Search for: rheumatoid arthritis    methotrexate    autoimmune disease    biomarker    gene expression    GWAS    HLA genes    non-HLA genes   

ID PMID Title PublicationDate abstract
1635171 [Hodgkin's disease associated with Behçet's disease]. 1992 Feb This paper reports a rare case of Hodgkin's disease with Sjögren syndrome in the course of Behçet's disease. A 43-year-old man developed arthralgia of bilateral knees, ankles, elbows and wrists in May, 1988. He had hazy vision and was diagnosed as having iridocyclitis and chorioretinitis in February, 1989. Gingival ulcer, penile ulcer, erythema nodosum on the right lower leg and superficial thrombophlebitis on the bilateral arms appeared in June, 1989. Therefore, he was diagnosed as Behçet's disease. He responded well to prednisolone. In November, 1989, he developed fever with positive CRP and elevated alkaline phosphatase. Multiple mass lesions in the liver and spleen with retrocrural lymphadenopathy were noticed on the abdominal CT and echogram. A cervical lymph node biopsy revealed Hodgkin's disease of the mixed cellularity type. At the same time, the patient had dry eyes and a dry mouth. Salivary gland biopsy revealed chronic sialoadenitis with lymphocytic infiltration compatible with Sjögren syndrome. The patient responded well to ABVD regimen. He is still free of disease as of May, 1991.
7525472 B-1 cells in systemic autoimmune responses: IgM+, Fc epsilon Rdull B cells are lost during 1994 Aug The potential role of B-1 cells (i.e. the CD5+ B cell and "sister" B cell subsets) in autoimmunity is controversial. CD5+ B cells have been shown to secrete antibodies of similar specificity as those found in many systemic autoimmune diseases; in addition, increases in CD5+ B cell frequency have been reported in patients suffering from rheumatoid arthritis, Sjögren's syndrome, myasthenia gravis, insulin-dependent diabetes mellitus and Hashimoto's thyroiditis. Whether these increases are due to expansion of B-1 lineage cells in the human or due to activation-induced expression of CD5 by conventional B cells is unclear. In the present study, we used three murine models of systemic autoimmunity: murine acquired immunodeficiency syndrome (MAIDS), chronic graft-versus-host disease (cGvHD), and collagen-induced arthritis (CIA) to determine whether increases in B-1 cell frequency are universally seen in models of autoimmunity which are mechanistically distinct. In contrast to the aforementioned human systemic autoimmune diseases which exhibit an increase in CD5+ B cell frequency, the percentage of CD5+ B cells declined in all three murine models of systemic autoimmune disease. Even though there was a decrease in the frequency of CD5+ B cells there was no change in the actual number of CD5+ B cells. Thus, the apparent decline in CD5+ B cell frequency was due to increases in either T cells, conventional Fc epsilon R+ B cells, or both. The only actual decline in a B cell subset was the loss of IgM+, Fc epsilon Rdull cells in both the spleen and peritoneal cavity of mice undergoing a chronic graft-versus-host reaction. Therefore, our data suggests that expansion of the B-1 subset does not occur as a general feature of murine systemic autoimmune disease. These observations, consistent with previous studies of Ig gene usage in autoreactive antibodies, support the view that expansion and differentiation of the CD5+ B cell subset is not a central event leading to autoantibody production.
1307073 [Rheumatic manifestations of acquired immunodeficiency syndrome (AIDS)]. 1992 Apr 120 AIDS patients (mean age 33 +/- 9 years, 108 males) were evaluated regarding rheumatic manifestations. According to CDC's classification, 18.3% belonged to group II, 28.3% to group III, and 53.4% to group IV. Arthralgia was present in 33 patients (27.5%), and in only 8 could be associated with infections other than HIV (5 cases of tuberculosis, 3 P. carinii, and 1 gonococcal infection). Incidence of arthralgia was equal in either sex. Arthritis was present in 8 patients, 2 of them with Reiter's syndrome. In 6 patients arthralgia was the first symptom (3 with arthritis) before AIDS diagnosis. There was a higher incidence of dry mouth, dry eyes, and muscular complaints in patients with arthralgia than in patients without arthralgia. Antinuclear antibodies and rheumatoid factor were absent in the serum of the patients studied. Arthritic manifestations possibly occur in AIDS, even in patients without other clinical manifestations, as a reactive state to HIV infection.
