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ID PMID Title PublicationDate abstract
8371503 [Anti-type II collagen antibodies in collagen disease]. 1993 Aug Using enzyme-linked immunosorbent assay (ELISA), we determined the incidence of serum IgG antibodies to native type II collagen in patients with collagen diseases such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), progressive systemic sclerosis (PSS) and overlap syndrome (OL). Raised serum IgG anti-type II collagen antibody levels were present in 11% of patients with RA, 30% with SLE, 44% with PSS and 42% with OL. There was, however, no correlation with clinical manifestations or other laboratory data.
8446824 Shoulder arthroscopy in the athlete. Practical applications. 1993 Feb Shoulder arthroscopy may be a useful tool to the surgeon in confirming a diagnosis for therapeutic treatment of a diagnosed condition. Shoulder arthroscopy has provided valuable information in establishing a diagnosis in the athletic individual when overlapping symptoms make a clinical diagnosis difficult. Shoulder arthroscopy for shoulder instability is in its developmental stages with early studies showing a high redislocation rate. Impingement syndrome is initially treated with conservative methods; however, if this is unsuccessful acromioplasty can be considered. Arthroscopic acromioplasty allows a thorough examination of the glenohumeral joint. Patients with rotator cuff tears may get pain relief with arthroscopic debridement. Inflammatory diseases such as rheumatoid arthritis can be treated with arthroscopic synovectomy. Shoulder arthroscopy is a valuable tool in the treatment and diagnosis of shoulder disorders.
1301592 Disease-modifying anti-rheumatic drugs: strategies for screening. 1992 Dec Rheumatoid arthritis, a disease of unknown aetiology, has a multifactorial pathogenesis which may result in irreversible connective tissue destruction and loss of joint function. The search for drugs which offer more than symptomatic relief is a long term, largely unachieved aim of many pharmaceutical companies. This review briefly outlines those features of the aetiopathogenesis which appear to offer targets for therapeutic intervention and the structured strategy and test systems that can be used to detect drugs which may be capable of halting disease progression.
25990997 Systemic necrotizing vasculitis. 1994 Jul Systemic necrotizing vasculitis may be idiopathic or associated with a variety of diseases of known etiology. A typical example is polyarteritis nodosa, which is characterized by fibrinoid necrosis and severe inflammation leading to destruction of the wall, narrowing of the lumen, and interference with blood circulation. In addition to the idiopathic form, histologically similar lesions are seen in hepatitis B, rheumatoid arthritis, Kawasaki mucocutaneous lymph node syndrome, and other diseases. Microscopic polyangitis involves mainly small vessels-venules more often than arterioles-but occasionally also small arteries. Its characteristic feature is leukocytoclasia of neutrophilic leukocytes, but fibrinoid necrosis also occurs. Churg-Strauss syndrome consists of granulomas in patients with a background of severe allergy, such as asthma, allergic rhinitis, or occasionally drug sensitization.
8952894 [Role of type II secreted phospholipase A2 in inflammatory processes]. 1996 Secreted phospholipase A2 has been detected in numerous inflammatory and infectious diseases. Since the cloning of the type II sPLA2 in 1989 from rheumatoid arthritis synovial fluid, a direct or indirect participation of type II sPLA2 in the production of lipid mediators has been purposed. This paper reviews the different studies from the literature alleging that type II sPLA2 participates to inflammatory processes and lipid mediators synthesis.
8724309 Intravenous immunoglobulin in the treatment of polyarticular juvenile rheumatoid arthritis 1996 May OBJECTIVE: To obtain preliminary information about the safety and efficacy of intravenous immune globulin (IVIG: Iveegam, Immuno AG, Vienna) in the treatment of polyarticular juvenile rheumatoid arthritis (poly-JRA) resistant to other forms therapy. METHODS: We used a multicentered, phase I/II blinded-withdrawal design with stratified entry. All patients began by receiving open infusions of IVIG at a dose between 1.5 and 2.0 g/kg/infusion (100 g maximum) bimonthly for the first 2 months, then monthly for up to 6 months. Beginning at Month 3, those who met the criteria for "clinically important improvement" were randomized to receive monthly infusions for 4 months of either placebo or IVIG in a double blind (DB) phase. Patients were permitted nonsteroidal antiinflammatory drugs, slow acting antirheumatic drugs, and low dose (< 10 mg/day) prednisone at constant doses. An "early escape" provision in the DB allowed those who showed "clinically important worsening" to again receive IVIG (if taking placebo) or a higher dose of IVIG (if taking the lower dose of IVIG). RESULTS: Efficacy. Twenty-five children entered the trial and 19 (76%) met the criteria for "clinically important improvement" during the open phase (OP) and entered the DB. Three patients completed the OP but failed to meet the criteria for response, and 3 patients dropped out of the OP, none of whom showed benefit from IVIG. Treatment effect sizes produced by IVIG were moderate to large for all variables in the OP. Patients who continued IVIG in the DB continued to show improvement over that achieved in the OP. Those given placebo showed a rapid loss of efficacy, suggesting IVIG has a limited duration of effect after discontinuation. Safety. No patient developed serious or unexpected adverse side effects in the open or DB phases, and none dropped out of the study due to toxicity or side effects. CONCLUSION: Substantial clinical improvement from IVIG is produced in about three-fourths of patients with poly-JRA during open administration, but the duration of the beneficial effect is short after discontinuation. Those with disease < 3 years' duration may be more likely to respond than those who have had their disease for > 5 years. Short term safety is excellent.
