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At least 667 records · Page 37Linked to original sources
PubMed1988

Synovial fluid and plasma kinetics of repeat dose sustained action tiaprofenic acid in patients with rheumatoid arthritis.

Tiaprofenic acid is a potent non-steroidal anti-inflammatory drug which, in conventional tablet form, has been shown to be rapidly absorbed and eliminated from the plasma, while synovial fluid concentrations remain constant for at least 8 hours. Recently, a sustained action formulation of tiaprofenic acid has been developed to provide the patient with the convenience of a once daily dosage. The purpose of this study was to measure plasma and synovial fluid concentrations over a 24-hour period following repeated administration of the sustained action formulation, and thus determine the pharmacokinetic profile. Eight patients suffering from rheumatoid arthritis were included in this open study (of whom 3 were subsequently excluded from the analysis). All were hospital outpatients requiring aspiration of the knee joint. The patients received sustained action tiaprofenic acid in a dosage of 600 mg once daily for a period of 7 days. Plasma and synovial fluid samples were taken on the final treatment day at 0, 4, 8, 12, and 18 hours following administration of the last treatment dose. Areas under the concentration-time curves, maximum plasma and synovial fluid concentrations, times to maximum concentration, and apparent elimination half-lives are presented and the findings compared and discussed. The drug was found to be retained in both the plasma and synovial fluid over a 24-hour period. Synovial fluid concentrations exceeded plasma concentrations at 24 hours in 4 of the 5 patients who were analysed, while in the fifth patient the levels were very similar.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1996

Elevated levels of nitric oxide in synovial fluid from patients with temporomandibular disorders.

OBJECTIVE: The objective of this study was to measure nitric oxide activity in synovial fluid samples taken from patients with temporomandibular disorders. STUDY DESIGN: We investigated six volunteers without symptoms and 56 patients with temporomandibular disorders. Nitric oxide activity was measured in temporomandibular joint synovial fluid with a highly sensitive and specific chemiluminescence detection method. RESULTS: A detectable nitrite concentration was found in only 1 of 10 joints in the control group. Measurable levels (> 0.001 mol/l) of nitrites in the synovial fluid were found in 8 (72.7%) of 11 joints with disk derangement with clicking, 24 (85.7%) of 28 joints with disk derangement with locking, and all 26 (100%) joints with osteoarthritis. The mean nitrite concentrations in the temporomandibular joint synovial fluid in the disk derangement with clicking, disk derangement with locking, and osteoarthritis groups were significantly higher than that in the control group (p < 0.05, p < 0.001, p < 0.001, respectively). CONCLUSIONS: These data clearly show increased nitric oxide production in certain temporomandibular disorders and suggest that nitric oxide may play a role in the pathogenesis of synovitis and degenerative changes of cartilaginous tissue and bone of the temporomandibular joint.

Adolescent↗
PubMed1985

Proliferating cells in the synovial fluid in rheumatic disease. An analysis with autoradiography-immunoperoxidase double staining.

The subtype of the proliferating cells in the synovial fluid of patients with rheumatoid arthritis (RA), ankylopoietic spondylarthrosis (SPA), and osteoarthritis (OA) was studied with autoradiography-immunoperoxidase double staining. Of all spontaneously proliferating synovial fluid cells in chronic arthritis, 59 +/- 4% displayed T8 differentiation marker, whereas T4 (21 +/- 4%) and B (2 +/- 1%) cells were few. Of all T4+ and all T8+ lymphocytes, 0.55 +/- 0.1% and 0.90 +/- 0.1%, respectively, incorporated [3H]thymidine. The [3H]thymidine labelling index for B cells was 0.30 +/- 0.1%. This was in contrast to OA, in which no proliferating lymphocytes were observed in the synovial fluid. Our findings suggest that the predominance of proliferating T8+ cells in the synovial fluid reflects an underlying chronic inflammation. Because RA and SPA synovium is a site of intense immunoglobulin production, our finding of the predominance of activated, proliferating T8+ cells may also reflect a dissociation between phenotype and function as a reason for the chronicity of the joint inflammation.

Adult↗
PubMed1975

A comparative study of the protein pattern in serum and synovial fluid.

A routine program for evaluation of the protein pattern in serum and synovial fluid has been tested on 25 patients in a consecutive study. The program comprised agar gel electrophoresis, total protein and albumin determination, and immunochemical determination of antitrypsin, orosomucoid, haptoglobin, IgR, and IgA. Linear correlation analysis of corresponding data in serum and synovial fluid gave r-values for the five latter components which varied from 0.74 to 0.87. On this basis reference intervals in synovial fluid could be established. Total protein, haptoglobin and IgG were elevated in rheumatoid arthritis, compared with osteoarthritis.

