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ID PMID Title PublicationDate abstract
9178972 [A case of Sjögren's syndrome associated with EDTA-dependent pseudothrombocytopenia]. 1997 Apr A 69-year-old woman was admitted to Department of Orthopedic Surgery in our hospital because of lumbago on April 4, 1995. Since laboratory data showed thrombocytopenia (platelet count 2.1 x 10(4)/mm3) on admission, she was transferred to Department of Internal Medicine for further examination on April 11. She noticed abnormal taste and showed remarkable sicca symptoms. Schirmer test, gum test and electrogustometry were positive, and parotid sialogram findings and histology of minor salivary glands of the lip were compatible with those of typical Sjögren's syndrome. Thus, she was diagnosed as Sjögren's syndrome. Although the antibodies to SS-A/SS-B were negative in her serum, anti-nuclear and anti-centromere antibodies were strongly positive (x1280). Serum IgM level was increased. The decreased platelet count was observed when EDTA was used as anticoagulant. The binding activity of the anti-platelet antibody activated by EDTA was dependent on temperature. Its immunoglobulin class was shown to be IgM by enzyme-labelled antibody method. We here report a case of Sjögren's syndrome associated with EDTA-dependent pseudothrombocytopenia.
11093603 Anti-cardiolipin autoantibodies and pulmonary embolism. A case for a common cause. 2000 A patient with primary Sjögren's syndrome developed pulmonary embolism following infection with influenza A virus. IgM anti-cardiolipin autoantibodies (aCL) evolved two weeks after hospitalisation, synchronously with antibodies against influenza A. IgG aCL developed three weeks after hospitalization, peaked during the recovery period, and gradually declined to undetectable levels 12 months after admission. Antibodies against beta2 glycoprotein I were not detected. Our results assign a high likelihood to the hypothesis that influenza A virus caused the patient's thromboembolic disease as well as development of aCL. aCL may have contributed to tissue pathology by forming immune-complexes with cardiolipin and rheumatoid factor.
10701693 Big prolactin 60 kDa is overexpressed in salivary glandular epithelial cells from patients 2000 Feb Characterization of endogenous synthesis of prolactin (PRL) proteins and their cellular localization in labial salivary glands of patients with Sjogren's syndrome (SS) were achieved. PRL, PRL-receptors (PRL-R), and S100A6 protein were detected by immunohistochemistry. In situ prolactin synthesis was investigated in controls and SS patients by ex vivo incubation of minor salivary glands biopsies and immunoprecipitation assay. Increased PRL-immunoreactivity was found in cytoplasmic acinar epithelial cells in SS patients compared with normal subjects. PRL-R was distributed only in ductal epithelial cells in which S100A6 protein (a PRL-R-associated protein) was also present. PRL, PRL-R, or S100A6-immunoreactivity was not detected in infiltrating mononuclear cells. Immunoprecipitation demonstrated that PRL synthesis occurred in minor salivary glands with increased synthesis of two distinct PRL-like proteins (one major band at 60 kDa and a minor at 16 kDa) in SS glands compared with normal glands. Expression of PRL gene was demonstrated in SS salivary glands using RT-PCR. A positive correlation was found between the presence of PRL-like proteins in acinar epithelial cells of SS patients and clinical extraglandular manifestations. The presence of anti-Ro and anti-La antibodies also positively correlated with a higher percentage of PRL in acinar epithelial cells. In conclusion, PRL-like proteins are synthetized and overexpressed in glandular epithelial cells of labial salivary glands from SS patients and correlate with the aggressiveness of the disease.
9153549 Role of nitric oxide in Sjögren's syndrome. 1997 May OBJECTIVE: To measure levels of salivary nitrite (NO2-) and to localize nitric oxide synthases (NOS) in the labial salivary glands (LSGs) of patients with Sjögren's syndrome (SS). METHODS: NO2- was measured by the Griess reaction. LSGs were analyzed using NADPH-diaphorase histochemical and immunohistochemical studies to determine the constitutive NOS (neuronal [ncNOS] and endothelial [ecNOS]) and inducible NOS (iNOS) isoforms. RESULTS: The NO2- concentration (mean +/- SEM 307 +/- 51 microM versus 97 +/- 16 microM; P < 0.05) and output (166 +/- 46 nmoles/minute versus 37 +/- 7 nmoles/minute) were increased in SS patients compared with healthy control subjects. NADPH-diaphorase was found in some nerve fibers and endothelial cells, and, in SS, was found in myoepithelial, acinar, and ductal epithelial cells, but in only a few inflammatory cells. In SS, ncNOS-immunoreactive nerve fibers were sparse and ecNOS was found in a minority of the CD31-positive vascular endothelial cells and acinar cells, whereas iNOS was localized in myoepithelial, acinar, and ductal epithelial cells, often together with tumor necrosis factor alpha. CONCLUSION: Nitrite was found in normal human saliva. NO produced by ncNOS probably acts as a nonadrenergic, noncholinergic neurotransmitter, whereas that produced by ecNOS exerts a vasodilatory effect. SS patients had increased NO2- concentrations, with most of the superfluous salivary NO being produced not by the immigrant inflammatory cells, but rather, by the resident salivary gland cells. NO may contribute to inflammatory damage and acinar cell atrophy in SS.
