Background: Curcumin contained in Curcuma xanthorrhiza is an immunomodulator that has similar biological effect as vitamin D. Combination of curcumin and vitamin D3 is expected to work synergistically.
Objective: To determine the effect of Curcuma xanthorrhiza supplementation on vitamin D3 administration to SLEDAI, IL-6, and TGF-β1 serum in SLE patients with hypovitamin D.
Methods: This was a double-blind RCT conducted in Saiful Anwar Hospital, Malang, in January 2016-March 2017. Subjects were SLE active (SLEDAI > 3) with levels of 25(OH)D3 ≤ 30 ng/ml and divided into two groups: those receiving cholecalciferol 3 × 400 IU and placebo 3 × 1 tablets (group I) and those receiving 3 × 400 IU cholecalciferol and Curcuma xanthorrhiza 3 × 20 mg for 3 months (group II). SLEDAI, levels of vitamin D, IL-6, and TGF-β1 in serum were evaluated before and after the treatment.
Results: There were no significant differences in SLEDAI reduction, decreased serum levels of IL-6, and increased levels of TGF-β1 serum among groups after the treatment. Decreased levels of serum IL-6 have a positive correlation with SLEDAI reduction. Conclusion. Curcuma xanthorrhiza supplementation on vitamin D3 had no effects on SLEDAI and serum levels of IL-6 and TGF-β1. This clinical trial is registered with NCT03155477.
背景:姜黄中所含的姜黄素是一种与维生素d具有相似生物学效应的免疫调节剂。姜黄素与维生素D3联合使用有望发挥协同作用。目的:探讨补充姜黄对低维生素d SLE患者血清中维生素D3给药SLEDAI、IL-6、TGF-β1的影响。方法:采用双盲随机对照试验，于2016年1月- 2017年3月在马琅赛富安华医院进行。受试者SLE活动期(SLEDAI > 3)， 25(OH)D3水平≤30 ng/ml，分为两组:服用胆骨化醇3 × 400 IU +安慰剂3 × 1片(I组)和服用胆骨化醇3 × 400 IU +姜黄3 × 20 mg，疗程3个月(II组)，评估治疗前后血清SLEDAI、维生素D、IL-6、TGF-β1水平。结果:治疗后各组患者SLEDAI降低、血清IL-6水平降低、血清TGF-β1水平升高均无显著差异。血清IL-6水平降低与SLEDAI降低呈正相关。结论。姜黄补充维生素D3对SLEDAI和血清IL-6、TGF-β1水平无影响。该临床试验注册号为NCT03155477。
{"title":"Effect of <i>Curcuma xanthorrhiza</i> Supplementation on Systemic Lupus Erythematosus Patients with Hypovitamin D Which Were Given Vitamin D<sub>3</sub> towards Disease Activity (SLEDAI), IL-6, and TGF-<i>β</i>1 Serum.","authors":"C Singgih Wahono, Cameleia Diah Setyorini, Handono Kalim, Nurdiana Nurdiana, Kusworini Handono","doi":"10.1155/2017/7687053","DOIUrl":"https://doi.org/10.1155/2017/7687053","url":null,"abstract":"<p><strong>Background: </strong>Curcumin contained in <i>Curcuma xanthorrhiza</i> is an immunomodulator that has similar biological effect as vitamin D. Combination of curcumin and vitamin D<sub>3</sub> is expected to work synergistically.</p><p><strong>Objective: </strong>To determine the effect of <i>Curcuma xanthorrhiza</i> supplementation on vitamin D<sub>3</sub> administration to SLEDAI, IL-6, and TGF-<i>β</i>1 serum in SLE patients with hypovitamin D.</p><p><strong>Methods: </strong>This was a double-blind RCT conducted in Saiful Anwar Hospital, Malang, in January 2016-March 2017. Subjects were SLE active (SLEDAI > 3) with levels of 25(OH)D3 ≤ 30 ng/ml and divided into two groups: those receiving cholecalciferol 3 × 400 IU and placebo 3 × 1 tablets (group I) and those receiving 3 × 400 IU cholecalciferol and <i>Curcuma xanthorrhiza</i> 3 × 20 mg for 3 months (group II). SLEDAI, levels of vitamin D, IL-6, and TGF-<i>β</i>1 in serum were evaluated before and after the treatment.</p><p><strong>Results: </strong>There were no significant differences in SLEDAI reduction, decreased serum levels of IL-6, and increased levels of TGF-<i>β</i>1 serum among groups after the treatment. Decreased levels of serum IL-6 have a positive correlation with SLEDAI reduction. <i>Conclusion. Curcuma xanthorrhiza</i> supplementation on vitamin D<sub>3</sub> had no effects on SLEDAI and serum levels of IL-6 and TGF-<i>β</i>1. This clinical trial is registered with NCT03155477.</p>","PeriodicalId":51715,"journal":{"name":"International Journal of Rheumatology","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2017/7687053","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35831492","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-01-01Epub Date: 2017-05-07DOI: 10.1155/2017/1824794