8431217 Prevention of autoimmune inflammatory polyarthritis in male New Zealand black/KN mice by t 1993 Feb OBJECTIVE: To prevent polyarthritis in male New Zealand black/KN (NZB/KN) mice by transplantation of both bone marrow cells (BMC) and bone (to recruit stromal cells) from normal mice. METHODS: Arthritic lesions in male NZB/KN mice injected intravenously with BMC plus bone from C57Bl/10 mice were compared with those in untreated male NZB/KN mice. RESULTS: Male NZB/KN mice engrafted with BMC plus bone were both radiologically and histopathologically normal, and had decreased production of anti-single-stranded DNA antibodies and rheumatoid factors at 8-12 months of age. CONCLUSION: Bone marrow transplantation prevented polyarthritis in male NZB/KN mice.
7686945 Human rheumatoid B-1a (CD5+ B) cells make somatically hypermutated high affinity IgM rheum 1993 Jul 1 To analyze the structure and formally ascertain the B-1a cellular origin of IgM rheumatoid factor (RF) autoantibodies, we generated 4 IgM RF mAb-producing cell lines using sorted (surface CD5+) B-1a cells from a patient with active rheumatoid arthritis. The RF mAb111, mAb112, mAb113, and mAb114 were monoreactive and displayed a relatively high affinity for human IgG Fc fragment (Kd, 3.1 x 10(-7) to 6.8 x 10(-7) M). The B-1a origin of the lymphocytes that gave rise to the IgM RF was confirmed by the expression of surface CD5 and specific CD5 mRNA by all mAb-producing cell lines. Analysis of the genes encoding the RF mAb VH and VL regions revealed that members of the VHI and VHIII families were utilized in conjunction with V kappa IIIa, V kappa IIIb, or V lambda I genes. JH3 and JH4 genes were each utilized twice. The H chain CDR3 sequences were divergent and variable in length. The RF mAb VH genes were identical or closely related to those expressed in the "restricted" fetal B cell repertoire and/or were JH-proximal. For instance, mAb111 VH gene likely constituted a mutated variant of the expressed fetal 20P3 which is the second most JH-proximal gene (125 kb from JH). In addition, the expressed VH and VL genes were among those that have been found to encode other RF, different autoantibodies, high affinity antibodies induced by exogenous Ag, and natural autoantibodies in the adult and neonatal B cell repertoires. When compared with those of known germline genes, the expressed V gene sequences displayed a number of differences. By cloning and sequencing DNA from PMN of the same patient whose B lymphocytes were used for the mAb generation, we showed that such differences resulted from somatic hypermutation in the RF mAb112 VH gene. The germline gene (112GL) that presumably gave rise to the RF mAb112 VH segment was identical to the expressed fetal 51P1 gene. The distribution and the high replacement to silent mutation ratio of the nucleotide mutations in RF mAb112 VH segment were highly consistent with their selection by Ag. RF mAb113 was clonally related to RF mAb112, as shown by the utilization of the same sets of VHI-D-JH4 and V kappa IIIb-J kappa 4 genes, displaying identical junctional sequences, and the presence of two identical replacement and one silent mutations.(ABSTRACT TRUNCATED AT 400 WORDS)
8605703 Soluble forms of P-selectin and intercellular adhesion molecule-3 in synovial fluids. 1996 Mar A number of adhesion molecules have been identified in synovial tissues of patients with rheumatoid arthritis (RA). Some of them are upregulated and may play an important role in the inflammatory processes of the diseased joint. In addition to synovial tissue cell surface expression, synovial fluids contain soluble forms of many adhesion molecules, such as intercellular adhesion molecule-1, E-selectin (sE-selectin), and L-selectin. In this study, we investigated the expression of soluble P-selectin (sP-selectin) and intercellular adhesion molecule-3 (sICAM-3) in synovial fluids from patients with RA, osteoarthritis (OA), and other forms of arthritis. sP-selectin and sICAM-3 levels in RA synovial fluids were significantly increased compared to those in OA. The levels of sP-selectin++ in synovial fluids correlated with sICAM-3 and sE-selectin in synovial fluids. The levels of sICAM-3 in synovial fluids correlated with synovial fluid leukocyte counts and erythrocyte sedimentation rate. In vitro, synovial fluid mononuclear cells produced sICAM-3 spontaneously. Elevated levels of sP-selectin and sICAM-3 in RA synovial fluids compared to OA may indicate inflammatory interactions between endothelial cells, leukocytes, and other synovial cells in the diseased joint.
