Search for: rheumatoid arthritis methotrexate autoimmune disease biomarker gene expression GWAS HLA genes non-HLA genes
| ID | PMID | Title | PublicationDate | abstract |
|---|---|---|---|---|
| 1882666 | The infected knee arthroplasty. A 6-year follow-up of 357 cases. | 1991 Aug | The incidence of deep infection after 12,118 primary knee arthroplasties performed in Sweden from October 1, 1975 through 1985 with a median follow-up of 6 years was 1.7 percent for arthrosis and 4.4 percent for rheumatoid arthritis. Risk factors for infection were large prostheses, postoperative wound-healing complications, rheumatoid arthritis, a prior deep infection, and skin infections. We have analyzed the treatment of 357 knee arthroplasties with a deep infection. Systemic antibiotics alone were primarily used in 225 knees, with healing of the infection in 44 knees, 20 of which had a functioning prosthesis at the final follow-up; the treatment did not compromise later revision surgery. Soft-tissue surgery was used in 154 knees--37 healed, 15 of which had a functioning prosthesis. Resection arthroplasty resulted in healing of the infection in 11 of 22 knees. Revision arthroplasty was performed in 107 knees, with eventual healing of the infection in 81 knees, 36 of which had a functioning prosthesis; there were no differences in the outcome of one-stage and two-stage procedures. Arthrodesis was attempted in 135 knees, with eventual healing of the infection in 120 knees and fusion in 105. Twenty-two patients were amputated. Thus, the infection healed in 315 knees (88 percent), but only 71 (20 percent) recovered with a functioning prosthesis, and 8 patients died of the infection. Attention should therefore focus on prophylactic measures directed towards the soft-tissue problems--by avoiding conflicting skin incisions, by gentle handling of the periarticular soft tissues, by avoiding the use of constrained prostheses and oversized compartmental prostheses, by letting wound healing take priority over motion in knees with compromised soft tissues, and by using prophylactic antibiotic treatment for skin ulcers until these have healed. | |
| 2428883 | Apoptotic keratin bodies as autoantigen causing the production of IgM-anti-keratin interme | 1986 Oct | The presence of numerous keratin bodies in the upper dermis is a characteristic finding in skin lesions of patients with various dermatoses such as cutaneous graft-versus-host disease, lichen planus, or chronic discoid lupus erythematosus. These keratin bodies are generated by apoptotic keratinocyte death, consist largely of keratin intermediate filaments (KIF), and are constantly covered with immunoglobulins, mainly IgM. Apoptosis is also thought to occur under physiologic conditions in the skin as it does in other organs, but keratin bodies are not frequently reported as being found in nonlesional skin. In order to assess the frequency of keratin bodies in normal skin, we examined serial sections of 10 normal human skin specimens and 5 dermal sheets prepared from normal human skin for the presence of keratin bodies. They were visualized by direct immunofluorescence using a fluorescein isothiocyanate (FITC) rabbit antihuman IgM conjugate. In addition the KIF origin of keratin bodies was demonstrated by a double-staining immunofluorescence procedure using a FITC-conjugated rabbit antihuman IgM followed by a mouse monoclonal antibody against keratin and a sheep antimouse immunoglobulin conjugated with Texas Red. One specimen was also examined for keratin bodies at the ultrastructural level. In serial sections, all 10 normal human skin specimens had numerous keratin bodies as assessed by visualization of globular IgM deposits. Evaluated on dermal sheets, the number of keratin bodies ranged from 39-262 per mm2. Nearly all keratin bodies also stained with the antikeratin antibodies. Ultrastructurally the remarkable number of keratin bodies, which consist of filaments measuring approximately 10 nm in diameter or of more granular material, in normal human skin was confirmed. In order to investigate the capacity of KIF material in keratin bodies to function as autoantigen, we examined the sera of the 10 skin donors and, in addition, of 30 normal healthy individuals and 10 patients with rheumatoid arthritis for the occurrence and specificity of IgM-anti-KIF autoantibodies by an enzyme-linked immunosorbent assay and by immunoblot. IgM-anti-KIF autoantibodies were found in all 50 test sera. In the majority of the sera the specificity of these autoantibodies included the 51 kD and the 58 kD KIF protein, which are constituents of KIF in keratin bodies and basal keratinocytes. Quantitatively, the antibody activity of the IgM-anti-KIF autoantibodies varied from serum to serum, being highest in the sera of patients with rheumatoid arthritis.(ABSTRACT TRUNCATED AT 400 WORDS) | |
