Statin or Nonsteroidal Anti-Inflammatory Drug Use Is Associated With Lower Erythrocyte Sedimentation Rate in Patients With Giant Cell Arteritis

Hegg, Ryan M.; Lee, Andrew G.; Tagg, Nathan T; Zimmerman, M. Bridget

doi:10.1097/wno.0b013e31820c4421

Cited by 20 publications

(10 citation statements)

References 10 publications

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“…However the number of patients receiving statins in the study by Hegg et al was small (24/161 patients with GCA), and most of the patients received concomitant statins and NSAIDs (19/24). Therefore, it was difficult to draw conclusions regarding the role of NSAIDs or statins on levels of inflammatory markers in the study reported by Hegg et al (26). …”

Section: Discussionmentioning

confidence: 97%

Statin Use in Giant Cell Arteritis: A Retrospective Study

Schmidt

Kermani²,

Muratore³

et al. 2013

J Rheumatol

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Objectives 1) To examine the association between statin use and giant cell arteritis (GCA). 2) To compare the clinical features and disease course of GCA among statin users and non-users. Methods For this retrospective study, we reviewed the medical records of all patients with biopsy-positive GCA diagnosed between 1998 and 2008. Using a case-control design we compared the frequency of statin use in GCA patients to non-GCA population-based subjects who were randomly selected and individually matched by sex, age, and calendar year to the GCA case. Statin use at diagnosis or index date, and, during follow-up was abstracted. In subjects with GCA, clinical information at diagnosis and follow-up was collected. Results We included 594 patients, 297 patients with GCA (73 % female), mean age at diagnosis 75 years. The rate of statin exposure at index date was 18.1 % for GCA patients, versus 33.3 % for controls (p < 0.001). Patients using statins were less likely to develop GCA compared with patients not using statins (odds ratio 0.31, 95 % CI 0.15–0.6, p < 0.001), even after adjustment for cardiovascular risk factors. Among patients with GCA, the presenting clinical features and acute phase reactants were similar in patients receiving statins compared to those not on statin therapy. These two groups were also similar with regards to relapse rate, prednisone tapering and overall survival. Conclusion Patients using statins may be less likely to develop GCA compared to patients who are not using statins. However, statin use does not appear to modify the clinical presentation or the course of the disease.

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Section: Discussionmentioning

confidence: 97%

Statin Use in Giant Cell Arteritis: A Retrospective Study

Schmidt

Kermani²,

Muratore³

et al. 2013

J Rheumatol

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“… 19 The anti-inflammatory properties of statins are also evident in reducing the level of erythrocyte sedimentation rate in patients with GCA. 20 Statin use during the course of GCA facilitates more rapid tapering of prednisolone dose. 10 Furthermore, the anti-inflammatory effect of statins may be due to reduction of CD4+CD28 null T lymphocyte levels 21 and reduction of tumour necrosis factor-alpha or interlukin 6 levels.…”

Section: Discussionmentioning

confidence: 99%

Cardiovascular drug treatment, statins and biopsy-confirmed giant cell arteritis: a population-based case–control study

2020

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ObjectiveTo determine whether exposure to cardiovascular medications and statins is associated with increased risk of giant cell arteritis (GCA).DesignThe population-based case–control study comprised a cohort of patients with biopsy-confirmed GCA linked to the Swedish Prescribed Drug Register to identify all exposure to drugs prior to diagnosis of GCA. Ten controls per GCA case, matched for age, sex and residential area, were included. Using corresponding Anatomical Therapeutic Chemical codes, ACE inhibitors, angiotensin II receptor blockers, beta-blocking agents, calcium antagonists, diuretics, statins and cardiac therapy drugs were investigated from July 1, 2005 to the diagnosis/index date. A conditional logistic regression model was fitted adjusted for income, education level and marital status. We repeated the analyses including only new drug users excluding those with any prescription during the year from July 1, 2005 to July 1, 2006.Results574 cases (29% men) of diagnosed GCA and 5740 controls (29% men) were included. The mean age at diagnosis is 75 years (SD 8). Of the GCA cases, 71% had at least one dispensation of a cardiovascular drug prior to the index date, compared to 74% of controls. The ORs for the association of target drug exposure with GCA were <1 for most drugs, but close to 1 in the analysis of new users. Statins were consistently associated with lower risk of GCA, OR 0.74 (95% CI 0.61 to 0.90).ConclusionStatins may be associated with lower risk of incident biopsy-confirmed GCA. No association was evident for other studied drugs.

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“…However, CRP and ESR do not have enough specificity for each pathway and are elevated in all of them, so we cannot recognize which one was responsible. Furthermore, some pain killers like NSAIDs (nonsteroidal anti-inflammatory drugs), usually taken by TAO patients, can influence the result of ESR [153].…”

Section: Controversial Biomarkersmentioning

confidence: 99%

Recent Updates and Advances in Winiwarter-Buerger Disease (Thromboangiitis Obliterans): Biomolecular Mechanisms, Diagnostics and Clinical Consequences

et al. 2021

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Thromboangiitis obliterans (TAO) or Buerger’s disease is a segmental inflammatory, thrombotic occlusive peripheral vascular disease with unknown aetiology that usually involves the medium and small-sized vessels of young male smokers. Due to its unknown aetiology and similarities with atherosclerosis and vasculitis, TAO diagnosis is still challenging. We aimed to review the status of biomolecular and laboratory para-clinical markers in TAO compared to atherosclerosis and vasculitis. We reported that, although some biomarkers might be common in TAO, atherosclerosis, and vasculitis, each disease occurs through a different pathway and, to our knowledge, there is no specific and definitive marker for differentiating TAO from atherosclerosis or vasculitis. Our review highlighted that pro-inflammatory and cell-mediated immunity cytokines, IL-33, HMGB1, neopterin, MMPs, ICAM1, complement components, fibrinogen, oxidative stress, NO levels, eNOS polymorphism, adrenalin and noradrenalin, lead, cadmium, and homocysteine are common markers. Nitric oxide, MPV, TLRs, MDA, ox-LDL, sST2, antioxidant system, autoantibodies, and type of infection are differential markers, whereas platelet and leukocyte count, haemoglobin, lipid profile, CRP, ESR, FBS, creatinine, d-dimer, hypercoagulation activity, as well as protein C and S are controversial markers. Finally, our study proposed diagnostic panels for laboratory differential diagnosis to be considered at first and in more advanced stages.

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Statin or Nonsteroidal Anti-Inflammatory Drug Use Is Associated With Lower Erythrocyte Sedimentation Rate in Patients With Giant Cell Arteritis

Cited by 20 publications

References 10 publications

Statin Use in Giant Cell Arteritis: A Retrospective Study

Statin Use in Giant Cell Arteritis: A Retrospective Study

Cardiovascular drug treatment, statins and biopsy-confirmed giant cell arteritis: a population-based case–control study

Recent Updates and Advances in Winiwarter-Buerger Disease (Thromboangiitis Obliterans): Biomolecular Mechanisms, Diagnostics and Clinical Consequences

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