11688830 Hemophagocytic syndrome and adult Still's disease associated with meningoencephalitis and 2001 Oct We describe a 19-year-old woman with hemophagocytic syndrome and adult Still's disease who showed rare features of central neurological involvement, including cerebellar symptoms and the sudden onset of unconsciousness with pleocytosis in the cerebrospinal fluid during the early course of the illness. As this patient's serum showed a high level of interferon-gamma and soluble interleukin 2 receptor, this might play a pathologic role in the development of central nervous system symptoms. Intensive treatment consisting of methylprednisolone pulse therapy followed by the oral administration of methylprednisolone and cyclosporine, as well as plasma exchange, was found to achieve good results.
9330880 Autoimmune ataxic neuropathies (sensory ganglionopathies). 1997 Oct Autoimmune ataxic neuropathies are a subset of the sensory ataxic neuropathies which are characterized by ataxia as the dominant presenting feature. The major known causes of autoimmune ataxic neuropathies include sensory variants of the Guillain-Barré syndrome, including Miller-Fisher syndrome, subsets of immunoglobulin M paraproteinaemic neuropathy, paraneoplastic neuropathy and the neuropathy associated with Sjögren's syndrome. Identified antigens as targets for autoantibodies include gangliosides, myelin associated glycoprotein, Hu antigen and extractable nuclear antigens. Some recent studies support the pathogenic role of anti-GD1b ganglioside antibody in autoimmune ataxic neuropathies. The major site of pathology in autoimmune ataxic neuropathies is the dorsal root ganglion, but dorsal roots and peripheral nerve myelin and axons may also be affected.
11794743 Effects of mouthrinses with linseed extract Salinum without/with chlorhexidine on oral con 2001 Dec OBJECTIVES: To study the effect of mouthrinses with salivary replacement substances on oral conditions in patients with primary Sjögren's syndrome. DESIGN: Cross-over, double-blind study. SETTING: Facilities at the Centre for Oral Health Sciences, Malmö University and at Malmö University Hospital, Malmö, Sweden. SUBJECTS: Twenty-two patients with Sjogren's syndrome. INTERVENTION: Linseed extract Salinum alone (Sal) or with addition of chlorhexidine (Sal/Chx) was used for mouthrinsing during 3-week periods of rinsings separated by a 3-week "wash-out" period. MEASUREMENTS: Recordings of percentages of sites with dental plaque and bleeding on probing, mirror friction test and microbiological analyses. Questionnaire on oral symptoms due to reduced salivation. RESULTS: Dental plaque and bleeding on probing were reduced after Sal and after Sal/Chx. Friction was reduced after both treatments. No significant differences for counts of studied microbial groups were seen after Sal but the total anaerobically cultured microorganisms and of mutans streptococci fell after Sal/Chx (p<0.05 and p<0.001). Symptoms of oral dryness improved following Sal and Sal/Chx (p<0.05 and p<0.001 respectively). Speaking problems and burning mouth symptoms improved after use of Sal (p<0.05). CONCLUSIONS: Positive effects on symptoms in patients with Sjögren's syndrome were seen after use of Salinum without or with chlorhexidine.
