Synovial Fluid Leukocyte Count Research Articles

Intra-articular distribution and residence time of Hylan A and B: a study in the goat knee

This study evaluates the viscosupplementation material Hylan A and B in relation to its: (1) joint distribution, residence time and mechanism of removal and/or degradation, and (2) associated synovial fluid leukocyte response, in a goat model. One green fluorophore was covalently bound to the Hylan A low molecular weight (MW) molecule (viscous fluid fraction) and a second red fluorophore was covalently bound to Hylan B high MW molecule (globule gel-like fraction). Goats were anesthetized and the right knee received 0.5 ml of test material or unbound fluorophore dyes. Gross and histological serial evaluations were performed over an 8-week period. By 24 h, the non-covalently linked control labels were not present in the tissues. For the covalently linked labels, the green fluorophore Hylan A diminished rapidly in intensity grossly but persisted to 28 days within the superficial synovial and articular cartilage layers in histologic sections. The red fluorophore linked Hylan B was seen only as globules in the synovial fluid. Mononuclear cells remained attached to these globules for 28 days and showed phagocytosis of the globules as well as the green fluorophore Hylan A. The globules were absent at 56 days after injection. The synovial fluid leukocyte count peaked at 24h (mean 9767 cells/mm(3) +/- 8574 S.D.) and declined by 7 days. The smaller MW Hylan was removed more rapidly than the higher MW Hylan. The globules were degraded by a different mechanism involving monocytes/macrophages on the surface of the higher MW globules.

Pseudomonas aeruginosa Septic Arthritis Treatment Failure With Ceftazidime and Amikacin in a Chronic Hemodialysis Patient Successfully Treated With Meropenem

Pseudomonas aeruginosa Septic Arthritis Treatment Failure With Ceftazidime and Amikacin in a Chronic Hemodialysis Patient Successfully Treated With Meropenem

Familial Mediterranean fever mimicking septic arthritis

We report the case of a young Lebanese female who presented with recurrent episodes of left knee and calf swelling and a synovial fluid leucocyte count suggestive of septic arthritis, however bacteriologic cultures were negative. Familial Mediterranean fever (FMF) was suspected in view of a positive family history and genetic analysis for the mutations in the pyrin/marenostrin (MEFV) gene revealing a homozygote mutation at methionine-694-valine. The arthritis was controlled with prophylactic colchicine therapy. FMF should be considered in the differential diagnosis of acute monoarticular arthritis with elevated synovial fluid white blood cells counts in regions with high incidence of FMF.

Synovial fluid leukocyte count and differential for the diagnosis of prosthetic knee infection

Criteria for the interpretation of synovial fluid are well established for native joint disorders but lacking for the evaluation of prosthetic joint failure. Our aim was to define cutoff values for synovial fluid leukocyte count and neutrophil percentage for differentiating aseptic failure and prosthetic joint infection. We performed a prospective study of 133 patients in whom synovial fluid specimens were collected before total knee arthroplasty revision between January 1998 and December 2003. Patients with underlying inflammatory joint disease were excluded. Aseptic failure was diagnosed in 99 patients and prosthetic joint infection was diagnosed in 34 patients. The synovial fluid leukocyte count was significantly higher in patients with prosthetic joint infection (median, 18.9 x 10(3)/microL; range, 0.3 to 178 x 10(3)/microL) than in those with aseptic failure (median, 0.3 x 10(3)/microL; range, 0.1 to 16 x 10(3)/microL; P <0.0001); the neutrophil percentage was also significantly higher in patients with prosthetic joint infection (median [range], 92% [55% to 100%] vs. 7% [0% to 79%], P <0.0001). A leukocyte count of >1.7 x 10(3)/microL had a sensitivity of 94% and a specificity of 88% for diagnosing prosthetic joint infection; a differential of >65% neutrophils had a sensitivity of 97% and a specificity of 98%. Staphylococcus aureus was the only pathogen associated with leukocyte counts >100 x 10(3)/microL. A synovial fluid leukocyte differential of >65% neutrophils (or a leukocyte count of >1.7 x 10(3)/microL) is a sensitive and specific test for the diagnosis of prosthetic knee infection in patients without underlying inflammatory joint disease.

