Biomedical subjects

J D Ji

Publications and source records attributed to J D Ji.

At least 19 recordsLinked to original sources

PubMed2006

The PTPN22 C1858T functional polymorphism and autoimmune diseases--a meta-analysis.

OBJECTIVE: To assess whether combined evidence shows the association between the protein tyrosine phosphatase non-receptor 22 (PTPN22) C1858T polymorphism and autoimmune diseases, and to summarize the effect size of the polymorphism associated with susceptibility of autoimmune diseases. METHODS: We surveyed studies on the PTPN22 C1858T polymorphism and autoimmune diseases using comprehensive Medline search and review of the references. Meta-analysis was performed for genotypes T/T (recessive effect), T/T + C/T (dominant effect) and T-allele in random effects models. RESULTS: Twenty-nine studies with 43 comparisons including 13 rheumatoid arthritis (RA), six systemic lupus erythematosus (SLE), six type-1 DM (T1D), three Grave's disease (GD), four inflammatory bowel diseases (IBD), three juvenile idiopathic arthritis (JIA), two psoriasis, two multiple sclerosis, two Addison's disease and two Celiac disease were available for the meta-analysis. The overall odds ratios (ORS) for T-allele, T/T and T/T + C/T genotypes were significantly increased in RA, SLE, GD and T1D (OR for T-allele = 1.58, 1.49, 1.85, 1.61, respectively, P < 0.00001). This meta-analysis showed the association between the T-allele and the T/T genotype and JIA (OR = 1.34, P = 0.03; OR = 1.97, P = 0.02) but did not reveal the association between the PTPN22 C1858T polymorphism and IBD, psoriasis, multiple sclerosis, Addison's disease and Celiac disease. CONCLUSION: This meta-analysis demonstrates that the PTPN22 1858T allele confers susceptibility to RA, SLE, GD, T1D and JIA, supporting evidence of association of the PTPN22 gene with subgroup of autoimmune diseases.

Autoimmune Diseases↗

PubMed2005

Genome scan meta-analysis of rheumatoid arthritis.

OBJECTIVE: Genome scans for rheumatoid arthritis (RA) have yielded inconsistent results. The absence of replication of linkage might be due to lack of power of individual studies. We performed a genome scan meta-analysis of published data to increase statistical power and to assess evidence for linkage of RA across genome scan studies. METHODS: Four RA whole-genome scans containing 767 families with 964 sibling pairs were included for the genome scan meta-analysis (GSMA). The GSMA method was applied to pool the results obtained from four genome scans. For each study, 120 genomic bins of approximately 30 centimorgans were defined and ranked according to maximum evidence for linkage within each bin. Bin ranks were weighted and summed across all studies. The summed rank for each bin was assessed empirically for significance using permutation methods. RESULTS: A total of nine bins lay above the 95% confidence level (P=0.05) and four bins were above the 99% confidence level (P=0.01) in the RA GSMA, suggesting that these bins contain RA-linked loci: bins 6.2, 6.4, 8.1, 18.3, 12.3, 12.2, 1.5, 6.3 and 16.2. The strongest evidence for linkage occurred on chromosome 6p22.3-6p21.1 (bin 6.2), containing the HLA region (P(sumrnk)=0.0000008). CONCLUSION: This RA GSMA confirmed the evidence for HLA loci as the greatest susceptibility factor to RA and showed evidence for linkage at non-HLA loci, such as chromosomes 1p, 6, 8p, 12, 16 and 18q, across studies. These data may provide a basis to carry out targeted linkage and candidate gene studies, particularly in the regions.

Arthritis, Rheumatoid↗

PubMed2005

Inhibition of IL-10-induced STAT3 activation by 15-deoxy-Delta12,14-prostaglandin J2.