8996859 Antirheumatic agents. II. Novel methotrexate derivatives bearing an alkyl-substituted benz 1996 Dec Novel methotrexate (MTX) derivatives with either a mono- or dialkyl-substituted benzene ring were synthesized and initially tested for in vitro anti-proliferative activities using human peripheral blood mononuclear cells (hPBMC) derived from healthy volunteers and synovial cells (hSC) derived from patients with rheumatoid arthritis (RA). Compounds with potent activities were further evaluated in an in vivo adjuvant arthritis model. In comparison with MTX, a glutamate derivative 3a was more potent as a suppressor of the in vitro cell proliferation and the in vivo experimental arthritis, and a homoglutamate derivative, 3e, exhibited fairly good activities in vitro and considerable activity in vivo in a dose-dependent manner. As expected, 3e did not act as a substrate of folylpolyglutamate synthetase (FPGS), and thus did not undergo polyglutamation, which is thought to be responsible for side-effects that occur during MTX therapy.
1283924 Expression of decay-accelerating factor on synovial lining cells in inflammatory and degen 1992 The decay-accelerating factor (DAF) is a complement regulatory cell surface protein that protects cells from complement-mediated lysis. We analysed synovial tissue biopsies from patients with chronic arthritides for the presence of DAF using immunohistochemistry. DAF was expressed in the synovial lining cell layer both in rheumatoid arthritis (RA) and in osteoarthritis (OA). DAF was also on vascular endothelial cells of synovial tissue. A significant correlation was found between the expression of DAF and of HLA-DR in the lining layer, suggesting that DAF may be induced during a local inflammatory response. In addition, C5b-9 terminal complement complexes were found in several DAF-positive cases, suggesting that complement activation might, in itself, induce DAF expression. We propose that the occurrence of DAF may represent a physiological mechanism for local complement regulation in synovial tissue.
8453819 Hypertrophic cranial pachymeningitis causing progressive unilateral blindness: MR findings 1993 Mar A case of hypertrophic cranial pachymeningitis is described and the MR appearance presented. A gadopentetate-dimeglumine-enhanced MR scan enhanced markedly suggesting thickening and inflammation of dura and falx cerebri. The patient, a 72-year-old elderly man, had surprisingly little clinical abnormality. His only neurological manifestation was progressive unilateral blindness. The exact cause of his pachymeningitis was unknown, though neither rheumatoid arthritis nor other collagen disease was completely excluded.
7910643 Bilateral acetylsulfapyridine nephrolithiasis associated with chronic sulfasalazine therap 1994 Jun We report on formation of bilateral renal calculi secondary to sulfasalazine therapy for juvenile rheumatoid arthritis. The condition was successfully treated with extracorporeal shock wave lithotripsy. Analysis of the fragments with thin layer chromatography and nuclear magnetic resonance revealed acetylsulfapyridine, a metabolite of sulfasalazine.
8007408 [Collagen disease and vasculitis with manic and depressive symptoms]. 1994 May Collagen diseases and vasculitis diseases are known to have severe disorders in many organs. Manic and depressive symptoms are also found in these diseases as one of central nervous system disorders. They are frequently observed in systemic lupus erythematosus, primary Sjögren's syndrome and rheumatoid arthritis. It is very difficult to diagnose and treat the manic-depressive states because there are many origins that cause the psychological disorder; immunological disorders (anti-cardiolipin antibodies, anti ribosomal protein P etc.), cerebral vasculitis, thrombosis, infections, endocrinological disorders, steroid induced psychosis and so on. There are few pathogenic studies to explain the manic-depressive symptom in these diseases.
