[Antibiotic treatment in rheumatoid arthritis?].
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Anti-Bacterial Agents↗
Biomedical subjects
M Leirisalo-Repo
Publications and source records attributed to M Leirisalo-Repo.
High frequency of silent inflammatory bowel disease in spondylarthropathy.
OBJECTIVE: To search for an association between gut infection, gut inflammation, and spondylarthropathies. METHODS: Ileocolonoscopy was performed in 118 patients with various inflammatory and noninflammatory joint diseases and in 24 patients with uncomplicated acute bacterial gastroenteritis. RESULTS: Endoscopic lesions were more frequent in patients with spondylarthropathy (44%) compared with those with other inflammatory arthritides (6%; P = 0.001). Ileal changes were observed only in patients with spondylarthropathy (20% versus 0%; P = 0.01). Inflammatory bowel disease was the endoscopic diagnosis in 19% of the arthritis patients. Possible or definite Crohn's disease was diagnosed in 26% of patients with chronic spondylarthropathy, and ulcerative colitis in 1 patient with rheumatoid arthritis and in 1 with chronic uroarthritis. Histologic evidence of inflammation differed less distinctly than endoscopy findings between patients groups. There was no association of gut lesions with the use of nonsteroidal antiinflammatory drugs or with the presence of HLA-B27. CONCLUSION: Gut inflammation is frequent in patients with spondylarthropathy, and one-fourth of the patients who have chronic disease have early features of Crohn's disease.
Adolescent↗
Type I collagen degradation product in serum of patients with early rheumatoid arthritis: relationship to disease activity and radiological progression in a 3-year follow-up.
The new assay of cross-linked carboxyterminal telopeptide of type I collagen (ICTP), a serum marker for bone collagen degradation, was evaluated in serial measurements of 66 patients with early RA during a 3-yr prospective study. Initially 51% of RA patients had elevated levels of serum ICTP compared to healthy controls. During the subsequent months after starting anti-rheumatic treatment, the mean ICTP levels decreased in parallel with the clinical and laboratory variables measuring disease activity. Despite marked clinical improvement with anti-rheumatic treatment, a steady increase in radiological progression of joints was observed. Throughout the follow-up serum ICTP levels correlated with inflammatory parameters and from the first year on with the radiological changes assessed annually. However, initial serum ICTP levels correlated better than the other variables of disease activity with the subsequent erosive progression of joints indicating that measurement of serum ICTP may serve as one of the prognostic markers for joint damage in early RA.
Adult↗
Reactive arthritis following an outbreak of Salmonella infection in Finland.
The incidence and clinical features of reactive arthritis (ReA) following an outbreak of enteritis caused by Salmonella enterica ssp. enterica serovar 4,5,12:b:-were studied in the autumn of 1992. The outbreak occurred in several municipalities and originated from sprouted mung beans. A questionnaire on extra-enteric manifestations such as joint and eye symptoms was mailed 2 to 5 months after the outbreak to all bacteriologically proven cases. Two hundred and forty-six of the 272 (90%) subjects responded to the questionnaire; 224 (91%) reported having had enterocolitis, 22 (9%) were asymptomatic. Sixteen subjects fulfilled the criteria for ReA, and one had irities only. Thus, the incidence of ReA/iritis after S. enterica was 6.9%. Only four of the 155 (3%) subjects aged less than 16 yr developed ReA, as compared with 12 of the 91 (13%) older patients (P < 0.001). The only patient with iritis was also more than 16 yr old. The joint symptoms were oligoarticular in 10 (63%), monoarticular in five (31%) and polyarticular in one (6%). The most frequently affected joints were the wrists, knees and ankles. Joints of upper extremities only were affected in three (19%), of the lower extremities only in six (37%) and of both in seven (44%) subjects. In the majority of the patients ReA was mild. The joint symptoms persisted for less than 1 month in six, 2 to 6 months in five and more than 6 months in five. Thirteen subjects with ReA/iritis were tissue-typed for HLA; four (33%) had HLA-B27.(ABSTRACT TRUNCATED AT 250 WORDS)
Adolescent↗
Enteropathic arthritis, Whipple's disease, juvenile spondyloarthropathy, and uveitis.
An association between inflammatory bowel disease and enteroarthritis and the spondyloarthropathies has been known of for a while. Within the past few years, ileocolonic studies have expanded the diagnostic accuracy of asymptomatic gut inflammation, and it now seems evident that chronic gut inflammation is either associated with or is even the cause of chronicity of peripheral arthritis and the development of ankylosing spondylitis. This situation, previously studied in adult patients, now appears also to affect pediatric patients with spondyloarthropathies, who seem to have similar genetic and inflammatory bowel findings. Chronic infection in the gut has been demonstrated in Whipple's disease. Analogously, infection or immunologic aberrations probably contribute to chronicity in other forms of spondyloarthropathy. Infection also might be involved, at least partly in attacks of uveitis, but activation of immunologic mechanisms can mediate tissue destruction during eye inflammation.