| 3541728 | A century of American rheumatology. | 1987 Feb | In reviewing the development of rheumatology in the United States, I begin with the understanding of rheumatic diseases in the previous century and then consider subsequent scientific and organizational events that were important in the creation of rheumatology as a recognized medical specialty. The perception had to evolve that rheumatic diseases can be analyzed beyond their gross clinical description and that effective therapy is possible. The virtual coincidence of the discoveries of the rheumatoid factor, the lupus erythematosus cell, and cortisone in 1948-49 satisfied these requirements. The publicity that was generated is considered to have been most responsible for the unusually abrupt recognition of rheumatology as a specialty. | |
| 2324975 | Sinus tarsi syndrome in a patient with talipes equinovarus. | 1990 Apr | The literature reports that 70% of the cases of sinus tarsi syndrome are post-traumatic, following an inversion sprain, and that 30% result from inflammatory disorders, such as rheumatoid arthritis, ankylosing spondylitis, and gouty arthritis. However, in the case presented, talipes equinovarus deformity and sinus tarsi syndrome coexisted. One of the corrective goals in the management of the talipes equinovarus deformity is the realignment of the articulation between the medial plantarly deviated talar head and the anteromedial segment of the calcaneus. The calcaneus must be rotated from a plantarflexed position into a dorsiflexed position. The posterior tubercle will be moved down and in, with the anterior process moved up and out away from the talar head. By correcting the plantarflexed varus attitude of the calcaneus, it is put in a valgus position that often closes down the sinus tarsi upon weightbearing. This compression may result in pain over the lateral aspect of the midfoot with hindfoot instability, as seen in the case presented. As a result of the abnormal anatomical relationship of the talus and calcaneus, the patient developed severe pain in the sinus tarsi. Based on the medical history and present postoperative results, the authors find a long-term sequela of talipes equinovarus deformity to be sinus tarsi syndrome. | |
| 3126745 | Inhibition of in vitro proliferative response of cultured T lymphocytes to interleukin-2 b | 1988 Feb | Gold sodium thiomalate (GST), in concentrations attainable during chrysotherapy for rheumatoid arthritis, significantly inhibited the proliferative responses of cultured T cells stimulated by interleukin-2 (IL-2). The observed suppression was not related to altered kinetics, cell death, or interference with the binding of IL-2 to cell surface receptors. It appeared that GST affected an early step in the proliferative process, since maximum inhibition was obtained by the addition of GST within 4 hours of stimulation; progressive reduction of suppression was observed when GST was added later. Significant inhibition occurred when cultured T cells were preincubated for 24 hours with GST and washed prior to IL-2 stimulation, although the degree of suppression was decreased. Thus, inhibitory activity was not dependent on the continued presence of GST throughout culture. These findings suggest that there is a direct inhibition of T lymphocytes by GST, which may be important in immunomodulation by gold compounds. | |
| 3499655 | [Loss of digital substance in rheumatic diseases. Apropos of 43 cases]. | 1987 Jul | The authors briefly summarize 16 cases involving digital necrosis observed in the course of rheumatic disorders (3 carpal tunnel syndromes, 2 cases of panarteritis, 2 of rheumatoid arthritis, 2 of lupus erythematosus, 2 of scleroderma, 2 of dermatomyositis, 1 of adult form of Still's disease, 1 of gout, and 1 case of cryoglobulinemia). In addition the case reports of 129 patients with connective tissue disease were reviewed (74 cases of disseminated lupus erythematosus, 43 of scleroderma, and 12 mixed connective tissue disorders). Soft tissue destruction of digits was observed in 15, 39 and 25% of these patients respectively, and true tissue necrosis of varying extent in 7, 9 and 0% of these cases. The incidence and pathogenic mechanisms responsible for these disorders and lesions were discussed. | |
