Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “SYNOVIAL FLUID”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,585 records · Page 88Linked to original sources

Free-radical oxidation (peroxidation) products in serum and synovial fluid in rheumatoid arthritis.

Free-radical oxidation (peroxidation) products were measured in (a) 65 synovial effusions and (b) 30 sera from normal subjects and 58 sera from patients with rheumatoid arthritis (RA). Free-radical oxidation products were detectable in 90% of synovial fluids, their concentration being higher in "inflammatory" than in "degenerative" joint disease. Free-radical oxidation products in serum were significantly elevated in patients with RA compared to normal controls; the levels declined after treatment with a variety of antiinflammatory agents.

Adult↗

Effects of gold therapy on the synthesis and quantity of serum and synovial fluid IgM, IgG, and IgA rheumatoid factors in rheumatoid arthritis patients.

Eleven patients with active rheumatoid arthritis were monitored prospectively while receiving up to 1 gm of gold sodium thiomalate. There was a significant decrease in serum and synovial fluid IgG, IgA, and IgM rheumatoid factor (RF) levels over the period of study. Comparison of changes in serum RF and total immunoglobulin levels indicated a selective effect on RF production. These observations were supported by changes in the spontaneous in vitro production of IgM-RF and total IgM by peripheral blood mononuclear cells. Studies of synovial membrane synthesis showed a downward trend in immunoglobulin and RF production, but this did not reach statistical significance. A differential effect on the various RF classes was also noted. The most profound effect was on IgM-RF production; whereas, changes in IgG-RF production were least affected. These results suggest a selective and differential effect of gold salts on RF production.

Adult↗

Synovial fluid lactate determinations as a diagnostic aid in cases of monoarticular arthritis.

The concentration of synovial fluid lactate was determined by an enzymatic kit method in 16 patients with various types of monoarticular arthritis and in 2 patients with non-inflammatory lesions and no joint effusion. Lactate concentrations in control cases were 1.2 mmol/l, in septic arthritis above 10 mmol/l, in pseudogout and yersinia arthritis around 7 mmol/l, and in other cases of inflammatory, nonseptic arthritis around 3.0 mmol/l.

Adolescent↗

Inorganic pyrophosphate generation from adenosine triphosphate by cell-free human synovial fluid.

OBJECTIVE: To quantify inorganic pyrophosphate (PPi) production from extracellular adenosine triphosphate (ATP) by human synovial fluids (SF). METHODS: Serial measurements of ATP hydrolysis rate (t1/2) were performed by the luciferase method from a starting concentration of 500 nM in 21 pathologic and one normal cell-free SF samples incubated under physiologic conditions. ATP was then pumped into a sample of each fluid, using the rate constant derived from the t1/2 of that fluid, to provide steady state levels simulating those reported in SF. Trace [32P] gamma ATP was added at the start of the infusion; conversion to [32P] Pi and to [32P] PPi was determined by precipitation of Pi as reduced phosphomolybdate before and after treatment with yeast inorganic pyrophosphatase. Finally, the pumping experiment was repeated and PPi production was calculated from direct measurement of PPi at time zero and at 60 min. PPi hydrolysis was measured in each fluid by [32P] Pi precipitation from [32P] PPi tracer added at time zero. RESULTS: ATP was hydrolyzed by all SF. The mean t1/2 (seconds) in 8 osteoarthritis (OA) samples was 72 s, in 5 calcium pyrophosphate dihydrate (CPPD) 30 s (p < 0.02), in 3 rheumatoid arthritis (RA) 1160 s, in normal 86 s, in 3 olecranon bursal (OB) 54 s, and in 2 total knee replacement fluid samples 17 and 121 s. The major product of ATP hydrolysis was PPi in all but 2 fluids (1 RA, 1 OB), even at lower than steady state levels. At simulated in vivo steady state ATP levels, mean conversion of APT to PPi was stoichiometric in OA and CPPD fluids. PPi hydrolysis was < 4% in all noninflammatory fluids. CONCLUSION: PPi is the major product of extracellular ATP catabolism in most SF. Hydrolysis rates were significantly faster in SF containing CPPD crystals. Mean PPi production by these fluids at simulated in vivo steady state levels was 6-fold that of OA SF (p < 0.01). Hydrolysis of extracellular ATP by ectonucleotide pyrophosphohydrolases can account for all PPi produced by joint issues previously estimated from [32P] PPi pool and turnover studies in human knee joints.