Arthritis is linked to local and systemic activation of coagulation and fibrinolysis pathways

Activation of coagulation and fibrinolysis play a role in the pathophysiology of experimental arthritis. To determine the extent of activation of the coagulation and fibrinolytic pathways in different joint diseases in humans and to ascertain the factors that may influence fibrin deposition within the joint. Plasma from normal subjects (controls, n= 21) and plasma and synovial fluid samples from patients with rheumatoid arthritis (RA; n = 64), osteoarthritis (OA; n = 29), spondyloarthropathy (SpA; n = 22) and crystal arthritis (CA; n = 25) were analyzed for the levels of TF (tissue factor) and tissue factor pathway inhibitor (TFPI) activities, thrombin-antithrombin III (TAT) complexes, and F1 + 2 (thrombin fragment), fibrin d-dimer and thrombin-activated fibrinolysis inhibitor (TAFI) antigenic levels. The measurements were analyzed by pairwise correlation with each other as well as with standard parameters of inflammation [C-reactive protein (CRP), joint leukocyte count]. Inter-group comparisons were performed to look for disease-specific differences. Compared with healthy controls, patients with joint diseases had higher levels of TAT, F1 + 2 and d-dimers in their plasma. In the synovial fluid, TF activity, TAT, d-dimers, and TAFI were significantly higher in inflammatory arthritides than in OA. The levels were highest in RA patients. In the plasma, TF activity was correlated with TAT and d-dimer levels with CRP, TFPI, and TAT. In the synovial fluid, TF activity correlated with plasma CRP levels, synovial fluid leukocyte count, and synovial TAT and TAFI levels. In addition, synovial d-dimers correlated with CRP, and synovial TAFI levels were correlated with synovial F1 + 2 and TAT. Activation of the coagulation and fibrinolytic cascades in the joint and in the circulation is evident in both inflammatory and degenerative joint diseases. Within the joint, inflammatory mechanisms leading to TF-mediated activation of the coagulation pathway and subsequent fibrin deposition is the most likely explanation for the observed findings. In the plasma, the link between inflammation (CRP increase) and TF activation is weak, and a non-TF-mediated mechanism of coagulation activation could explain these findings. RA is characterized by significantly higher levels of TAT in the synovial fluid and plasma than other arthritides. Although fibrinolytic activity is linked to inflammation, the increased amounts of TAFI in the joint, particularly in RA, may explain why fibrin formation is so prominent in this condition compared with other joint diseases.

Concomitant septic and gouty arthritis--an analysis of 30 cases.

To analyse the clinical features and outcomes of gouty patients with concomitant septic arthritis in a medical centre. From the hospital database, we collected 30 hospitalized cases with concomitant septic arthritis and gouty arthritis from 1987 to 2001. All patients had positive bacterial culture and monosodium urate crystals in the affected joints. Medical records of the patients were analysed in detail. The mean age of patients was 52.8+/-12.5 yr. One-third of patients were afebrile at presentation, 30% had a normal blood leucocyte count and 10% had a synovial fluid leucocyte count less than 6000/mm3. The knee joint was the most common site of involvement, followed by the ankle, shoulder and wrist joints. Most patients had long-standing disease and subcutaneous tophi. Subcutaneous tophi rupture with secondary wound infection is the most common route of infection. Causative micro-organisms were Staphylococcus aureus (16 cases, 7 of whom were oxacillin-resistant), Streptococcus sp. (5 cases), Pediococcus sp. (1 case), and Gram-negative bacilli (9 cases). Fourteen patients received surgical debridement, among them two patients had an arthrodesis owing to severe joint destruction and one received above-knee amputation. Two patients died. One died of septic complications and the other died of acute myocardial infarction. Septic arthritis coexistent with gout presented a diagnostic difficulty. An early diagnosis requires a high level of suspicion. Prompt aspiration and analysis of the synovial fluid is imperative, regardless of the absence of fever or leucocytosis. Culture of the aspirated synovial fluid is warranted in gouty attack, even when it has a low white cell count or the Gram stain reveals no organisms.