OBJECTIVES: 15-Deoxy-Delta12,14-prostaglandin J2 (15d-PGJ2) is a natural ligand that activates the peroxisome proliferator-activated receptor (PPAR)-gamma, a member of the nuclear receptor family implicated in the regulation of lipid metabolism and adipocyte differentiation. Recent data have shown that 15d-PGJ2 exerts anti-inflammatory action via inhibition of the interferon gamma (IFN-gamma)-induced Jak-STAT signalling pathway. The anti-inflammatory effect of IL-10 is mediated via activated STAT3 (signal transducer and activator of transcription 3). In this study, we investigated whether 15d-PGJ2 inhibit IL-10-induced STAT activation. METHODS: We used western blotting, flow cytometric analysis and a real-time polymerase chain reaction. RESULTS: 15d-PGJ2 blocked IL-10-induced STAT1 and STAT3 activation in primary human monocytes, macrophages and THP-1 cells. Inhibition was not specific for IL-10, as induction of STAT activation by IFN-gamma and IL-6 was also inhibited by 15d-PGJ2. Inhibition of IL-10 signalling was induced within 1 h after pretreatment of 15d-PGJ2. Other PPARgamma agonists, such as troglitazone, did not inhibit IL-10 signalling. Treatment with GW9662, a specific PPARgamma antagonist, had no effect on 15d-PGJ2-mediated inhibition of IL-10 signalling even at higher concentrations (50 microM), indicating that 15d-PGJ2 affects the IL-10-induced Jak-STAT signalling pathway via an PPARgamma-independent mechanism. Actinomycin D had no effect on 15d-PGJ2-mediated inhibition of IL-10 signalling, indicating that inhibition of IL-10 signalling occurs independently of de novo gene expression. Also, inhibitors of extracellular signal-regulated kinase (ERKs) (PD98059), p38 MAPK (mitogen-activated protein kinase) (SB203580) and protein kinase C (PKC) (GF109203X, calphostin C) had no effect on 15d-PGJ2-mediated inhibition of IL-10 signalling. These results show that MAPKs and PKC are not involved in the inhibition of IL-10 signalling. CONCLUSIONS: We showed that 15d-PGJ2 non-specifically inhibits STAT signalling of the anti-inflammatory cytokine IL-10 as well as the proinflammatory cytokine IFN-gamma. These findings indicate the possibility that 15d-PGJ2 can have adverse effects in the management of diseases in which IL-10 plays a critical role in the suppression of inflammation.

Blotting, Western↗

PubMed2005

The functional p53 codon 72 polymorphism is associated with systemic lupus erythematosus.

The aim of the study is to investigate whether the functional p53 codon 72 polymorphism is associated with susceptibility to SLE and its clinical features. A polymerase chain reaction of genomic DNA-restriction fragment length polymorphism was used to determine genotypes of the p53 codon 72 in 90 SLE patients and 114 healthy controls. Clinical/serological manifestations were analysed in each patient and correlated with the genotypes. The OR of the association of the Pro allele with SLE was 1.70 (95% CI, 1.15-2.53, P = 0.0079) and the OR of the Pro/Pro (a recessive model) was significantly increased (OR = 2.58, 95% CI = 1.24-5.39, P = 0.0093). The Armitage's trend test indicated a significant dosage effect of the Pro allele for SLE (OR = 1.73, chi-square = 7.08, P = 0.0078). However, there was no significant association of the polymorphism with clinical/serological manifestations studied here. In conclusion, our finding suggests the functional p53 codon 72 polymorphism may be associated with SLE susceptibility, suggesting individuals who carry the Pro allele may have a higher risk to SLE susceptibility than those with the Arg allele. Further studies for replications are needed to confirm that the p53 polymorphism contributes to SLE.

Adolescent↗

PubMed2004

Platelet-derived growth factor-AA increases IL-1beta and IL-8 expression and activates NF-kappaB in rheumatoid fibroblast-like synoviocytes.

The effect of platelet-derived growth factor (PDGF)-AA on the inflammation in rheumatoid arthritis (RA) and osteoarthritis (OA) was investigated using cultured fibroblast-like synoviocytes (FLS) obtained from RA and OA patients as well as control nonarthritic (NA) individuals. PDGF-AA increased the mRNA and protein expressions of proinflammatory cytokines, interleukin (IL)-1beta and IL-8 in RA FLS. Biological activity of IL-1 in the culture supernatant of RA FLS was also increased by PDGF-AA stimulation. Interestingly, PDGF-AA synergized with tumour necrosis factor (TNF)-alpha to upregulate the protein expressions of IL-1beta and IL-8. PDGF-induced enhancement of the IL-1beta and IL-8 mRNA expressions was also observed in OA FLS. However, the expression of these proinflammatory cytokines in NA FLS did not change by PDGF treatment, suggesting that the inflammatory condition might have modified the biological effects of PDGF. In accordance with the enhanced expression of inflammatory cytokines, the activity of nuclear factor kappaB was also induced in response to PDGF-AA in RA FLS. These results suggest that PDGF-AA plays an important role in the progression of RA inflammation, and inhibiting PDGF activity may be useful for the effective RA treatment.

