Search for: rheumatoid arthritis methotrexate autoimmune disease biomarker gene expression GWAS HLA genes non-HLA genes
ID | PMID | Title | PublicationDate | abstract |
---|---|---|---|---|
11123077 | Autologous hemopoietic stem-cell transplantation for children with refractory autoimmune d | 2000 Aug | Autologous stem cell transplantation (ASCT) has been proposed as a possible treatment for severe autoimmune diseases such as rheumatoid arthritis (RA), multiple sclerosis (MS), systemic sclerosis, and systemic lupus erythematosus (SLE). To date, more than 250 patients with various autoimmune disorders have undergone an ASCT since 1996. Among them, there is a very limited number of children. This review summarizes the experience with ASCT for pediatric rheumatic diseases. Most reported cases concern juvenile idiopathic arthritis (JIA). Experience with ASCT for childhood SLE, Scleroderma, or Dermatomyositis is very limited. To date, 12 children with severe systemic or polyarticular JIA, all with progressive disease activity despite the use of corticosteroids, MTX, CsA, or Cyclophosphamide were treated in our center with ASCT. Rheumatologic follow-up at 3-month intervals up to 36 months showed a marked decrease in arthritis severity as expressed by the core-set criteria for juvenile chronic arthritis (JCA) activity. However, these children remain at risk for severe viral infections due to the prolonged lymfopenia. ASCT in this severely ill patient group induces a very significant and drug-free remission of the disease, but carries a significantly risk of developing fatal MAS. | |
11018357 | Characteristics of chronic arthritis and other rheumatic condition-related ambulatory care | 2000 Oct 1 | PURPOSE: To characterize ambulatory medical care visits among persons with arthritis and other rheumatic conditions, the leading cause of disability.METHODS: The 1997 National Ambulatory Medical Care Survey (NAMCS) and National Hospital Ambulatory Medical Care Survey (NHAMCS) collect annual data on the utilization of ambulatory medical services provided by non-federal office-based physicians and hospital outpatient and emergency departments. Arthritis-related visits were defined using a predetermined set of ICD9-CM diagnostic codes developed by an expert panel and designed to include all potential diagnoses for arthritis and other rheumatic conditions. Visits related to acute conditions such as injuries were not included. National estimates and rates of arthritis-related ambulatory care visits were calculated by age, race, and sex groups.RESULTS: In 1997, there were an estimated 959.3 million ambulatory care visits, of which over 38 million (4.0%) were related to arthritis and other rheumatic conditions. Arthritis-related visits were more likely to be made by females (65.4%), white persons (82.2%), non-Hispanic persons (72.7%) and persons aged 25-64 years (61.9%). More than one-third of arthritis-related visits were for osteoarthritis, rheumatoid arthritis and unspecified myalgia/myositis. About half (50.2%) of the office visits for arthritis were made to general/family physicians or internists, while an additional 16.2% were to rheumatologists. Counseling or education related to exercise, diet/nutrition and injury prevention were provided at 18.9%, 9.2% and 2.2% of office and outpatient department visits respectively.CONCLUSIONS: Arthritis and other rheumatic conditions are common conditions associated with ambulatory medical care. These results suggest missed opportunities for counseling patients regarding public health prevention messages for arthritis, including increasing moderate physical activity, weight management and injury prevention. | |
11407706 | Germinal center reaction in the joints of mice with collagen-induced arthritis: an animal | 2001 Jun | OBJECTIVE: To establish an animal model and provide a basis for investigating the role of germinal center (GC) reaction in autoimmune arthritis. METHODS: DBA/1 mice were immunized with bovine type II collagen (CII) to elicit collagen-induced arthritis (CIA). Sections of arthritic joints were examined by in situ immunohistochemical studies, and purified cells from affected joints were subjected to flow cytometry analysis. RESULTS: De novo GC reaction was induced in the arthritic joints of male DBA/1 mice by immunization with bovine CII. In comparison with GCs formed in lymphoid tissues, such as spleen and lymph nodes, we found that these GCs formed in the joint tissues of mice with CIA were morphologically typical, as determined by immunohistologic and flow cytometric assays. CONCLUSION: The local immune responses in murine CIA induced ectopic GC formation, as observed in the synovial tissues of patients with rheumatoid arthritis. This system will allow for the first time the direct study of the role of the GC reaction in autoimmune arthritis in an animal model. | |