Adenosine Triphosphate↗

Immunoglobulins, anti-IgG antibodies and antinuclear antibodies in paired serum and synovial fluid samples. A comparison between juvenile and adult rheumatoid arthritis.

Paired samples of serum and synovial fluid (SF) from 13 patients with juvenile rheumatoid arthritis (JRA) and 10 patients with adult rheumatoid arthritis (RA) were examined regarding the level of immunoglobulins and the occurrence and titres of anti-IgG antibodies and antinuclear antibodies (ANA). The levels of immunoglobulins were lower in SF than in serum. In JRA the SF/serum ratio of IgG was equal to that of albumin, pointing to a local production of IgG. The SF/serum ratio of IgM was equal to that of alpha 2-macroglobulin. In JRA the SF/serum ratios of immunoglobulins tended to be lower than in RA, the difference being significant for IgM. IgD autoantibodies and IgA anti-IgG were not found in JRA. IgE autoantibodies occurred in some cases, but in RA in more than 60%. In JRA the SF titres of anti-IgG and ANA were most often lower than the serum titres. In RA the SF titres were often higher than the serum titres. In 9 of 10 paired SF samples from patients with RA the SF/serum ratios were mutually different with regard to one or several immunoglobulins. Evidence of synovial production of anti-IgG antibodies of classes other than IgG distinguished RA from JRA. Otherwise the differences were quantitative.

Adolescent↗

Chondroitin sulphation patterns in synovial fluid in osteoarthritis subsets.

OBJECTIVES: To determine concentrations of chondroitin sulphate (CS) disaccharides in knee synovial fluid (SF) from normal subjects and patients with osteoarthritis (OA) or rheumatoid arthritis (RA), to test whether these variables differ between different diseases and subsets of OA. METHODS: OA was subdivided into large joint OA (LJOA), nodal generalised OA (NGOA), and OA with calcium pyrophosphate crystal deposition (CPA), with 25, 9, and 11 people in each subset respectively. The SF of 13 normal subjects was also volunteered for analysis along with 15 RA patients. Clinical assessment of inflammation (0-6) was undertaken on OA and RA knees. Concentrations of unsaturated CS disaccharides Deltadi6S and Deltadi4S were measured by capillary zone electrophoresis. RESULTS: Concentrations of Deltadi6S were lower in RA (5.90 ng/ml) and OA (13.24 ng/ml) fluids compared with normal (21.0 ng/ml) but no significant differences were seen between disease and normal fluids for Deltadi4S (about 4-6 ng/ml). The ratio of Deltadi6S:Deltadi4S were RA<OA<normal subjects (p<0.001 for all comparisons). The disaccharide concentration values along with the ratios are below. Higher Deltadi6S:Deltadi4S ratios were obtained for LJOA and CPA compared with NGOA. Uninflamed knees had lower concentrations of Deltadi6S than inflamed knees (p<0.01). In patients with bilateral samples, there were strong correlations between right and left knees for all SF variables. CONCLUSIONS: Altered ratios of CS sulphation patterns occur in OA and within OA subsets. These further justify considering NGOA as a subset with a different aetiopathogenesis.

Adult↗

The redox states of serum and synovial fluid of patients with temporomandibular joint disorders.

The redox states of albumin in serum and synovial fluid (SF) were analyzed in 35 female patients with temporomandibular joint disorders and 9 asymptomatic female healthy volunteers by high-performance liquid chromatographic (HPLC) analysis. Human serum albumin (HSA) is divided by HPLC analysis into three fractions: mercaptalbumin (HMA, reduced form) and nonmercaptalbumin (HNA-1 and HNA-2, oxidized forms). It was found that the characterized values of albumin in SF of patients with the disorders were the fraction of HMA (f (HMA), 65.8 +/- 9.1%), the fraction of HNA-1 (f (HNA-1), 31.3 +/- 8.8%), and the fraction of HNA-2 (f (HNA-2), 2.9 +/- 0.9%), respectively, and similarly the values of albumin in serum of same subjects were f (HMA), 79.4 +/- 4.0%; f (HNA-1), 18.7 +/- 3.8%; and f (HNA-2), 1.9 +/- 0.5%. The HNA fractions in SF were significantly higher than those in serum (p < 0.0001). The SF of patients and even control showed more oxidative condition compared with sera of the same subjects. Each fraction of SF showed significant difference in control (p < 0.05), and greater significance in patients (p < 0.0001). Furthermore, the HNA-2 fraction (f (HNA-2), 2.9 +/- 0.9%) in SF of the patients with temporomandibular joint disorders revealed a significantly higher value (p < 0.01) than that (f (HNA-2), 1.7 +/- 0.3%) of controls. These findings suggested that SF of the temporomandibular joint is more locally oxidized than serum; thus oxidative factors are concerned in the pathogenesis of the temporomandibular joint disorders. It was also suggested that synovial albumin may play a scavenging role against the intraarticular oxidative stress.