| 2060158 | Local immunoglobulin production in synovial tissue in patients with Lyme borreliosis. | 1991 Mar | A study was made to find out whether immunoglobulins are produced locally in synovial tissue in patients with Lyme borreliosis. Synovial fluid specimens from six patients with Lyme borreliosis were compared with those from 25 patients with rheumatoid arthritis, psoriatic arthritis, unspecified oligoarthritis or arthrosis (control group). Agarose electrophoresis revealed local oligoclonal IgG and IgM bands in the synovial fluid of two patients with Lyme borreliosis, but no local bands were observed in the control group. An index for local synthesis of immunoglobulins in synovial fluid was calculated in analogy with the IgG index for cerebrospinal fluid. The two patients with Lyme borreliosis in whom oligoclonal bands were seen in the synovial fluid showed the highest synovial fluid IgG indices and the highest concentrations of specific IgG antibodies against Borrelia spirochetes in synovial fluid. The presence of local oligoclonal immunoglobulin bands and a high synovial fluid IgG index suggest that immunoglobulins are produced locally within the synovial tissue in some patients with Lyme borreliosis. The increase in immunoglobulins may be a response to a local invasion of Borrelia spirochetes or may represent an immune reaction which continues after the spirochetes no longer are viable. | |
| 3172101 | Jaccoud's arthritis and panvasculitis in the hypocomplementemic urticarial vasculitis synd | 1988 | We describe a woman who developed hypocomplementemic urticarial vasculitis syndrome, and who demonstrated 2 rare features. As well as vasculitis of the small cutaneous vessels, vasculitis affected the femoral, cystic and renal arteries. Her arthritis led to subluxation of the metacarpophalangeal joints, without radiological evidence of rheumatoid-like erosions. This deformity could be passively corrected, and therefore conformed to the pattern described by Jaccoud. | |
| 2467628 | Serum IgA, acute phase proteins, and glycosylation of alpha 1-acid glycoprotein in ankylos | 1989 Feb | Several investigators have suggested that gastrointestinal inflammation has a role in the pathogenesis of ankylosing spondylitis. To test this hypothesis markers of gastrointestinal immunostimulation, as manifested by serum IgA concentrations, were compared with serum markers of inflammation, as manifested by acute phase proteins. Serum samples from 45 unrelated Caucasian patients with ankylosing spondylitis (AS) were tested for correlation of serum IgA and six acute phase proteins: C reactive protein (CRP), alpha 1-antitrypsin, alpha 1-antichymotrypsin, caeruloplasmin, alpha 1-acid glycoprotein (AGP), and haptoglobin. Serum IgA was shown to be significantly positively correlated with four of these six acute phase proteins: CRP (r = 0.58, p less than 0.001), alpha 1-antitrypsin (r = 0.29, p less than 0.05), AGP (r = 0.61, p less than 0.01), and haptoglobin (r = 0.58, p less than 0.001), suggesting that gastrointestinal immunostimulation does have a role in the pathogenesis of inflammation in AS. In addition, the microheterogeneity of the pattern of glycosylation of AGP, expressed as reactivity coefficients, was examined. The AGP reactivity coefficient has been shown to increase in infection, remain the same in systemic lupus erythematosus, and decrease in rheumatoid arthritis. It was found that the AGP reactivity coefficient was significantly decreased in patients with AS as compared with healthy controls (p less than 0.006). As recent studies have indicated that patterns of glycosylation reflect intrahepatocellular biosynthetic processes induced by cytokines our data suggest that cytokine-hepatocellular mechanisms in AS may be similar to those occurring in rheumatoid arthritis, but different from those in systemic lupus erythematosus or infection. | |