Anand N Malaviya, Roopa Rawat, Neha Agrawal, Nilesh S Patil
Since 1984 the diagnosis of ankylosing spondylitis (AS) has been based upon the modified New York (mNY) criteria with mandatory presence of radiographic sacroiliitis, without which the diagnosis is not tenable. However, it may take years or decades for radiographic sacroiliitis to develop delaying the diagnosis for long periods. It did not matter in the past because no effective treatment was available. However, with the availability of a highly effective treatment, namely, tumour necrosis factor-α inhibitors (TNFi), the issue of early diagnosis of AS acquired an urgency. The Assessment of SpondyloArthritis International Society (ASAS) classification criteria published in 2009 was a significant step towards this goal. These criteria described an early stage of the disease where sacroiliitis was demonstrable only on MRI but not on standard radiograph. Therefore, this stage of the disease was labelled "nonradiographic axial SpA" (nr-axSpA). But questions have been raised if, in search of early diagnosis, specificity was compromised. The Federal Drug Administration (FDA, USA) withheld approval for the use of TNFi in patients with nr-axSpA because of issues related to the specificity of these criteria. This review attempts to clarify some of these aspects of the nr-axSpA-AS relationship and also tries to answer the question whether ASAS classifiable radiographic axial spondyloarthritis (r-axSpA) term can be interchangeably used with the term AS.
{"title":"The Nonradiographic Axial Spondyloarthritis, the Radiographic Axial Spondyloarthritis, and Ankylosing Spondylitis: The Tangled Skein of Rheumatology.","authors":"Anand N Malaviya, Roopa Rawat, Neha Agrawal, Nilesh S Patil","doi":"10.1155/2017/1824794","DOIUrl":"https://doi.org/10.1155/2017/1824794","url":null,"abstract":"<p><p>Since 1984 the diagnosis of ankylosing spondylitis (AS) has been based upon the modified New York (mNY) criteria with mandatory presence of radiographic sacroiliitis, without which the diagnosis is not tenable. However, it may take years or decades for radiographic sacroiliitis to develop delaying the diagnosis for long periods. It did not matter in the past because no effective treatment was available. However, with the availability of a highly effective treatment, namely, tumour necrosis factor-<i>α</i> inhibitors (TNFi), the issue of early diagnosis of AS acquired an urgency. The Assessment of SpondyloArthritis International Society (ASAS) classification criteria published in 2009 was a significant step towards this goal. These criteria described an early stage of the disease where sacroiliitis was demonstrable only on MRI but not on standard radiograph. Therefore, this stage of the disease was labelled \"nonradiographic axial SpA\" (nr-axSpA). But questions have been raised if, in search of early diagnosis, specificity was compromised. The Federal Drug Administration (FDA, USA) withheld approval for the use of TNFi in patients with nr-axSpA because of issues related to the specificity of these criteria. This review attempts to clarify some of these aspects of the nr-axSpA-AS relationship and also tries to answer the question whether ASAS classifiable radiographic axial spondyloarthritis (r-axSpA) term can be interchangeably used with the term AS.</p>","PeriodicalId":51715,"journal":{"name":"International Journal of Rheumatology","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2017/1824794","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35037527","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