Adult↗
Alkali-treated LPS of Yersinia enterocolitica does not induce expression of E-selectin, ICAM-1 or VCAM-1 on endothelial cells but may mediate antibody- and complement-dependent cell injury.
Lipopolysaccharide (LPS) prepared from a rough mutant of Salmonella typhimurium and deacylated enzymatically (dLPS) does not promote neutrophil adherence to human umbilical vein endothelial cells (HUVECs). This paper reports that similarly, a smooth form of LPS prepared from Yersinia enterocolitica O:3, a serotype known to trigger reactive arthritis in humans, and treated with alkali (yersinia LPS-OH) failed to augment neutrophil adherence to HUVECs. Studies of the mechanism underlying the poor augmentation revealed that neither enzymatically deacylated LPS from Escherichia coli J5 (J5 dLPS) nor yersinia LPS-OH stimulated expression of endothelial cell adhesion molecules E-selectin, VCAM-1 and ICAM-1, whereas both intact J5 LPS and yersinia LPS were stimulatory. Impaired up-regulation could not be explained by decreased binding of yersinia LPS-OH to HUVECs. Furthermore, 51Cr-labelled HUVECs treated with different concentrations of yersinia LPS-OH released 51Cr in the presence of anti-yersinia anti-O antibody and complement. J5 dLPS and yersinia LPS-OH inhibited up-regulation of the adhesion molecules induced by J5 LPS and yersinia LPS but not that induced by tumour necrosis factor alpha. Taken together, the results suggest that although yersinia LPS-OH can depress development of acute inflammation by inhibiting up-regulation of endothelial-cell adhesion molecules, sufficient LPS-OH is bound to induce cell injury and thereby inflammation in the presence of specific antibody and complement. The findings may have pathogenetic implications in yersinia-triggered reactive arthritis characterized by dissemination of yersinia LPS throughout the body.
ABO Blood-Group System↗
Different DRB1*04 alleles predominate in the Finnish random population and in HLA-B27-positive subpopulations.
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Alleles↗
The present knowledge of the inflammatory process and the inflammatory mediators.
Endothelial damage, synovial oedema, fibrin deposition, polymorphonuclear cell (PMN) invasion, and mild lining cell hyperplasia characterize acute inflammatory arthritis. Later on, perivascular tissue is infiltrated by mononuclear cells. The early events are mediated by interactions between PMNs and endothelial cells. Both parts in the adhesion event are activated with multiple stimuli resulting in complex interactions of varying intensity and duration. Adhesion molecules present on the surface of PMNs (L-selectin) or induced by inflammatory stimuli (beta 2-integrins) mediate PMN adhesion to activated endothelium, which has counter receptors (E-selectin for L-selectin and ICAM-1 and ICAM-2 for beta 2-integrins). At the initial phase L-selectin initiates the rolling of PMNs on endothelial cells. Further stimuli result in a more prolonged adhesion between PMNs and endothelium. At the side of endothelium, induction of P-selectin and PAF by histamine, thrombin and LTC4 contribute to the acute rolling of PMNs on endothelial surface. Tumor necrosis factor (TNF), interleukin-1 (IL-1) and lipopolysaccharide activate endothelial cells to synthesize interleukin-8 (IL-8), a potent chemotactic and proadhesive mediator for PMNs, and further adhesion molecule (E-selectin), a mediator of long-term adhesion between PMN and endothelium. After adhesion and migration to the focus of inflammation, PMNs induce inflammation by aggregating, releasing hydrolyzing enzymes, generating lipid peroxidation products such as prostaglandins and LTB4, and oxygen derived free radicals. In studies on the pathogenesis of seronegative spondyloarthropathies, we have shown persistently aberrant PMN function evidenced by enhanced chemotaxis and high production of toxic oxygen derived free radicals by PMN.(ABSTRACT TRUNCATED AT 250 WORDS)
Arthritis, Reactive↗
HSP70-Hom NcoI polymorphism and HLA-associations in the Finnish population and in patients with ankylosing spondylitis or reactive arthritis.