7738955 The natural history of juvenile chronic arthritis: a population based cohort study. II. Ou 1995 Feb OBJECTIVE: To investigate the outcome in a population based cohort of patients with juvenile chronic arthritis (JCA) who were in the process of being transferred from pediatric to adult rheumatology care. METHODS: The cohort of patients born in 1968 through 1972, recruited from a population based epidemiological study in southwestern Sweden, were called to a followup after a median disease duration of 7.1 years. The study group consisted of 124 patients with a median age of 17.7 years. The disability and discomfort dimensions were evaluated using the Childhood Health Assessment Questionnaire (C-HAQ). The impact of the disease on social life was evaluated by patients and parents. RESULTS: The median C-HAQ disability index was 0.19 with a range from 0 to 2.75 (maximum possible score = 3). Sixty percent of the patients indicated some difficulty in daily activities. Female sex and a polyarticular disease course were risk factors for disability. The strongest determinants for disability were continuing disease activity and a positive IgM rheumatoid factor. Social impact of the disease was strongly linked to a raised C-HAQ disability index. CONCLUSION: Even in a population based study of JCA, which includes many mild cases, the majority of patients experienced some difficulty in daily activities when judged by themselves. This underlines the necessity to use the patient's own values in outcome studies, rather than the physician's. Further development of internationally accepted, standardized instruments to evaluate the handicap dimension of childhood arthritis is called for.
8923360 Aberrant vascularity and von Willebrand factor distribution in inflamed synovial membrane. 1996 Nov OBJECTIVE: Von Willebrand factor (vWF) is an adhesive glycoprotein produced and secreted constitutively by endothelial cells. vWF is released upon endothelial stimulation and/or vascular injury, and mediates adhesion and aggregation of platelets. Our aim was to quantify synovial vasculature and to evaluate vWF distribution in situ in synovial membranes in various arthritides. METHODS: Immunohistochemical staining of vWF in synovial membranes from patients with rheumatoid arthritis (RA) (N = 9), psoriatic (PsA) (N = 3), and reactive (ReA) (N = 4) arthritis, and from 6 noninflammatory controls: osteoarthritis (N = 1), chondromatosis (N = 1), meniscus lesion (N = 4). Morphometric assessments were performed with an image analyzer. RESULTS: In RA, mean number of blood vessels/mm2 in the thickened synovium was relatively low (131 +/- 57 vs control 257 +/- 115, p = 0.0137, ReA 346 +/- 83, p = 0.0002, PsA 434 +/- 157, p = 0.0127). In particular, the superficial layer, corresponding to the thickness of normal synovial membrane (i.e., 56 +/- 5 microns), was sparsely vascularized (70 +/- 37 in the superficial vs 219 +/- 104 in the deeper layer, p = 0.0047). Synovial thickening was not seen in ReA and PsA. In accordance with its constitutive metabolism, vWF was found in the endothelial cells, inside the blood vessels, and in the subendothelium. In addition, RA was characterized by weak endothelial immunoreactivity and perivascular vWF. In ReA, perivascular vWF staining was visible in areas of inflammatory cell infiltrates. CONCLUSION: Morphometric findings indicate decreased vascularization of the superficial synovial membrane in RA. Second, vWF may play a role in the inflammatory/reparative responses in synovium in RA and ReA, which were characterized by vascular stimulation/injury and abnormal vWF distribution.
