There is a relationship between cardiovascular morbidity, inflammatory activity, and changes in the lipid profile in rheumatoid arthritis (RA), although the mechanisms are not fully elaborated. ...Recent know-ledge that white adipose tissue (WAT) is a producer of immunologically and metabolically active substances gives another perspective to study.
To evaluate the relationship between interleukin-1 receptor antagonist (IL-1Ra) and variables associated with WAT and inflammation in RA.
Anthropometric, inflammatory and metabolic variables were assessed in 23 women with RA and 23 matched controls. Spearman, partial correlation and factor analyses were performed.
Inflammatory markers were increased in patients. In both groups, IL-1Ra correlated with leptin independent of age and BMI. IL-1Ra also correlated with haptoglobin and apolipoprotein (Apo) B in patients and with soluble TNF receptor (sTNFR) 1 in controls. In factor analysis, three latent factors were identified among patients. The first loaded on IL-1Ra, leptin, BMI, ApoB and body fat content (BF%), the second loaded on IL1-Ra and sTNF-receptors and the third showed inverse loadings on ApoA-I together with loadings on ESR, haptoglobin, orosomucoid, BF% and BMI.
IL-1Ra was associated with markers of inflammation and with fat-related factors in RA patients, suggesting a dualistic relationship of IL-1Ra in RA. IL-1Ra correlated independently with leptin in both patients and controls, indicating a relationship between inflammation and leptin.
Förekomst och dödlighet i hjärt–kärlsjukdomar är överrepresenterade vid inflammatoriska reumatiska sjukdomar.
Risken är särskilt stor hos patienter med reumatoid artrit med persisterande ...sjukdomsaktivitet och/eller extraartikulär sjukdom samt vid systemisk lupus erythematosus (SLE).
En arbetsgrupp inom Svensk reumatologisk förening har tagit fram riktlinjer för kardiovaskulär primärprevention för dessa patientgrupper.
Patienter med reumatisk sjukdom bör screenas regelbundet och vid behov behandlas för påverkbara riskfaktorer såsom högt blodtryck, lipidrubbningar, diabetes mellitus, rökning och bukfetma.
Vid riskintervention bör patienter med reumatoid artrit med persisterande hög sjukdomsaktivitet eller med SLE betraktas som om de hade en extra riskfaktor.
Att behandla grundsjukdomen optimalt är viktigt även ur kardioprotektivt perspektiv.
There is an increased risk for cardiovascular (CV) comorbidity among patients with rheumatoid arthritis (RA), with premature atherosclerosis, and a higher incidence of CV events, compared with the ...general population. Disease related factors add to the CV risk, and interact with the traditional CV risk factors. The underlying mechanism for this is not completely understood. In active RA there is a loss of muscle mass and an increase in body fat content. Production of cytokines, i.e., adipokines, in the adipose tissue could link the inflammation with the CV system. Control of the inflammation has been suggested to modify the CV risk in RA, and the recently introduced biological drugs, such as the tumor necrosis factor inhibitors (TNFi), have opened up new treatment opportunities. The aim of this thesis was to evaluate aspects of the interaction between inflammation and CV comorbidity in RA using biochemical and epidemiological methods. Methods In the first two studies, patients with established RA were examined for clinical disease activity, and blood samples were analysed for cytokines and adipokines using ELISAs and multiplex technology. In Study I (n RA=23) anthropometric measurements were assessed and in Study II (n RA=51) measurements of intima-media thickness (IMT), and endothelial function (FMD). From a subgroup of patients (Study II, n RA=13) samples of abdominal subcutaneous adipose tissue (SAT) were analysed for content of adipokines. In study III and IV associations between treatment with TNFi and acute coronary syndromes (ACS) were analysed using data from the Swedish Rheumatology Register; in Study III regarding early RA (n TNFi exposed=1,271, n bionaïve RA=4,729), and in Study IV comprising patients with RA of all stages (n TNFi exposed=7,213, n bionaïve RA=17,769) and with a matched general population comparator cohort (n=32,161). Associations between response to TNFi therapy and risk for ACS in the early RA cohort were evaluated in a nested case-control design (cases n=24, controls n=81). Results Serum levels of the cytokines/adipokines interleukin-1 receptor antagonist (IL-1Ra), IL-6, osteopontin, visfatin and TNF were increased in patients compared with controls (p≤0.001-0.036). The amount of TNF receptor II extracted from SAT was greater in patients (p=0.006). The serum (s-) levels of IL-1Ra correlated with s-leptin (r=0.71, p≤0.001) and s-haptoglobin in RA patients (r=0.56, p≤0.01). The result from a factor analysis indicated IL-1Ra to be associated with both adipose tissue and inflammation. Levels of s-visfatin (p=0.019) and s-IL-1Ra (p=0.023), respectively, were positively associated with IMT independently of inflammatory activity and CV risk factors. PAI-1 and MCP-1 extracted from SAT showed inverse associations with IMT. Patients with RA, whether exposed to TNFi or bio-naïve, had a doubled risk for ACS compared with the general population; HR 2.09 (95%CI 1.58-2.76) and 1.80 (1.49-2.17), respectively. No significant associations between risk for ACS and TNFi exposure were detected after adjustments; HR 0.80 (0.52-1.24) in early RA and HR 1.08 (0.82-1.41) in RA of any duration. Furthermore, no association between the risk for ACS and response to TNFi treatment in patients with early RA was observed, OR 1.5 (0.3-6.9). Conclusions The results indicate that cytokines/adipokines may have a role in the development of atherosclerosis in RA patients. A continuing increase in the risk of ACS in RA compared with the general population, despite modern therapeutic strategies, was noted. Neither exposure nor response to treatment with TNFi was associated with any modification of the risk for ACS.