10494947 | Optic disc edema in neonatal onset multisystem inflammatory disease (NOMID). | 1999 Sep | PURPOSE: To inform ophthalmologists about neonatal onset multisystem inflammatory disease (NOMID), a rare condition with ophthalmologic manifestations. METHODS: We report a single case of NOMID with optic disc edema. RESULTS: A 28-month-old child with neonatal rash, arthropathy, central nervous system (CNS) involvement, and optic disc edema was diagnosed with NOMID. CONCLUSIONS: The finding of posterior uveitis or optic disc edema in a child with juvenile onset arthritis may allow the differentiation of NOMID from juvenile rheumatoid arthritis. | |
10934883 | [Various clinical patterns of relapsing polychondritis in six cases]. | 2000 Jun 18 | Relapsing polychondritis is a relatively rare disease characterized by episodic inflammation and progressive destruction of cartilage involving ears, nasal and laryngotracheal cartilage, cardiovascular system and the eyes. The increasing awareness of its clinically distinct has resulted in recognition of at least 550 reported cases. Six cases are reported to demonstrate the wide variety of clinical pattern. The most common features of the disease are auricular and nasal cartilage inflammation and nondeforming arthritis. Ocular symptoms and vasculitis is relatively rare. Two cases of relapsing polychondritis with laryngotracheobronchial manifestations illustrate the severe clinical features of the disease. Relapsing polychondritis may associate with diverse forms of connective tissue disease, such as rheumatoid arthritis. It seems interesting to note the onset in childhood. Treatment has been primarily symptomatic. In situations of mild symptoms, initial treatment is with nonsteroidal antiinflammatory drugs. For cases with serious manifestation, corticosteroids and immunosuppressants are indicated. | |
10367688 | Animal models of arthritis: relevance to human disease. | 1999 Jan | Animal models of arthritis are used to evaluate potential antiarthritis drugs for clinical use. Therefore capacity of the model to predict efficacy in human disease is one of the most important criteria in model selection. Animal models of rheumatoid arthritis (RA) with a proven track record of predictability include rat adjuvant arthritis, rat type II collagen arthritis, mouse type II collagen arthritis, and antigen-induced arthritis in several species. Agents currently in clinical use (or trials) that are active in these models include corticosteroids, methotrexate, nonsteroidal anti-inflammatory drugs, cyclosporin A, leflunomide, interleukin-1 receptor antagonist, and soluble tumor necrosis factor receptors. For some of these agents, the models also predict that toxicities seen at higher doses for prolonged periods would preclude dosing in humans at levels that might provide disease-modifying effects. Animal models of osteoarthritis (OA) include mouse and guinea pig spontaneous OA, meniscectomy and ligament transection in guinea pigs, meniscectomy in rabbits, and meniscectomy and cruciate transection in dogs. None of these models have a proven track record of predictability in human disease because there are no agents that have been proven to provide anything other than symptomatic relief in human OA. Efficacy data and features of the various models of RA and OA are discussed with emphasis on their proven relevance to human disease. | |
10366103 | Association of the course of collagen-induced arthritis with distinct patterns of cytokine | 1999 Jun | OBJECTIVE: To quantitate changes in cytokine and chemokine messenger RNA (mRNA) levels during the development and progression of collagen-induced arthritis (CIA) in mice. METHODS: Mice with CIA were scored for arthritis and killed at weekly intervals. Cytokine and chemokine mRNA levels were determined by RNase protection assays of total paw RNA. RESULTS: Arthritic paws exhibited mRNA levels of interleukin-1beta (IL-1beta), IL-2, macrophage inflammatory protein 2 (MIP-2), IL-6, IL-1 receptor antagonist, RANTES, tumor necrosis factor alpha (TNFalpha), TNFbeta, MIP-1alpha, IL-11, transforming growth factor beta1 (TGFbeta1), TGFbeta2, and TGFbeta3 that were increased above mRNA levels in paws of normal, unimmunized mice and that exhibited distinct temporal patterns of mRNA expression. Clinically uninvolved paws also exhibited an increase in mRNA levels of IL-11, RANTES, TNFalpha, TNFbeta, and MIP-1alpha. CONCLUSION: The observed differential temporal cytokine and chemokine mRNA expression patterns suggest that specific cytokines and chemokines have defined roles at various times during the course of autoimmune arthritis. Since most of these cytokines and chemokines are found in human rheumatoid arthritis (RA) synovium and synovial fluids, these findings may have relevance to RA. | |