Albumins↗
PubMed2004

Neprilysin levels in plasma and synovial fluid of juvenile idiopathic arthritis patients.

OBJECTIVE: Neprilysin (neutral endopeptidase, 3:4:24:11, CD10) (NEP) is a Zn metallopeptidase linked to controlling inflammation through the degradation of neuropeptides involved in neurogenic inflammation of chronic rheumatic diseases. The aim of our study was to evaluate circulating activity and cellular expression of NEP in the plasma of 58 children with juvenile idiopathic arthritis (JIA) and 52 controls. In 20 subjects requiring local steroid injection, NEP was measured in synovial fluid. METHODS: Plasma and synovial NEP were evaluated using a fluorimetric technique. Neprilysin, expressed as the antigen CD10, was determined on circulating and synovial fluid cells as mean fluorescence intensity (MFI) and as percentage of positive cells by two-color immunofluorescence. RESULTS: Circulating NEP levels were lower in JIA patients than in controls (42.0+/-16.6 vs 76.5+/-24 pmol/ml per min, P<0.001), while synovial fluid NEP values were higher than circulating levels (241.4+/-86.2 vs 40+/-15.3 pmol/ml per min, P<0.001). In monocytes, the percentage of CD10-positive circulating cells and the MFI in JIA were lower than in controls (11.6+/-5.2% vs 41.4+/-13%, P<0.001 and 18.1+/-7.5 vs 31.2+/-5.4, P<0.05, respectively). On synovial monocytes, the percentage of CD10-positive cells and the MFI were higher than on circulating monocytes (35.2+/-14.6% vs 9.1+/-2.4%, P<0.001 and 66.4+/-5.4 vs 22.8+/-14.7, P<0.001, respectively). CONCLUSIONS: The downregulation of CD10 expression in monocytes and the reduction in NEP activity may be linked to the enzyme's role in the control of peptides involved in the inflammation. The increased levels of NEP, MFI, and CD10-positive monocytes in synovial fluid, even though in plasma, might reflect a reactive effort to control synovial proliferation.

Arthritis, Juvenile↗
PubMed1988

Interaction between fibronectin and C1q in rheumatoid synovial fluid and normal plasma.

The interaction between fibronectin and C1q was studied in the presence of normal human plasma and rheumatoid synovial fluid by solid phase binding assay. Fibronectin-C1q binding occurred in the presence of rheumatoid synovial fluid but not in the presence of normal plasma. Binding was strongest at 4 degrees C and in the presence of EDTA. Fibronectin-C1q binding could be induced in the presence of normal plasma by hypotonicity, augmentation of the concentration of solution-phase fibronectin or by the addition of heat-aggregated IgG. The C1q present in rheumatoid synovial fluid bound to both aminoterminal collagen-binding and carboxyterminal noncollagen binding fibronectin fragments although binding to the aminoterminal fragment was stronger. The interaction between fibronectin and C1q in rheumatoid synovial fluid may modulate immune-complex deposition and complement activation in the inflamed joint.

Arthritis, Rheumatoid↗
PubMed1984

Synovial fluid and blood monocytes/macrophages in rheumatoid arthritis. Influence on polyclonal activation of autologous B lymphocytes.

The regulatory role of synovial fluid monocytes/macrophages from patients with rheumatoid arthritis in terms of B lymphocyte activation was evaluated by a reverse haemolytic plaque-forming cell (PFC) assay. Macrophage-depleted blood mononuclear cells (BMC) failed to respond to pokeweed mitogen (PWM). With autologous synovial fluid macrophages added, the PFC responses of macrophage-depleted BMC increased, and optimal concentration for full restoration of the PFC responses ranged from 8 to 35%. Synovial fluid mononuclear cells (SMC) as well as macrophage-depleted SMC were not able to respond to PWM. Addition of irradiated autologous blood macrophages to SMC did not increase the SMC PFC responses. It is concluded that the regulatory properties of synovial fluid macrophages do not explain the low PFC response of SMC to PWM.

Adult↗
PubMed1987

Paired serum and synovial fluid values of alpha 2-macroglobulin and TIMP in rheumatoid arthritis.

The levels of alpha 2-macroglobulin and tissue inhibitor of metalloproteinases (TIMP) were determined in paired serum and synovial fluid samples from rheumatoid arthritis patients. Serum levels of alpha 2-macroglobulin (mean 1580 +/- 340 mg/l) were always higher than the corresponding synovial fluid although the spread of synovial fluid levels was broad (mean 520 +/- 340 mg/l). Tissue inhibitor of metalloproteinases was always higher in synovial fluid (mean 4.59 +/- 1.8 mg/l) than serum (mean 1.3 +/- 0.39 mg/l) indicating that local synthesis occurred within the joint.

