Search for: rheumatoid arthritis methotrexate autoimmune disease biomarker gene expression GWAS HLA genes non-HLA genes
| ID | PMID | Title | PublicationDate | abstract |
|---|---|---|---|---|
| 1969825 | Clinical evidence supporting the radical scavenger mechanism of 5-aminosalicylic acid. | 1990 May | 5-Aminosalicylic acid, the therapeutically active metabolite of sulfasalazine, was exposed to oxygen-derived free radicals produced by the Fenton reaction in vitro, and several metabolites were detected and characterized by high performance liquid chromatography and ultraviolet spectrophotometry. The majority of these metabolites were present in methanolic extracts of feces samples from sulfasalazine-treated patients with inflammatory bowel disease but not in rheumatoid arthritis patients with normal bowel function. The presence of these metabolites, which have not been demonstrated in vivo before, provides evidence of an interaction between 5-aminosalicylic acid and oxygen-derived free radicals in sulfasalazine-treated patients with inflammatory bowel disease. Since the concentration of lipid peroxides, which is dependent on the release of oxygen-derived free radicals, was significantly increased in pretreatment rectal biopsies of the patients, and further was normalized concomitantly with a significant improvement in disease activity over the 5-wk treatment period, an important role of the radical scavenger mechanism of 5-aminosalicylic acid in sulfasalazine therapy of chronic inflammatory bowel disease is strongly suggested. | |
| 2319132 | A conserved anti-DNA antibody idiotype associated with nephritis in murine and human syste | 1990 Apr 1 | In order to identify unique structural features of pathogenic autoantibodies to DNA in SLE, a murine anti-anti-DNA (anti-Id) mAb (mAb 1C7) was produced in response to immunization of lupus mice with a syngeneic anti-DNA mAb (mAb 3E10). Immunization of lupus mice with mAb 3E10 inhibited production of native anti-DNA antibodies, suppressed development of lupus kidney disease (nephritis), and induced production of anti-anti-DNA (anti-Id) antibodies. mAb 1C7 bound F(ab')2 fragments of mAb 3E10, and it bound other murine anti-DNA mAb, but not murine mAb or polyclonal serum antibodies unreactive with DNA. Moreover, binding of mAb 1C7 anti-Id to mAb 3E10 was inhibited by DNA, suggesting anti-Id binding within or near the binding site for DNA. Furthermore, mAb 1C7 bound serum IgG immunoglobulins from 9/12 patients with lupus nephritis and serum anti-DNA antibodies compared to only 3/12 SLE patients with comparable serum levels of anti-DNA antibodies, but without nephritis (p = 0.04), and only 1/53 SLE patients without serum anti-DNA antibodies, 0/49 patients with rheumatoid arthritis, and 1/47 healthy subjects (p less than 0.001). These results provide evidence that mAb 1C7 identifies a conserved Id associated with anti-DNA antibodies in murine and human SLE and may be useful as a structural probe to characterize pathogenic anti-DNA antibodies in SLE. | |
| 2112196 | Inhibitory effects of gold sodium thiomalate on the proliferation and interferon-gamma ind | 1990 Apr | Our study was undertaken to investigate the effects of gold sodium thiomalate (GSTM) on the proliferation and HLA-DR antigen expression of human umbilical vein endothelial cells (EC). The proliferation of the EC was determined by 3H-thymidine incorporation into the EC. The expression of HLA-DR antigen on the surface of the EC was detected by an indirect immunofluorescent method using a fluorescent flow cytometer. When GSTM was added at the start of the EC culture, GSTM at a low concentration could inhibit the proliferative response of the EC to endothelial cell growth supplement. Furthermore, when the EC were cultured with recombinant interferon-gamma (rIFN-gamma) and GSTM, GSTM was also able to suppress the HLA-DR antigen expression on the surface of EC induced by rIFN-gamma. On the time-kinetic study of the effects of GSTM on the HLA-DR antigen expression induced by rIFN-gamma, the pretreatment of GSTM was able to suppress the HLA-DR antigen expression, whereas GSTM did not affect the HLA-DR antigen expression already induced by rIFN-gamma. Our findings suggest that the therapeutic effects of gold compounds in patients with rheumatoid arthritis may be attributed to the interference of the proliferation and HLA-DR antigen expression of the EC. | |