9783764 | Comparison of clinical and self-reported diagnoses for participants on a community-based a | 1998 Sep | OBJECTIVE: With the advent of community-based arthritis education programmes, it is important to determine the accuracy of participants' self-reported diagnoses. The purpose of this study was to determine the level of agreement between general practitioner (GP)-recorded and self-reported diagnoses of participants attending an Arthritis Self-Management Programme (ASMP). METHODS: Participants enrolling on the ASMP were asked to (a) identify their type of arthritis via a self-administered postal questionnaire and (b) obtain a written confirmation of their diagnosis from their GP. The sample (n = 613) comprised mainly women (83%) with a mean age of 58.8 yr (S.D. 12.6) and a mean disease duration of 15.4 yr (S.D. 12.5). RESULTS: Participants' self-reported diagnoses were confirmed by GPs in 534 cases [87.1%, 95% confidence interval (CI): 84.4 89.8%]. Confirmed diagnoses were reported by 86.9% (95% CI: 83.1-90.7%) of those with osteoarthritis (OA) and 96.1% (95% CI: 93.6 98.6%) of those with rheumatoid arthritis (RA). The concordance rate for all other types of arthritis combined was lower at 60.5% (95% CI: 49.5-71.5%). There were no significant differences with respect to age, gender, education, physical functioning, duration of disease and number of GP visits between those who correctly identified their type of arthritis and those who did not. CONCLUSIONS: This study suggests that the majority of RA and OA participants attending an arthritis education programme can correctly identify their specific type of arthritis. | |
10553101 | Bone marrow-derived cells are responsible for the development of autoimmune arthritis in h | 1999 Nov 15 | Previously, we reported that human T cell leukemia virus type I env-pX region-introduced transgenic (pX-Tg) mice developed an inflammatory polyarthropathy associated with a development of autoimmunity. To elucidate roles of autoimmunity in the development of arthritis, the immune cells were reciprocally replaced between pX-Tg mice and non-transgenic (Tg) mice. When bone marrow (BM) cells and spleen cells from pX-Tg mice were transferred into irradiated non-Tg mice, arthritis developed in these mice. In contrast, arthritis in pX-Tg mice was completely suppressed by non-Tg BM and spleen cells. Similar results were obtained with BM cells only. After the transplantation, T cells, B cells, and macrophages were replaced completely, whereas cells in the joints were replaced partially. In those mice, serum Ig and rheumatoid factor levels correlated with the disease development, and inflammatory cytokine expression was elevated in the arthritic joints. Furthermore, involvement of T cells in the joint lesion was suggested, because the incidence was greatly reduced in athymic nu/nu mice although small proportion of the mice still developed arthritis. These observations suggest that BM stem cells are abnormal, causing autoimmunity in pX-Tg mice, and this autoimmunity plays an important, but not absolute, role in the development of arthritis in this Tg mouse. | |
10355966 | Sjögren's syndrome in mice carrying the Ipr(cg) gene and the therapeutic efficacy of an i | 1999 Feb | The influence of the Ipr(cg) gene on the development of Sjögren's syndrome was followed up to 5 months of age in male and female mice of MRL, CBA and C3H strains. In MRL-Ipr(cg) mice, focal mononuclear cell infiltration started at 2 months and became conspicuous after 3 months of age in the lacrimal and submandibular glands but was minimal in the parotid and sublingual glands, even at 5 months of age, without any apparent sex effects found. In CBA and C3H mice carrying the Ipr(cg) gene, this manifestation of Sjögren's syndrome was much less prominent, indicating that the participation of some genes of the MRL strain may be indispensable for the development of Sjögren's syndrome in mice carrying this gene. In MRL-Ipr(cg) mice, an immunosuppressive agent, FK506, improved the serological abnormalities (decreased levels of anti-double-stranded DNA antibody of IgG2a and IgG3 subclasses) and proteinuria. It also reduced the manifestations of Sjögren's syndrome when it was intraperitoneally administered three times weekly at a dose of 2 mg/kg from 6 weeks (before disease onset) until 5 months of age (the termination of the experiment). Although VP8.2+ T cells have been demonstrated to be responsible for causing several autoimmune diseases, the selective deletion of Vp8.2+ T cells with the superantigen encoded by mouse mammary tumor virus did not affect the disease severity at all, suggesting that this T cell repertoire may not play a crucial role in induction of Sjögren's syndrome. | |
