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PubMedDate not supplied

Hormone concentrations in synovial fluid of patients with rheumatoid arthritis.

OBJECTIVE: Alterations in local concentrations of hormones, affecting directly synovial cells, could be involved in the modulation of the rheumatic inflammatory processes. The aim of present study was to investigate the levels of selected hormones (steroids, peptide and thyroid hormones) in synovial fluid of knee joint of patients with rheumatoid arthritis (RA) and control individuals with non-rheumatic exudate (with osteoarthrosis, OA). METHODS: Thirty-eight patients, 22 female and 16 males, with rheumatoid arthritis (RA) and 12 subjects with osteoarthrosis (OA, control group, 6 females and 6 males) participated in the study. Concentrations of cortisol (CS), 17-beta-estradiol (ES), dehydroepiandrosterone (DHEA), progesterone (PRG), aldosterone ALD), prolactin (PRL), insulin (INS), and C-peptide were determined by radioimmunoassay in synovial fluid. Insulin binding to isolated cell membrane of cells from synovial sediment was estimated by using radioiodine labeled insulin. In a group of patients (10 with RA and 4 with OS), the levels of free threeiodothyronine (FT3), TSH and growth hormone (GH) were also determined in synovial fluid. RESULTS: Increased levels of ES in synovial fluid of RA patients were observed, and higher differences were noted in men. TE concentrations were moderately elevated in synovial fluid of RA patients, however the ratio of ES/TE was significantly higher in male RA compared to OA patients. Higher levels of PRG, ALD and growth hormone were noted in synovial fluid of RA patients. Besides the steroid hormones the presence of insulin and C-peptide was noted in synovial fluid and the correlation between the levels of these two peptides was highly significant. The concentrations of INS and C-peptide in synovial fluid of patients from RA and OA group were not significantly different, however, highly significant increase of insulin binding to isolated membrane of synovial cells was found. Concentrations of cortisol, dehydroepiandosterone, prolactin, TSH and FT3 in synovial fluid were not significantly different in RA and OA groups. CONCLUSIONS: Besides the steroids also insulin, c-peptide, GH and FT3 were found in synovial fluid. The elevated ALD and GH levels in synovial fluid of RA patients and the presence of INS in synovial fluid with increase of INS binding to plasma membranes of cells from synovial fluid of RA patients suggest that besides the gonadal steroids also these hormones may affect the local inflammatory processes.

Arthritis, Rheumatoid↗
PubMed1984

Diminished activity of a chemotactic inhibitor in synovial fluids from patients with familial Mediterranean fever.

Synovial fluids from patients with osteoarthritis contain a chemotactic inhibitor that acts by antagonizing the complement-derived chemotactic anaphylotoxin, C5a. The activity of this inhibitor in synovial fluids from patients with several forms of inflammatory arthritis (rheumatoid arthritis, systemic lupus erythematosus, ankylosing spondylitis, and gout) were comparable to the activity present in osteoarthritic synovial fluids. In contrast, levels of inhibitory activity in synovial fluids from 9 patients with familial Mediterranean fever were decreased to less than 20% of those found in osteoarthritis fluids. The possibility was considered that the diminished inhibitory activity in fluids from patients with familial Mediterranean fever plays a part in the pathogenesis of the inflammatory attacks characteristic of this disease.

Adult↗
PubMed1985

A pharmacokinetic comparison of tenoxicam in plasma and synovial fluid.

In view of the paucity of information of the synovial fluid pharmacokinetics of nonsteroidal anti-inflammatory drugs with a long half-life, we have compared the pharmacokinetics of tenoxicam (TILCOTIL, MOBIFLEX) in plasma and synovial fluid in six patients with polyarthritis causing knee effusion. Plasma and synovial fluid concentrations of tenoxicam were measured up to 96 hours after an oral dose of a single 40 mg tablet. A full pharmacokinetic analysis was performed. Tenoxicam passed into synovial fluid attaining a peak concentration significantly later than that for plasma. However, the mean half-life for synovial fluid (45 hours) was not significantly different from that for plasma (42 hours). Comparison of area under the curve (AUC) indicated the total exposure of the synovial fluid to tenoxicam was consistent in different patients, comprising 50-60% of the corresponding plasma levels in every case. In the case of tenoxicam, synovial fluid exhibits the pharmacokinetic properties of a peripheral "tissue" compartment.