| 2312159 | A human fetal monoclonal DNA-binding antibody shares idiotypes with fetal and adult murine | 1990 Mar | A human DNA-binding monoclonal antibody was produced by fusing the hepatocytes from a 12-week-old human fetus with the lymphoblastoid cell line GM 4672 using polyethylene glycol. This antibody, designated BEG 2, binds to single-stranded (ss) DNA but also binds to double-stranded (ds) DNA, poly(dT), polyI and poly(ADP-ribose), but not to RNA, cardiolipin or K-30. The binding of BEG 2 to these polynucleotides can be inhibited by incubation with polynucleotides in the fluid phase. A rabbit polyclonal anti-idiotype was raised, and using this reagent it was shown that the BEG 2 idiotype is present in normal human serum (7%), systemic lupus erythematosus (SLE) sera (8%) and rheumatoid arthritis sera (23%). The extent of idiotypic sharing between BEG 2 and murine monoclonal DNA-binding antibodies, in particular monoclonal antibody (mAb) 423 (derived from a 15-day-old fetal MRL/Mp-lpr/lpr mouse) and mAb 402 (derived from an adult MRL/lpr mouse), was also investigated. Using a competition ELISA, it was shown that preincubation of BEG 2 with rabbit anti-423 and rabbit anti-402 inhibits the binding of BEG 2 to DNA, and the binding of 402 to DNA by anti-BEG 2 and anti-423. These data suggest that mAb BEG 2, 423 and 402 share common idiotypes, that autoreactivity is present in early fetal life, and that autoantibodies may be encoded for by germline genes, which have been conserved through evolution. | |
| 2183533 | Autoantibodies to insulin do appear in non-diabetic patients with autoimmune disorders: co | 1990 Mar | Insulin- and anti-immunoglobulin-antibodies have been recently reported in pre-diabetic subjects: the former has been proposed as a predictive marker of Type I diabetes in non-diabetic-subjects. To evaluate the diabetes-related specificity of these antibodies, the presence of insulin autoantibodies, using a recently developed and highly sensitive competitive radioimmune assay, and of anti-immunoglobulin antibodies together with that of immune complexes and of other autoantibodies has been investigated in patients with organ- or non-organ-specific autoimmune diseases. One hundred and eleven serum samples were assayed from patients with Graves' disease, primary hypothyroidism, chronic autoimmune thyroiditis, Addison's disease, chronic autoimmune hepatitis, pernicious anemia, lupus erythematosus, and rheumatoid arthritis, together with 45 serum samples from normal subjects. From patients with autoimmune diseases, 32.4% of all sera revealed values of insulin autoantibodies above the limit of positivity (p less than 0.001); anti-immunoglobulin antibodies were present in 4.1% of patients (NS); immune complexes were found in 19.5% (NS) of all patients, but in 38% of patients with Graves' disease and chronic hepatitis (p less than 0.02). There was a trend for multiple autoantibody positivity to be associated with high levels of insulin autoantibodies (p less than 0.05). Thus, whereas contrary to expectation anti-immunoglobulin antibodies are not associated with non-diabetes-related autoimmune diseases, increased humoral immunoresponsiveness to endogenous insulin appears to be related to autoimmunity in general rather than restricted to Type I diabetes. | |
| 2663276 | The health effects of oral contraceptives: misperceptions, controversies, and continuing g | 1989 Jun | ||
| 2503443 | Inhibition of human platelet aggregation and secretion by ant venom and a compound isolate | 1989 Apr | Venom from the tropical ant, Pseudomyrmex triplarinus, has activity against rheumatoid arthritis. Since platelets are involved in inflammatory responses, they were employed to study the effects of venom on prostaglandin-dependent human platelet aggregation and secretion. The assay is very sensitive and uses microliter volumes, which makes it useful as a screen during isolation and characterization of venom components. Whole venom inhibited arachidonic acid- and U46619-induced platelet aggregation with IC50s of 45 and 39 micrograms/ml, respectively. This suggested that venom prevented the action of prostaglandins. Pure venom was fractionated by gel filtration and at least three materials with antiplatelet activity were detected. The smallest component (factor F) was most active and was purified by additional molecular filtration and characterized by UV absorbance, thin-layer chromatography, nuclear magnetic resonance spectra, and activity to platelets. Factor F was identified as adenosine, which is known to stimulate platelet adenylate cyclase and has not been previously reported to be a component of insect venom. | |