| 3036026 | Retinoid modulation of collagenase production by adherent human mononuclear cells in cultu | 1987 May | Previous observations have suggested that retinoids might be useful for the treatment of rheumatoid arthritis. In this study we examined the effects of various retinoids on collagenase production by adherent human peripheral blood mononuclear cells in culture. We have previously shown that these cells, consisting predominantly of monocyte-macrophages, actively synthesize and secrete collagenase upon stimulation with concanavalin A. The cells were incubated in serum free medium with all-trans-retinoic acid, 13-cis-retinoic acid, all-trans-retinal, or Ro 10-9359 (trimethylmethoxyphenyl retinoic acid ethyl ester) for up to 72 hours, and the collagenase activity was determined with [3H]proline labelled type I collagen as substrate. The incubation of mononuclear cells with all-trans-retinoic acid in the concentration range 10(-7)-10(-5) mol/l resulted in a dose dependent inhibition of the collagenase production. All-trans-retinal was also a potent inhibitor, whereas 13-cis-retinoic acid and Ro 10-9359 in a concentration of 10(-5) mol/l had a lesser effect. Control experiments indicated that the inhibition of collagenase production by all-trans-retinoic acid did not result from inhibition of total protein synthesis nor could it be explained by induction of an inhibitory molecule. These results indicate that retinoids with distinct structural features can inhibit collagenase production by monocyte-macrophages, and suggest a role for retinoids in the treatment of rheumatoid arthritis. | |
| 2544599 | Heat shock of rabbit synovial fibroblasts increases expression of mRNAs for two metallopro | 1989 Jun | Two metalloproteinases, collagenase and stromelysin, are produced in large quantities by synovial fibroblasts in individuals with rheumatoid arthritis. These enzymes play a major role in the extensive destruction of connective tissue seen in this disease. In this study, we show that heat shock of monolayer cultures of rabbit synovial fibroblasts increases expression of mRNA for heat shock protein 70 (HSP-70), and for collagenase and stromelysin. We found that after heat shock for 1 h at 45 degrees C, the mRNA expression for HSP-70 peaks at 1 h and returns to control levels by 3 h. Collagenase and stromelysin mRNA expression is coordinate, reaching peak levels at 3 h and returning to control levels by 10 h. The increase in mRNA is paralleled by an increase in the corresponding protein in the culture medium. 3 h of heat shock at a lower temperature (42 degrees C) is also effective in inducing collagenase and stromelysin mRNAs. Concomitant treatment with phorbol myristate acetate (PMA; 10(-8) or 10(-9) M) and heat shock is not additive or synergistic. In addition, all-trans-retinoic acid, added just before heat shock, prevents the increase in mRNAs for collagenase and stromelysin. Our data suggest that heat shock may be an additional mechanism whereby collagenase and stromelysin are increased during rheumatoid arthritis and perhaps in other chronic inflammatory stress conditions. | |
| 2493048 | Heterogeneous effects of IFN-gamma in adjuvant arthritis. | 1989 Mar 1 | In an attempt to evaluate the role of IFN-gamma in autoimmune arthritis, we tested the effects of IFN-gamma and anti-IFN-gamma mAb (DB-1) in various phases of arthritis development in a rat model for rheumatoid arthritis; the adjuvant arthritis (AA) model, induced by immunization with CFA. In addition, the effects of IFN-gamma were tested in vitro on T cell clones derived from rats afflicted with AA. T cell clone A2b, which has been shown to be arthritogenic secreted low amounts of IFN-gamma and its Ag-specific proliferation was inhibited by IFN-gamma. In contrast, clone A2c, which can inhibit the development of AA, produced high amounts of IFN-gamma and its proliferation was increased by IFN-gamma. In vivo administration of IFN-gamma 24 h before CFA caused an enhancement of arthritis, whereas giving IFN-gamma 24 to 48 h after CFA suppressed the disease. Administration of IFN-gamma between day +4 to +12 or between day +12 to +24 increased the severity of the first phase of the disease, but had no effect later. Administration of DB-1 1 to 2 days before adjuvant or between day +4 to +8 substantially decreased the disease, whereas DB-1 given from day +12 to +24 significantly enhanced it. Taken together, these results illustrate the heterogeneity of IFN-gamma in autoimmune arthritis and suggest a rational explanation for the possibly conflicting reports regarding the role(s) and effects of IFN-gamma in autoimmune processes. The multistage nature of T cell-mediated autoimmune arthritis may be due to the predominance of distinct T cell populations at different stages of the disease. The differences in the biologic activities of these T cells may be due to their patterns of lymphokine production. | |