Arthritis, Rheumatoid↗

PubMed2004

Intron 4 polymorphism of the endothelial nitric oxide synthase gene is associated with the development of lupus nephritis.

The objective was to investigate whether the functional polymorphism of intron 4 in the endothelial nitric oxide synthase (eNOS) gene is associated with susceptibility to systemic lupus erythematosus (SLE) and its clinical features. The 27-bp repeat polymorphism in intron 4 of the eNOS gene was determined by polymerase chain reaction in 88 SLE patients and 95 healthy control subjects. Clinical manifestations were analysed in each patient and correlated with the genotypes. The genotype distribution of the intron 4 of the eNOS did not differ between SLE patients and control subjects (aa, ab, bb genotypes 0, 15, 73 versus 2, 19, 74 controls respectively, chi-squared = 2.21, 2 df, P = 0.331). In the lupus patients according to the intron 4 genotypes of the eNOS, there was no clinically significant difference in age at onset, anti-dsDNA titre, C3, C4 level, SLEDAI, SLICC/ACR Damage Index, or autoantibodies such as RF, anti-Ro, La, RNP, Sm, or phospholipid antibodies. However, renal involvement was higher in patients with ab genotypes than in those with bb genotypes (53% versus 26%), but it did not reach statistical significance (P = 0.062). Logistic regression showed that having the ab genotype was a significant risk factor for the development of lupus nephritis (odds ratio = 3.28, 95%CI: 1.04-10.2, P = 0.04). In conclusion, our data show that the eNOS ab genotypes may be associated with the development of lupus nephritis, suggesting individuals who carry the 'a' allele are more susceptible to lupus nephritis than those with the 'b' allele.

Adolescent↗

PubMed2003

Actinomycin D renders cultured synovial fibroblasts susceptible to tumour necrosis factor related apoptosis-inducing ligand (TRAIL)-induced apoptosis.

OBJECTIVE: To investigate the expression of tumour necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) receptors in cultured synovial fibroblasts from rheumatoid arthritis (RA) and osteoarthritis (OA) patients, and to examine their susceptibility to TRAIL-induced apoptosis in the presence or absence of metabolic inhibitors. METHODS: The expression of TRAIL receptors in synovial fibroblasts was examined by Western blot and immunohistochemistry. Expression of TRAIL-receptor 1 (TRAIL-R1), FLICE-inhibitory protein (Fas-associating protein with death domain-like interleukin-1-converting enzyme), and Bcl-2 was assessed by Western blot. Synovial cell viability was measured by 2,3-bis(2-methoxy-4-nitro-5-sulfophenyl)-2H-tetrazolium-5-carboxanilide assay (XTT), and apoptosis was determined both by DNA content analysis after propidium iodide staining and Annexin V stain. RESULTS: TRAIL-R1 was constitutively expressed on cultured synovial fibroblasts from RA and OA, however, expression of TRAIL-R2 and TRAIL-R3 was not observed by immunohistochemistry and Western blot. Cultured synovial fibroblasts were resistant to apoptosis by TRAIL alone, but combined treatment of TRAIL with actinomycin D (ActD: 200 ng/mL), cycloheximide (CHX: 10 microg/mL), or proteasome inhibitor (MG132: 20 microM) induced apoptosis in a dose-dependent manner. The apoptosis was completely or partially inhibited by various caspase inhibitors, implicating an involvement of caspase pathway in TRAIL-induced apoptosis in the presence of these metabolic inhibitors. Expression of TRAIL-R1, FLIPL, and Bcl-2 did not account for the apoptosis by the combined treatment of TRAIL with ActD. CONCLUSIONS: Although TRAIL-R1 was constitutively expressed; cultured synovial fibroblasts were resistant to apoptosis by TRAIL. ActD, CHX, and MG132 rendered cultured synovial fibroblasts susceptible to TRAIL-induced apoptosis by a caspase-dependent mechanism. However, the exact mechanism of sensitization by these metabolic inhibitors remains to be determined.