7835974 Reduced galactosyltransferase mRNA levels are associated with the agalactosyl IgG found in 1994 Nov MRL-lpr/lpr strain mice have defectively glycosylated IgG. This may be related to the rheumatoid arthritis (RA)-like disease that occurs in these mice, because a similar glycosylation defect is seen in human subjects with RA. Whilst it is known that this defect is associated with reduced activity of the beta-1,4-galactosyltransferase (beta-1,4-GalTase) enzyme, the cause of this reduced activity is at present unknown. We have therefore examined the molecular genetics of beta-1,4-GalTase in MRL-lpr/lpr mice. Using 10 different restriction endonucleases we found no evidence for a polymorphic variant of the gene in glycosylation-defective mice. However, the level of mRNA for beta-1,4-GalTase was lowest in the MRL-lpr/lpr mice, the strain with the most poorly galactosylated IgG of the four strains examined. Thus, the reduced level of IgG oligosaccharide galactosylation found in MRL-lpr/lpr strain mice appears to be related to either an altered transcriptional level of, or altered mRNA stability for, beta-1,4-GalTase in lymphocytes from these mice.
1537526 A prospective study of risk for peptic ulcer disease in Seventh-Day Adventists. 1992 Mar Cross-sectional and prospective data were collected and analyzed to identify risk factors for the development of peptic ulcer disease in a population of 34,198 white, non-Hispanic Seventh-Day Adventists. On a life-style questionnaire administered in 1976, 3853 subjects reported ever having had a physician-diagnosed peptic ulcer for a lifetime prevalence of 13.5% for men and 11.0% for women. Odds ratios of greater than 2.0 (P less than 0.0001) were observed for use of "stronger pain relievers," current cigarette smoking, and history of rheumatism or other arthritis and coronary disease. For both sexes, lower but statistically significant odds ratios (P less than 0.05) were found for eating white bread, "snacking," ever having smoked cigarettes, low church involvement, poor dietary adherence, high blood pressure, rheumatoid arthritis, aspirin use, job frustration and dissatisfaction, having a "blue collar household," and having less education. During 3 years of follow-up, 154 incident cases of ulcer were identified. The average annual incidence was 1.7 per 1000. Multivariate adjusted relative risks were statistically significant for using stronger pain relievers (P less than 0.001), having rheumatic conditions (P = 0.006), and using aspirin (P = 0.013). These findings suggest that rheumatic disease and use of aspirin and stronger pain relievers are more important risk factors for development of peptic ulcer disease in certain populations than diet, life-style, or psychological or socioeconomic characteristics.
7497521 Suppression of collagen-induced arthritis by an angiogenesis inhibitor, AGM-1470, in combi 1995 Dec Pannus formation characterized by neovascularization is a prominent pathologic finding in both rheumatoid arthritis (RA) and rat collagen-induced arthritis (CIA). CIA is a T-cell-dependent process induced by immunization of inbred LOU rats with native type II collagen in incomplete Freund's adjuvant. AGM-1470 is a highly specific inhibitor of new blood vessel formation by its effects on endothelial cell migration, endothelial cell proliferation, and capillary tube formation. Cyclosporin A (CSA) is an immunomodulating agent that inhibits IL-2 and other cytokine production involved in early antigen activation of T-cells. In this study the effects of single and combination therapy with AGM-1470 (27 mg/kg alternate days) and low-dose CSA (4 mg/kg/day continuous infusion via osmotic pump) on established CIA (total n = 62) were examined. At Day 18 post arthritis onset, clinical arthritis was significantly reduced in rats treated with single-agent AGM-1470 (1.88 +/- 0.33) or combination therapy (1.13 +/- 0.32) (P < 0.00001 and 0.000001, respectively) versus control. Single-agent CSA-treated rats, even if given CSA beginning on the day of immunization, did not attenuate arthritis severity. THe longitudinal mean arthritis score of combination-treated rats was significantly lower than that of rats receiving AGM-1470 (P < 0.0001), reflecting a more moderate early disease course in combination-treated rats. Disease severity in rats treated with single-agent CSA was not significantly different from control rats. Mean WBC counts, differentials, and delayed-type hypersensitivity responses were similar in all groups. CII antibody levels were lower in AGM-1470 protocols compared to CSA or controls. Flow cytometry of peripheral blood, spleen, and lymph nodes demonstrated decreased levels of CD4+ cells in rats given CSA. TNF-alpha levels remained elevated, even in treated rats, while vascular endothelial growth factor levels were reduced in rats receiving AGM-1470 compared to both arthritic controls and naive rats. Both single-agent and combination therapies were well tolerated. This is the first study to examine the effects of AGM-1470 together with CSA. Combination therapy was more effective than single-agent therapy. The results suggest that the use of interventions with distinct mechanisms of action may be efficacious in the treatment of RA.