M. M. Rahman, Jacek A. Kopec, C. Goldsmith, A. Anis, J. Cibere
Objectives. The validity of administrative osteoarthritis (OA) diagnosis in British Columbia, Canada, was examined against X-rays, magnetic resonance imaging (MRI), self-report, and the American College of Rheumatology criteria. Methods. During 2002–2005, 171 randomly selected subjects with knee pain aged 40–79 years underwent clinical assessment for OA in the knee, hip, and hands. Their administrative health records were linked during 1991–2004, in which OA was defined in two ways: (AOA1) at least one physician's diagnosis or hospital admission and (AOA2) at least two physician's diagnoses in two years or one hospital admission. Sensitivity, specificity, and predictive values were compared using four reference standards. Results. The mean age was 59 years and 51% were men. The proportion of OA varied from 56.3 to 89.7% among men and 77.4 to 96.4% among women according to reference standards. Sensitivity and specificity varied from 21 to 57% and 75 to 100%, respectively, and PPVs varied from 82 to 100%. For MRI assessment, the PPV of AOA2 was 100%. Higher sensitivity was observed in AOA1 than AOA2 and the reverse was true for specificity and PPV. Conclusions. The validity of administrative OA in British Columbia varied due to case definitions and reference standards. AOA2 is more suitable for identifying OA cases for research using this Canadian database.
{"title":"Validation of Administrative Osteoarthritis Diagnosis Using a Clinical and Radiological Population-Based Cohort","authors":"M. M. Rahman, Jacek A. Kopec, C. Goldsmith, A. Anis, J. Cibere","doi":"10.1155/2016/6475318","DOIUrl":"https://doi.org/10.1155/2016/6475318","url":null,"abstract":"Objectives. The validity of administrative osteoarthritis (OA) diagnosis in British Columbia, Canada, was examined against X-rays, magnetic resonance imaging (MRI), self-report, and the American College of Rheumatology criteria. Methods. During 2002–2005, 171 randomly selected subjects with knee pain aged 40–79 years underwent clinical assessment for OA in the knee, hip, and hands. Their administrative health records were linked during 1991–2004, in which OA was defined in two ways: (AOA1) at least one physician's diagnosis or hospital admission and (AOA2) at least two physician's diagnoses in two years or one hospital admission. Sensitivity, specificity, and predictive values were compared using four reference standards. Results. The mean age was 59 years and 51% were men. The proportion of OA varied from 56.3 to 89.7% among men and 77.4 to 96.4% among women according to reference standards. Sensitivity and specificity varied from 21 to 57% and 75 to 100%, respectively, and PPVs varied from 82 to 100%. For MRI assessment, the PPV of AOA2 was 100%. Higher sensitivity was observed in AOA1 than AOA2 and the reverse was true for specificity and PPV. Conclusions. The validity of administrative OA in British Columbia varied due to case definitions and reference standards. AOA2 is more suitable for identifying OA cases for research using this Canadian database.","PeriodicalId":51715,"journal":{"name":"International Journal of Rheumatology","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2016-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2016/6475318","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64480596","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
M. S. Mosleh-Shirazi, M. Ibrahim, P. Pastides, Wasim Khan, H. Rahman, L. Jahangiri
[This corrects the article DOI: 10.1155/2015/140143.].