Apoptosis↗

PubMed2003

Functional polymorphisms in matrix metalloproteinase-1 and monocyte chemoattractant protein-1 and rheumatoid arthritis.

The aim of this study is to investigate whether the functional polymorphisms in the promoter of matrix metalloproteinase-1 (MMP-1) and in the regulatory region of the monocyte chemoattractant protein-1 (MCP-1) gene are associated with susceptibility to rheumatoid arthritis (RA) and its clinical features. The MMP-1 1G/2G polymorphism and the MCP-1 promoter A/G polymorphism were determined by polymerase chain reaction-restriction fragment length polymorphism in 117 RA patients and 97 healthy controls. The genotype distribution of the MMP-1 promoter did not differ between RA patients and control subjects. However, in the 2G/2G genotype, ESR and Plat were higher than the 1G/1G genotype. The genotype distribution of the MCP-1 promoter did not differ between the RA and control groups. Clinically there was no significant difference among RA patients according to the MCP-1 promoter genotypes. Our data show that the functional promoter polymorphism in the MMP-1 promoter may not play an important role in the susceptibility of RA, but the polymorphism may be related to clinical phenotypes.

Adolescent↗

PubMed2001

Effects of peroxisome proliferator-activated receptor-gamma (PPAR-gamma) on the expression of inflammatory cytokines and apoptosis induction in rheumatoid synovial fibroblasts and monocytes.

This study was performed to investigate whether peroxisome proliterator-activated receptor-gamma (PPAR-gamma) exerted an anti-inflammatory effect on rheumatoid synovial cells and inhibited dysregulated proliferation. The expression of PPAR-gamma mRNA in cultured human synoviocytes and THP-1 cells was analysed by RT-PCR. PPAR-gamma was expressed in normal, osteoarthritis (OA), rheumatoid arthritis (RA) synovial cells as well as a human monocytic cell line, THP-1. In RA and OA synoviocytes, the induction of inflammatory cytokine mRNA expression such as TNF-alpha and IL-1beta was significantly inhibited by the natural PPAR-gamma agonist, 15 deoxy-Delta(12,14)prostaglandin J(2)(15d-PGJ(2)). The effect of PPAR-gamma on the nuclear factor (NF)-kappaB activity was tested by electrophoretic mobility shift assay (EMSA). Both troglitazone and 15d-PGJ(2)markedly inhibited TNF-alpha-induced NF-kappaB activation at 30 microM. However, PPAR-gamma agonist neither reduced proliferation nor induced apoptosis in RA synoviocytes when measured by XTT assay and fluorescence activated cell sorter (FACS) analysis. In contrast, it induced apoptosis in a dose-dependent manner in THP-1 cells and augmented TNF-related apoptosis-inducing ligand (TRAIL)-induced apoptosis as well. In conclusion, these data demonstrate that PPAR-gamma is expressed in human synoviocytes and THP-1 cells, and the PPAR-gamma activation inhibits expression of inflammatory cytokines in RA synoviocytes. Furthermore, PPAR-gamma activation induces apoptosis by itself and augments TRAIL/Apo2L-induced apoptosis in THP-1 cells. These results suggest that PPAR-gamma agonists may provide a new therapeutic approach for RA.

Apoptosis↗

PubMed2001

Polymorphsims of CTLA-4 exon 1 +49, CTLA-4 promoter -318 and Fas promoter -670 in spondyloarthropathies.