1519270 Historic reflection on steroids: Lederle and personal aspects. 1992 Aug Steroid research at Lederle was initiated in 1946 and continued until about 1971. The areas of research interest involved primarily a study of delta 5,7-steroids, provitamin D3 variants, dehydroepiandrosterone variants, steroidal ketals, corticoids, and steroid conjugates. One of the principal goals was to develop novel antiinflammatory steroids for the treatment of, e.g., rheumatoid arthritis. A rational design led to the development of 16 alpha-hydroxycorticoids, culminating in the synthesis and therapeutic use of triamcinolone and related compounds.
1546338 Case report 707: Hemorrhagic Baker's cyst of the right calf. 1992 A 50-year-old woman with juvenile rheumatoid arthritis presented with painful swelling of the right calf. Roentgenograms, sonograms, magnetic resonance images, and arthrograms were obtained. A diagnosis of hemorrhagic Baker's cyst was made, and surgical excision was performed. The etiology, clinical features, and radiological evaluation of simple and complicated Baker's cysts are discussed and the differential diagnosis considered.
7594561 The effect of pregnancy on polymorphonuclear leukocyte function. 1995 Dec 1 Pregnancy exerts suppressive effects on a number of chronic inflammatory conditions, particularly rheumatoid arthritis. We isolated peripheral blood polymorphonuclear leukocytes (PMN) from pregnant women at 30 to 34 wk (n = 34) and showed significant reductions in respiratory burst activity compared with nonpregnant controls (n = 34), as determined by lucigenin-enhanced chemiluminescence (LUCL). Responses to FMLP were reduced by 54% (p = 0.0046) and to zymosan-activated serum (ZAS) by 69% (p = 0.0043). Following LUCL responses to these agonists in women throughout the course of their pregnancy (n = 7) revealed significantly reduced responses by the second and third trimesters (p < 0.005). Intracellular H2O2 production in PMN at 30 to 34 wk gestation was significantly reduced (p = 0.0454) in response to FMLP, compared with the nonpregnant controls. Investigation of adhesion molecule expression revealed no differences in CD11b or CD18. However, loss of CD62L from the PMN surface in response to FMLP and ZAS was significantly reduced at 30 to 34 wk, as compared with controls (FMLP, p = 0.049; ZAS, p = 0.01; n = 34). There were no significant differences in cell surface formyl peptide receptor expression, although there were statistical differences in LUCL responses to all concentrations of FMLP used (p < 0.05). Incubating PMN with TNF, IL-8, and granulocyte-macrophage CSF increased formyl peptide receptor expression but revealed no differences between the two groups. Priming of pregnancy PMN with the same cytokines gave significantly reduced LUCL when cells were subsequently stimulated with FMLP (p < 0.05; n = 6). Our results show a reduction in PMN NADPH-oxidase activity during pregnancy and may offer a partial explanation for the remission of symptoms observed in rheumatoid arthritis.
7784648 [Posterior luxation of the tibia on total knee prosthesis: apropos of 6 cases]. 1994 PURPOSE OF THE STUDY: Posterior dislocation of Total knee arthroplasty is an infrequent but serious complication. Six cases of this complication were treated from 1979 to december 1993, all occurring on primary arthroplasties. MATERIAL AND METHODS: Knee arthroplasty was performed once for rheumatoid arthritis, five times for osteoarthritis. All cases occurred with a semi constrained prosthesis sacrifying posterior cruciate ligament: 2 Total condylar without posterior stabilisation, and 4 posterior stabilised prosthesis. In one case the dislocation occurred on a very severe rheumatoid arthritis: the patient, confined in a wheel chair, was not reoperated. In two patients, the dislocation was due to rotatory malposition of the tibial component. In the last three cases, we did not found any cause to the dislocation, except ligament laxity: 2 of these patients had, pre operatively, a valgus deformity. In 6 cases, we found only 2 problems on extensor system (one patellar dislocation and one patellectomy). RESULTS: 5 patients required a surgical treatment In 2 cases, we used a more constrained prosthesis, with poor results, but the knee was stable. Once, by changing the position of the tibial component, and using a thicker plate. In 2 patients we only put a thicker tibial polyethylene component. These 3 patients had a good stability: 2 have an excellent result with H.S.S. rating system, the third one has a poor result explained by patellar pseudoarthrosis occurring after traumatic patellar fracture. DISCUSSION: With our patients and cases published in North American works, we have studied the different mechanisms of such a posterior dislocation: rotatory disorder on tibial component, ligament laxity in flexion, extensor system deficiency, valgus deformity with important postero lateral release. CONCLUSION: The causes of posterior dislocation on Total knee arthroplasties must be known: we have to try to prevent such a complication. If it occurs, a precise analysis will permit a logical curative treatment, which must avoid constrained prosthesis.
