA. SAA levels fell from 110·5 ± 118·5 μg/ml (mean ± standard deviation) at treatment initiation to 15·3 ± 13·3 μg/ml after 4 weeks treatment with tofacitinib. The reduction in SAA levels was greater in patients receiving tofacitinib plus methotrexate compared with those receiving tofacitinib monotherapy. Tofacitinib was also associated with reduced serum interleukin (IL)-6, but had no effect on serum levels of soluble IL-6 receptor. Patients were divided into groups with adequate (normalization) and inadequate SAA responses (without normalization). Serum IL-6 levels were reduced more in the group with adequate SAA response compared with those with inadequate SAA response. These results suggest that tofacitinib down-regulates the proinflammatory cytokine, IL-6, accompanied by reduced serum SAA levels in patients with active RA. The ability to regulate elevated serum IL-6 and SAA levels may explain the anti-inflammatory activity of tofacitinib.

Effect of storage conditions and freeze/thaw cycles on serum and plasma levels of anti-acetylcholine receptor (AChR) antibody

Article Effect of storage conditions and freeze/thaw cycles on serum and plasma levels of anti-acetylcholine receptor (AChR) antibody was published on June 1, 2014 in the journal Clinical Chemistry and Laboratory Medicine (CCLM) (volume 52, issue 6).

Clinical significance of serum soluble T cell regulatory molecules in clear cell renal cell carcinoma.

To clarify the role of serum soluble T cell regulatory molecules in clear cell renal cell carcinoma (CCRCC), we measured the serum levels of soluble interleukin-2 receptor (sIL-2R), soluble B7-H3 (sB7-H3), and soluble cytotoxic T lymphocyte associated antigen-4 (sCTLA-4) in 70 CCRCC patients and 35 healthy controls. We investigated correlations between the serum levels of these soluble T cell regulatory molecules and the pathological grade, clinical stage, and prognosis of CCRCC. We also assessed the relations among each of these soluble molecules. As a result, the serum level of sIL-2R was significantly higher in CCRCC patients than in healthy controls (P < 0.05). In addition, elevation of serum sIL-2R was significantly correlated with the clinical stage (P < 0.001), and the survival of patients with high sIL-2R levels was shorter than that of patients with low sIL-2R levels (P < 0.05). Furthermore, the serum level of sB7-H3 was also significantly correlated with the clinical stage (P < 0.05), while the sIL-2R and sB7-H3 levels showed a positive correlation with each other (R = 0.550, P < 0.0001). These results indicate that the serum level of sIL-2R reflects tumor progression in CCRCC patients. In addition, the possibility was suggested that the IL-2/IL-2R and B7-H3 pathways may be involved in the progression of CCRCC.

Correlation between soluble triggering receptor expressed on myeloid cells-1 and endoscopic activity in intestinal Behçet's disease.

PurposeThe serum levels of soluble triggering receptor expressed on myeloid cells-1 (sTREM-1) have recently been shown to be correlated highly with disease activity in patients with intestinal Behçet's disease (BD). However, it remains unclear whether sTREM-1 levels reflect endoscopic activity in intestinal BD. This study aimed to evaluate the correlation of sTREM-1 levels with endoscopic activity in intestinal BD.Materials and MethodsA total of 84 patients with intestinal BD were enrolled. Endoscopic activity was compared with sTREM-1 levels as well as other laboratory findings, including erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP).ResultssTREM-1 levels were significantly increased in intestinal BD patients compared with controls (37.98±27.09 pg/mL vs. 16.65±7.76 pg/mL, p=0.002), however, there was no difference between endoscopically quiescent and active diseases (43.53±24.95 pg/mL vs. 42.22±32.68 pg/mL, p=0.819). Moreover, serum sTREM-1 levels did not differ in terms of number, shape, depth, size, margin, or type of ulcer in patients with intestinal BD. However, mean ESR and CRP levels in patients with active disease were significantly higher than those in patients with quiescent disease (p=0.001, p<0.001, respectively). In addition, endoscopic activity scores for intestinal BD were correlated significantly with both CRP levels (γ=0.329) and ESR (γ=0.298), but not with sTREM-1 levels (γ=0.166).ConclusionUnlike CRP levels and ESR, serum sTREM-1 levels were not correlated with endoscopic activity in patients with intestinal BD.