The aim of the study was to investigate a possible association between the CTLA-4 exon 1 +49, CTLA-4 promoter -318 and Fas promoter -670 and spondyloarthropathies (SpA). Polymerase chain reaction of genomic DNA-restriction fragment length polymorphism was used to determine genotypes of the CTLA-4 exon 1 +49, CTLA-4 promoter -318 and Fas promoter -670 in 54 SpA patients, 84 healthy control subjects and 87 bronchial asthma patients as disease controls. There were no significant differences in the genotype and allele frequencies of the CTLA-4 exon 1, promoter and Fas promoter genes among SpA, asthma patients and controls. No significant differences were found in age at onset, sex, disease duration, history of enthesopathy, peripheral arthritis and uveitis, Schober test, chest expansion, white blood cell count, C-reactive protein and erythrocyte sedimentation rate among patients with SpA according to the CTLA-4 exon 1, CTLA-4 promoter and Fas promoter polymorphisms. We found no association between the polymorphisms of the CTLA-4 exon 1 +49, CTLA-4 promoter -318 and Fas promoter -670 genes and SpA. However, further studies are required to discover the possible contribution of the polymorphisms of the CTLA-4 and Fas to the pathogenesis of SpA.

Abatacept↗

PubMed2001

Polymorphisms of the CTLA-4 exon 1 and promoter gene in systemic lupus erythematosus.

The objective of this study was to determine whether the polymorphisms of the CTLA-4 exon 1 (+49) and promoter (-318) are associated with susceptibility to systemic lupus erythematosus (SLE) and its clinical features. Polymerase chain reaction of genomic DNA-restriction fragment length polymorphism was used to determine genotypes of the CTLA-4 exon 1 (+49) and promoter (-318) in 80 SLE patients and 86 healthy control subjects. The genotype distribution of the CTLA-4 exon 1 (+49) differed between SLE patients and controls (chi2 = 6.74, 2 degrees of freedom (d.f.), P = 0.03). The CTLA-4 AG genotype occurred more frequently in patients with SLE (46.3% vs 33.7% controls). On the other hand, the CTLA-4 AA genotype as well as the CTLA-4 GG genotype was less frequent among SLE patients than among control subjects (1.3% vs 9.3% and 52.5% vs 57.0%, respectively). The genotype distribution of the CTLA-4 promoter (-318) differed between SLE patients and control subjects (CT, TT, CC; genotypes 27.5%, 0%, 72.5% vs 16.3%, 4.7%, 79.1% controls respectively, chi2 = 6.36, 2 d.f., P = 0.04). However, Fischer's exact or chi2 P-values for each genotypes of the CTLA-4 exon 1 (+49) and promoter (-318) between SLE and control group were > 0.05. Clinically, in the lupus patients there was no significant difference according to the CTLA-4 polymorphisms. In conclusion, no correlation was found between CTLA-4 exon 1 (+49) and promoter (-318) polymorphisms and SLE in our study.

Abatacept↗

PubMed2001

A case of BOOP developed during bucillamine treatment for rheumatoid.

We describe a patient with rheumatoid arthritis(RA) who developed bronchiolitis obliterans organizing pneumonia(BOOP) during the treatment of bucillamine. A 51 year-old man was admitted to the hospital for an abnormal shadow on his chest radiograph. He had been diagnosed as having RA 3 years previously and had been receiving 200 mg of bucillamine for 21 months. Two months prior to admission, he presented with a cough and his chest X-ray showed opacities in both lower lungs. He was treated with antibiotics for 2 months after the development of cough and lesions on the chest X-ray, but the symptoms and lung lesions became more aggravated. On admission, an HRCT revealed airspace consolidations in the subpleural space of both basal lungs and a CT-guided fine needle aspiration biopsy showed Masson's body filling air space, interstitial infiltration of acute and chronic inflammatory cells and type II cell hyperplasia, consistent with BOOP. Bucillamine was stopped and 50 mg of prednisolone was administered. His symptoms and infiltrations on the chest X-ray resolved. We suggest that bucillamine should be considered as a drug possibly associated with BOOP.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed2001

Fas promoter -670 polymorphism is associated with development of anti-RNP antibodies in systemic lupus erythematosus.