| 2500276 | Modulation of monocyte complement synthesis by lymphocytes and lymphocyte-conditioned medi | 1989 Apr | Culture supernatants from mitogen- and antigen-stimulated human peripheral blood lymphocytes (PBL), stimulated synthesis of the second complement component (C2) by human monocytes, but not as effectively as the stimulated PBL themselves, which adhered to the monocytes and caused marked spreading. In contrast to PBL, lymphocytes isolated from the synovial membranes (SML) of patients with rheumatoid arthritis and their culture supernatants were able to stimulate C2 synthesis without exposure to mitogens or antigens. Depletion of B and T populations showed that T cells were responsible for stimulation of C2 synthesis. Further studies of synthesis rates of C2, C3 factor B (B), C1 inhibitor, and properdin (P) were undertaken, and it was found that lymphocytes and their supernatants increased synthesis of C2, B and C1 inhibitor, and reduced synthesis of C3 and P. This profile of activity was identical to that produced by the addition of recombinant gamma-interferon (rIFN-gamma) to the cultures. Furthermore the addition of a monoclonal antibody to rIFN-gamma to cultures abrogated the effects of rIFN-gamma, and almost completely reversed the effects of lymphocytes and their supernatants. Thus it appears that gamma-interferon is the lymphocyte product which is responsible for the modulation of monocyte complement synthesis. The results of studies with synovial membrane lymphocytes raise the possibility that this process occurs in vivo. Monocyte C2 had a higher specific functional activity (SpFA) than serum C2 isolated from serum or C2 produced by HepG2 cells. Monocyte C2 formed a C3 convertase which had a longer half-life than that found with both serum C2 or HepG2 C2. Thus monocyte C2 behaves like oxidized C2. Monocytes exposed to rIFN-gamma, lymphocytes or lymphocyte-conditioned medium (LCM) produced C2 which had an even higher SpFA. Although antibody to IFN-gamma prevented any increase in C2 synthesis in monocyte cultures containing lymphocytes or LCM, C2 SpFA was still increased. Thus a second lymphocyte product is responsible for this 'oxidation' effect. This production of 'oxidized' C2 by monocytes and further 'oxidation' by the action of either lymphocytes or gamma-interferon might play a significant role in the perpetuation of complement activation at sites of inflammation. | |
| 3218609 | D-penicillamine metabolism in an in-vivo model of inflamed synovium. | 1988 Dec | Oxidation to disulphides is the chief metabolic transformation of D-penicillamine (D-pen) in patients with rheumatoid arthritis. Oxidation also occurs in many biological fluids in-vitro. Reduction of oxygen species may accompany the oxidation of D-pen under appropriate conditions and may mediate the anti-rheumatic action of D-pen. The transformation of D-pen therefore was examined in an in-vivo model of inflamed synovium. Subcutaneous air-pouches of groups of rats were treated with saline, 10% serum or 10% zymosan activated serum (ZAS). The transformation of D-pen to low molecular weight (LMW) metabolites and protein conjugates within the pouch was then assessed. The concentrations of total protein were significantly higher in the serum and ZAS-treated groups than in the saline-treated group and the inflammatory cell counts were significantly higher in the ZAS-treated group than in either of the other groups, as expected. D-pen oxidised rapidly to LMW metabolites and smaller amounts of D-pen-protein conjugate (D-pen-protein) in the air pouches of all animals. The rates of oxidation to LMW metabolites were greater in the ZAS-treated animals than the saline-treated group (p less than 0.005). The concentrations of D-pen-protein conjugate were also greater for the serum-treated and ZAS-treated animals than for the saline controls (p less than 0.005 in each case) at all times. Oxidation of D-pen therefore occurs at this site of inflammation and is influenced by local conditions. This may be important to understanding the forms in which D-pen exists in inflamed synovial joints and the way it may exert its antirheumatic activity. | |