| 2066957 | Deforming arthropathy complicating primary biliary cirrhosis. | 1991 Apr | A 53-year-old woman with concurrent systemic lupus erythematosus (SLE) and primary biliary cirrhosis (PBC) developed a deforming but minimally symptomatic arthropathy. The simultaneous occurrence of SLE and PBC is believed to be rare. Moreover, destructive arthritis, in the absence of serum rheumatoid factor, has not been previously reported with either disease. We review the association of liver disease with arthritis and propose a possible mechanism to account for the severe joint destruction seen in our patient. | |
| 2070558 | Quantification of cross-reactive idiotype-positive rheumatoid factor produced in autoimmun | 1991 Jul | The aetiology of sustained autoantibody production in human autoimmune diseases is unknown. Evidence for structural similarities and common clonal origin among autoantibodies have been demonstrated through the expression of cross-reactive idiotype (CRI). In the present study we use four monoclonal antibodies (MoAbs) with specificity for non-overlapping CRI on human rheumatoid factor (RF) autoantibodies to define the structural features of polyclonal RF characteristic of patients with autoimmune rheumatic diseases. The pattern of CRI expression in the serum of 12 patients with rheumatoid arthritis (RA), eight with systemic lupus erythematosus (SLE) and 20 with primary Sjögren's syndrome and 34 normal individuals were determined in parallel with the level of IgM RF, IgA RF and autoantibodies to the cellular antigens SS-A, SS-B, Sm, nRNP and dsDNA and cryoglobulins. The results demonstrate significant elevation in the level of IgM and IgA expressing VHI (G6 and G8) and VHIII (B6 and D12) associated CRI in the serum of patients with autoimmune rheumatic diseases compared with normal individuals. These increases paralleled, but did not equal the increase in the level of immunoglobulins and RF. However, when expressed as proportion of immunoglobulin, only the VHI-associated CRI were significantly elevated in patients compared with normal individuals. The proportion of IgM RF expressing the VHI-associated CRI was higher in patients with Sjögren's syndrome compared with SLE and RA. Furthermore, the proportion of IgA RF expressing the G6 CRI was higher than G6+ IgM RF. These findings imply that different mechanisms contribute to RF production in autoimmune diseases. It is suggested that polyconal B cell activation is likely to be a contributing mechanism. However, such polyclonal activation is unlikely to be random since a selective elevation in the level of specific autoantibodies and VHI-associated CRI is observed. Furthermore, the data demonstrate that a proportion of autoantibodies in autoimmune diseases are immunoglobulin germline gene encoded. This is more evident in some patients with primary Sjögren's syndrome, where RF is likely to be oligoclonal or monoclonal in individuals with lymphoproliferation. | |
| 3131434 | Determination of the affinity of monoclonal 19 S IgM rheumatoid factor for IgG by modified | 1988 May 25 | In rheumatoid arthritis (RA), the pathogenicity of IgM rheumatoid factor (RF), an autoantibody whose antigen is IgG, is still unclear although RF-IgG complexes appear to be important mediators of immune injury. The polyclonality of RF in RA makes it difficult to characterize certain qualitative properties such as specificity and affinity which may be very important in determining pathogenicity. Monoclonal IgM RF can be used to circumvent this problem. Monoclonal RF secreting cells can be produced via hybridizations with RA B lymphocytes fused with mouse or human myeloma cell lines. Another source of monoclonal RF is the sera of patients with Waldenström's macroglobulinemia (WM). One particular WM IgM RF (Kas) was chosen for our experiments to measure affinities and specificities to eight different monoclonal IgGs (three IgG1s, three IgG3s, one IgG2, and one IgG4). 19 S IgM RF, a pentavalent molecule, was mildly reduced with DTT to make 7 S univalent fragments (7 S IgM RF). 7 S IgM RF was incubated with each of the different IgGs at several different concentrations. These mixtures were allowed to come to equilibrium. An aliquot was then used to determine the amount of free 7 S IgM RF by ELISA. By plotting the reciprocal of the fraction of bound RF versus the reciprocal of the concentration of free antigen at equilibrium, different affinities were determined. The results of these determinations compare favorably with published IgM RF affinities determined by more traditional methods. This method can also be used with proteolytic digest fragments of IgG and short synthetic peptides of the IgG molecule to better locate the antigen binding site. The technique may also help us to determine whether there are select clones of RSC producing RF with different affinities that could complex to a particular type of IgG which, in vivo, could produce greater inflammatory tissue damage. Furthermore, this methodology should be useful in the study of other autoimmune diseases characterized by pathogenic autoantibodies of differing affinities. | |