OBJECTIVE: To evaluate whether the polymorphism of Fas promoter -670 is associated with susceptibility to systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) and their clinical features. METHODS: A polymerase chain reaction of a genomic DNA-restriction fragment length polymorphism was used to determine genotypes of the Fas promoter -670 in 87 patients with SLE, 87 with RA, and 87 healthy controls. A second cohort of SLE patients (n = 85) was included. Clinical manifestations were analyzed in each patient and correlated with the genotypes. RESULTS: The genotype distribution of the Fas promoter -670 did not differ between patients with SLE and control subjects (AA, GA, GG genotypes 31, 54, 15% vs 30, 55, 15% controls, respectively; chi-squared = 0.03, 2 df, p = 0.99) and between RA patients and controls (AA, GA, GG genotypes 38, 44, 18% vs 30, 55, 15% controls, respectively; chi-squared = 2.30, 2 df, p = 0.32). Regarding the clinical status of lupus patients according to Fas promoter -670 genotypes, there was no significant difference in age at onset, anti-dsDNA titer, C3, C4 level, renal involvement, number of American College of Rheumatology (ACR) criteria met, SLE Disease Activity Index, SLE International Collaborating Clinics/ACR Damage Index, or autoantibody profiles. However, the frequency of anti-RNP antibody was significantly different in the AA, GA, and GG groups (71, 25, 30%; chi-squared = 13.29, 2 df, p = 0.001). To confirm this finding, the Fas promoter -670 genotype was examined in a second cohort of SLE patients (n = 85). The result in the second cohort replicated the association shown in the first. In patients with RA, there was no significant difference in clinical and laboratory findings according to the Fas promoter -670 genotypes. CONCLUSION: Our data suggest that the Fas promoter -670 polymorphism is associated with development of anti-RNP antibodies in SLE.

Adolescent↗

PubMed2001

p53 codon 72 polymorphism and rheumatoid arthritis.

OBJECTIVE: To investigate whether the p53 codon 72 polymorphism is associated with susceptibility to rheumatoid arthritis (RA) and its clinical features. METHODS: A polymerase chain reaction of genomic DNA-restriction fragment length polymorphism was used to determine genotypes of the p53 codon 72 in 114 patients with RA and 114 healthy controls. Clinical/serological manifestations were analyzed in each patient and correlated with the genotypes. RESULTS: The genotype distribution of the p53 codon 72 did not differ between patients with RA and controls (Arg/Arg, Arg/Pro, Pro/Pro genotypes 38, 58, 18 vs 37, 60, 17 controls, respectively; chi-square = 0.08, 2 df, p = 0.96). No significant difference was found in allele frequencies between the groups. Clinically there was no significant difference in age at onset, functional class, physician's global assessment, ESR, CRP, RF titer, extraarticular and cervical spine involvement, frequencies of joint operation, and admission in RA patients according to the p53 codon 72 genotypes. However, the number of patients within each group was extremely small, for example only 5 patients with cervical spine involvement. No firm conclusions could safely be reached about clinical manifestations from this study. CONCLUSION: No association was found between the p53 codon 72 polymorphism and RA. Studies are needed to clarify the role of the p53 polymorphism in the pathogenesis of RA.

Adolescent↗

PubMed2000

Lipoprotein(a) and lipids in relation to inflammation in rheumatoid arthritis.

The aim of this study is to evaluate whether lipoprotein(a) (Lp(a)) acts as the acute phase reactant and whether changes of lipids are related to inflammation in rheumatoid arthritis (RA). Lp(a) and lipids were measured after an overnight fast, before and after 14 days use of antiinflammatory agents and correlated with laboratory findings in 21 untreated RA patients and 19 healthy controls. Nine (42.3%) of 21 RA patients and 6 (31.6%) of 19 controls had high Lp(a) levels (> 30 mg/dl) and the Lp(a) level was higher in RA patients compared with controls (27.1 +/- 5.3 vs 19.0 +/- 4.2 mg/dl) without significant difference (p > 0.05). There was no significant correlation between ESR and Lp(a) and lipids in RA patients except for HDL cholesterol (r = -0.563, p = 0.008). After antiinflammatory agent use for 14 days, change in ESR (ESRsample1-ESRsample2) was significantly and negatively correlated to changes in total and HDL cholesterols in RA patients. In conclusion, although Lp(a) tended to be higher in RA, we could not find a distinct acute phase pattern of Lp(a). But changes in total and HDL cholesterols were negatively correlated with inflammation in RA. Our data support the phenomenon that dyslipoproteinemia observed in RA is associated with inflammation.