Adult↗
PubMed1988

Interleukin 2 inhibitor in synovial fluid.

Since evidence for the presence of IL-2 activity in rheumatoid synovial fluid is conflicting, we have assayed IL-2 activity in synovial fluid from patients with rheumatoid arthritis (RA) and other articular diseases (OAD). Using the IL-2-dependent murine T cell line CTLL, IL-2 activity was not demonstrable in synovial fluid tested at concentrations ranging from 50% to 0.02%. There was an inhibitory effect on IL-2 activity in the bioassay of synovial fluid from 16 of the 22 patients with RA and 15 of the 16 with OAD. This inhibitory activity was heat-labile, precipitable by ammonium sulphate, reversible with excess IL-2 and was not significantly altered by preincubation of synovial fluid with CTLL. The mean inhibitory activity of synovial fluid from patients with RA was significantly reduced in comparison with that of synovial fluid from patients with OAD. Sera also had an inhibitory effect on IL-2 activity; however sera from patients with RA were less inhibitory than control sera but were more inhibitory than sera from patients with systemic lupus erythematosus. The deficiency in synovial fluid of an inhibitor of IL-2 activity may be relevant to the pathogenesis of RA.

Adult↗
PubMed1991

Neutrophil chemotactic factors in synovial fluids of patients with Lyme disease.

We examined synovial fluid samples from 14 patients with Lyme arthritis for the presence of neutrophil chemotactic factors. Thirteen of the synovial fluids stimulated chemotaxis of normal human neutrophils. The chemotactic activity was heat-sensitive and was not inhibited by antibody to C5a or antibody to interleukin-8, or by a competitive inhibitor of the chemotactic peptide f-Met-Leu-Phe. A culture supernatant of Borrelia burgdorferi also contained neutrophil chemoattractants. Chromatography demonstrated that the chemoattractants in the synovial fluid samples were different from those in the B burgdorferi culture supernatant. One of the major chemotactic factors in Lyme disease synovial fluid had a calculated molecular weight of 13,900. We conclude that a novel, host-derived chemoattractant is present in the synovial fluid of patients with Lyme disease.

Chemotactic Factors↗
PubMed1992

Synovial fluid ferritin in traumatic hemarthrosis, rheumatoid arthritis and osteoarthritis.

Synovial fluid ferritin levels in patients with traumatic hemarthrosis (HA), rheumatoid arthritis (RA), and osteoarthritis (OA) were measured by double antibody radioimmunoassay. Synovial fluid ferritin levels were significantly higher in 60 patients with HA (mean +/- S.D., 536 +/- 536 ng/ml) and 39 patients with RA (614 +/- 486 ng/ml) than in 20 patients with OA (130 +/- 119 ng/ml) (p < 0.01). Individual levels, however, considerably varied. In HA patients, the synovial fluid ferritin level correlated well with the duration of hemarthrosis, but not with hemoglobin, hematocrit, or an inflammatory synovial fluid index such as the leukocyte count. In RA patients, there was no significant correlation between the synovial fluid ferritin levels and any inflammatory parameter, such as catalase activity, synovial leukocyte counts (including polymorphs and monocytes) or the duration of arthritis. Our results indicate that the synovial fluid ferritin level reflects primarily hemoglobin degradation and appears unrelated to inflammation in joint diseases.

Adolescent↗
PubMed1991

Evidence for a promoter of urate crystal formation in gouty synovial fluid.

The effect of serum and synovial fluid obtained from six healthy subjects and from 12 patients with gout, six with rheumatoid arthritis and 18 with calcium pyrophosphate dihydrate arthropathy (CPPD) on the rate of in vitro urate crystal formation was measured. Gouty and normal serum produced similar results. Gouty synovial fluids promoted urate crystal formation significantly more than did rheumatoid or CPPD fluids. The promotion of urate crystal formation by gouty synovial fluid was not due to native urate crystals nor to an effect on the level of urate supersaturation. The development of gout in some, but not other, hyperuricaemic subjects may relate to the presence of promoters (or relative lack of inhibitors) of urate crystal formation in the group who develop gout.