Adolescent↗

Synovial fluid interleukin-8 and neutrophil function in rheumatoid arthritis and seronegative polyarthritis.

The relationships between synovial fluid (SF) interleukin-8 (IL-8) and neutrophil turnover as measured by cytidine deaminase (CD), and SF metabolites were studied in 28 patients, 16 with rheumatoid arthritis (RA; median age and disease duration 62 and 14 yr, respectively) and 12 with seronegative polyarthritis (SNP; median age and disease duration 32 and 5 yr, respectively). Knee SF samples were aspirated using indwelling cannulae following a period of rest for 1 h. SF IL-8 levels (measured by an ELISA) were significantly elevated in RA compared to SNP (median 2.35 vs 0.22 ng/ml, P < 0.001), as were median levels of CD (55.8 vs 8.11 U/ml, P < 0.01), lactic acid (29.6 vs 16.6 mg/dl, P < 0.001), glucose (57.9 vs 84.5 mg/dl, P < 0.05) and the lactate to glucose ratio (0.85 vs 0.19, P < 0.001). Measures of disease activity, C-reactive protein, plasma viscosity and articular index were also elevated in RA compared to SNP (P < 0.05). SF IL-8 levels correlated strongly with CD, lactate, glucose and the lactate to glucose ratio when both disease groups were considered together (P < 0.001). These parameters also showed some association with the measures of disease activity (P < 0.05). All these associations were less marked when the individual disease groups were analysed separately. These results suggest that factors responsible for neutrophil accumulation and priming (probably IL-8) are present in SF, and these coincide with products of their activation (CD). The degree of neutrophil turnover is linked to the anaerobic metabolism of the synovial cavity.

Adult↗

Cytomorphological, ultrastructural and immunological particularities of the synovial fluid in seronegative rheumatoid arthritis.

Our studies on the cytomorphological and ultrastructural analysis of 15 Synovial Fluid (SF) samples from patients diagnosed with seronegative Rheumatoid Arthritis (RA) and 10 SF from patients with Hydroarthrosis considered as controls were carried out. By cytomorphological studies we determined the cellularity, ragocytosis and synoviocytogram. SF in seronegative RA is characterized by leucocytosis (7,656/mm3) with polynucleosis (65.38%) and ragocytosis (59.27%) versus hydroarthrosis SF defined morphologically by lymphocytosis (47%). Degenerative forms of ragocyte-like polymorphonuclears (PMN) cells, individualized by an ultrastructural alteration less evident than recorded in seropositive Rheumatoid Arthritis (RA), associated with a remarkable capacity of endocytosis. The ultrastructural alterations, immune complexes (CIC), the immunoglobulins (MG) and the anticollagen II antibodies, suggest the early implication of these immune parameters in etiopathogenesis. The corroboration of the cytomorphological, ultrastructural and immunological data allows the profound study of the etiopathogenic mechanism and may represent a paraclinical criterion for differentiated seronegative RA field.

Antigen-Antibody Complex↗

Excitatory amino acids, TNF-alpha, and chemokine levels in synovial fluids of patients with active arthropathies.