Syfte Syftet med den här studien var att undersöka förekomst av prestationsbaserad självkänsla (PBS) hos unga manliga ishockeyspelare samt vilka coping-strategier de använder sig av i idrottsliga ...situationer de upplever utmanande och stressande. Detta för att undersöka om det finns ett samband mellan PBS och olika coping-strategier samt om det finns ett samband mellan de olika strategierna inom coping. Metod Genom en kvantitativ ansats användes två enkäter i studien. En enkät undersökte grad av prestationsbaserad självkänsla och den andra enkäten mätte val av coping-strategier inför en utmanande och stressande situation. Enkäterna delades ut till två olika hockeyföreningar. De 65 enkäterna som kom tillbaka fördes sedan in i Statistica för analys. Resultat Resultatet visade att de unga ishockeyspelarna inte hade en särskilt hög tendens till prestationsbaserad självkänsla. De coping-strategier de var mest benägna att använda var aktiv coping, planering och positivt tänkande. De strategier som i sin tur visade sig korrelera med PBS var aktiv coping, egen skuldbeläggning och önsketänkande. Det starkaste sambandet återfanns mellan PBS och önsketänkande. I delskalorna inom coping-enkäten korrelerade flertalet strategier med varandra och bland dessa var de mer aktiva förhållningssätten: planering, aktiv coping och undantryckande av andra aktiviteter. Slutsats De unga spelarna verkade inte i stor grad koppla deras självkänsla till prestation. När det kom till hantering av utmanande och stressande situationer uppvisade de ett mestadels aktivt förhållningssätt. De med en något högre tendens till PBS hade även en ökad benägenhet att använda sig av strategin önsketänkande som ett sätt att hantera stressande situationer. Man kan dra slutsatsen att de flesta spelarna ifråga planerar och har struktur på sitt spel och hanterar stressande situationer på ett effektivt och positivt sätt i form av aktiva coping-strategier. De som har större tendens till prestationsbaserad självkänsla hanterar dessa situationer på ett sätt som kan liknas vid drömmande och visualisering vilket även det kan räknas som ett positivt förhållningssätt.
Introduction Co-morbidity and mortality due to cardiovascular disease (CVD) are increased in patients with rheumatoid arthritis (RA). Most published studies in this field are retrospective or cross ...sectional. We investigated the presence of traditional and disease related risk factors for CVD at the onset of RA and during the first 5 years following diagnosis. We also evaluated their potential for predicting a new cardiovascular event (CVE) during the 5 year follow-up period and the modulatory effect of pharmacological treatment.
Methods All patients from the four northern-most counties of Sweden with early RA are since December 1995 consecutively recruited at diagnsosis (T0) into a large survey on the progress of the disease. Information regarding cardiovascular co-morbidity and related predictors was collected from clinical records and supplemented with questionnaires. By April 2008, 700 patients had been included of whom 442 patients had reached the 5-year follow-up (T5).
Result Among the 442 patients who reached T5 during the follow-up period, treatment for hypertension increased from 24.5 to 37.4% ( p<0.001)), diagnosis of diabetes mellitus (DM) from 7.1 to 9.5%(p<0.01) whilst smoking decreased from 29.8 to 22.4 % ( p<0.001) and the BMI from 26.3 to 25.8( p<0.05) , respectively. By T5, 48 patients had suffered a new CVE of which 12 were fatal. A total of 23 patients died during the follow-up period. Age at disease onset, male sex, a previous CVE, DM, treatment for hypertension, triglyceride level, cumulative disease activity (AUC DAS28), extra-articular disease, corticosteroid use, shorter duration of treatment with DMARDs and use of COX-2 inhibitors increased the hazard rate for a new CVE. A raised ESR at inclusion and AUC DAS28 at 6 months increased the hazard rate of CVE independently whilst DMARD treatment was protective in multiple Cox extended models adjusted for sex and CV risk factors. The risk of a CVE due to inflammation was potentiated by traditional CV risk factors.
Conclusion The occurrence of new CV events in very early RA was explained by traditional CV risk factors and was potentiated by high disease activity. Treatment with DMARDs decreased the risk. The results may have implications for cardio-protective strategies in RA.
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