8603428 The effect of minocycline in rat models of inflammatory arthritis: correlation of arthriti 1996 Feb 1 Adjuvant and collagen arthritis in the rat are widely accepted T-cell-dependent counterparts of rheumatoid arthritis and were used to examine the antiinflammatory properties of minocycline. Administration of oral minocycline, a semisynthetic tetracycline, significantly decreased (P < 0.01) the incidence of arthritis in both models. In vivo exposure to minocycline also significantly increased the percentage of splenocytes exhibiting a rise in free intracellular calcium concentration ([Ca2+]i) following concanavalin A stimulation (P < 0.05 in adjuvant and P < 0.01 in collagen). This enhancement was mitogen dose-dependent and supported exclusively by extracellular Ca2+. Resting [Ca2+]i levels were unaffected by minocycline and predominantly the CD4+ subset was involved. No changes were observed in weight, IgG antibodies to collagen, synoviocyte release of collagenase and prostaglandin E2, acute inflammation in an air-pouch system, or cell surface expression of activation markers (interleukin-2 and transferrin receptors) by splenocytes or lymph node cells. As a controlled [Ca2+]i rise is a critical event in normal T cell activation, minocycline's antiarthritic profile in vivo may relate to perturbed Ca2+ influx during T cell activation, an alteration that could promote the development of clinical tolerance to otherwise arthritogenic stimuli.
7655463 A novel allelic variant of serum amyloid A, SAA1 gamma: genomic evidence, evolution, frequ 1995 Jun Reactive systemic amyloidosis, also called AA-amyloidosis is a rare fatal complication of common chronic inflammatory diseases such as rheumatoid arthritis. It has been proposed that as yet undefined factors other than persistent elevation of serum level of the precursor protein, serum amyloid A (SAA), are also important for the development of AA-amyloidosis. In this work we show genomic evidence for a novel allelic variant of human SAA, SAA1 gamma, which we have recently identified at the protein level. The SAA1 gamma [Ala52(GCC), Ala57(GCG)] differed from SAA1 alpha [Val52(GTC), Ala57(GCG)] only at one base, indicating a single point mutation. On the other hand, SAA1 beta [Ala52(GCC), Val57(GTG)] had not only one, but additional differences in a nearby intron and this portion was identical to the SAA2 gene, suggesting a crossing-over between the SAA1 and SAA2 genes. Furthermore, we report that there was a significant difference in the observed numbers of SAA1 alleles between rheumatoid arthritis patients with AA-amyloidosis and the control population (chi 2(2) = 11.59, p = 0.003) with a higher frequency of gamma-allele in the AA-amyloid group (0.70 vs. 0.37). There was also a notable difference in the distribution of SAA1 genotypes (chi 5(2) = 14.63, p = 0.012) with an increased frequency of gamma/gamma-homozygotes in the AA-amyloid group (0.60 vs. 0.18). Thus our findings indicate that this novel allelic variant may be an important risk factor for the development of AA-amyloidosis.
7694864 Radicicol, a microbial cell differentiation modulator, inhibits in vivo angiogenesis. 1993 Sep 14 Angiogenesis plays a significant role in various pathological states, including the progressive growth of solid tumors, rheumatoid arthritis, psoriasis, and diabetic retinopathy, in addition to its crucial role in embryonic development. Recent studies have revealed that an angiogenesis inhibitor is efficacious for these so-called angiogenic diseases. In the previous studies, we found that retinoids and vitamin D3 analogs, which are known to exhibit cell differentiation-modulating activity, effectively inhibit angiogenesis in vivo, thus forming the basis of our working hypothesis that a modulator of cell differentiation is capable of affecting angiogenesis. In this study, to verify this hypothesis further, radicicol (syn. monorden; 5-chloro-6-(7,8-epoxy-10-hydoxy-2-oxo-3,5-undecadienyl)-beta -resorcylic acid mu-lactone), a microbial cell differentiation modulator from a fungus, a strain of Neocosmospora tenuicristata, was examined for its anti-angiogenic activity in a bioassay system involving chorioallantoic membranes of growing chick embryos. The microbial cell differentiation modulator dose dependently inhibited embryonic angiogenesis, the ID50 value being 200 ng/egg. Radicicol also inhibited both the proliferation of and plasminogen activator production by vascular endothelial cells in the nM concentration range in a concentration-dependent manner, suggesting the possible involvement of these inhibitory effects in the anti-angiogenic action of the microbial product. These results indicate that radicicol might be a potential drug for treating different angiogenesis-dependent diseases, such as solid tumors, psoriasis, rheumatoid arthritis, and diabetic retinopathy.