Synovial fluid levels of E-selectin and intercellular adhesion molecule-1: relationship to joint inflammation in children with chronic arthritis

E-selectin and intercellular adhesion molecule (ICAM)-1 are crucial to the inflammatory response in chronic inflammatory arthritis. Soluble (s) levels of these molecules in sera and synovial fluid (SF) correlate with some clinical parameters and synovial tissue expression of the same molecules in rheumatoid arthritis. Studies of sera from children with chronic inflammatory arthritis corroborate this information; corresponding SF data are relatively lacking. We thus studied SF sE-selectin and sICAM-1 in 28 children with active juvenile rheumatoid arthritis or a spondyloarthropathy. Levels were correlated with erythrocyte sedimentation rate (ESR), SF leukocyte counts, duration of disease, and duration of response to concomitant intra-articular corticosteroid injection. Levels were compared according to use of methotrexate and/or sulfasalazine. Synovial fluid sE-selectin correlated with ESR and SF leukocyte counts. There was a trend toward lower sICAM-1 in patients treated with sulfasalazine and/or methotrexate. We conclude that SF levels of sE-selectin accurately reflect intra-synovial inflammation. Soluble ICAM-1 levels may reflect the effects of disease-modifying agents.

Leukocyte count in the synovial fluid of children with culture-proven brucellar arthritis.

Brucellosis is an important cause of paediatric septic arthritis in endemic areas. Because the Gram stain is frequently negative and culture results are unavailable at the time of the patient's admission, the diagnosis of brucellar arthritis is usually entertained on the bases of epidemiological considerations and cytological examination of the synovial fluid aspirate. The aim of this study was to assess the sensitivity of a synovial fluid leukocyte count >50 000 WBC/mm(3) for detecting culture-proven brucellar arthritis in children. The medical records of all children with brucellar arthritis diagnosed since 1994 in a hospital serving an endemic area for brucellosis in southern Israel were reviewed. Nine patients (six males and three females), aged 3-14 years, were identified. A single joint was affected in all patients. The median leukocyte count in the synovial fluid was 9500 WBC/mm(3) (range 300-61 500 WBC/mm(3)), and in eight of the nine patients it was less than 50 000 WBC/mm(3). Brucella melitensis was recovered from the synovial fluid culture in all patients. The diagnosis of brucellar septic arthritis cannot be excluded on the basis of a low leukocyte count in the joint aspirate. A high index of suspicion and use of modern culture techniques are recommended to improve the diagnosis of brucellar arthritis.

Placenta growth factor (PlGF) induces vascular endothelial growth factor (VEGF) secretion from mononuclear cells and is co-expressed with VEGF in synovial fluid.

The aims of this study were (i) to determine whether PlGF, VEGF and PlGF/VEGF heterodimers are detected in synovial fluid (SF) and plasma samples from patients with a range of arthropathies; (ii) to describe whether any correlation exists between SF PlGF, VEGF and PlGF/VEGF heterodimer levels and the total and differential SF leucocyte counts; and (iii) to investigate the regulation of peripheral blood mononuclear cell (PBMC) VEGF secretion by stimuli relevant to inflammatory joints. PlGF, VEGF and PlGF/VEGF heterodimer levels were measured in the SF and plasma of patients with a range of arthropathies and normal controls by ELISA. Western blotting for PlGF was performed on SF from three patients with rheumatoid arthritis (RA) and primary inflammatory arthropathies. VEGF was quantified in cell culture supernatants after stimulation with lipopolysaccharide (LPS), PlGF or cobalt ions of PBMC isolated from RA patients and controls. PlGF and VEGF were detected in all SF samples. PlGF/VEGF heterodimers were detected in 10.2% of SF samples, most frequently in RA samples. Western blotting confirmed the presence of PlGF in RA SF. PlGF was detected in 52% of RA and 31% of control plasma samples, and VEGF was detected in 38% of RA and 38% of control plasma samples. PlGF/VEGF heterodimers were detected in 21% of RA samples and none of the control samples. In primary inflammatory arthropathy patients, SF PlGF and VEGF levels correlated significantly with the SF total leucocyte count and the neutrophil count. PlGF was the most potent inducer of PBMC VEGF production in both RA and control subjects. This is the first report of the detection of PlGF and PlGF/VEGF heterodimers in the SF of patients with inflammatory arthropathies, and we have shown for the first time that PlGF up-regulates PBMC VEGF production. PlGF may therefore play a key role in the production of VEGF in the inflammatory joint.