The aim of this study was to assess the synovial fluid (SF) neurotransmitter excitatory amino acid (EAA) levels, including glutamate (Glu) and aspartate (Asp), in the context of SF levels of other amino acids, TNF-alpha and chemokines from patients with active arthropathies. The SF was collected from patients with active rheumatoid arthritis (RA), gout, or osteoarthritis (OA). The SF samples were analysed for levels of neurotransmitters glutamate and aspartate, tumour necrosis factor-alpha (TNF-alpha), Regulated upon Activation Normally T-cell Expressed and Secreted (RANTES), macrophage inhibitory factor-1 alpha (MIP-1alpha) and interleukin 8 (IL-8). SF WBC counts were also determined. Correlations between SF EAA, TNF-alpha and chemokines were determined by the Pearson product-moment correlation. Primary cultures derived from SF from active RA and gout patients were incubated with added l-glutamate, to assess if exposure to Glu could increase TNF-alpha levels. There were significant elevations in SF EAA, SF TNF-alpha and SF RANTES in RA patients compared to gout or OA patients. Significant correlations between SF EAA and SF RANTES, MIP-1alpha and IL-8 levels were seen, and SF EAA and SF TNF-alpha or SF WBC levels approached significance. Addition of exogenous neurotransmitter glutamate significantly increased TNF-alpha levels in primary cell cultures derived from RA and gout patients. The SF neurotransmitter EAA levels significantly correlated to selected SF chemokine levels, in clinically active RA, gout and OA patients, independent of disease. Added Glu resulted in significantly increased TNF-alpha levels in primary synovial cell cultures. These data expand the relationship of SF neurotransmitter EAA levels to SF cytokines and chemokines in patients with clinically active arthritis, and suggest that neurotransmitters Glu and Asp contribute to peripheral inflammatory processes.

Adult↗

RANTES and chemotactic activity in synovial fluids from patients with rheumatoid arthritis and osteoarthritis.

A massive accumulation of inflammatory cells in synovial tissues is a major pathological feature of rheumatoid arthritis (RA). Neutrophiles dominate synovial fluid while rheumatoid synovium is infiltrated with mononuclear cells. Mechanisms regulating influx of particular subpopulations of leukocytes into articular cavity and synovium compartment are not completely defined. An increasing amount of data supports a crucial role of a C-C chemokine RANTES in the RA pathogenesis. Our objective is to evaluate chemotactic activity for neutrophils (NCA), lymphocytes (LCA), and monocytes (MoCA) in SFs obtained from patients with RA and osteoarthritis (OA). We also aimed to characterise the relation between chemotactic activity, RANTES, and percentage distribution of leukocytes in SF. SFs from 11 patients with RA and 6 with OA were included in the study. Modified microchamber Boyden method was employed to assess chemotactic activity. Cytological and biochemical analysis of SF was performed. RANTES was measured with ELISA. Rheumatoid SFs were rich in cells with predominance of neutrophiles while osteoarthritic fluids were lymphocytic. RA SFs were also characterised by increased lactoferrin level. Both NCA and LCA were higher in SF from patients with RA (62 +/- 12 and 24 +/- 6 cells/HPF, resp) as compared to patients with OA (23 +/- 6; P < .05 and 6 +/- 2 cells/HPF; P < 0.05). The chemoattractive effect of RA SF was more pronounced on neutrophiles than on lymphocytes. RA SF expressed high RANTES levels (145+/- 36 pg/mL), while OA SF was characterised by only trace amount of this chemokine (2 +/- 1 pg/mL). We found positive correlation of RANTES with chemotactic activity for mononuclear cells (LCA + MoCA; R = 0.61; P < .05). Surprisingly, RANTES correlated also positively with neutrophiles number (R = 0.77; P < 0.001). Rheumatoid SF possesses strong chemotactic potency for leukocytes. RANTES is overexpressed in RA SF and is a potential mediator influencing intensity and composition of cellular infiltration in joints affected with inflammatory arthritis.

Aged↗

Altered formation of leukotriene B4 in vitro by synovial fluid neutrophils in rheumatoid arthritis.

The synthesis of products of the 5-lipoxygenase pathway by synovial fluid (SF) and peripheral blood neutrophils of 12 patients with rheumatoid arthritis was compared in 3 experimental conditions using high performance liquid chromatographic analysis. Major differences were observed when blood and SF neutrophils were incubated with ionophore A23187, the formation of all 5-lipoxygenase products being lower (p less than 0.0005) in the SF neutrophils. Addition of exogenous arachidonic acid to the A23187 stimulated cells partially overcame the difference in 5-lipoxygenase product synthesis between the 2 neutrophil populations. In contrast, upon incubation with arachidonic acid alone, SF neutrophils produced significantly larger amounts of 5-lipoxygenase products. The increased reactivity of the SF neutrophil 5-lipoxygenase to arachidonic acid and the decreased 5-lipoxygenase product synthesis upon A23187 stimulation may be the consequence of the previous activation of the cells and 5-lipoxygenase product synthesis in situ.