11263778 Polymorphisms of the Ro52 gene associated with anti-Ro 52-kd autoantibodies in patients wi 2001 Mar OBJECTIVE: To screen for the Ro52 gene encoding the 52-kd Ro autoantigen for possible mutations and polymorphisms associated with primary Sjogren's syndrome (SS). METHODS: The restriction enzyme fragment-single-strand conformation polymorphism method was used to search for mutations and polymorphisms in the Ro52 gene in 97 patients with primary SS and 72 healthy control subjects. The results were verified by automated DNA sequencing and natural or amplification-created restriction site tests. RESULTS: A single-nucleotide polymorphism (SNP) was discovered in intron 3 (137 bp upstream of exon 4). The C/T genotype was significantly more prevalent among patients who were positive for anti-Ro 52-kd (20 of 38) than among healthy controls (9 of 72) (P = 0.00003); significant differences were not seen in patients who were negative for anti-Ro 52-kd. Furthermore, the frequency of the T allele in this position among groups of anti-Ro 52-kd-positive patients, anti-Ro 52-kd-negative patients, and control subjects was significantly increased in the patients who were positive for anti-Ro 52-kd compared with the controls. CONCLUSION: We present the results of a complete screening for the Ro52 gene in patients with primary SS and the results of an association study. An SNP in intron 3 was found to be strongly associated with the presence of anti-Ro 52-kd autoantibodies in primary SS. This finding is interesting in light of the fact that an alternative messenger RNA is made by deleting exon 4, which encodes a putative leucine zipper domain, to generate a shorter version of the Ro 52-kd protein.
10658904 Sjögren's syndrome and MALT lymphomas of salivary glands: a DNA-cytometric and interphase 2000 Jan Few and conflicting cytogenetic data are available concerning the chromosomal constitution of (mainly gastric) extranodal marginal zone B-cell non-Hodgkin's lymphoma arising from mucosa-associated lymphoid tissue (MALT)-type lymphoma. The majority of salivary gland MALT lymphomas are thought to develop from longstanding Sjögren's syndrome/benign lymphoepithelial lesion (BLEL). We tried to achieve a better comprehension of related cytogenetic alterations by comparing DNA-ploidy and numerical chromosomal (#) aberrations, assessed by different techniques of DNA cytometry (image cytometry) and interphase cytogenetics using nonradiographic in situ hybridization (centromere specific probes for #3, 7, 12, 18) on 12 cases of BLEL, 13 low-grade MALT lymphomas (LG-MALT-L) and 4 high-grade MALT lymphomas (HG-MALT-L) of salivary gland. Both techniques were applied on tissue sections preferentially, enabling a reliable measurement of histomorphologically identified areas. No case of BLEL showed cytogenetic abnormalities. Three of 4 HG- and 2 of 13 LG-MALT-L exhibited complex chromosomal gains in nonisotopic in situ hybridization, which were reflected by DNA nondiploidy in image cytometry. In 6 of 13 LG- and lof 4 HG-MALT-L, one or two numerical chromosomal aberrations were demonstrated by nonisotopic in situ hybridization, which could not be resolved by image cytometry. In the 11 DNA-diploid LG-MALT-L, trisomies 18, 3, and 12 were found in 36, 12, and 9%, respectively. In conclusion, comparing BLEL, which showed no chromosomal aberrations, with LG- and HG-MALT-L, an increase in frequency and number of numerical aberrations and DNA nondiploidy was seen. Peritetraploid DNA nondiploidy might be characteristic for HG-MALT-L of salivary gland as it is a rare finding in MALT lymphomas of other sites. It is unclear whether the documented chromosomal aberrations in LG-MALT-L, especially increased rate of trisomy 18, indicate a pathogenic impact or merely reflect genetic instability.
10446867 Correlation of increased susceptibility to apoptosis of CD4+ T cells with lymphocyte activ 1999 Aug OBJECTIVE: To investigate whether a change in the CD95-related apoptosis of T lymphocytes might have a share in the development of the disease in patients with primary Sjögren's syndrome (SS). METHODS: Two-color cytometric analysis was used to study the phenotype of freshly separated mononuclear cells, while Western blotting was used to detect CD95 ligand (CD95L) expression in total homogenates of isolated CD4+ T lymphocytes. The ability of various subpopulations of T cells to undergo apoptosis was investigated in 1-day cultures in medium alone or following various (anti-CD3, anti-CD95 monoclonal antibody, calcium ionophore) treatments. Apoptosis was detected using 7-aminoactinomycin D dye. RESULTS: Compared with the findings in healthy controls, the number of CD4+ T lymphocytes was decreased, while their expression of CD95, HLA-DR, and CD45RO was significantly increased in patients with primary SS. A positive correlation was found between the activity of disease, the decrease in the CD4+ T cell number, and the increase in the expression of CD95, CD95L, HLA-DR, and CD45RO molecules within the CD4+ T cell subset. An increased rate of spontaneous, anti-CD3-, or anti-CD95-induced apoptosis was found in the T cells of SS patients, and this was more pronounced in the CD4+ T cell population, correlated with the decreased CD4+ T cell number, increased CD45RO expression, and activity of disease, and concerned mainly the CD95+ cells. CONCLUSION: These observations indicate that the increased susceptibility to apoptosis of peripheral CD4+ T cells from SS patients correlates with disease activity. These findings support the hypothesis that the chronic activation of the immune system that occurs in this autoimmune disease is the primary mechanism responsible for this cell-deletion process.