Acute Gouty Arthritis Involving a Prosthetic Knee Joint

A painful and swollen prosthetic joint, accompanied by fever, is considered to be an intra-articular infection until proven otherwise. Acute gout is one of the rare causes of arthritis in a prosthetic joint, and it may be misdiagnosed as an infection, especially when a high leukocyte count is present in the joint fluid. We report a case of crystal-proven, gouty arthritis with a low synovial fluid leukocyte count presenting with pain and swelling in a prosthetic knee and responding to treatment with colchicine and corticosteroids. Physicians taking care of patients with prosthetic joints should be aware that acute gout can occur in an artificial joint and that aspirated prosthetic joint fluid should be routinely screened for crystals independently from the WBC counts obtained.

Soluble Forms of P-Selectin and Intercellular Adhesion Molecule-3 in Synovial Fluids

A number of adhesion molecules have been identified in synovial tissues of patients with rheumatoid arthritis (RA). Some of them are upregulated and may play an important role in the inflammatory processes of the diseased joint. In addition to synovial tissue cell surface expression, synovial fluids contain soluble forms of many adhesion molecules, such as intercellular adhesion molecule-1, E-selectin (sE-selectin), and L-selectin. In this study, we investigated the expression of soluble P-selectin (sP-selectin) and intercellular adhesion molecule-3 (sICAM-3) in synovial fluids from patients with RA, osteoarthritis (OA), and other forms of arthritis. sP-selectin and sICAM-3 levels in RA synovial fluids were significantly increased compared to those in OA. The levels of sP-selectin in synovial fluids correlated with sICAM-3 and sE-selectin in synovial fluids. The levels of sICAM-3 in synovial fluids correlated with synovial fluid leukocyte counts and erythrocyte sedimentation rate.In vitro,synovial fluid mononuclear cells produced sICAM-3 spontaneously. Elevated levels of sP-selectin and sICAM-3 in RA synovial fluids compared to OA may indicate inflammatory interactions between endothelial cells, leukocytes, and other synovial cells in the diseased joint.

Synovial fluid and serum concentrations of aminoterminal propeptide of type III procollagen in healthy volunteers and patients with joint disease.

To analyse synovial fluid and serum concentrations of the amino-propeptide of the type III procollagen (PIIINP) in normal individuals and patients with joint disease, and to explore the relationship between synovial fluid PIIINP concentrations and the rheumatological diagnosis, local inflammation, and joint disease. A radioimmunoassay was used to measure the PIIINP concentrations in serum and knee joint synovial fluid from 16 healthy volunteers and patients with osteoarthritis (OA) (n = 40), rheumatoid arthritis (RA) (n = 30), and psoriatic arthritis (PsA) (n = 12). The PIIINP measurements were related to demographic data, synovial fluid leucocyte counts, and radiographic changes at the knee. Serum PIIINP concentrations were greater in each of the disease groups than in control subjects, but there were no differences between the disease groups. Synovial fluid concentrations of PIIINP were much greater than those in serum, indicating local production, and were significantly greater in RA than in other disease groups (p < 0.001). There was only a weak positive correlation between synovial fluid leucocyte counts, some radiographic changes, and synovial fluid PIIINP concentrations. These data suggest that synovial fluid PIIINP concentrations may reflect local synovial proliferative processes in joint disease, and that they could be of diagnostic and prognostic value in inflammatory arthropathies.