The NcoI polymorphism of the HSP70-Hom gene was investigated in the Finnish population and in two HLA-B27-associated autoimmune diseases. The two HSP70-Hom alleles were shown to be strongly associated to some specific HLA-B/DR haplotypes in random Finnish population and the segregation of the alleles as a part of these haplotypes was confirmed in 18 families. In addition, the HSP70-Hom alleles of 31 patients with ankylosing spondylitis (AS) and 38 with reactive arthritis (ReA) were compared with each other and with 56 unrelated healthy HLA-B27 positive individuals. The results indicated that the HSP70-Hom polymorphic variation is not connected independently to the different pathogenesis of AS and ReA, as no statistically significant differences between the patient groups and/or controls could be found. The HSP70-Hom status was investigated also in 28 homozygous HLA typing cells and when compared with previously published results of HSP70-l and HSP70-2 polymorphisms, it appeared that these three MHC Class-III linked HSP70 genes segregated in fixed allelic combinations.
Arthritis, Reactive↗
Side effects of sulphasalazine in patients with rheumatic diseases or inflammatory bowel disease.
We compared sulphasalazine (SSZ) toxicity in 140 patients (196 treatment periods) of two patient groups, those with rheumatoid disease (RD) (rheumatoid arthritis, RA, ankylosing spondylitis, AS), and those with inflammatory bowel disease (IBD). Adverse events occurred in 64% of all patients (highest 85% in AS and lowest 50% in ulcerative colitis, CU). There were more recorded adverse events in patients with RD than in patients with IBD. Hepatic side effects were more frequent in patients with IBD than in patients with RD. Adverse events were the most common reason for discontinuing the treatment (in 34.8% of AS patients, in 46.2% of RA patients, in 21.7% of the Crohn's disease patients and in 32.6% of CU patients). There were no lethal or permanent adverse events. Age, sex, rheumatoid factor and HLA-B27 antigen positivity did not influence on the appearance of adverse events.
Adult↗
[How to facilitate the rehabilitation of patients with musculoskeletal symptoms].
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Absenteeism↗
[Relationship between intestinal inflammation and arthritis].
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Adolescent↗
Antibodies to Klebsiella pneumoniae, Escherichia coli, and Proteus mirabilis in ankylosing spondylitis: effect of sulfasalazine treatment.
OBJECTIVE: To make a longitudinal study of antibodies to Klebsiella pneumoniae in patients with ankylosing spondylitis (AS) and to assess treatment effects. As a comparison we measured antibodies of 2 other gut associated bacteria, Escherichia coli and Proteus mirabilis. METHODS: In a double blind study in 84 Finnish outpatients with AS before and after 26 weeks' treatment with sulfasalazine or placebo we measured serum antibodies to Klebsiella pneumoniae, E. coli and Proteus mirabilis with ELISA: Serum samples of 100 healthy blood donors served as controls. RESULTS: The levels of IgA class antibodies to all 3 bacteria were statistically significantly higher in the sera of the patients compared to the controls. During sulfasalazine treatment significant decreases were observed in concentrations of the IgA class antibodies to Klebsiella and E. coli whereas only a slight decrease was observed in the concentrations of IgA antibodies to Proteus mirabilis. There were no correlations between the clinical and laboratory results observed with sulfasalazine and decrease in concentrations of IgA class antibodies. CONCLUSION: Our results agree with the role of gut associated lymphoid tissue in the pathogenesis of AS, but do not totally exclude Klebsiella pneumoniae as a specific agent contributing to the development of AS.
Adult↗
Subcutaneously administered recombinant interferon-gamma in humans: pharmacokinetics and effects on chemiluminescence responses of alveolar macrophages, blood neutrophils, and monocytes.
A Phase I trial was conducted to investigate the clinical toxicity, pharmacokinetics, and chemiluminescence (CL) responses of alveolar macrophages (AMs), peripheral blood neutrophils, and monocytes after subcutaneous injection of recombinant interferon-gamma (rIFN-gamma). Six patients with lung cancer received rIFN-gamma subcutaneously as single doses of 0.2, 0.6, and 1.8 mg. Bronchoalveolar lavage was performed three times: 21 h before as well as 6-7 and 27 h after injection. Serum samples were taken five times during the 27-h follow-up. IFN concentrations were measured from alveolar epithelial lining fluid (ELF) and serum by using an antiviral bioassay. IFN-gamma was not detectable in ELF after subcutaneous injection. AMs did not effect an increase in CL responses to N-formyl-methionyl-leucyl-phenylalanine or to phosphate-buffered saline. Circulating IFN-gamma was detectable at 3-12 h after an injection of 1.8 mg of rIFN-gamma, the highest dose given. CL responses of peripheral blood monocytes increased in all patients after injection, whereas the responses of neutrophils were less clear-cut. All patients developed systemic side effects such as transient fever, nausea, headaches, and flu-like symptoms. The findings suggest that rIFN-gamma passes poorly from the blood to the pulmonary alveoli. On the basis of this and our previous findings of increased CL responses in AMs and measurable IFN concentrations in ELF after inhalation of rIFN-gamma, we recommend inhalation rather than the parenteral route of IFN-gamma for the treatment of respiratory diseases.