[这更正了文章DOI: 10.1155/2015/140143]。
{"title":"Corrigendum to “An Insight into Methods and Practices in Hip Arthroplasty in Patients with Rheumatoid Arthritis”","authors":"M. S. Mosleh-Shirazi, M. Ibrahim, P. Pastides, Wasim Khan, H. Rahman, L. Jahangiri","doi":"10.1155/2016/1741420","DOIUrl":"https://doi.org/10.1155/2016/1741420","url":null,"abstract":"[This corrects the article DOI: 10.1155/2015/140143.].","PeriodicalId":51715,"journal":{"name":"International Journal of Rheumatology","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2016-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2016/1741420","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64240185","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jirun Apinun, P. Sengprasert, P. Yuktanandana, S. Ngarmukos, A. Tanavalee, Rangsima Reantragoon
Osteoarthritis is a condition of joint failure characterized by many pathologic changes of joint-surrounding tissues. Many evidences suggest the role of both innate and adaptive immunity that interplay, resulting either in initiation or in progression of osteoarthritis. Adaptive immune cells, in particular T cells, have been demonstrated to play a role in the development of OA in animal models. However, the underlying mechanism is yet unclear. Our aim was to correlate the frequency and phenotype of tissue-infiltrating T cells in the synovial tissue and infrapatellar fat pad with radiographic grading. Our results show that CD8+ T cells are increased in osteoarthritic patients with higher radiographic grading. When peripheral blood CD8+ T cells were examined, we show that CD8+ T cells possess a significantly higher level of activation than its CD4+ T cell counterpart (P < 0.0001). Our results suggest a role for CD8+ T cells and recruitment of these activated circulating peripheral blood CD8+ T cells to the knee triggering local inflammation within the knee joint.
{"title":"Immune Mediators in Osteoarthritis: Infrapatellar Fat Pad-Infiltrating CD8+ T Cells Are Increased in Osteoarthritic Patients with Higher Clinical Radiographic Grading","authors":"Jirun Apinun, P. Sengprasert, P. Yuktanandana, S. Ngarmukos, A. Tanavalee, Rangsima Reantragoon","doi":"10.1155/2016/9525724","DOIUrl":"https://doi.org/10.1155/2016/9525724","url":null,"abstract":"Osteoarthritis is a condition of joint failure characterized by many pathologic changes of joint-surrounding tissues. Many evidences suggest the role of both innate and adaptive immunity that interplay, resulting either in initiation or in progression of osteoarthritis. Adaptive immune cells, in particular T cells, have been demonstrated to play a role in the development of OA in animal models. However, the underlying mechanism is yet unclear. Our aim was to correlate the frequency and phenotype of tissue-infiltrating T cells in the synovial tissue and infrapatellar fat pad with radiographic grading. Our results show that CD8+ T cells are increased in osteoarthritic patients with higher radiographic grading. When peripheral blood CD8+ T cells were examined, we show that CD8+ T cells possess a significantly higher level of activation than its CD4+ T cell counterpart (P < 0.0001). Our results suggest a role for CD8+ T cells and recruitment of these activated circulating peripheral blood CD8+ T cells to the knee triggering local inflammation within the knee joint.","PeriodicalId":51715,"journal":{"name":"International Journal of Rheumatology","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2016-12-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2016/9525724","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64619466","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hala M Lofty, H. Marzouk, Y. Farag, M. Nabih, Iman Khalifa, Noha Mostafa, A. Salah, L. Rashed, Kamal El Garf
Background and Objectives. SAA is an acute-phase reactant detected during an FMF attack or other inflammatory conditions. High SAA levels may increase the risk of amyloidosis. The aim of the study is to measure the serum amyloid A (SAA) level in a group of Egyptian children with familial Mediterranean fever (FMF) and study its various correlates, if any. Methods. The study enrolled seventy-one children with FMF. Results. SAA level was high in 78.9% of the studied patients with a mean of 81.62 ± 31.6 mg/L, and CRP was positive in 31% of patients. There was no significant releation between SAA level and any demographic or clinical manifestation. High SAA was more frequent in V726A allele (16.9%) followed by M694V allele (12.3%). Elevated SAA levels were more frequent in patients on low colchicine doses. Forty-five percent (45%) of patients have low adherence to colchicine therapy. Interpretation and Conclusion. High SAA levels were detected two weeks after last FMF attack in a large percentage of Egyptian FMF children. This indicates that subclinical inflammation continues during attack-free periods, and SAA could be used as a marker of it.