Adult↗
PubMed1995

Functional analysis of synovial fluid and peripheral blood T cells from patients with rheumatoid arthritis.

Rheumatoid arthritis is a T cell-mediated autoimmune disease. The lack of knowledge of the involved target antigens severely hampers research on relevant T cells in patients. Here we describe the functional analysis of freshly isolated T cells from the peripheral blood and the site of the lesion (synovial fluid or synovial membrane) of patients with rheumatoid arthritis. Healthy donors and osteoarthritis patients served as controls. Using various polyclonal stimuli, we analyzed CD4+ T cells with respect to proliferation and their ability to produce lymphokines. Our data show that lesion-derived CD4+ T cells of patients with rheumatoid arthritis are severely defective in proliferation and lymphokine (interleukin-2, interleukin-4, tumor necrosis factor-alpha, interferon-gamma) production. This activation defect was most pronounced at lower cell densities and was present in both synovial fluid derived and synovial membrane derived CD4+ T cells of all patients tested. No difference was found between responses of synovial fluid derived CD4+ T cells from osteoarthritis patients and those observed with peripheral blood derived T cells from all groups. The observed defect in lesion-derived CD4+ T cells from rheumatoid arthritis patients was not due to the effect of inflammatory factors in the synovial fluid because preincubation with synovial fluid could not induce a similar defect in control T cells. Together, our data show a rheumatoid arthritis specific, general defect in the activation of lesion-derived CD4+ T cells.

Adult↗
PubMed1981

Synovial fluid lactic acid levels in septic arthritis.

Synovial fluid lactic acid estimations were carried out on 50 samples by gas liquid chromatography. Specimens from 4 patients with bacteria arthritis, other than gonococcal, had a mean lactic acid concentration of 215 mg/dl. One patient with gonococcal arthritis had a synovial fluid lactic acid of 30 mg/dl. Forty-one patients with inflammatory arthritis and 4 patients with degenerative arthritis had mean synovial fluid lactic acid levels of 27 and 23 mg/dl respectively. The estimation of synovial fluid lactic acid is reliable in differentiating septic arthritis from inflammatory and degenerative arthritis except when the infecting organism is NEisseria gonorrhoeae.

Arthritis, Infectious↗
PubMedDate not supplied

Detection of bacteria in equine synovial fluid by use of the polymerase chain reaction.

Equine synovial fluid aliquots were inoculated with Salmonella enteritidis, Escherichia coli, Actinobacillus equuli, Staphylococcus aureus, and Streptococcus zooepidemicus to obtain approximate concentrations of 1000, 100, 10, and 1 colony forming U/mL. Synovial fluid aliquots were also inoculated with an unquantitated inoculum of Bacteroides fragilis and Clostridium perfringens. Inoculated synovial fluid was incubated in trypticase-soy broth or Columbia broth for approximately 12 hours. Then aliquots were removed for DNA extraction and polymerase chain reaction (PCR) analysis for detection of a 531 base-pair segment of bacterial DNA corresponding to a region of the 16S ribosomal gene. Duplicate samples of inoculated synovial fluid were prepared for microbial culture. Bacteria were detected in all samples inoculated with bacteria but not in control synovial fluid samples. Under experimental conditions there was no difference between microbial culture and PCR analyses for detection of bacteria. Experimentally, PCR was able to detect bacteria in synovial fluid within 24 hours of inoculation.

Actinobacillus↗
PubMed2004

Characterization of plasmacytoid dendritic cells in inflammatory arthritis synovial fluid.