Adult↗

PubMed2000

Serum creatine kinase in patients with rheumatic diseases.

Serum creatine kinase (CK) activity is reduced in some conditions, including rheumatic diseases, but the aetiology and significance remain to be clarified. The aim of this study was to investigate relationships between serum CK activity and other muscle enzymes, muscle mass, renal function, steroid use and disease activity in patients with rheumatic diseases. Serum CK activity was measured in sera from 498 patients with rheumatic diseases: rheumatoid arthritis (RA, n = 145), systemic lupus erythematosus (SLE, n = 31), spondyloarthropathies (SpA, n = 35), polyarthralgia/arthritis (Poly, n = 74), miscellaneous group (MI, n = 46), and in non-inflammatory arthropathies (NIA, n = 167) as controls. Serum CK level was significantly reduced in RA (45.4 +/- 1.9 IU/l), SLE (46.4 +/- 4.2 IU/l), SpA (64.7 +/- 5.6 IU/l) and MI (63.4 +/- 4.8 IU/l), but not in poly (70.2 +/- 3.1 IU/l), compared to controls (78.9 +/- 2.4 IU/l) (P < 0.05). CK values correlated with aspartate aminotransferase (AST), erythrocyte sedimentation rate (ESR), body mass index (BMI) and platelets (Plat) in RA; ESR and haemoglobin (Hb) in SLE, AST, ESR and Hb in SpA; lactate dehydrogenase (LDH), AST, ESR and Hb in Poly; LDH, AST, ESR, Hb and Ccr in MI; and LDH, AST and ESR in controls. In all patients with rheumatic diseases CK level was significantly correlated with LDH, AST, alanine aminotransferase (ALT), ESR, C-reactive protein (CRP) and BMI and prednisolone dose, but not with Ccr, age and disease duration. In conclusion, our data support the possibility that reduced CK activity is inversely correlated with inflammatory activity and correlated with other muscle enzymes, muscle mass and steroid use, but not with renal function, age and disease duration in rheumatic diseases.

Adult↗

PubMed2000

Expression of cyclooxygenase-1 and -2 in rheumatoid arthritis synovium.

The aim of this study was to investigate the expression and localization of cyclooxygenase-1 and -2 (COX-1 and COX-2) in synovial tissues from patients with rheumatoid arthritis (RA). Synovial tissues from 9 patients with RA and 5 patients with osteoarthritis (OA) were examined for COX-1 and COX-2 expressions by immunohistochemical staining using 2 polydonal COX-1 and COX-2 antibodies. In RA synovia, synovial lining cells showed intense immunostaining for COX-1, whereas slight to moderate staining was observed in inflammatory cells, stromal fibroblast-like cells and vascular endothelial cells. There was no significant difference in COX-1 expression between RA and OA synovia. The localization of COX-2 expression dearly differed from that of COX-1 expression, being most intense in inflammatory cells. However, there was no difference in COX-1 and COX-2 expressions between RA and OA synovial tissues. Our observations support that inflammatory mechanisms modulated by COX-1 and COX-2 in chronic RA synovium might be similar to those in chronic OA synovium.

Adult↗

PubMed2000

Dermatomyositis without elevation of creatine kinase presented as bronchiolitis obliterans organizing pneumonia.

A case of dermatomyositis presented as bronchiolitis obliterans organizing pneumonia has been rarely reported. We describe a 46-year-old female patient with dermatomyositis without elevation of creatine kinase presented as bronchiolitis obliterans organizing pneumonia. She was treated with prednisolone and azathioprine. Over a 2-year follow-up she has had no elevation of creatine kinase. The patient remains asymptomatic and has no medication for dermatomyositis and bronchiolitis obliterans organizing pneumonia two years after initial treatment. It has been suggested that the prognosis of dermatomyositis without creatine kinase elevation may be poor. Because the prognosis of bronchiolitis obliterans organizing pneumonia is generally believed to be good, we tentatively suggest that the normal value of creatine kinase in dermatomyositis does not always seem to herald a poor prognosis, an associated malignancy or severe interstitial lung disease.

Azathioprine↗