8624631 Correlates of disablement in polyarticular juvenile chronic arthritis--a cross-sectional s 1996 Jan To assess the impact of disease on the functional outcome of patients with polyarticular juvenile chronic arthritis (JCA), the relationship between impairments and functional limitations was studied. Therefore, variables from the impairment domain were correlated with variables of the functional limitation domain and outcome variables were analysed for differences as a result of inflammatory disease, rheumatoid factor (RF), disease duration and age at onset. Twenty-three patients with polyarticular JCA were subjected to auxologic evaluation, a laboratory check, radiographic evaluation, joint count on tenderness and swelling, joint mobility/deformity examination, functional assessment of skills, health assessment and psychosocial evaluation. Inflammatory disease parameters, like CRP, ESR, thrombocytosis and leucocytosis, were increased in 6/23 patients. The parameters of the impairment domain, like joint tenderness and swelling, showed mild outcome, while parameters of the functional limitation domain showed more severe outcome. Generally, perceived competence was found to be normal. A clinically relevant number of patients (10/13) showed low scores on the activity factor of the Child Behaviour Check List (CBCL). A significant relationship was found between inflammatory disease variables and functional limitation outcome. RF seropositivity was not a good outcome predictor. Disease duration and age of onset showed no significant difference in the outcome of the domains. Significant correlation was found between the parental report of the Childhood Health Assessment Questionnaire (CHAQ) and all impairment parameters. Joint swelling showed a significant relationship with CHAQ and Juvenile Arthritis Functional Assessment Report (JAFAR). Disability outcome did not correlate with functional limitation. In general, children with polyarticular JCA function rather well when using a multidomain evaluation approach. Compensatory and adaptational mechanisms might contribute to the poor correlation between impairment and functional limitation parameters. Laboratory evaluation of inflammatory disease, a joint count of swollen joints and parent's report of the child's health status related best in our study.
9239815 Decay-accelerating factor (DAF, CD55)-negative T lymphocytes in the peripheral blood of Sj 1996 Oct OBJECTIVE: To clarify possible associations of decay-accelerating factor (DAF, CD55), expressed on circulating lymphocyte subsets and other hematologic cells, with corresponding cytopenias observed in primary Sjögren's syndrome (SS). METHODS: DAF expression on peripheral blood (PB) cells was determined in 21 patients with SS and 11 healthy controls by single or 2 color flow cytometry. RESULTS: In the PB from SS patients, anemia, monocytopenia, neutropenia, and lymphocytopenia were observed. Compared to the controls, the percentages of DAF-negative cells were higher in CD4+ and CD8+ T cell subsets from SS patients, but the expression of DAF was similar in the other PB cells, including CD19+ B cells, CD56+ NK cells, monocytes, granulocytes, and erythrocytes. The percentages of DAF-negative cells among the CD4+ and CD8+ cells were positively correlated in SS patients, but the numbers of cells in both subsets were decreased in those patients being treated with prednisolone. However, these proportional changes are thought to reflect a decrease in the numbers of DAF-positive CD4+ and CD8+ cells, because the absolute numbers of circulating DAF-positive CD4+ and CD8+ cells, but not DAF-negative cells, were significantly decreased in SS patients. In addition, DAF-negative cells were detectable in both CD45RA+ (naive) and CD45RO+ (memory) T cells from healthy individuals, and the expression of DAF was remarkably increased in both subsets after in-vitro activation with concanavalin-A. CONCLUSION: DAF-negative cells are proportionally increased among circulating CD4+ and CD8+ T cells in SS patients, although such changes are due to decreased numbers of DAF-positive cells within each subset. When considering previous observations, the DAF-negative CD4+ and CD8+ cells probably belong to activated T cell subsets in both SS patients and controls. However, the patterns of DAF expression seemed to be different between activated T cells recognized in the PB, and those induced by in vitro-stimulation.