Cathepsin G and elastase in synovial fluid and peripheral blood in reactive and rheumatoid arthritis.

The purpose of the study was to evaluate the involvement of serine proteinases cathepsin G and elastase on pathomechanisms in synovial fluid (SF) of patients with reactive (ReA) and rheumatoid, (RA) arthritis. Cathepsin G, elastase, and their endogenous inhibitors alpha1-antichymotrypsin (alpha1-ACT) and alpha1-proteinase inhibitor (alpha1-PI) were identified immunohistochemically from SF and peripheral blood (PB) of patients with ReA and RA. Cathepsin G and elastase activities in SF and PB were measured spectrophotometrically. Dot-immunostaining was used to identify cathepsin G, elastase, but also alpha1-ACT and alpha1-PI from SF and PB. Cathepsin G and elastase-like activities (IU/I) were slightly elevated in ReA SF compared to the corresponding peripheral blood values (11.4 +/- 9.2 vs 4.8 +/- 1.7, NS, and 5.1 +/- 2.8 vs 2.3 +/- 2.2, NS), which was similar to what was seen in RA (16.4 +/- 6.2 vs 0.53 +/- 0.4, p < 0.05, and 6.51 +/- 1.8 vs 1.22 +/- 0.58, p < 0.05). Although some samples did not contain cathepsin G and/or elastase-like activities, all samples contained immunoreactive enzyme, but also alpha1-ACT and alpha1-PI. In ReA SF, in contrast to monocytes, all polymorphonuclear (PMN) cells contained cathepsin G and elastase. Cathepsin G and elastase activities correlated with each other (r = 0.78, p < 0.05) suggesting PMN / primary granules as their likely source. There was a closer association between the cathepsin G or elastase and SF leukocyte count in ReA than in RA. In ReA and RA SF elevated cathepsin G and elastase activities are detected compared to activity levels in PB suggesting local production mainly from PMNs. The co-existence of highly cellular SF and cathepsin G and elastase activity in the documented presence of endogenous inhibitors in ReA SF together with the, known, usually self-remitting clinical course of ReA, suggest a brisk and even exaggerated local PMN serine proteinase release; sparing of joints does not seem to be due to lack or inhibition of PMN responses but rather to a successful down-regulation or cessation of the responses initially elicited.

Changes in cartilage metabolism in arthritis are reflected by altered serum and synovial fluid levels of the cartilage proteoglycan aggrecan. Implications for pathogenesis.

The metabolism of the cartilage proteoglycan aggrecan was studied in patients with osteoarthritis (OA, n = 83), rheumatoid arthritis (RA, n = 127), and in controls (n = 117) using monoclonal antibody-based radioimmunoassays for glycosaminoglycans in the serum and synovial fluid (SF) to detect epitope 846 on chondroitin sulfate (probably only on recently synthesized molecules) and a keratan sulfate (KS) epitope AN9PI, present on intact and degraded molecules. Epitope 846 levels were always elevated in SF over serum (mean 38-fold in OA and 8.6-fold in RA) being highest in OA patients with the longest disease duration and greatest loss of cartilage, and lowest in RA joints with high leucocyte counts. Serum levels were more often elevated in RA (56%) than in OA (19%) and probably reflect increased aggrecan synthesis in diseased joints. KS levels were higher in SF than in serum in 69% of patients (up to 2.3-fold); levels were inversely (OA) and directly (RA) related to SF leucocyte counts. Serum KS was reduced in both diseases and in RA was inversely related to both systemic and joint inflammation markers. SF 846 levels were inversely related to SF KS in both diseases. These epitopes may provide a measure of the balance between cartilage synthesis and degradation in these diseases.