| 3072382 | Immunogenetics of collagen-induced arthritis in rats. | 1988 Sep | CIA can be viewed as a multifactorial animal model of experimentally-induced autoimmunity that is targeted to joint tissues and under multiple gene control. Thus, although induction of CIA requires immune reactivity to type II collagen, a high immune response to type II collagen is not pathognomonic of CIA, indicating that determinant specificity is of crucial importance. Also, both RT1-linked and non-RT1-linked gene directed functions are involved in the final clinical response to immunization with type II collagen. RT1-linked control is likely exerted at the level of Class II (Ia) molecules (as it is in mice) with inherent selectivity of arthritogenic vs non-arthritogenic epitopes for presentation to the immune response system; non-RT1-linked control may reflect genes controlling T-cell receptors, immunoglobulin subtypes or complement components. There is also evidence that the effects of potentially pathological anti-collagen autoimmunity may in some strains be muted or even obviated by other non-RT1 gene controlled traits that are not directly related to the immune system. These general conclusions are in close accord with those of other investigators who have carefully conducted extensive and in-depth studies of the immunogenetics of CIA in mice. CIA is obviously not an exact model of any one of the more common rheumatic diseases, such as rheumatoid arthritis or systemic lupus erythematosus. In fact, it is more closely analogous to polychondritis and some of the other sero-negative connective tissue diseases. However, CIA remains an extremely useful model in attempts to understand the genetic and environmental factors which influence a specific and definable autoimmune process--anti-collagen reactivity. In turn, autoimmunity to collagen, and to other autoantigens, is a contributing or complicating aspect of most of the diverse human rheumatic disease syndromes which have been identified to date. The characteristics of the CIA model in rats which have been discussed in this article, i.e., genetically controlled variations in incidence, severity, rate of progression and expression of clinical disease, are also characteristic of the human rheumatic disease patient population. Likewise, the probable contribution of multiple genes to these syndromes is recognized. Continued investigation of the CIA model can be expected to yield important information that can be used to better understand its human counterparts. | |
| 1953736 | Oncostatin M stimulates urokinase-type plasminogen activator activity in human synovial fi | 1991 Oct 31 | Cytokine regulation of synovial cell function has been considered to be involved in the pathogenesis of rheumatoid arthritis. Synoviocyte urokinase-type plasminogen activator (u-PA) expression may be relevant to the tissue remodelling, as well as to the cell migration and transformation occurring in rheumatoid joints. We report here that purified recombinant human oncostatin M (greater than or equal to approximately 0.2 U/ml = 1 pM) stimulated within six hr the u-PA activity of non-rheumatoid synovial fibroblast-like cells and raised their u-PA mRNA levels. Oncostatin M could augment PGE2 production and DNA synthesis in these cells; however, the increase in PGE2 was small compared with that caused by IL-1. Since oncostatin M is produced by immune cells, it may have a role in immune and inflammatory reactions by interacting with fibroblast populations, such as synoviocytes, in the manner described. | |