| 3313660 | Interference of cartilage surface with interaction of granulocyte elastase with alpha 1-pr | 1987 | Synovial fluids of patients suffering from rheumatoid arthritis contain elevated levels of granulocyte (PMN) elastase in complex with alpha 1-proteinase inhibitor (alpha 1-PI), whereas free-elastase activity is usually not detectable. This absence of free enzymatic activity in joint effusions has cast some doubt on the pathophysiological relevance of PMN elastase in inflammatory joint destruction. Our in vitro experiments using bovine nasal cartilage demonstrate that incubation with elastase and alpha 1-PI in equimolar concentrations to or even in excess of the serum proteinase inhibitor resulted in significant tissue destruction as assessed by histological staining for proteoglycans, release of uronic acid from the matrix and loss of mechanical stability. Though in the supernatants containing alpha 1-PI, free-elastase activity was not detectable, immunofluorescent staining for elastase evidenced penetration of the enzyme into the matrix. Simultaneous measurements of the incubation media employing a sandwich enzyme-linked immunoadsorption assay (ELISA) revealed PMN elastase in complex with alpha 1-PI but without correlation to the parameters of tissue degradation. In comparison with the results obtained using the chromogenic substrate Suc-Ala-Ala-Ala-pNA (SAPA) for titration of alpha 1-PI against elastase, the employment of cartilage matrix showed that a fourfold increase in inhibitor concentration was necessary to achieve 100% enzyme inhibition. Hence, cartilage surface obviously interferes with the interaction between alpha 1-PI and elastase. Measurements of elastase-inhibitor concentrations or free enzymatic activity in synovial fluid seem to have limited value in predicting cartilage destruction. | |
| 3490288 | Heterogeneity of large granular lymphocyte proliferations: delineation of two major subtyp | 1986 Nov | Two major types of lymphocytosis of large granular lymphocytes (LGLs) were observed. The proliferating LGLs in each type had distinct immunophenotypes, functional characteristics, and probably belonged to different cell lineages. The more common form (Type A) consisted of cells derived from the T cell lineage and had the T suppressor/cytotoxic phenotype (T11+, T3+, T8+). The expression of the Leu 7 and HLA-DR antigen was variable. These cells did not have natural killer (NK) function but showed a variable degree of antibody-dependent cell-mediated cytotoxic (ADCC) activity. Neutropenia was invariably present and rheumatoid arthritis and autoantibodies were frequent associations. These lymphocytes had many similarities to the major type of LGLs present in normal adult bone marrow. The other type of LGL lymphocytosis (Type B) consisted of cells lacking the antigens T3 and T8 but expressing M1 and NKH1. These cells possessed strong NK and ADCC activity but their cell lineage was not clear. Neutropenia and autoimmune phenomena were not detected. The cytochemical characteristics of the LGL granules from both types of patients were similar but differences in ultrastructure were observed. LGLs from Type B patients proliferated in the presence of Interleukin 2 (IL-2) and 12-O-tetradecanoyl-phorbol-13 acetate (TPA). Significant changes in their basic T11+, T3-, T8- phenotype were not observed. IL-2 and TPA, however, had profound influence on the NK function of the cells with enhancement in the case of IL-2 and marked suppression when stimulated by TPA. | |
| 3484437 | The IgG detected in the C1q solid-phase immune-complex assay is not always of immune-compl | 1986 Jan | The properties of the solid-phase C1q immune-complex assay as well as the nature of the IgG detected by this assay in patients' sera were investigated. Aggregated IgG was used as a model for immune complexes. Aggregated IgG bound to solid-phase C1q was detected by 125I-anti-IgG. Fluid-phase C1q (either in normal human serum or purified) neither inhibited the binding of aggregated IgG to solid-phase C1q nor dissociated bound aggregated IgG from the solid-phase C1q. Therefore, we concluded that the solid-phase C1q has a higher affinity for aggregated IgG than the fluid-phase C1q, probably because of the polymerization of the solid-phase C1q. To get more insight into the nature of the IgG detected by the C1q solid-phase assay in patients' sera, we investigated whether C4 and/or C3 were present on it. With the use of 125I-anti-C4 and 125I-anti-C3 