8033415 The role of tumour necrosis factor-alpha and IL-1 in polymorphonuclear leucocyte and T lym 1994 Jul The mediators involved in leucocyte recruitment to joints during arthritis are not fully defined, but two important proinflammatory cytokines, IL-1 and tumour necrosis factor-alpha (TNF-alpha), are produced in joints in rheumatoid arthritis (RA). We investigated in the rat adjuvant arthritis model whether endogenous IL-1 and TNF-alpha contribute to joint inflammation and polymorphonuclear leucocyte (PMNL) and T lymphocyte infiltration. The migration of 51Cr-labelled rat blood PMNL and 111In-labelled T lymphocytes to the joints of rats with adjuvant arthritis was measured along with plasma protein extravasation, which was quantified using 125I-labelled human albumin. Rats with active arthritis of 5 days' duration received i.p. non-immune serum, polyclonal neutralizing anti-serum to rat TNF-alpha, antiserum to IL-1 alpha and IL-1 beta, or both anti-TNF plus anti-IL-1 for 5 days. Treatment with anti-IL-1 alpha and IL-1 beta did not affect plasma protein extravasation, or PMNL or T lymphocyte accumulation in the joints (i.e. talar joint, hind paws, and tail) despite the fact that this treatment inhibited 80-90% of the PMNL migration into dermal sites injected with IL-1 alpha or IL-1 beta. In contrast, anti-TNF-alpha treatment significantly improved clinical scores, decreased plasma protein extravasation by 60-80%, inhibited PMNL accumulation by 40-50% and decreased T lymphocyte accumulation by 30-50%. Treatment with anti-IL-1, together with anti-TNF-alpha, significantly potentiated the inhibition of T lymphocyte accumulation observed with anti-TNF-alpha alone. These results indicate that endogenous TNF-alpha production may play an important role in the inflammatory changes and leucocyte recruitment in this experimental model of human arthritis, while IL-1 may have a less important role in leucocyte recruitment to these joints.
8822585 A sensitive bioimmunoassay for thrombin-cleaved two-chain urokinase-type plasminogen activ 1996 Jun Thrombin cleaves single-chain urokinase-type plasminogen activator (scu-PA) into a two-chain form (tcu-PA/T), which is virtually inactive in plasminogen activator assays. Little is known about the physiological importance of tcu-PA/T. To examine the occurrence of tcu-PA/T in vivo, we developed a sensitive and specific bioimmunoassay (BIA) for the assessment of tcu-PA/T in human body fluids. In this BIA, urokinase antigen was immuno-immobilized in microtiter plates and treated with cathepsin C, a specific activator of tcu-PA/T, after which plasminogen activator activity was measured. The occurrence of tcu-PA/T was examined in the plasma of 27 healthy individuals and of 17 sepsis patients, and in the synovial fluid of 16 rheumatoid arthritis patients. In addition, the concentration of urokinase antigen and scu-PA were measured in all three groups. In the plasma of the healthy individuals no measurable amounts of tcu-PA/T could be found(< detection limit of 0.2 ng/ml). In the plasma of almost all sepsis patients tcu-PA/T could be detected (median value 0.4 ng/ml). The amount of tcu-PA/T was 12% of the amount of scu-PA and accounted for about 9% of urokinase antigen. In the synovial fluid of all rheumatoid arthritis patients tcu-PA/T could be measured (median value 5.4 ng/ml) at a concentration which was twofold higher than the concentration found for scu-PA. In this group tcu-PA/T contributed to about 47% of the urokinase antigen. From these data we conclude that inactivation of scu-PA by thrombin can take place in vivo under pathological conditions which involve the production of large amounts of thrombin. This way thrombin may regulate fibrinolysis and extracellular proteolysis. The BIA for tcu-PA/T can be of use for further research on the physiological role of tcu-PA/T.