9712092 | Hypofunction of the stress axis in Sjögren's syndrome. | 1998 Aug | OBJECTIVE: To examine the functional integrity of the hypothalamic-pituitary-adrenal (HPA) and thyroid axes in Sjögren's syndrome (SS) via the assessment of basal and stimulated adrenocorticotropin (ACTH), cortisol, thyroid stimulating hormone (TSH), and prolactin levels. METHODS: Pituitary function of the HPA axis was assessed by determining the basal plasma levels of ACTH in the late afternoon, as well as the ACTH released to ovine corticotropin releasing hormone (oCRH) stimulation; adrenal function was assessed by measuring plasma cortisol levels in the late afternoon at baseline and after release of the endogenous ACTH during oCRH stimulation. Basal and thyrotropin releasing hormone (TRH) stimulated levels of TSH and prolactin were also assessed. Healthy volunteers were used as controls. RESULTS: Patients with SS, compared to controls, were characterized by significantly lower ACTH levels (pg/ml), (5.1 +/- 0.5 vs 11.4 +/- 1.5, respectively; p < 0.05) and cortisol levels (microg/ml), (2.4 +/- 0.6 vs 5.9 +/- 1.2, respectively; p < 0.05). Furthermore, a blunted pituitary and adrenal response to oCRH compared to controls was observed: peak plasma ACTH and cortisol levels for patients with SS were 46.2 +/- 5.4 pg/ml and 15.7 +/- 1.6 microg/ml, respectively, and for controls 61.5 +/- 3.8 and 19.6 +/- 0.7, respectively (p < 0.05). Basal TSH levels were significantly elevated in patients (1.3 +/- 0.3 microIU/ml vs 0.9 +/- 0.05 microIU/ml; p < 0.05). CONCLUSION: The above findings indicate hypoactivity of the HPA axis in patients with SS. Further studies are needed to definitively identify the locus of the defects and assess the significance of the pattern of the perturbations to the pathogenesis and expression of SS. | |
9506579 | Collagen-induced arthritis in nonhuman primates: multiple epitopes of type II collagen can | 1998 Mar | OBJECTIVE: To define which regions of the type II collagen (CII) molecule result in anticollagen antibody production and the subsequent development of autoantibodies in a collagen-induced arthritis (CIA) nonhuman primate model. METHODS: Male and female cynomolgus monkeys (2-6 of each sex per group) were immunized with either chicken (Ch), human, or monkey (Mk) CII, or with cyanogen bromide (CB)-generated peptide fragments of ChCII emulsified in Freund's complete adjuvant. Monkeys were observed for the development of arthritis, and sera were collected and analyzed for anticollagen antibody specificity by enzyme-linked immunosorbent assay. RESULTS: Overt arthritis developed in all groups of monkeys immunized with intact CII and with all major CB peptide fragments of ChCII except CB8. Onset and severity of arthritis correlated best with serum anti-MkCII antibody levels. The levels of IgG autoantibody to MkCII were a result of the cross-reactivity rate of anti-heterologous CII antibodies with MkCII, which was based on the genetic background of individual monkeys rather than on sex differences. CONCLUSION: CII from several species and disparate regions of the CII molecule were able to induce autoantibody-mediated arthritis in outbred cynomolgus monkeys. The strong anti-MkCII response suggests that epitope spreading or induction of broad-based CII cross-reactivity occurred in these animals. Autoantibody levels to MkCII were higher in CIA-susceptible monkeys than in resistant monkeys, despite comparable antibody levels in response to the various immunizations of CII. These results closely parallel the type of anticollagen responses found in sera from rheumatoid arthritis patients. Perhaps this can be accounted for by similar major histocompatibility complex heterogenicity associated with an outbred population, or maybe this is a primate-specific pattern of reactivity to CII. | |