instead of 125I-anti-IgG, C4 and C3, respectively, were easily detected on the aggregated IgG that had bound to the solid-phase C1q. The lower limit of detection of these assays was 30 micrograms aggregated IgG/ml of normal human serum. Sera of patients suffering from rheumatoid arthritis and systemic lupus erythematosus were tested with these assays and, despite positive results with 125I-anti-IgG, no positive results were obtained with either 125I-anti-C4 or 125I-anti-C3. So, on the IgG detected by the C1q solid-phase assay in patients' sera, neither C4 nor C3 are present. Furthermore, in five of the six sera tested, this IgG sedimented as monomeric IgG. Therefore, it seems unjustified to refer to this IgG as circulating immune complexes. | |
| 1864055 | Uncemented total hip arthroplasty. Prospective analysis of the tri-lock femoral component. | 1991 Aug | Fifty consecutive hip disease patients (56 hips) with total hip arthroplasties (THA) utilized the uncemented Tri-Lock femoral component. Forty-five patients (51 hips) were followed for an average of 46 months (range, 24-66). Forty-two patients (47 hips) were followed with clinical examination and roentgenographs, three (four hips) by telephone interview, four (four hips) were deceased, and one (one hip) was lost to follow-up evaluation. The diagnoses included osteoarthritis (30 hips), avascular necrosis (11 hips), juvenile rheumatoid arthritis (two hips), and degenerative joint disease secondary to childhood hip disorder (four hips). Of 47 hips, 34 were graded excellent, seven good, three fair, and three poor using the Harris hip score. The incidence of thigh pain was 19% at one year, but only 6% at final follow-up evaluation. Limp persisted in 19% of the patients. Of the three patients with four hips contacted by telephone, two had slight pain and two had no pain. The roentgenographic results found an alarming 38% incidence of varus shift of the components, relative to their preoperative position. The presence of a varus shift did not adversely affect the clinical results. Early experience with the Tri-Lock femoral component shows results comparable to those reported in the literature. The high incidence of femoral component shift, presumably because of geometry of the stem is of concern. Longer follow-up evaluation will be necessary to determine the fate of these uncemented THA operations. | |
| 2302835 | Liver membrane antibodies (LMA) recognize a 26-kD protein on the hepatocellular surface. | 1990 Jan | Sera from 82 patients with chronic inflammatory liver diseases and from patients with systemic lupus erythematosus (SLE), rheumatoid arthritis (RA) and Hashimoto's thyroiditis were studied by immunoblotting against purified liver plasma membranes (LPM) and soluble liver protein (SLP) fractions from different species after previous separation by SDS-PAGE. Eighteen of 19 sera with LMA of IgG type in immunofluorescence assay and six LMA-negative sera (three sera from patients with RA) showed antibodies of the IgG or IgM classes against a protein with a molecular weight of 26 kD which was present in LPM and SLP fractions from rats, rabbits, pigs and humans. The reaction with 26-kD liver protein did not correlate with other known autoantibody-antigen systems. All sera were negative in the 26-kD region with liver mitochondria, liver microsomes and soluble proteins of kidney (with one exception), heart and gut from the rat. The 26-kD protein was purified by affinity chromatography on immobilized anti-26-kD protein antibodies from patients, eluted from the 26-kD band of immunoblots. Studies with purified 26-kD liver protein and with SLP as antigens after separation in two-dimensional electrophoresis confirmed that patient serum and experimental rabbit antiserum react with the same protein. Eluted patient antibodies and rabbit antisera showed a linear fluorescence pattern on isolated hepatocytes from rat and rabbit. The data indicate that one of the target antigens of LMA is a species-nonspecific 26-kD protein located on the hepatocellular surface. | |