{"title":"Serum Amyloid A Level in Egyptian Children with Familial Mediterranean Fever","authors":"Hala M Lofty, H. Marzouk, Y. Farag, M. Nabih, Iman Khalifa, Noha Mostafa, A. Salah, L. Rashed, Kamal El Garf","doi":"10.1155/2016/7354018","DOIUrl":"https://doi.org/10.1155/2016/7354018","url":null,"abstract":"Background and Objectives. SAA is an acute-phase reactant detected during an FMF attack or other inflammatory conditions. High SAA levels may increase the risk of amyloidosis. The aim of the study is to measure the serum amyloid A (SAA) level in a group of Egyptian children with familial Mediterranean fever (FMF) and study its various correlates, if any. Methods. The study enrolled seventy-one children with FMF. Results. SAA level was high in 78.9% of the studied patients with a mean of 81.62 ± 31.6 mg/L, and CRP was positive in 31% of patients. There was no significant releation between SAA level and any demographic or clinical manifestation. High SAA was more frequent in V726A allele (16.9%) followed by M694V allele (12.3%). Elevated SAA levels were more frequent in patients on low colchicine doses. Forty-five percent (45%) of patients have low adherence to colchicine therapy. Interpretation and Conclusion. High SAA levels were detected two weeks after last FMF attack in a large percentage of Egyptian FMF children. This indicates that subclinical inflammation continues during attack-free periods, and SAA could be used as a marker of it.","PeriodicalId":51715,"journal":{"name":"International Journal of Rheumatology","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2016-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2016/7354018","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64517374","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
E. Tchetina, G. Markova, A. Poole, D. Zukor, J. Antoniou, S. Makarov, A. N. Kuzin
This study reports the effects of the iron chelator deferoxamine (DFO) on collagen cleavage, inflammation, and chondrocyte hypertrophy in relation to energy metabolism-related gene expression in osteoarthritic (OA) articular cartilage. Full-depth explants of human OA knee articular cartilage from arthroplasty were cultured with exogenous DFO (1–50 μM). Type II collagen cleavage and phospho-adenosine monophosphate-activated protein kinase (pAMPK) concentrations were measured using ELISAs. Gene expression studies employed real-time PCR and included AMPK analyses in PBMCs. In OA explants collagen cleavage was frequently downregulated by 10–50 μM DFO. PCR analysis of 7 OA patient cartilages revealed that 10 μM DFO suppressed expression of MMP-1, MMP-13, IL-1β, and TNFα and a marker of chondrocyte hypertrophy, COL10A1. No changes were observed in the expression of glycolysis-related genes. In contrast, expressions of genes associated with the mitochondrial Krebs cycle (TCA), AMPK, HIF1α, and COL2A1 were upregulated. AMPK gene expression was reduced in OA cartilage and increased in PBMCs from the same patients compared to healthy controls. Our studies demonstrate that DFO is capable of suppressing excessive collagenase-mediated type II collagen cleavage in OA cartilage and reversing phenotypic changes. The concomitant upregulation of proanabolic TCA-related gene expressions points to a potential for availability of energy generating substrates required for matrix repair by end-stage OA chondrocytes. This might normally be prevented by high whole-body energy requirements indicated by elevated AMPK expression in PBMCs of OA patients.