10882055 | Potent adjuvant effect by anti-CD40 in collagen-induced arthritis. Enhanced disease is acc | 2000 Jun | Collagen type II-induced arthritis (CIA) is an experimental model of rheumatoid arthritis, an autoimmune inflammatory disease of the peripheral joints in humans. CD40 interaction with its ligand CD154 (CD40L) has been shown to be an obligatory step in the initiation of autoimmune disease in several animal models. In this study we report on the effect of CD40 stimulation in CIA induced by immunization with type II collagen (CII) in CFA or IFA. We found that the administration of stimulatory anti-CD40 mAb resulted in earlier onset and more severe disease in IFA-CII-immunized mice. The mAb treatment resulted in markedly elevated titers of CII-specific IgG2a antibodies whereas CII-specific IgG1 titers were unaffected. Draining lymph node cell cultures from mice treated with anti-CD40 exhibited significantly increased IFN-gamma production compared to cultures from control antibody-treated mice. In conclusion, our results indicate that the level of CD40 activation during the induction of an autoimmune response may determine the severity of the resulting disease. | |
9776475 | Anti-arthritic effects of the novel dipeptidyl peptidase IV inhibitors TMC-2A and TSL-225. | 1998 Jul | We evaluated the immunopharmacological effects of two novel dipeptidyl peptidase IV (DP IV) inhibitors, TMC-2A [(2S,2S',2S'')-2-[2'-[2''-amino-3''-(-indol-3'''-yl)-1''-oxopropyl]-1',2 ',3',4'-tetrahydro-6',8'-dihydroxy-7'-methoxyisoquinol-3-yl-car bonylamino]-4-hydroxymethyl-5-hydroxypentanoic acid] and TSL-225 (tryptophyl-1,2,3,4-tetrahydroisoquinoline-3-carboxylic acid). TMC-2A, produced by Aspergillus sp. A374, inhibited rat kidney DP IV uncompetitively, with a Ki value of 5.3 microM. In vivo, TMC-2A suppressed alkyldiamine (N,N-dioctadecyl-N',N-bis(2-hydroxyethyl)propanediamine)-induced arthritis. We developed a chemically modified inhibitor, TSL-225, with potency similar to that of TMC-2A. TSL-225 inhibited DP IV uncompetitively, with a Ki value of 3.6 microM. TSL-225 was also effective against adjuvant-induced arthritis. These results suggest that TMC-2A and its derivatives may have therapeutic potential for the treatment of inflammatory diseases such as rheumatoid arthritis. | |
9717083 | Immunological abnormality associated with the augmented nitric oxide synthesis in adjuvant | 1998 Jan | Excessive nitric oxide (NO) synthesis, by inducible NO synthase (iNOS), has been implicated in the pathogenesis of inflammatory diseases such as rheumatoid arthritis. We investigated the pathophysiological role of NO using an adjuvant-induced arthritis model. Kinetics of iNOS mRNA expression in paw and spleen showed that it was induced from an early stage of the disease. To further characterize the pathophysiological relevance of iNOS induction in spleen, the mitogenic response of spleen cells was examined. ConA-induced proliferation of spleen cells from arthritic rats was completely suppressed in comparison to normal rats. Elevation of nitrite, which could be converted from NO, was also observed in the culture supernatants. Addition of three NOS inhibitors, S-(2-aminoethyl) isothiouronium bromide (ITU), aminoguanidine (AG) and LNG-nitroarginine methyl ester (L-NAME) all reduced the nitrite level and restored the proliferative response dose-dependently. These NOS inhibitors also showed anti-arthritic effects. Daily subcutaneous administration of either ITU at 50 mg/kg or AG at 200 mg/kg suppressed the paw swelling by 50% in arthritic rats on day 18. Oral administration of L-NAME at 30 mg/kg showed a tendency to suppress the development of arthritis from day 11 to day 15. However, drug-induced hypertension was observed with L-NAME due to poor selectivity for iNOS isozyme. These results suggest that augmented NO synthesis, via iNOS induction, may be partly involved in the pathogenesis of adjuvant-induced arthritis by causing defects in lymphocyte function. Thus, selective inhibition of iNOS might be beneficial for the treatment of immunological abnormalities associated with inflammatory diseases. | |
11361221 | Therapeutic effect of anti-Fas antibody on a collagen induced arthritis model. | 2001 May | OBJECTIVE: To investigate the therapeutic effect of anti-Fas monoclonal antibody (Mab, RK-8) in collagen induced arthritis (CIA). METHODS: CD1F1 mice were immunized with bovine type II collagen to induce CIA and were treated with RK-8 intravenously. The effect of RK-8 was monitored by visual scoring. ELISA to detect serum anti-type II collagen antibody was performed on Day 47 and 70. Histopathological analysis was performed on Days 31 and 72. Digital micrography was performed on Day 72. RESULTS: RK-8 treatment almost completely prevented CIA. This suppressive effect continued after RK-8 was discontinued. RK-8 significantly suppressed the serum anti-type II collagen antibody level on Day 47. Histological analysis revealed that RK-8 significantly reduced joint histopathology, as determined by the infiltration of inflammatory cells and cartilage damage, consistent with digital micrography. CONCLUSION: Administration of anti-Fas Mab may be a useful therapeutic strategy for rheumatoid arthritis if used early in the disease. | |