OBJECTIVE: To examine the phenotype of dendritic cell subsets in synovial fluid and peripheral blood from patients with rheumatoid arthritis (RA) or spondyloarthropathy (SpA). METHODS: Multiparameter flow cytometry was used to identify and characterize dendritic cells in mononuclear cell populations isolated from synovial fluid and peripheral blood. RESULTS: Synovial fluid contained two subsets of dendritic cells (DC), myeloid and plasmacytoid. These subsets could also be identified in peripheral blood, but there were lower numbers of DC in peripheral blood compared with synovial fluid. Plasmacytoid DC were distinguished from the myeloid subset by high expression of CD123 and lack of expression of CD11c. In comparison with myeloid dendritic cells, the plasmacytoid subset were less mature, similar to those in peripheral blood. They failed to express CD83 and DC-LAMP, and had relatively low levels of CD40 and CD86. Comparison of dendritic cells in synovial fluid from RA and SpA patients showed increased numbers of the plasmacytoid subset in SpA. CONCLUSIONS: This is the first demonstration of the plasmacytoid subset of dendritic cells in synovial fluid. Since these cells are major producers of type I interferons, their increased numbers in SpA might be relevant to pathogenesis, but the immature phenotype in SpA synovial fluid may also indicate that conditions for maturation of this subset do not pertain in SpA synovium.

Antigens, Surface↗
PubMed1982

Different molecular forms of fibronectin in rheumatoid synovial fluid.

The concentration of fibronectin in rheumatoid synovial fluid was found to be 2-3 times higher than in the corresponding plasma. Normal plasma revealed a homogeneous precipitate by cross- immunoelectrophoresis using antifibronectin, while rheumatoid plasma and rheumatoid synovial fluid exhibited a heterogeneous precipitate. The heterogeneous precipitate in rheumatoid plasma was found to be a complex between fibronectin and fibrinogen as evidenced by cross-immunoelectrophoresis. Synovial fluid fibronectin demonstrated a lower molecular weight by gelfiltration on Sepharose CL6B than did normal plasma fibronectin. We suggest that the presence of degraded fibronectin in rheumatoid synovial fluid may be the result of either the degradation of fibrin-fibronectin complexes or the destruction of matrix fibronectin from the synovial tissue.

Adult↗
PubMed1981

Protection against superoxide and hydrogen peroxide in synovial fluid from rheumatoid patients.

1. On exposure of synovial fluid to superoxide and hydrogen peroxide, generated enzymically or by activated polymorphonuclear leucocytes, hyaluronic acid is depolymerized and the fluid loses its lubricating properties. The ability of synovial fluid from rheumatoid patients to scavenge superoxide and hydrogen peroxide was therefore examined. 2. Synovial fluid from a range of rheumatoid patients contained no superoxide dismutase activity, insufficient caeruloplasmin to scavenge any superoxide radical and little, if any, catalase activity. 3. Total ascorbate (reduced ascorbate + dehydroascorbate) concentrations in the plasma and synovial fluid of rheumatoid patients were similar in each case. The values are at the low end of the normal range. 4. These results are discussed in relation to the role of oxygen radicals in inflammatory joint disease.

Arthritis, Rheumatoid↗
PubMed1989

Concentrations of sulphadimidine, oxytetracycline and penicillin G in serum, synovial fluid and tissue cage fluid after parenteral administration to calves.

Drug concentrations in serum, synovial fluid and tissue cage fluid (TCF) in calves were measured after single i.m. doses of oxytetracycline hydrochloride (OTC), procaine penicillin G (PPG) and potassium penicillin G (KPG) and single i.v. doses of sulphadimidine (SDM) and OTC. For all drugs, concentration-time curves in serum and synovial fluid were not identical but they had similar profiles, with peak levels occurring at about the same time. Concurrent concentrations were lower in synovial fluid than in serum. For each drug, elimination half-lives from synovial fluid and from serum were similar, except for penicillin G after KPG administration which had a significantly longer half-life from synovial fluid than from serum (P less than 0.05). Of the two penicillin G preparations, PPG gave a significantly higher synovial fluid:serum area under curve (AUC) ratio than did KPG; 0.76 +/- 0.10 and 0.54 +/- 0.12, respectively (P less than 0.05). For OTC, the synovial fluid:serum AUC-ratio was 0.33 +/- 0.12 after i.m. and 0.34 +/- 0.08 after i.v. administration. Drug concentration-time curves of TCF had different profiles compared with serum, with relatively low and delayed peak levels and slow elimination from TCF. TCF:serum AUC-ratios did not differ significantly for i.m. and i.v. administration of OTC; 0.10 +/- 0.10 and 0.19 +/- 0.03 respectively (P greater than 0.05). Potassium penicillin G (KPG), however, gave a significantly higher TCF:serum AUC-ratio than PPG; 0.55 +/- 0.21 and 0.19 +/- 0.07, respectively (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1997

Immunocytochemical analysis of tissue kallikrein and the kinin moiety in rheumatoid synovial fluid neutrophils.