| 3326144 | Evaluation of CD5-positive B cells in blood and synovial fluid of patients with rheumatic | 1987 | CD5 (OKT1, Leu-1) is an antigen originally associated only with T cells. This antigen has recently been detected on a population of B cells that have been implicated in autoimmune diseases, particularly in rheumatoid arthritis (RA). We determined the percentage of these cells in the peripheral blood (PB) and synovial fluid (SF) of patients with RA and other joint diseases (OJD) using flow cytometry and two-colour fluorescence. No significant difference was observed between the percentages of CD5-positive B cells in the PB of these two patient groups or healthy individuals. In comparison with PB, significantly higher percentages of these cells were observed in the SF of patients with RA, but not in SF of OJD patients. Higher percentages of B cells were also noted in RA SF. However, when B-cell percentages were accounted for, no significant difference was observed between the numbers of B cells expressing CD5 in SF. No correlation was observed between the percentages of CD5-positive B cells and the levels of rheumatoid factor (RF) or C-reactive protein (CRP). We conclude that CD5-positive B cells are an integral part of the B-cell pool of PB and that there is increased representation of B cells in SF. The increased percentages of B cells in RA SF, compared with OJD, may reflect the autoimmune phenomenon occurring in the rheumatoid joint. | |
| 2059091 | Advances in patient education in rheumatic disease. | 1991 Jun | Education of patients with arthritis began with an emphasis on conveying knowledge, grew to include behaviour change, compliance, and more general coping and management of disease and then progressed to consider physical and psychosocial health outcomes. Research continues in all these areas. Control, in many forms (locus of control, self perceived efficacy, learned helplessness), is now suggested to be a central mediating variable. Evaluation of programmes is moving away from programme v usual care towards comparison of alternative methods of delivery and matching of method to learner. The first generation of researchers in arthritis education tended to be care givers with little formal education in behavioural sciences and evaluation methodology; the programmes they designed were often empirically based. The current generation, nurtured in large part by funds from the Arthritis Foundation and the National Institutes of Health, is better trained in designing programmes grounded in behavioural sciences and educational theory. In the long run, collaborations with care givers and patients will considerably strengthen the effectiveness of education programmes for patients. A variety of educational strategies have been shown to change the knowledge, behaviour, and health of patients with arthritis for the better. Many methods seem to work, so long as the programme is planned, has a goal, and is accountable. There is much work still to be done to teach care givers to be better teachers, and patients to be better managers of their diseases, in concert with their doctors, and to focus on high risk groups. Although most work has been done with patients with rheumatoid arthritis and osteoarthritis, many of these findings can and should be safely generalised to less studied rheumatic diseases. Finally, we need to consider the patient first as a person, and to provide education through all avenues, not just the medical care system. | |
| 1982677 | The role of continuous passive motion following total knee arthroplasty. | 1990 Dec | A retrospective review of 25 knees with postoperative continuous passive motion (CPM) treatment following total knee arthroplasty (TKA) was compared with a control group of 25 knees without postoperative CPM. The diagnoses were similar in both groups, with osteoarthritis in 43 knees, traumatic arthritis in 2 knees, rheumatoid arthritis in 2 knees, osteonecrosis in one knee, and gouty arthritis in one knee. Average knee flexion at discharge was 93.2 degrees in the CPM group and 86.5 degrees in the control group (p less than 0.01). Eighty percent of the CPM group and 64% of the control group had achieved 90 degrees of flexion before hospital discharge. The time required to achieve 90 degrees of flexion after TKA averaged 9.6 days in the CPM group and 11 days in the control group (p less than 0.01). There was no significant difference in flexion at 3 months or at 1 year postoperatively between the two groups. The duration of hospitalization was not significantly different between the two groups. One knee in the CPM group and 3 knees in the control group required manipulation. Wound hemovac drainage and transfusion requirements were not significantly different. The number of pain medication was not significantly different between the two groups. The CPM made the TKA knee achieve motion earlier with fewer complications. |