8966840 Risk factors of calcium stone formation in patients with primary Sjögren's syndrome. 1996 Distal renal tubular acidosis (dRTA), which occurs in patients with primary Sjögren's syndrome (SS), is a risk factor for the development of urolithiasis. Twenty-seven patients with SS were evaluated with respect to biochemical risk factors of calcium stone formation. Sixteen had no history of urolithiasis (group 1) whereas 11 had such a history (group 2). The stone composition was known for seven of the patients, and calcium phosphate was the major stone constituent in all of them. dRTA was present in all patients in group 2, and in 7 of the 16 patients in group 1. Hypocitraturia was common in both groups, and the urinary excretion of citrate did not differ between the two groups. There was a higher urinary excretion of calcium and urate in group 2 and this group also had a higher urine volume. The risk of forming a urine supersaturated with calcium oxalate (CaOx) expressed in terms of AP(CaOx)index(s), which is an approximate estimate of the ion-activity product of CaOx calculated for a 24-h urine volume of 1500 ml, was higher in stone formers. A similarly derived estimate of the ion-activity product of calcium phosphate, AP(CaP)index(s), was calculated for a urine pH of 7. Although AP(CaP)index(s) was not significantly higher in group 2, there was a good correlation between AP(CaP)index(s) and AP(CaOx)index(s). We conclude that the urine composition in patients with SS, dRTA and urolithiasis is similar to that of other stone-forming patients with dRTA, and recurrence preventive therapy can be designed as for these patients.
8176076 Salivary gland dysfunction: causes, symptoms, treatment. 1994 Apr The three most common known causes of salivary gland dysfunction are medication usage, radiation therapy and Sjogren's syndrome. Current therapeutic options to treat salivary dysfunction are limited. Clinical considerations as well as the outlook for individuals experiencing salivary dysfunction are discussed.
8129768 Clinical significance of antibodies to native or denatured 60-kd or 52-kd Ro/SS-A proteins 1994 Jan OBJECTIVE: To evaluate the clinical significance of antibodies to native or denatured (anti-n or anti-d) 60- or 52-kd Ro/SS-A proteins (60K or 52K) in Sjögren's syndrome (SS). METHODS: The presence of antibodies to denatured and native Ro/SS-A proteins was determined by immunoblotting and immunoprecipitation, respectively. Salivary gland dysfunction was evaluated by salivary function scintigraphy. RESULTS: The incidence of anti-d-60K without anti-d-52K was lower among patients with systemic lupus erythematosus with SS (SLE/SS) and among those with primary SS, compared with patients who had SLE without SS, whereas anti-d-52K without anti-d-60K was more common in SLE/SS patients and primary SS patients than in SLE patients without SS. All of the patients with anti-Ro/SS-A had anti-n-60K. Serologic abnormalities and salivary gland dysfunction were associated with anti-n-60K in SS, whereas Hashimoto's thyroiditis in SS was related to anti-d-60K. Anti-d-52K was not associated with any extraglandular or glandular symptoms in SS. CONCLUSION: The data indicate that anti-n-60K, which appears to recognize conformational epitopes, is associated with clinical features of SS characterized by glandular dysfunction.
8312661 Mixed connective tissue disease presenting myasthenia gravis. 1993 Aug We herein describe a 41-year-old female patient with an association of myasthenia gravis (MG) with anti-acetylcholine receptor (AcR) antibody, mixed connective tissue disease (MCTD) and Sjögren's syndrome (SjS). We reviewed the reported association of MG and MCTD, systemic lupus erythematosus, progressive systemic sclerosis, polymyositis and dermatomyositis, and SjS. Since we could find only two patients who fulfilled the diagnostic criteria for MCTD in the previous literature, we concluded that the association of MG and MCTD is rare. We also discuss the coexistence of SjS as one of the underlying pathological conditions for the association of MG and various connective tissue diseases including MCTD.