| 2207443 | Chronically inflamed tissue activates plasma mediators of vascular permeability. | 1990 | 1. After inflammation was induced in the foot-pad of rats with nistatin or BCG, injection of "non-activated" homologous plasma at the inflamed site caused a significant increase in the vascular permeability of the lesions (Evans blue test), which was more intense in older lesions, increasing from 7.83 +/- 1.11 to 8.70 +/- 1.18 (nistatin, 4 and 21 days) and 7.30 +/- 0.66 to 7.54 +/- 0.80 (BCG, 4 and 21 days). 2. Steroidal (acetyltriamcinolone, 2 mg/kg) and non-steroidal (indomethacin, 25 mg/kg) [corrected] anti-inflammatory drugs markedly decreased this effect on 14-day old lesions induced by nistatin plus "non-activated" plasma (2.37 +/- 0.10 for acetyltriamcinolone treatment vs 8.15 +/- 1.22 for untreated animals; 3.34 +/- 0.41 for indomethacin treatment vs 8.15 +/- 1.22 for untreated animals) and BCG plus "non-activated" plasma (1.67 +/- 0.11 for acetyltriamcinolone treatment vs 10.27 +/- 0.52 for untreated animals; 5.87 +/- 0.35 for indomethacin treatment vs 9.14 +/- 0.23 for untreated animals). 3. These data suggest that an increase in exudation in chronic lesions might result in "reactivation" of the process as observed clinically, for example, in rheumatoid arthritis in man. | |
| 1972874 | Cytokines and osteoporosis. | 1990 | Bone remodeling is controlled by systemic factors such as parathyroid hormone (PTH), calcitonin (CT), and 1,25(OH)2 vitamin D and by local factors including cytokines and growth factors such as IL-1, IL-2, TNF alpha, TGF beta, IFN alpha, and IFN gamma. Derangement of such control mechanisms leading to an imbalance between osteoclastic bone resorption and osteoblastic bone formation could cause osteoporosis. Conditions associated with immune dysfunction such as aging, corticosteroid therapy, and rheumatoid arthritis are associated with osteoporosis, which is also more common in females than in males, like most of the autoimmune-collagen diseases. Peripheral lymphocyte subsets CD4/CD8 were higher in patients with senile osteoporosis than in the age-matched controls, and returned to normal after 1 month of 1 alpha(OH)vitamin D3 treatment. On multiple regression analysis of histomorphometric data and lymphocyte subsets, a negative correlation was found between CD4 lymphocytes and bone resorption. High CD4 is thus associated with a low level of osteoclastic bone resorption or low turnover osteoporosis. Plasma interferon reflecting macrophage function decreased with advance in age and increased in response to 1 alpha(OH)D3 treatment. As one of the immunoregulators, vitamin D tends to stimulate the macrophage-natural killer system and suppress the lymphocyte system, stimulating TGF beta and TNF alpha activity. Senile osteoporosis of low turnover thus appears to be associated with vitamin D deficiency, low macrophage function, high CD4 lymphocyte proportion, low IL-1 and high IL-2 activity, low IFN alpha and high IFN gamma activity, and low TGF beta and TNF alpha activity. Treatment with vitamin D derivatives tends to reverse these changes. | |
| 2725926 | [Sulglicotide in the prevention of gastric disease induced by NSAID. Double-blind controll | 1989 Jan | Non-steroidal anti-inflammatory drugs, essential for the treatment of rheumatic diseases, are frequently associated with significant adverse effects on the integrity of the gastrointestinal mucosa. Sulglicotide (S), a natural product, has been found to possess gastromucosal protective properties. Aim of the present study was to evaluate whether (S) 200 mg t.i.d prevented or reduced the severity of gastric and/or duodenal mucosal injury induced by Diclofenac. A total of 30 patients with either rheumatoid arthritis (RA) or osteoarthritis (OA) who required NSAID therapy for at least 8 weeks were enrolled into a double-blind randomized placebo-controlled study. The main criteria for entry into the trial was the absence of gastrointestinal symptoms, and gastric/duodenal lesions assessed by endoscopy. At the end of the treatment endoscopy and relative symptoms were assessed. Six out of 15 patients, in both groups of treatment developed mucosal injury, but only in the placebo group the gastric damage was important (ulcer and petechiae) while in the group (S) we observed only hyperemia of the gastric mucosa. These preliminary data indicate the usefulness of Sulglicotide in preventing or reducing mucosal injury from NSAID treatment. | |