Soluble Intercellular Adhesion Molecule-1 in Arthritis

The objective of this study is to determine whether soluble intercellular adhesion molecule-1 (siCAM-l) is found in rheumatoid arthritis (RA) and other inflammatory disorders and to identify which cells are responsible for sICAM-1 production. Synovial fluid, blood and cells isolated from RA synovial fluids, and synovial tissues from 59 patients were studied. In addition, normal peripheral blood was obtained. sICAM-1 was assayed by an enzyme-linked immunoabsorbant assay. Synovial fluids from patients with RA and other inflammatory arthritides had significantly higher sICAM-1 levels than did osteoarthritis (OA) synovial fluids. Synovial fluid sICAM-1 levels were significantly positively correlated with synovial fluid leukocyte counts. RA synovial tissue fibroblasts released low levels of sICAM-1. Neutrophils (PMNs) isolated from synovial fluids of RA patients spontaneously released sICAM-1. However, mononuclear cells isolated from RA synovial fluid produced the largest quantities of sICAM-1. Phytohemagglutinin but not lipopolysaccharide enhanced mononuclear sICAM-1 release. sICAM-1 was increased in synovial fluids from RA compared to OA. This sICAM-1 may be important in modulating the trafficking of inflammatory leukocytes into diseased RA synovial tissue and fluid.

The effects of orally administered calcium pentosan polysulfate on inflammation and cartilage degradation produced in rabbit joints by intraarticular injection of a hyaluronate-polylysine complex.

To determine the antiinflammatory and cartilage-protecting activities of orally administered calcium pentosan polysulfate (CaPPS) in a rabbit model of inflammatory arthritis. A single intraarticular injection of a preformed polycation complex (PC) of poly-D-lysine and hyaluronan was used to induce joint inflammation; saline was injected into the contralateral joint as a control. Animals were killed 1, 4, 7, or 10 days post-PC injection. CaPPS, at 5 mg/kg, 10 mg/kg, or 75 mg/kg, was given every 48 hours commencing 7 days prior to PC injection. Serum interleukin-6 (IL-6), synovial fluid (SF) prostaglandin E2, cell numbers, and cartilage proteoglycan (PG) content, composition, and biosynthesis were determined for PC- and saline-injected joints. In PC-injected, non-drug-treated animals, serum IL-6 activity, SF leukocyte numbers, and prostaglandin E2 levels were elevated, while cartilage PG content and biosynthesis were reduced. CaPPS at 10 mg/kg, but not at 5 mg/kg, decreased serum IL-6 levels but maintained cartilage PG concentration and biosynthesis. However, SF leukocyte counts and prostaglandin E2 levels (except on day 1) were not reduced. The ability of CaPPS to attenuate serum IL-6 levels and preserve cartilage PGs in inflamed rabbit joints suggests that this substance could be of value as an effective orally administered chondroprotective, antiarthritic drug.

Soluble E-Selectin in Arthritis

Cellular adhesion molecules, such as E-selectin, function to recruit leukocytes into inflammatory lesions. Recently, a soluble form of this adhesion molecule, sE-selectin, has been described. In this study we determined soluble E-selectin (sE-selectin) in synovial fluid (SF) and blood samples from patients with rheumatoid arthritis (RA) and other inflammatory disorders and correlated sE-selectin levels with clinical parameters of disease activity. SF, blood, and cells isolated from RA SFs and synovial tissues (STs) were examined from 76 patients. In addition, normal plasma as well as supernatants from cultured human umbilical vein endothelial cells (HUVECs) were obtained. sE-selectin levels were assayed in these fluids and cell supernatants by an enzyme-linked immunoabsorbant (ELISA) assay. SFs from patients with RA had significantly higher sE-selectin levels than did those from osteoarthritis (OA) SFs ( P < 0.05). SF sEselectin levels were correlated with SF leukocyte counts. HUVECs, or RA ST cells enriched in endothelial cells, produced sE-selectin. Neutrophils isolated from RA SFs did not release sE-selectin. SF soluble intercellular adhesion molecule-1 levels correlated positively with sE-selectin levels. We conclude that sE-selectin levels are increased in SFs from RA compared to those from OA. Endothelial cells derived from umbilical vein or from RA STs release sE-selectin. Thus, sE-selectin may be important in the migration of inflammatory leukocytes into diseased RA STs and SFs.