Arthritis, Rheumatoid↗
PubMed1989

A tissue kallikrein in the synovial fluid of patients with rheumatoid arthritis.

Tissue kallikrein is an enzyme that forms the vasoactive peptide kallidin from an endogenous substrate L-kininogen. Tissue kallikrein has been identified in joint fluids and in inflammatory infiltrates within synovial membranes. It is suggested that tissue kallikrein and kinins have an important role in synovitis and joint damage. Immunoreactive tissue kallikrein and amidase activity were both measured in the synovial fluid of 24 patients with rheumatoid arthritis (RA) and 12 with osteoarthritis (OA). Active enzyme concentrations were higher in RA than in OA and correlated well with the lysosomal enzymes beta-glucuronidase and lactate dehydrogenase. Both total immunoreactive tissue kallikrein and the proenzyme values were similar in RA and OA. Tissue kallikrein was localised by immunocytochemistry to the polymorphonuclear leucocytes present in the synovial fluid and membranes of patients with RA.

Adult↗
PubMed2003

Procollagen II C propeptide level in the synovial fluid as a predictor of radiographic progression in early knee osteoarthritis.

OBJECTIVE: To investigate the prognostic value of procollagen type II carboxy-terminal propeptide (PIICP) level in synovial fluid in relation to early tibiofemoral joint osteoarthritis (OA). METHODS: Data were collected on 172 women (age 40 to 59 years) who had knee pain and tibiofemoral joint OA in the early stage. Standing semiflexed knee radiographs were obtained by fluoroscopy at baseline and at four year follow up and a computerised, magnification corrected measurement system was applied to measurement of minimal joint space width in the tibiofemoral compartment. Synovial fluid sampling was performed at baseline and at the four year follow up. Levels of PIICP in the synovial fluid were measured by enzyme immunoassay. The outcome measures were assessed by radiographic joint space narrowing (JSN) in the tibiofemoral joints over four years. Multiple linear regression analyses were used to examine the relation between radiographic JSN and synovial fluid level of PIICP. RESULTS: The number of women available at both baseline and at four year follow up was 110. The average of radiographic JSN over four years was 0.53 mm (range 0.00-2.01). Body mass index showed a slightly positive association with baseline PIICP level. In multiple linear regression analyses adjusted for age and body mass index, radiographic JSN over four years had a direct positive correlation with baseline PIICP level (r=0.395; 95% confidence interval (95% CI) 0.231 to 0.529; p<0.001). CONCLUSION: In a four year prospective study of women, quantification of synovial fluid PIICP was able to predict subsequent radiographic progression in early tibiofemoral joint OA.

Adult↗
PubMed1997

Concentrations of keratan sulfate in plasma and synovial fluid from clinically normal horses and horses with joint disease.

OBJECTIVE: To determine whether keratan sulfate concentrations in plasma or synovial fluid from clinically normal horses were different from concentrations in horses with joint disease and whether concentrations varied with type of joint disease. DESIGN: Case-control study. ANIMALS: 67 clinically normal horses, 10 clinically normal foals, and 160 horses with joint disease. PROCEDURE: ELISA was used to measure keratan sulfate concentrations. RESULTS: Mean plasma keratan sulfate concentration (mean +/- SEM, 580 +/- 124 ng/ml) in foals peaked at 10 weeks of age. Mean plasma keratan sulfate concentration in clinically normal horses was 200 ng/ml (95% confidence interval, 157 to 251 ng/ml). Horses with osteochondral (chip) fractures, other closed intraarticular fractures, inflammatory arthritis (synovitis), infectious arthritis, or osteochondrosis had significantly higher plasma keratan sulfate concentrations than did clinically normal horses, but horses with osteoarthritis did not. Breed, gender, and type of joint disease affected keratan sulfate concentration in synovial fluid. Standard-breds with chip fractures of the metacarpophalangeal/ metatarsophalangeal joints had significantly higher keratan sulfate concentrations in synovial fluid than did Thoroughbreds. Keratan sulfate concentrations in synovial fluid from osteoarthritic carpal joints were lower than concentrations in normal carpal joints and tarsocrural joints with inflammatory joint disease. CLINICAL IMPLICATIONS: Keratan sulfate concentration alone was not a specific marker of joint disease but was affected by various joint diseases.

Aging↗
PubMed2005

Synovial fluid and plasma selenium, copper, zinc, and iron concentrations in patients with rheumatoid arthritis and osteoarthritis.