9811052 Accumulation of human T lymphotropic virus type I-infected T cells in the salivary glands 1998 Nov OBJECTIVE: To clarify the involvement of human T lymphotropic virus type I (HTLV-I) in the pathogenesis of Sjogren's syndrome (SS). METHODS: In HTLV-I-seropositive patients with SS, HTLV-I proviral DNA in the labial salivary glands (SG) was detected by polymerase chain reaction (PCR) amplification of the extracted cellular DNA, and the localization in the SG was examined by in situ PCR hybridization. RESULTS: The cellular DNA extracted from the SG contained full HTLV-I proviral DNA, which was present in the nucleus of the infiltrating T cells, but not in either the SG epithelial cells or the acinar cells. Furthermore, the viral loads in the SG were approximately 8 times to 9 x 10(3) times higher than those in the peripheral blood mononuclear cells. CONCLUSION: Accumulation of HTLV-I-infected T cells in the SG suggests that HTLV-I likely causes the self-reactive T cells to proliferate, which, as a result, induces SS.
10363633 Lupus nephritis in juvenile myelomonocytic leukemia. 1999 May A 13-year-old girl developed lupus nephritis and Hashimoto thyroiditis in the chronic phase of juvenile myelomonocytic leukemia (JMML). At age 7 months, she was diagnosed as having JMML based on the hepatosplenomegaly, leukocytosis, thrombocytopenia, increased levels of fetal hemoglobin, and spontaneous in vitro growth of granulocyte-macrophage progenitors. At the onset of JMML, she had hypergammaglobulinemia, antinuclear antibodies, rheumatoid factors and anti-smooth muscle antibody. She had been placed on oral 6-mercaptopurine for about 12 years, with clinical improvement. At age 13 years, she was found to have hematuria and proteinuria. She also developed arthritis and Raynaud's phenomenon as well. She had antinuclear antibodies, rheumatoid factors, LE phenomenon, beta-1C (C3) nephritic factor (C3NeF), antithyroid antibodies, and hypocomplementemia. The renal biopsy specimens revealed a diffuse increase in the mesangial cells and matrix by light microscopy, and intense staining of IgG, Clq and C3 by immunofluorescence microscopy. The hormonal study ultimately showed decreased thyroid functions. So she was diagnosed as lupus nephritis and Hashimoto thyroiditis. The patient is the first example to show close relationship between stem cell abnormalities in JMML and development of overt autoimmune disorders.
11714393 Early response genes induced in chondrocytes stimulated with the inflammatory cytokine int 2001 Recent work has established that IL-1beta plays a central role in the inflammation and connective tissue destruction observed in both rheumatoid arthritis and osteoarthritis. These processes result from the ability of this inflammatory cytokine to activate expression of genes for neutral proteases, such as the matrix metalloproteinases. While IL-1beta activates matrix metalloproteinase genes within several hours, it also activates immediate early genes, which are required for the later expression of matrix metalloproteinases and other arthritis-perpetuating genes, are also activated. To identify putative immediate early genes involved in IL-1beta-mediated arthritic disease, a chondrocytic cell line (SW1353) was stimulated with this cytokine for 2 hours, total RNA was isolated, and expressed genes were identified by microarray analysis. This analysis identified alterations in the expression of multiple transcription factors, cytokines, growth factors and their receptors, adhesion molecules, proteases, and signaling intermediates that may contribute to inflammation and cartilage destruction in arthritis. Interestingly, confirmation of the expression of activating protein-1 family members by reverse transcriptase polymerase chain reaction revealed a preferential increase in junB, a known transcriptional antagonist of c-jun. The failure to observe induction of early growth response gene-1, which was detected by reverse transcriptase polymerase chain reaction to be substantially and transiently induced by 1 hour of IL-1 treatment, may be explained by the known instability of the message after early induction. However, this analysis has identified numerous IL-1beta-responsive genes that warrant further investigation as mediators of disease in arthritis.