Adult↗

Biochemical investigation of cell motile activity in rheumatoid synovial fluid.

OBJECTIVE: We have suggested that autocrine motility-like factor is expressed in rheumatoid synovial fluid (SF). We examined the biochemical features of the motile activity. METHODS: We investigated chemokinetic activities of SF from patients with osteoarthritis and joint trauma as well as rheumatoid arthritis (RA) using a unique protein-free culture fibrosarcoma system. We then investigated biochemical features and the signal transduction pathway of the motile activity expressed in RA. RESULTS: We found chemokinetic activity in SF from all patients. However, ability to block binding of the monoclonal antibody to the receptor for autocrine motility factor (AMF) was observed only in rheumatoid SF on immunoblots. Biochemical investigation indicated motile activity to be heat labile, trypsin sensitive, and eluted at high salt concentration from an anion exchange column. Stimulated motility of rheumatoid SF was inhibited by the pertussis toxin, staurosporine (C kinase inhibitor), and genistein (tyrosine kinase inhibitor), but not by A kinase inhibitor, H-8. CONCLUSION: The cell motility activity expressed in rheumatoid SF appears to be AMF, and the cytokine may be essential for communication among leukocytes in rheumatic disease.

Animals↗

Immunoelectronmicroscopic characterization of intracellular inclusions in synovial fluid cells of patients with rheumatoid arthritis.

Qualitative immunoelectronmicroscopic (IEM) analysis of intracellular inclusions in synovial fluid (SF) cells in rheumatoid arthritis (RA) was performed using the peroxidase-antiperoxidase (PAP) method. Cells from patients with chronic RA were fixed in glutaraldehyde containing 0.05% saponin to permeabilize membranes before immunologic treatments. Intracellular inclusions of IgG, IgM, and C3 were observed in vacuoles of greater than 75% of both polymorphonuclear leukocytes (PMNs) and mononuclear phagocytic cells. IgA- and fibrinogen-containing inclusions were less frequent. Intracellular staining for albumin was minimal. Other membranous, vesicular, and granular unstained materials of potential importance were also often present in the same vacuoles. Stained inclusions were clearly distinct from lipid bodies, which were negative for immunostaining. Control samples had only occasional, scattered and weak stain that was easily recognizable as nonspecific and thus established the specificity of the reactions. A few lymphocytes in 2 patients showed positive staining for IgG in vacuoles. Extracellular staining of clumps of immunoglobulins, C3, and fibrinogen was also present. The various materials phagocytized by the different SF cells may be important in perpetuation of joint inflammation.

Antigen-Antibody Reactions↗

The effect of inflammatory synovial fluid on the breaking strength of new "long lasting" absorbable sutures.

The effect of inflammatory synovial fluid upon several absorbable sutures potentially useful for arthroscopic procedures, e.g., meniscus repair and shoulder stabilization, was studied by implanting lengths of these sutures into unstable, arthritic rabbit knees and testing their breaking strength after varying time periods (up to 18 weeks). Polyglyconate (Maxon) sutures retained no significant strength at 6 weeks. Polydioxanone (PDS) sutures began to lose breaking strength at 3 weeks, retained only 40% of their original strength 6 weeks after implantation, and had no measurable strength at 9 weeks. Polycaprolactone (LTS) sutures showed a slow reduction in strength and retained approximately 90% of their original breaking strength after 18 weeks of implantation. Green braided polyester (Mersiline) sutures showed no loss of breaking strength over the testing period. Measurements of inherent viscosity were made to give an indirect indication of the decline in molecular weight of these sutures. These data paralleled the breaking strength decline in every case. The surgeon selecting an absorbable suture must consider the length of time the suture will hold the target tissue. This information should be helpful to surgeons considering an absorbable suture for procedures such as meniscus repair and shoulder stabilization.

Absorption↗

Evidence for locally synthesized and clonally restricted immunoglobulin in the synovial fluid from rheumatoid arthritis patients.