In recent years, a great number of studies have investigated the possible role of trace elements in the etiology and pathogenesis of rheumatoid arthritis (RA) and osteoartritis (OA). We studied synovial fluid and plasma concentrations of selenium (Se), zinc (Zn), copper (Cu), and iron (Fe) in patients with RA and OA and compared them with sex- and age-matched healthy subjects. Plasma albumin levels were measured as an index of nutritional status. Plasma Se, Cu, and Zn concentrations were determined by atomic absorption spectrophotometry and Fe concentrations were determined by the colorimetric method. Although plasma and synovial fluid Se concentration were found to be significantly lower (p < 0.05, and p < 0.05, respectively), Cu concentrations were significantly higher in patients with RA than those of healthy subjects and OA (p < 0.05 and p < 0.05, respectively). There were no significant differences in plasma and synovial fluid Zn concentrations and albumin levels among three groups (p > 0.05). On the other hand, synovial fluid Cu and Fe concentrations were significantly higher in patients with OA than those of healthy subjects (p < 0.05). There was a significantly positive correlation between synovial fluid Se-Cu values and Zn-Fe values in patients with RA. Our results showed that synovial fluid and plasma trace element concentrations, excluding Zn, change in inflammatory RA, but not in OA. These alterations in trace element concentrations in inflammatory RA might be a result of the changes of the immunoregulatory cytokines.

Adult↗
PubMed1985

The effect of non-inflamed synovial fluid on neutrophil function in vitro.

In neutrophils preincubated with non-inflamed synovial fluid, opsonized zymosan-induced O2- production was increased by 232.7 +/- 19.1% and degranulation induced by zymosan or phorbol myristate acetate was increased by 152.8 +/- 21.8% and 217.4 +/- 26.3 respectively. Unstimulated neutrophils were not directly activated by the fluid, nor did it affect their chemotactic response. The activity was not abolished by heat (56 degrees C, 30 min, or 100 degrees C, 3 min) or by treatment with trypsin or hyaluronidase. The activity was not present in the serum albumin-bound lipid extract of the synovial fluid. Thus, this activity may represent a heat- and trypsin-resistant factor which is neither a complement component nor hyaluronic acid. It is proposed that this synovial fluid factor plays a role in increasing the neutrophil killing potential during the inflammatory process.

Chemotaxis↗
PubMed2004

Soluble tumour necrosis factor receptors in synovial fluids from temporomandibular joints with painful anterior disc displacement without reduction and osteoarthritis.

The objective of this study was to detect soluble-form tumour necrosis factor receptors (sTNFRs) in temporomandibular joint (TMJ) synovial fluid aspirates, and to compare the sTNFR concentrations between painful anterior disc displacement without reduction and osteoarthritis (ADDwoR/OA) and asymptomatic TMJs. Synovial fluid was sampled from the superior TMJ cavity of 11 painful ADDwoR/OA cases (mean age: 36.9 years) and 10 asymptomatic females (mean age: 24.7 years) by diluted aspiration. The concentrations of sTNFR-I and -II in the synovial fluid were measured using human sTNFR-I and -II enzyme-linked immunosorbent assays. The total protein concentrations in synovial fluids were measured using a bicinchoninic acid protein assay kit. All data were normalised to the total protein concentration of each sample.Two-way factorial analysis of variance and post hoc multiple comparison revealed that: (1). mean normalised sTNFR-I and -II concentrations were higher in TMJ synovial aspirates from ADDwoR/OA patients than from healthy controls; (2). in the ADDwoR/OA patients and the healthy controls, the sTNFR-I concentration in TMJ synovial aspirates was higher than the sTNFR-II concentration; and (3). high TMJ synovial aspirate sTNFR-II seemed to be associated with less TMJ pain and a less restricted range of mouth opening in the ADDwoR/OA patients. The concentrations of sTNFRs in TMJ synovial fluid are higher in the presence of painful ADDwoR/OA, which could modulate intracapsular inflammation.

Adolescent↗
PubMed1980

Increased biosynthesis of complement components by cultured monocytes, synovial fluid macrophages and skynovial membrane cells from patients with rheumatoid arthritis.