11316141 Reduced incidence of gastroduodenal ulcers with celecoxib, a novel cyclooxygenase-2 inhibi 2001 Apr OBJECTIVE: Nonsteroidal anti-inflammatory drugs (NSAIDs) block prostaglandin production by inhibiting cyclooxygenase (COX); they are believed to cause gastroduodenal damage by inhibiting the COX-1 isoform and to have analgesic and anti-inflammatory effects by inhibiting the COX-2 isoform. As compared to conventional NSAIDs, celecoxib, a COX-2 specific inhibitor, has been shown in previous single posttreatment endoscopy studies to be associated with lower gastroduodenal ulcer rates. In response to concerns that such studies may under-represent ulceration rates, the present serial endoscopy study was designed to compare cumulative gastroduodenal ulcer rates associated with the use of celecoxib to those of naproxen, a conventional NSAID. METHODS: In this double-blind, parallel-group, multicenter study, 537 patients with osteoarthritis (OA) or rheumatoid arthritis (RA) were randomized to treatment with celecoxib 200 mg b.i.d. (n = 270) or naproxen 500 mg b.i.d. (n = 267) for 12 wk. Gastroduodenal damage was determined from esophagogastroduodenoscopy after 4, 8, and 12 wk of therapy. Arthritis efficacy was evaluated with Patient's and Physician's Global Assessments. RESULTS: Gastroduodenal ulcer rates after celecoxib and naproxen treatment were 4% versus 19% in the 0-4 wk interval (p < 0.001), 2% versus 14% in the 4-8 wk interval (p < 0.001), and 2% versus 10% in the 8-12 wk interval (p < 0.001), respectively. After 12 wk of treatment, the cumulative incidence of gastroduodenal ulcers was 9% with celecoxib and 41% with naproxen. In the celecoxib group, gastroduodenal ulcers were significantly associated with Helicobacter pylori status (p < 0.05), concurrent aspirin usage (p = 0.001), and a history of ulcer (p = 0.010), but not with disease type (OA/RA), age, gender, other relevant medical histories, or concurrent corticosteroid or disease-modifying antirheumatic drugs usage (p > 0.05). Celecoxib produced a significantly lower incidence rate of both gastric (p < 0.001) and duodenal (p < 0.030) ulcers. The two agents produced similar improvements in Patient's and Physician's Global Assessments of arthritis efficacy. The incidence of adverse events and withdrawal rates did not differ significantly between treatments. CONCLUSIONS: As compared to naproxen (500 mg b.i.d.), use of celecoxib (200 mg b.i.d.), a COX-2 specific agent, at the recommended RA dose and twice the most frequently prescribed OA dose, was associated with lower rates of gastric, duodenal, and gastroduodenal ulcers but had comparable efficacy, in patients with OA and RA.
9616158 A new strategy for treatment of autoimmune diseases in chimeric resistant MRL/lpr mice. 1998 Jun 15 A new strategy for the treatment of autoimmune diseases in chimeric resistant MRL/lpr mice is established. The strategy includes injection of cyclophosphamide (CY), fractionated irradiation (5 Gy x 2), bone grafts (to recruit stromal cells), and two transplantations of whole bone marrow cells (WBMCs) from allogeneic normal C57BL/6 mice (CY/2X/Bone/2BMT). MRL/lpr mice, thus treated, survived more than 40 weeks (1 mouse survived for >40 weeks, 7 for >50 weeks, and 4 for >60 weeks after these treatments). Immunohistological studies showed that the mice were completely free from both lymphadenopathy and autoimmune diseases such as systemic lupus erythematosis and rheumatoid arthritis. The levels of autoantibodies (IgM/IgG rheumatoid factors and IgM/IgG anti-ssDNA antibodies [Abs]) in the treated mice decreased to those in the normal mice. In addition, successful cooperation among T cells, B cells, and antigen-presenting cells (APCs) was observed. Abnormal T cells with immunophenotypes of B220+/Thy-1+/CD3+/CD4-/CD8- present in untreated MRL/lpr mice disappeared, and the hematolymphoid cells of the treated mice were of donor origin. However, the mice that had been irradiated with 8.5 Gy and then reconstituted with T-cell-depleted BMCs plus bone grafts died within 2 weeks due to the side effect of irradiation. The depletion of CD8+ cells (not CD4+ cells) from WBMCs resulted in graft failure; 60% of the recipient mice, thus treated, died within 2 weeks, and all recipients died by 15 weeks. Furthermore, limiting dilution assays showed that approximately more than 0.5% of T cells contained in the BMCs are necessary not only for engraftment of BMCs but also for long-term disease-free survival of the recipients. In contrast, recipients that had received CD4-depleted BMCs with CY plus fractionated irradiation (5Gy x 2) survived for more than 40 weeks without showing graft-versus-host reaction (GVHR). This indicates that CD8(+)cells in the BMCs are essential for the successful engraftment of the donor-type hematolymphoid cells.