In this study, we examined the immunoglobulin (Ig) present in synovial fluid (SF) from patients with rheumatoid arthritis (RA) to determine if it was locally produced and to assess the presence of clonally restricted (oligoclonal) immunoglobulin. We studied SF/serum pairs from 55 RA patients and 23 patients with degenerative joint disease (DJD). We found increases in total protein, IgG, IgA, and IgM in RA vs DJD SF (P less than 0.01). The immunoglobulin present in RA appeared to be locally produced as evidenced by significant increases (P less than 0.01) in the immunoglobulin indices. Regression analysis among the levels of IgG, IgA, and IgM RF and the Ig indices suggested that only a minority of the locally synthesized Ig present was specific for RF. To provide evidence of clonal restriction, we further analyzed the SF specimens by isoelectric focusing and assessed the presence of oligoclonal bands present only in RA SF. In 7/55 RA specimens (13%) we found unique SF IgG bands. All bands were of similar isoelectric point (pI), being quite cathodic with pI greater than 7.5. Our evidence supports synthesis of Ig within RA synovium, with a minority of patients showing prominent and unique SF Ig bands. This suggests an oligoclonal response in SF of some patients, but polyclonal Ig synthesis in most.

Arthritis, Rheumatoid↗

Synovial fluid calcium pyrophosphate dihydrate crystals and alizarin red positivity: analysis of 3000 samples.

Three thousand synovial fluids (1312 patients: chronic pyrophosphate arthropathy (CPA), 41%; osteoarthritis (OA), 12%; rheumatoid arthritis (RA), 16%) were examined for crystals, including calcium pyrophosphate dihydrate (CPPD), by polarized microscopy (score 0-3); calcific particles, by alizarin red positivity (ARP; 0-3); and total cell count. For 1150 fluids, local joint inflammation was assessed as 'active' or 'inactive' using a summated score of six clinical variables. CPPD and ARP scores did not correlate, but each showed positive correlation with age (P less than 0.01, P less than 0.02 respectively). Pseudogout had the highest mean CPPD score (P less than 0.001); intermittent CPPD positivity (range 8-100%) was seen in serially aspirated CPA joints, and there was no difference in CPPD positivity or score between active and inactive CPA. ARP was most frequent in OA subsets (72% of CPA, 46% of OA, 31% of RA; P less than 0.001). ARP was more frequent in active than inactive OA (P less than 0.05) but showed no association with inflammation in CPA or RA. Cell counts were higher in RA and pseudogout compared to OA and CPA, and in active compared to inactive RA. No correlation was found between ARP or CPPD scores and cell count. Cholesterol crystals were uncommon (0.2%) and showed no disease or joint predilection. In arthritic joints, CPPD and calcific particles particularly associate with the OA process and ageing. CPPD may contribute to acute and other calcific particles to chronic inflammation in OA.

Adolescent↗

Expression of lactoferrin on neutrophil granulocytes from synovial fluid and peripheral blood of patients with rheumatoid arthritis.

OBJECTIVE: To analyze lactoferrin expression on synovial fluid (SF) and peripheral blood neutrophils of patients with rheumatoid arthritis (RA) and to compare it with the lactoferrin expression on neutrophils from patients with osteoarthritis (OA). METHODS: Paired samples of peripheral blood and SF were obtained from 14 patients with RA and 9 patients with OA. Lactoferrin expression was evaluated on cell surfaces by cytofluorimetric analysis utilizing both polyclonal antibodies and the monoclonal anti-lactoferrin antibody AGM 2.29. Data are presented as mean fluorescence intensity. RESULTS: In patients with RA, the expression of membrane lactoferrin was significantly increased on SF neutrophils in comparison with those in peripheral blood. This increase was found using both polyclonal antibodies and AGM 2.29 (p = 0.0001, p = 0.0017, respectively). In patients with OA, the difference was not significant. In addition, lactoferrin expression on SF neutrophils of patients with RA was significantly increased compared with that found on SF neutrophils of patients with OA (polyclonal antibodies, p = 0.0015; AGM 2.29, p = 0.005). In patients with RA, no correlation was found between lactoferrin expression and disease activity. CONCLUSION: Our results provide evidence for an activation of neutrophil granulocytes at site of inflammation in RA and indicate that lactoferrin surface expression represents a reliable neutrophil activation marker.

Adult↗