{"title":"Deferoxamine Suppresses Collagen Cleavage and Protease, Cytokine, and COL10A1 Expression and Upregulates AMPK and Krebs Cycle Genes in Human Osteoarthritic Cartilage","authors":"E. Tchetina, G. Markova, A. Poole, D. Zukor, J. Antoniou, S. Makarov, A. N. Kuzin","doi":"10.1155/2016/6432867","DOIUrl":"https://doi.org/10.1155/2016/6432867","url":null,"abstract":"This study reports the effects of the iron chelator deferoxamine (DFO) on collagen cleavage, inflammation, and chondrocyte hypertrophy in relation to energy metabolism-related gene expression in osteoarthritic (OA) articular cartilage. Full-depth explants of human OA knee articular cartilage from arthroplasty were cultured with exogenous DFO (1–50 μM). Type II collagen cleavage and phospho-adenosine monophosphate-activated protein kinase (pAMPK) concentrations were measured using ELISAs. Gene expression studies employed real-time PCR and included AMPK analyses in PBMCs. In OA explants collagen cleavage was frequently downregulated by 10–50 μM DFO. PCR analysis of 7 OA patient cartilages revealed that 10 μM DFO suppressed expression of MMP-1, MMP-13, IL-1β, and TNFα and a marker of chondrocyte hypertrophy, COL10A1. No changes were observed in the expression of glycolysis-related genes. In contrast, expressions of genes associated with the mitochondrial Krebs cycle (TCA), AMPK, HIF1α, and COL2A1 were upregulated. AMPK gene expression was reduced in OA cartilage and increased in PBMCs from the same patients compared to healthy controls. Our studies demonstrate that DFO is capable of suppressing excessive collagenase-mediated type II collagen cleavage in OA cartilage and reversing phenotypic changes. The concomitant upregulation of proanabolic TCA-related gene expressions points to a potential for availability of energy generating substrates required for matrix repair by end-stage OA chondrocytes. This might normally be prevented by high whole-body energy requirements indicated by elevated AMPK expression in PBMCs of OA patients.","PeriodicalId":51715,"journal":{"name":"International Journal of Rheumatology","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2016-11-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2016/6432867","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64478841","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Objective. To determine whether the incidence of malignancy is increased in patients with rheumatoid arthritis (RA) compared to a matched comparison cohort and to identify risk for any individual malignancy in RA. Methods. A cohort of 813 Olmsted County, Minnesota, residents who first fulfilled 1987 ACR criteria for RA in 1980–2007 was previously identified by medical record review. Medical records of 813 RA cases and a comparison cohort of age and sex matched Olmsted County residents without RA were evaluated retrospectively for cancer occurrence. Patients in both cohorts were followed until death, migration from Olmsted County, or 12/31/2014. Results. The RA and non-RA cohorts (mean age at incidence/index date: 55.9 [SD: 15.7] years; 68.4% females in both cohorts) were followed on average of 14.1 (SD: 7.7) and 14.9 (SD: 8.1) years, respectively. Prior to RA incidence/index date, 52 RA patients and 66 non-RA subjects had malignancies excluding NMSC (p = 0.21). During follow-up, significantly more malignancies occurred in patients with RA (n = 143) than in comparator subjects (n = 118; hazard ratio: 1.32; p = 0.027). Inclusion of NMSC obviated this difference. Conclusion. After excluding NMSC, there was a small to moderately increased risk of malignancies in patients with RA. Cancer surveillance is imperative in all patients with RA.