9806371 Musculoskeletal manifestations and autoantibody profile in 90 hepatitis C virus infected I 1998 Oct OBJECTIVES: Recent interest has been expressed in rheumatic manifestations in hepatitis C virus (HCV)-infected populations. The aim of this study was to determine the prevalence and characteristics of the musculoskeletal manifestations and serological markers of autoimmunity in HCV-infected patients in Israel. METHODS: Ninety anti-HCV-positive patients were consecutively interviewed and examined. The prevalence of autoantibodies and their association with rheumatologic symptoms were also determined. RESULTS: Rheumatic manifestations were found in 28 subjects (31%), and included arthralgias (9%), arthritis (4%), cryoglobulinemia (11%), sicca symptoms (8%), cutaneous vasculitis (2%), polymyositis (1%), and antiphospholipid syndrome (1%). Rheumatic complications were not associated with liver disease severity, or subjects' gender. In addition, myalgia was reported by 22 patients (24%), and fibromyalgia was diagnosed in 14 (16%). Sixty-nine percent of the patients had at least one autoantibody detected in their serum, the most prevalent being rheumatoid factor (RF), 44%; antinuclear antibody (ANA), 38%; and IgM and IgG anticardiolipin antibodies (ac1), 28% and 22%, respectively. The frequency of autoantibodies was not associated with liver disease severity or rheumatic disorders. CONCLUSIONS: Musculoskeletal manifestations and autoimmune markers are common in HCV infection. An investigation of risk factors for HCV infection is pertinent in a patient presenting new rheumatic manifestations and should be included in the history of present illness. Future studies of these disorders may uncover the full spectrum of these associations and provide new insights into their operating mechanisms.
9694125 Ankle osteoarthritis scale. 1998 Jul Although there is a wide array of outcome tools for assessing patients with symptomatic ankle arthritis, no disease-specific instrument for ankle arthritis has been shown to be reliable and valid. The purpose of this study was to develop a simple, reliable, and validated outcome measure for the clinical assessment of ankle osteoarthritis. We modified the Foot Function Index, a visual analog-based scale used to assess rheumatoid foot problems, to measure patient symptoms and functional limitations stemming from osteoarthritis of the ankle joint. Test-retest reliability and criterion and construct validity were determined for the overall Ankle Osteoarthritis Scale and its two subscales (pain and disability). Overall reliability (r=0.97; 95% confidence interval [CI], 0.94-0.99), pain subscale reliability (r=0.95; 95% CI, 0.90-0.98), and disability subscale reliability (r=0.94; 95% CI, 0.88-0.97) were excellent. Criterion validity testing of the instrument with the WOMAC (a disease-specific scale for osteoarthritis) and the SF-36 (a general health survey) showed a high degree of concordance for related subscales. Construct validity using a physical measure of ankle function demonstrated sensitivity of the instrument to the degree of joint dysfunction. Normative data were obtained from 562 individuals who were not patients (264 men and 298 women). The responses were analyzed for trends in gender, body mass index, presence of arthritis, history of fracture in relation to the response levels, and age. A small but statistically significant main effect for gender was found, with women consistently reporting higher pain, disability, and total index scores. Body mass index and arthritis were also found to correlate with response answers across the subscale and total index scores; however, these factors only accounted for 12% of the variation. The Ankle Osteoarthritis Scale is a reliable and valid self-assessment instrument that specifically measures patient symptoms and disabilities related to ankle arthritis.