Monocytes, synovial fluid (SF) and synovial membrane (SM) macrophages from patients with rheumatoid arthritis (RA) were maintained in short-term tissue culture for up to 10 days, and the synthesis of C4, C2, C3, C5, factor B(B), D, properdin (P), C3b inactivator (C3bINA) and beta 1H globulin studied. Functionally active C2, B, D, P, C3bINA and beta 1H were synthesized by the cells in each type of culture. C4, C3 and C5 could be detected, but were functionally inactive. RA monocytes synthesized more C2 than monocytes from patients with degenerative joint disease (DJD) (P < 0.001). Similar studies revealed that SF macrophages synthesized more C3 than SM macrophages (P < 0.001) which in turn produced more C2 than monocytes (P < 0.001). Other experiments showed that SF macrophages synthesized more of each component than the other cell types. SM macrophages made more C2 than B than RA and DJD monocytes, but synthesized only small quantities of P, D and beta 1H. RA monocytes synthesized more of each component than DJD monocytes. The results of these studies show that (1) in RA, complement components can be synthesized locally in the inflamed joints, and (2) local factors in the joints probably stimulate complement synthesis.

Arthritis, Rheumatoid↗
PubMedDate not supplied

The primary plasmin inhibitor in rheumatoid synovial fluid.

In 20 consecutive rheumatoid arthritis patients, 14 women and 6 men, age 26--76, average 62 years, the concentration of the recently found "primary plasmin inhibitor" and phase proteins was estimated in plasma and synovial fluid. In 12 patients a complex between the inhibitor and plasmin could be demonstrated by crossed immunoelectrophoresis into immunoglobulins against the primary plasmin inhibitor and immunoglobulin against plasminogen. Only free inhibitor was found in corresponding plasma. All plasminogen present in synovial fluid could be activated to plasmin upon addition of urokinase (24 nM/1). In those patients where enzyme-inhibitor complex in synovial fluid was present, a higher concentration of phase proteins in synovial fluid was found, indicating an increased degree of inflammation despite identical scores in the Lansbury clinical index in the two groups. From these experiments it was concluded that the fibrinolytic capacity in rheumatoid synovial fluid is not decreased. It is suggested that the fibrin-like material in synovial tissue and upon the synovial membrane is a poor substrate for plasmin.

Adult↗
PubMed1999

Is routine synovial fluid analysis necessary? Lessons and recommendations from an audit.

This audit of 408 synovial fluid samples, analysed for cell counts and crystals, revealed that crystals were present in only 25 samples (6.1%). Of these, in only three patients was the diagnosis uncertain and therefore the analysis helpful. Cell counts and types generally reflected known underlying diagnoses of inflammatory arthritis or osteoarthritis. Routine synovial fluid analysis does not contribute to diagnosis or management in established rheumatic disorders and should be performed only when the underlying cause is uncertain or in newly presenting patients. Major savings can be made by abandoning routine synovial fluid analysis.

Diagnostic Tests, Routine↗
PubMed2006

Synovial fluid levels of anti-cyclic citrullinated peptide antibodies and IgA rheumatoid factor in rheumatoid arthritis, psoriatic arthritis, and osteoarthritis.

OBJECTIVE: To assess the levels of anti-cyclic citrullinated peptide (anti-CCP) and IgA rheumatoid factor (IgA-RF) in synovial fluids of patients with rheumatoid arthritis (RA), psoriatic arthritis (PsA), and osteoarthritis (OA). METHODS: Knee effusions of 29 patients with RA (23 women, 6 men; mean +/- SD age 60 +/- 15 years), 20 with PsA (6 women, 14 men; mean age 51 +/- 12 years), and 19 with OA (9 women, 10 men; mean age 73 +/- 11.8 years) were aspirated, tested for white blood cell (WBC) counts, centrifuged, and stored at -20 degrees . Sera of 22, 11, and 12 of these patients with RA, PsA, and OA, respectively, were similarly stored. IgG anti-CCP and IgA-RF were detected by enzyme-linked immunosorbent assay. Erythrocyte sedimentation rate and C-reactive protein levels were used as measures of disease activity. RESULTS: Mean levels of synovial fluid anti-CCP and IgA-RF were significantly increased in RA joint effusions compared with PsA and OA (anti-CCP: 150 +/- 134, 34 +/- 29, and 24 +/- 26 units, respectively [P < 0.003]; IgA-RF: 76 +/- 77, 15.7 +/- 10, and 18 +/- 20 units, respectively). No significant difference was noted between OA and PsA. A significant correlation was found between synovial fluid anti-CCP and serum anti-CCP and IgA-RF. In patients with RA, a significant correlation was found between synovial fluid WBC counts and IgA-RF (P = 0.03) and serum IgA-RF (P = 0.008), but not between synovial fluid and serum anti-CCP levels. In RA patients, C-reactive protein correlated with serum IgA-RF. CONCLUSION: Anti-CCP and IgA-RF were significantly increased in synovial fluid of RA in comparison with PsA and OA patients.

Aged↗