{"title":"Risk of Malignant Neoplasm in Patients with Incident Rheumatoid Arthritis 1980–2007 in relation to a Comparator Cohort: A Population-Based Study","authors":"Shafay Raheel, C. Crowson, K. Wright, E. Matteson","doi":"10.1155/2016/4609486","DOIUrl":"https://doi.org/10.1155/2016/4609486","url":null,"abstract":"Objective. To determine whether the incidence of malignancy is increased in patients with rheumatoid arthritis (RA) compared to a matched comparison cohort and to identify risk for any individual malignancy in RA. Methods. A cohort of 813 Olmsted County, Minnesota, residents who first fulfilled 1987 ACR criteria for RA in 1980–2007 was previously identified by medical record review. Medical records of 813 RA cases and a comparison cohort of age and sex matched Olmsted County residents without RA were evaluated retrospectively for cancer occurrence. Patients in both cohorts were followed until death, migration from Olmsted County, or 12/31/2014. Results. The RA and non-RA cohorts (mean age at incidence/index date: 55.9 [SD: 15.7] years; 68.4% females in both cohorts) were followed on average of 14.1 (SD: 7.7) and 14.9 (SD: 8.1) years, respectively. Prior to RA incidence/index date, 52 RA patients and 66 non-RA subjects had malignancies excluding NMSC (p = 0.21). During follow-up, significantly more malignancies occurred in patients with RA (n = 143) than in comparator subjects (n = 118; hazard ratio: 1.32; p = 0.027). Inclusion of NMSC obviated this difference. Conclusion. After excluding NMSC, there was a small to moderately increased risk of malignancies in patients with RA. Cancer surveillance is imperative in all patients with RA.","PeriodicalId":51715,"journal":{"name":"International Journal of Rheumatology","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2016-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2016/4609486","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64388393","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Makoto Tanaka, H. Yamada, S. Nishikawa, H. Mori, Y. Ochi, N. Horai, Minqi Li, N. Amizuka
The role of cathepsin K in joint degradation in a model of collagen-induced arthritis (CIA) in cynomolgus monkey was examined using biochemical markers and histology. Joint swelling, urinary C-telopeptide of type II collagen (CTX-II), deoxypyridinoline (DPD), and N- and C-telopeptides of type I collagen (NTX and CTX-I, resp.) were analyzed. Immunohistochemistry of type II collagen, cathepsin K, and CTX-II were performed using joints. Joint swelling reached peak on day 42 and continued at this level. The CTX-II level peaked on day 28 and declined thereafter, while CTX-I, NTX, and DPD reached plateau on day 43. Joint swelling was positively correlated with CTX-II increases on days 20 and 42/43, with increases in CTX-I and NTX/Cr on days 42/43 and 84, and with DPD increases throughout the study period. Intense cathepsin K staining was observed in osteoclasts and in articular cartilage and synovial tissue in arthritic joints. CTX-II was present in the superficial layer of articular cartilage in CIA monkeys. Evidence from biochemical markers suggests that matrix degradation in the CIA model starts with degradation of cartilage, rather than bone resorption. Cathepsin K expressed in osteoclasts, articular cartilage, and synovial tissue may contribute to degradation of cartilage.
{"title":"Joint Degradation in a Monkey Model of Collagen-Induced Arthritis: Role of Cathepsin K Based on Biochemical Markers and Histological Evaluation","authors":"Makoto Tanaka, H. Yamada, S. Nishikawa, H. Mori, Y. Ochi, N. Horai, Minqi Li, N. Amizuka","doi":"10.1155/2016/8938916","DOIUrl":"https://doi.org/10.1155/2016/8938916","url":null,"abstract":"The role of cathepsin K in joint degradation in a model of collagen-induced arthritis (CIA) in cynomolgus monkey was examined using biochemical markers and histology. Joint swelling, urinary C-telopeptide of type II collagen (CTX-II), deoxypyridinoline (DPD), and N- and C-telopeptides of type I collagen (NTX and CTX-I, resp.) were analyzed. Immunohistochemistry of type II collagen, cathepsin K, and CTX-II were performed using joints. Joint swelling reached peak on day 42 and continued at this level. The CTX-II level peaked on day 28 and declined thereafter, while CTX-I, NTX, and DPD reached plateau on day 43. Joint swelling was positively correlated with