Polymorphonuclear leucocytes (PMNs) from the synovial fluid of patients with rheumatoid arthritis (RA) showed reduced tissue kallikrein and kinin immunoreactivity in comparison with blood PMNs from healthy individuals as judged visually using confocal microscopy. Similarly, synovial fluid PMNs exhibited reduced tissue kallikrein immunoreactivity as compared with blood PMNs from the same RA patients. Blood PMNs stimulated to degranulate in vitro also displayed less immunostaining for tissue kallikrein and kinin than non-stimulated PMNs. By contrast, no difference in kininogen immunostaining was detected between RA synovial fluid PMNs and blood PMNs from healthy people. It is considered that the results support the hypothesis that tissue kallikrein, released from the granules of RA synovial fluid PMNs, cleaves the kinin moiety from multifunctional kininogen protein on the surface of the PMNs.

Adult↗
PubMed1985

Differences between plasma and synovial fluid fibronectin.

Fibronectin is a high molecular weight glycoprotein of plasma and tissue fluids, and one of its functions is to opsonise particulate material. Chromatographic and electrophoretic analyses showed that the main components of fibronectin are biochemically similar in rheumatoid patients' plasma and synovial fluid. But synovial fluid fibronectin also contains a slow-moving component seen on two-dimensional immunoelectrophoresis, suggesting the presence of fibronectin complexes. Affinity chromatography provided evidence that these involved IgG, and in vitro studies showed that fibronectin influenced the reaction between IgG and anti-IgG. Synovial fluid fibronectin is functionally active in binding to gelatin in an haemagglutination assay, and it gave a relatively higher degree of haemagglutination than did plasma fibronectin, supporting the concept of multivalent fibronectin complexes in synovial fluid. These results suggest synovial fluid fibronectin may be involved in the opsonic removal of IgG-containing complexes from synovial fluid.

Arthritis, Rheumatoid↗
PubMed1990

Determination of cathepsins B and H in sera and synovial fluids of patients with different joint diseases.

Synovial fluids and sera of patients with inflammatory and metabolic joint diseases contain different cysteine proteinases. The quantities of cathepsins B and H were determined by newly developed specific enzyme-linked immunoassay tests (ELISA), with detection limits of 0.5 microgram/l for cathepsin B and 3 micrograms/l for cathepsin H. The values of cathepsin B in normal sera ranged from 0.6 microgram/l to 2 micrograms/l, whereas in sera of patients with joint diseases they ranged from 1.7 micrograms/l to 18 micrograms/l. Cathepsin H was not found in sera (values below 3 micrograms/l), but was measurable in patients' synovial fluids. Patients with rheumatoid arthritis have on average the highest values of cathepsin B in synovial fluids, whereas patients with undifferentiated arthritis have the highest values of cathepsin H. The results show that cathepsins B and H are present in arthritic synovial fluids, where they may be implicated in destructive processes. There is yet no clear correlation between the quantity of each cathepsin released in synovia and the clinical diagnosis or the stage of the disease.

Antibodies↗
PubMed1978

[Biorheologic study of pathological synovial fluids].

Rheometric studies of 34 synovial fluids done using a rheometer with a cone and stage (Shirley-Ferranti type) showed that arthrotic synovial fluids had pseudoplastic characteristics (non-Newtonian) but in inflammatory rheumatisms, the characteristics index rises, the consistency decreases and the fluid tends to loose its pseudoplastic properties and to become Newtonian. Radioisotope synoviorthosis seems capable of restoring to a certain extent and in certain cases the rheometric characteristics of the pseudoplastic properties.

Adolescent↗