Synovial Leukocytosis in Infectious Arthritis

The clinical presentation of 41 adult patients with infectious arthritis has been reviewed with special emphasis on initial synovial fluid leukocytosis. Fifty percent of the patients with culture-proven joint-space infections had synovial fluid leukocyte counts below 28,000/mm3. Comparison of this investigation with previous studies of similar magnitude demonstrates a striking difference in the mean and median synovial fluid white cell counts. The population reviewed had a higher incidence of patients with potentially immunocompromising medical conditions than previous reports. Similarities between this and previous reports include predisposing conditions, the spectrum of pathogens cultured, associated clinical findings on admission, hospital course, and mortality. The data presented here document the magnitude of potential overlap between the synovial fluid leukocytosis in infected joints and in joints afflicted with other forms of inflammatory arthropathy. Three patients populations (malignant neoplasms, steroid use, and intravenous drug abuse) with positive cultures from synovial fluid aspirates but initial synovial fluid white cell counts averaging below 50,000 cells/mm3 were identified. Patients with moderate synovial fluid leukocytosis, especially those potentially immunocompromised, must be considered to have infectious arthritis unless other causes of inflammatory arthropathies are demonstrated.

Effects of Non-steroidal Anti-inflammatory Drugs and Prednisolone on Synovial Fluid White Cells, Prostaglandin E2, Leukotriene B4and Cyclic AMP in Patients with Rheumatoid Arthritis

Altogether 53 patients (31 women, 22 men) with definite rheumatoid arthritis were randomly divided into groups of 5-6 patients and treated for one day only with one of the following non-steroidal anti-inflammatory drugs (NSAIDs): acetylsalicylic acid, carprofen, diclofenac, indomethacin, naproxen, proquazone, timegadine, tolfenamic acid or paracetamol, and with prednisolone, in recommended doses. Synovial fluid samples were collected before and after the treatment. White cell count and its differentiation as well as the concentrations of protein, cyclic adenosine-3',5'-monophosphate (cAMP), prostaglandin E2 (PGE2) and leukotriene B4 (LTB4) were measured from the synovial fluid. Synovial fluid leukocyte counts correlated with PGE2 concentrations, but showed no correlation with LTB4 levels before treatment. Significant changes were seen in the form of lowered PGE2 values following treatment with the clinically and experimentally most potent NSAIDs, and as depressed LTB4 levels following prednisolone treatment. The other markers of inflammation are obviously more resistant, changing only slowly during prolonged treatment, and may thus be, at least in part, secondary to the changes in prostanoids.

Treatment of articular effusions with local deep microwave hyperthermia.

Local deep microwave hyperthermia (LDMWH) may be considered as a therapeutic tool for joint diseases because it has the advantage of heating the target organ e.g. synovium, while sparing the adjacent tissues, as demonstrated in animals. The effect of this new microwave device has been evaluated on seven rheumatoid arthritis patients with knee effusion. The hyperthermia apparatus consists of a 915 MHz power source with a cooling system to the skin. LDMWH was operated for one hour, twice a week for two weeks. Intra-articular knee temperature reached the level of 40.6 +/- 1.1 degrees C within 15 minutes, raised to 41.2 +/- 0.7 degrees C after 30 minutes and to 41.3 +/- 0.9 degrees C at one hour. The skin temperature over the heated knee joints remained at 24.3 +/- 1.1 degrees C during treatment. All patients noted a sensation of warmth in the treated knee. Aspiration of synovial fluid was performed before and immediately after each treatment. Walking time was improved (p = 0.04) and significant decrease in pain (p = 0.01) was noted following treatment. Synovial fluid leukocyte count and prostaglandin E2 level, knee circumference and range of motion did not change. Severity of pain, walking time, knee circumference and range of motion remained stable in the six weeks following the last hyperthermia application. No adverse reaction could be observed. These results suggest LDMWH to be safe and successful as an adjuvant treatment of chronic inflammatory joint effusions.