CTX-II increases on days 20 and 42/43, with increases in CTX-I and NTX/Cr on days 42/43 and 84, and with DPD increases throughout the study period. Intense cathepsin K staining was observed in osteoclasts and in articular cartilage and synovial tissue in arthritic joints. CTX-II was present in the superficial layer of articular cartilage in CIA monkeys. Evidence from biochemical markers suggests that matrix degradation in the CIA model starts with degradation of cartilage, rather than bone resorption. Cathepsin K expressed in osteoclasts, articular cartilage, and synovial tissue may contribute to degradation of cartilage.","PeriodicalId":51715,"journal":{"name":"International Journal of Rheumatology","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2016-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2016/8938916","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64590889","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-01-01Epub Date: 2016-04-20DOI: 10.1155/2016/4564531
G E M Reeves, N Collins, P Hayes, J Knapp, M Squance, H Tran, B Bastian
Pulmonary artery hypertension (PAH) is a disorder of elevated resistance in the pulmonary arterial vessels, reflected by elevation of measured pulmonary artery pressure (PAP), and presenting with breathlessness and, if untreated, progressing to right heart failure and death. The heightened prevalence of PAH in populations with underlying systemic autoimmune conditions, particularly scleroderma and its variants, is well recognised, consistent with the proposed autoimmune contribution to PAH pathogenesis, along with disordered thrombotic, inflammatory, and mitogenic factors. Rheumatoid arthritis (RA) is one of a group of systemic autoimmune conditions featuring inflammatory symmetrical erosive polyarthropathy as its hallmark. This study explored the prevalence of PAH in a population of unselected individuals with RA, using exercise echocardiography (EchoCG). The high prevalence of EchoCG-derived elevation of PAP (EDEPP) in this population (14%) suggests that, like other autoimmune conditions, RA may be a risk factor for PAH. Patients with RA may therefore represent another population for whom PAH screening with noninvasive tools such as EchoCG may be justified.
肺动脉高压（PAH）是一种肺动脉血管阻力升高的疾病，表现为肺动脉压力（PAP）测量值升高，并伴有呼吸困难，如不及时治疗，会发展为右心衰竭和死亡。PAH 在有潜在系统性自身免疫疾病（尤其是硬皮病及其变异型）的人群中发病率较高，这一点已得到广泛认可，这与所提出的自身免疫与血栓、炎症和有丝分裂紊乱因素共同导致 PAH 发病的观点是一致的。类风湿性关节炎（RA）是一组以炎症性对称侵蚀性多关节病为特征的全身性自身免疫性疾病之一。本研究利用运动超声心动图（EchoCG）探讨了 PAH 在未经筛选的 RA 患者中的患病率。在这一人群中，EchoCG 引起的血压升高（EDEPP）的发生率很高（14%），这表明与其他自身免疫性疾病一样，RA 也可能是 PAH 的一个危险因素。因此，使用 EchoCG 等无创工具对 RA 患者进行 PAH 筛查可能是合理的。
{"title":"SAPHIRE: Stress and Pulmonary Hypertension in Rheumatoid Evaluation-A Prevalence Study.","authors":"G E M Reeves, N Collins, P Hayes, J Knapp, M Squance, H Tran, B Bastian","doi":"10.1155/2016/4564531","DOIUrl":"10.1155/2016/4564531","url":null,"abstract":"<p><p>Pulmonary artery hypertension (PAH) is a disorder of elevated resistance in the pulmonary arterial vessels, reflected by elevation of measured pulmonary artery pressure (PAP), and presenting with breathlessness and, if untreated, progressing to right heart failure and death. The heightened prevalence of PAH in populations with underlying systemic autoimmune conditions, particularly scleroderma and its variants, is well recognised, consistent with the proposed autoimmune contribution to PAH pathogenesis, along with disordered thrombotic, inflammatory, and mitogenic factors. Rheumatoid arthritis (RA) is one of a group of systemic autoimmune conditions featuring inflammatory symmetrical erosive polyarthropathy as its hallmark. This study explored the prevalence of PAH in a population of unselected individuals with RA, using exercise echocardiography (EchoCG). The high prevalence of EchoCG-derived elevation of PAP (EDEPP) in this population (14%) suggests that, like other autoimmune conditions, RA may be a risk factor for PAH. Patients with RA may therefore represent another population for whom PAH screening with noninvasive tools such as EchoCG may be justified. </p>","PeriodicalId":51715,"journal":{"name":"International Journal of Rheumatology","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4854985/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34397847","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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