Adult↗
Flow cytometric determination of CD11b upregulation in vivo.
We describe a flow cytometric method to evaluate upregulation of peripheral blood neutrophil and monocyte integrin CD11b in vivo. To avoid spontaneous upregulation in vitro, buffy coat cells were separated on ice and all subsequent cell handling steps were carried out at 0-4 degrees C. Such leukocytes were 95-100% viable, as determined by PI staining. Buffy coat leukocytes were double-stained with CD11b PE-conjugated and CD14 FITC-conjugated monoclonal antibodies and, in addition, with the nucleic acid dye LDS-751. After staining, firstly, LDS-751 positive (+ve) leukocytes, and, secondly, CD14 +ve monocytes were collected in live mode. Aggregated and irrelevant cells were gated out on the basis of their LDS-751 staining pattern and cellular light scattering properties, and the CD11b expression on neutrophils and monocytes was determined. Upregulation of CD11b in vitro was significantly affected by factors such as cell handling temperature, pre-fixation of blood samples, and density gradient separation of the cells. Incubation of aliquots of buffy coat cell suspension supplemented with FMLP for 5 min or without FMLP supplement for 15 min at 37 degrees C significantly increased CD11b expression without affecting cell viability. We have demonstrated that CD11b is expressed at maximal levels on arthritic synovial fluid neutrophils and CD14 +ve cells, and at increased but submaximal levels on peripheral blood neutrophils and monocytes of patients recovering from sepsis. The results suggest that the method can be used to evaluate in vivo upregulation of CD11b.
Adult↗
Crossreaction between antibodies to oxidised low-density lipoprotein and to cardiolipin in systemic lupus erythematosus.
Serum lipoproteins contain phospholipids and modified low-density lipoprotein (LDL) may thus act as a target for antiphospholipid antibodies. Raised concentrations of IgG antibodies against oxidised LDL were found in 47 of 61 (80%) patients with systemic lupus erythematosus (SLE). 46% of patients also had raised concentrations of IgG anticardiolipin antibodies. Binding of anticardiolipin antibodies to solid-phase cardiolipin was inhibited by oxidised LDL but not by native LDL in 16 of 21 sera from SLE patients. These observations suggest crossreactivity between antiphospholipid antibodies, which are closely associated with thrombosis in SLE, and antibodies to oxidised LDL, thus providing a possible link between thrombotic and atherosclerotic complications in SLE.
Adult↗
Functions of polymorphonuclear leukocytes in early rheumatoid arthritis.
We carried out a prospective study on clinical variables and functions of polymorphonuclear leukocytes (PMNs) of 20 patients with early rheumatoid arthritis (RA) and compared the results with the presence of erosions before treatment and at a one-year follow-up. Migration of PMNs determined by agarose and filter assays and respiratory burst of PMNs determined by luminol-enhanced chemiluminescence (CL) test were studied both before starting RA-modifying treatment and 6-12 (mean 7.3) months later. PMNs of the patients without erosions at one year, as compared to the patients with erosions, showed significantly depressed migration into filter and significantly depressed CL responses to N-formyl-methionyl-leucyl-phenylalanine, both before starting the treatment and at 7.3 months. Although causality remains uncertain, the results suggest that depressed functional capacity of PMNs is associated with low risk of joint destruction in early RA.
Adult↗
Rheumatoid arthritis as a cause of cardiac compression. Favourable long-term outcome of pericardiectomy.
In order to clarify the significance of rheumatoid arthritis (RA) as a cause of cardiac compression, we scrutinized pericardiectomy files of 47 patients over a ten-year period at two university hospitals in Finland. Five patients with RA were found. All the patients with RA were men with seropositive disease and subcutaneous rheumatoid nodules. Two of the patients had pulmonary fibrosis, one had cutaneous vasculitis and three had had rheumatoid pleurisy. There was a mean delay of 10 months from the first cardiac symptom to the diagnosis of cardiac compression, the most common misdiagnosis being primarily a liver disease. On the basis of clinical and operative data, four out of the five patients had constrictive pericarditis and one had an effusive-constrictive form of the disease. The histopathological findings in all cases were consistent with chronic fibrosing pericarditis. A follow-up of seven to seventeen years of four patients has not revealed any signs of recurrent pericardial disease. Our results demonstrate that RA is an important aetiological factor for cardiac compression. The long-term outcome of this manifestation seems to be good after pericardiectomy.
Adult↗