9619894 Erosive arthritis in systemic lupus erythematosus: analysis of a distinct clinical and ser 1998 Apr Erosive arthritis (EA) in systemic lupus erythematosus (SLE) can be debilitating and deforming with uncertain factors for risk, although antibodies to the A2 hnRNP core protein, known as anti-RA33, have been associated with EA. Two hundred patients under long-term follow-up for SLE were evaluated for EA and associated clinical and serological abnormalities. In addition, sera were tested in a masked fashion for anti-RA33 antibodies in a total of 60 patients: 10 with EA and 50 age-, sex- and ethnically matched controls. Ten of 200 (5%) patients with SLE, mainly non-white women, had EA. There were trends for increased renal involvement (P = 0.06), Sjögren's syndrome (P = 0.07) and Raynaud's phenomenon (P = 0.03) in patients with EA compared to those without EA. Rheumatoid factor (RF) was increased in patients with EA (P < 0.02), as were antibodies to double-stranded DNA (P < 0.05), Sm (P < 0.01) and La/SS-B (P < 0.001). Anti-RA33 antibodies were present in 70% with EA compared to 28% without EA (P < 0.05). RF correlated with anti-RA33 antibodies in patients with EA, but not with the presence of anti-RA33 alone. Thus, anti-RA33 antibodies may identify those patients with SLE who are at risk for EA, and an association with RF suggests a common immune response or pathological mechanism in autoimmune erosive joint disease.
9558172 Prevalence and characterization of novel pANCA, antibodies to the high mobility group non- 1998 Apr OBJECTIVE: To determine the immunodiagnostic value of antibodies to the high mobility group non-histone chromosomal proteins HMG1 and HMG2, which have been identified as novel target antigens of perinuclear antineutrophil cytoplasmic antibodies (pANCA), in sera from patients with systemic rheumatic diseases. METHODS: Anti-HMG1 or HMG2 antibody was assayed by ELISA and Western blotting in sera from patients with systemic rheumatic diseases. These antibodies were analyzed for the relationship with pANCA detected by indirect immunofluorescence in these diseases, and with clinical features in rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). RESULTS: Anti-HMG1 or HMG2 antibody was frequently detected in sera from patients with RA (48%), SLE (45%), Sjögren's syndrome (SS) (44%), and systemic sclerosis (SSc) (41%). In these diseases, anti-HMG1 antibody was detected more frequently than anti-HMG2 antibody. In sera from patients with RA, the positivity for anti-HMG1 and HMG2 antibodies was significantly correlated with the positivity for pANCA (p < 0.0001). Anti-HMG1/HMG2 antibodies were associated with some disease activity variables, e.g., erythrocyte sedimentation rate, C-reactive protein, rheumatoid factor, joint score and hand grip strength in RA, and CH50, C3, C4, and IgG in SLE. CONCLUSION: Anti-HMG1/HMG2 antibodies are detected commonly in systemic rheumatic diseases, particularly in RA, SLE, SS, and SSc. HMGI and HMG2 seem to be the significant target antigens of pANCA in RA. These antibodies are significantly associated with disease activity indices in RA and SLE.
9492663 Risk of connective tissue disease and related disorders among women with breast implants: 1998 Feb 7 OBJECTIVE: To examine the relation between connective tissue disease and related conditions and breast implants. DESIGN: Retrospective cohort study of all women in the Swedish national inpatient registry who underwent breast augmentation surgery with artificial implants during 1964-93, compared with women who underwent breast reduction surgery during the same period. SETTING: Sweden. SUBJECTS: 7442 women with implants for cosmetic reasons or for reconstruction after breast cancer surgery and 3353 women with breast reduction surgery. MAIN OUTCOME MEASURES: Subsequent hospitalisation for definite connective tissue diseases (rheumatoid arthritis, systemic lupus erythematosus, systemic sclerosis, dermatomyositis, and Sjögren's syndrome) or related disorders. RESULTS: 29 women with implants were hospitalised for definite connective tissue disease compared with 25.5 expected based on general population rates (standardised hospitalisation ratio 1.1 (95% confidence interval 0.8 to 1.6)). There were no diagnoses of systemic sclerosis, and no significant excess in risk for polymyalgia rheumatica, fibromyalgia, and several related disorders. Among women who underwent breast reduction surgery, 14 were hospitalised for definite connective tissue disease compared with 10.5 expected (standardised hospitalisation ratio 1.3 (0.7 to 2.2)). Compared with the breast reduction group, women with breast implants showed a slight reduction for all definite connective tissue disease (relative risk 0.8 (95% confidence interval 0.5 to 1.4)). CONCLUSIONS: This large nationwide cohort study shows no evidence of association between breast implants and connective tissue disease.