| 2681034 | Phase IV evaluation of piroxicam in acute and chronic painful inflammatory disorders: an I | 1989 | We report the first phase-IV computerized study on Piroxicam in Indian patients. Comprehensive subject record sheets were distributed to 1,000 doctors. Piroxicam at 20 mg/day was given to patients categorized as suffering from rheumatoid arthritis (RA), osteoarthritis (OA), cervical spondylitis (CS), ankylosing spondylosis (AS), soft-tissue & other pains (ST) for up to 12 weeks. Assessments of pain, tenderness, swelling, range of movements, morning stiffness as well as the grip test and walking test, were made at 24 and 72 h, and 1, 4 and 8 weeks after therapy. All side-effects were noted. Data entry and statistical analysis (95% confidence interval) for proportions expressed as percentages) were handled by computer. A total of 174 doctors (17.4%) co-operated by giving data for 844 patients, consisting of the following cases: RA (306), OA (253), AS (52), CS (113) and ST (120). Piroxicam was found to be uniformly effective in the above disorders, a favourable response to the treatment being obtained in 82%-96% of the patients. The overall response rates (with 95% confidence interval in brackets) were 93% (91-95%) in pain, 93% (91-95%) in tenderness, 90% (80-93%) in swelling, 90% (87-92%) in range of movements and 86% (83-89%) in morning stiffness. The average duration of therapy ranged from 22 to 42 days. A total of 88 (10.4%) patients reported 224 incidences of side-effects, 91% of them being gastrointestinal, but no patient had ulcer or GI bleeding. In 1.9% of the patients, therapy was stopped due to an adverse reaction.(ABSTRACT TRUNCATED AT 250 WORDS) | |
| 2976831 | Chronic upper limb pain syndrome (repetitive strain injury) in the Australian workforce: a | 1988 Nov | The epidemic of chronic upper limb pain is the most important and controversial issue in industrial rheumatology in Australia today. Two hundred and twenty-nine consecutive patients referred with chronic upper limb pain which had been labelled "repetitive strain injury" or "overuse syndrome" were assessed according to a protocol designed to give insight into the questions: Is the pain genuine or falsely reported, i.e., malingering? If genuine is it due to a physical injury, a pain syndrome, or a mixture of both? Twenty-nine patients fulfilled criteria for specific rheumatological diagnoses (fibrositis 15, rotator cuff syndrome 3, rheumatoid arthritis 3, cervical referred pain 3, lateral epicondylitis 2, de Quervain's tenosynovitis 1, carpal tunnel syndrome 1, and psoriatic monoarthritis 1). In the remaining 200 (mean age 37 years, range 19-58, 91.5% female) many different pain patterns and nonspecific associated symptoms were recorded. Eighty-nine percent had greater than or equal to 2 Smythe tender points, 1.5% had 1 tender point, and 9.5% had no tender point. Diffuse pain and greater than 7 tender points is sufficient to diagnose fibrositis, and localized pain and a smaller number of tender points strongly suggests a genuine chronic rheumatic pain syndrome. Stress, personal susceptibility and poor motivation appeared important in some cases. The liberal workers' compensation system, early labeling as repetitive strain injury, and social acceptability appeared important in the development of the epidemic. | |
| 3142227 | In vivo effects of aurothioglucose and sodium thioglucose on rat tissue sulfhydryl levels | 1988 Aug | The active component of aurothioglucose (ATG) in effecting changes in plasma sulfhydryl (SH) levels and plasma SH reactivity with 5,5'-dithiobis-(2-nitrobenzoic acid) (DTNB) was determined. These two measurements are applied clinically to rheumatoid arthritis patients undergoing chrysotherapy. Normal rats were injected intramuscularly daily for seven days with 30 mumol of either ATG or sodium thioglucose (STG)/kg body wt or with an equivalent volume of the carrier, 0.05% benzyl alcohol. ATG but not STG significantly increased total SH levels in plasma, liver, and kidney. The seven-day treatment with ATG significantly increased glutathione levels in kidney but not in liver or plasma. Thus, gold(I) rather than thioglucose was the active moiety that affected SH levels in ATG-injected rats. In vivo, gold(I) was also the active moiety that stimulated plasma SH reactions with DTNB at pH 7.4, since injection of ATG but not STG stimulated the SH reactivity in fresh plasma. In vitro, ATG increased the rate of plasma reaction with DTNB at pH 7.4, thus, gold(I) ions acted as a catalyst in the SH-disulfide exchange reaction. This study demonstrates that gold(I) but not its thiol ligand strongly interacts with protein SH groups in the rat tissues. Such an interaction may play an important role in the biological actions of gold. |