11108829 | A novel anti-rheumatic drug suppresses tumor necrosis factor-alpha and augments interleuki | 2000 Dec 15 | Tumor necrosis factor-alpha (TNF-alpha) plays an important role in the pathology of rheumatoid arthritis. When N-[1-(4-¿[4-(pyrimidin-2-yl)piperazin-1-yl]methyl¿phenyl)cycloprop yl] acetamide (Y-39041) (3-30 mg/kg) was orally administered to rats with established arthritis from day 15 to day 20, hindpaw volume was significantly reduced. This inhibitory activity of Y-39041 was kept up after administration was stopped. On day 17 Y-39041 suppressed lipopolysaccharide-induced TNF-alpha and interleukin-6 production in serum at doses of 3-30 mg/kg, and augmented interleukin-10 production at doses of 10 and 30 mg/kg. The finding that Y-39041 suppresses TNF-alpha and interleukin-6 production and augments interleukin-10 production could be beneficial in the therapy of chronic inflammatory diseases. | |
10432196 | Primary Sjögren's syndrome (pSS): subjective symptoms and salivary findings. | 1999 Aug | We studied the relationship between dry mouth, general health and objective findings in 16 patients having primary Sjögren's syndrome (pSS) according to the 1993 European classification criteria as well as in healthy controls. Serum autoantibody to SSA/SSB (AB) was correlated to unstimulated whole saliva flow (UWS) and labial salivary gland focus score (FS). All patients had dry mouth symptoms and UWS < or = 0.10 ml/min, but patients with UWS < 0.05 ml/min and AB had more complaints of oral and ocular dryness. These patients also tended to have more exocrine and non-exocrine manifestations, and oral dryness had a greater impact on their self-reported general health than in patients with UWS > or = 0.05 ml/min. Accordingly, we consider rating of oral dryness by visual analogue scales or categorised questionnaires to be valuable for the evaluation of oral involvement in pSS. | |
11252942 | [Immunopathology of Gougerot-Sjogren syndrome]. | 2001 Jan 31 | Sjögren's syndrome presents as an autoimmune exocrinopathy, and the term autoimmune epitheliitis has recently been coined. The major lesion is a lymphocyte infiltrate affecting the salivary glands and consisting predominantly of activated CD4+ T cells. The remaining 20% B lymphocytes, first polyclonal, turn out to be monoclonal. Epithelial cells are endowed with a key-part in the play, inasmuch as they gather together most of the Sjögren's syndrome-specific target autoantigens within apoptotic bodies, and possess all the characteristics of antigen presenting cells. There appears to be every likelihood that the sequence is triggered off by a thus far unknown virus. | |
17249209 | Study of the role of parvo virus B19 in arthropathies of Egyptian adult cases. | 1998 | This work was done to assess the relation between HPV B19 infection and arthropathies in Egyptian adults cases. For this purpose 40 rheumatoid arthritis (RA) cases, 10 osteoarthritis cases and 10 systemic lupus erythematosus (SLE) cases were selected to represent different types of arthropathies. The selection of cases was based on clinical diagnosis and laboratory tests (ESR, Hb level, Rose waller, detection of antinuclear antibodies and detection of hidden rheumatoid factor). HPV B19 IgM and IgG were searched for by ELISA test in their sera as indicator of the state of HPV B19 infection. A control group was also included in this study, as 30 healthy persons with no previous complaint of rheumatic symptoms. HPV B19 IgM was detected in 60% of patients with RA, 40% of osteoarthritis cases and None of the SLE cases. Positive cases were more among females with long duration of illness affecting both big and small joints. These results indicated a possible causal association between acute HPV B19 and arthropathy. As regards HPV B19 IgG, it was detected in 57% of RA cases, 60% of osteoarthritis cases and 40% of SLE. The difference in IgG was statistically insignificant from the control group (46.7%). The presence of HPV B19 IgG antibodies indicates previous exposure to the virus but does not indicate its time. Detection of HPV B19 IgM or rising titer of HPV B19 IgG may lead to early diagnosis of HPV B19 arthropathies. |