8763097 [Sicca syndrome and hepatitis C virus infection: a Gougerot-Sjögren pseudo-syndrome?]. 1996 These last years, different virus have been incriminated in the etiopathogeny of the primary-Sjögren's syndrome and more particularly the hepatitis C virus. We have led a prospective study over 23 patients presenting a primary Sjögren's syndrome, searching for a sign of infection by the hepatitis C virus and over 23 patients presenting an active chronic hepatitis C virus searching for a Gougerot-Sjögren syndrome. The overcoming of the hepatitis C virus in the Sjögren group was 4.7% which was not significatively higher than in our sample of population. Parallelly, the search of the Sjögren's syndrome, in the hepatitis C virus group, found 4 patients (feminine, average age 48.5 years old) whose clinical board was compatible with this diagnostic. Antinuclear antibodies have not been found in any of the 23 patients. The lymphocytic typing of the infiltrate in the minor salivary glands biopsies showed a predominance of the CD8 lymphocytes in a proportion of 2/1, contrasting with what is observed in primary Sjögren's syndrome. We concluded that hepatitis C virus may be more associated with a chronic lymphocytic sialadenitis than an authentic primary Sjögren's syndrome.
7634859 Pulmonary findings in patients with primary Sjögren's syndrome. 1995 Aug STUDY OBJECTIVE: To evaluate pulmonary findings in patients with primary Sjögren's syndrome (SS). DESIGN: Prospective data collection. PATIENTS: Seventeen consecutive nonsmoking patients with primary SS. MEASUREMENTS AND RESULTS: Mild radiologic parenchymal changes were seen in two patients. Pulmonary hyperinflation (residual volume/total lung capacity [RV/TLC] percent ratio measured minus [-] RV/TLC percent ratio predicted > or = 8) was observed in 9 (53%) patients, whereas obstructive and restrictive changes were infrequently found in ordinary spirometry (FVC, FEV1, FEV%) (none and two cases, respectively). Patients with SS with hyperinflation had significantly lower maximal expiratory flow MEF50 (p < 0.05), MEF25 (p < 0.05), and higher total lung capacity (p < 0.05) and FRC (p < 0.05) values as compared with those patients with SS without hyperinflation. They were also more frequently dyspnoeic (six vs none, p < 0.02) and had higher mean serum beta 2-microglobulin levels (3.6 +/- 1.0 mg/L vs 2.6 +/- 0.7 mg/L, p < 0.025). The levels of serum beta 2-microglobulin correlated inversely with FVC (r = - 0.583, p < 0.01), FEV1 (r = - 0.533, p < 0.05), diffusing capacity for carbon monoxide (r = - 0.580, p < 0.01); its correlation with RV/TLC percent ratio was positive and relatively significant (r = 0.447, 0.05 < p < 0.10). CONCLUSIONS: Pulmonary hyperinflation associated with diminished peripheral spirometric flow values is frequently found in patients with primary SS. This together with the correlation of disturbed lung function parameters to elevated serum beta 2-microglobulin levels suggests that lungs and especially small airways may be an usual target organ in primary SS.
7748018 Cytokine and adhesion molecule expression in the minor salivary glands of patients with Sj 1995 Mar OBJECTIVE: To investigate the role of cytokines and cell adhesion molecules in the pathogenesis of Sjögren's syndrome (SS). METHODS: Using an indirect immunoperoxidase technique we assessed the expression of the cytokines interleukin-1 alpha (IL-1 alpha), interleukin-1 beta (IL-1 beta), interleukin-8 (IL-8), transforming growth factor beta (TGF beta) and granulocyte macrophage colony stimulating factor (GM-CSF), of the adhesion molecules intercellular adhesion molecule-1 (ICAM-1), lymphocyte function associated antigen-1 (LFA-1), the activated molecular form of LFA-1 (NKI-L16), CD2, and LFA-3, and of a panel of cellular markers in the minor salivary glands. RESULTS: In SS and chronic sialoadenitis (CS), the ductal epithelial cells and acini expressed all the cytokines examined. The percentage of glandular mononuclear cells which stained positive for cytokines did not differ significantly between SS and CS. NKI-L16 was detected on 33.6 (SD 10.1)% and 15.3 (4.3)% of LFA-1 cells in SS and CS, respectively (p < 0.002). CONCLUSION: SS and CS did not differ in the pattern of cytokines examined. The characteristic cell clustering seen in the salivary glands in SS may be caused by the upregulation of NKI-L16.