Serum Creatine Kinase in Patients with Rheumatic Diseases

Lee, Young Ho; Choi, Sung Jae; Ji, Jong Dae; Song, Gwan Gyu

doi:10.1007/s100670070049

Cited by 27 publications

(19 citation statements)

References 17 publications

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“…Additionally they showed a high predominance of the S3 allele and concluded causality. Lee et al [22] found elevated Lp(a) levels in RA patients compared to controls as well. Although Lp(a) tended to be higher in RA, they could not find a distinct acute phase pattern of Lp(a).…”

Section: Resultsmentioning

confidence: 99%

A Systematic Literature Review of the Association of Lipoprotein(a) and Autoimmune Diseases and Atherosclerosis

Missala

Kassner

Steinhagen‐Thiessen

2012

International Journal of Rheumatology

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Objective. To investigate the association of lipoprotein(a) and atherosclerosis-related autoimmune diseases, to provide information on possible pathophysiologic mechanisms, and to give recommendations for Lp(a) determination and therapeutic options. Methods. We performed a systematic review of English language citations referring to the keywords “Lp(a)” AND “autoimmune disease” AND “atherosclerosis,” “Lp(a)” AND “immune system” OR “antiphospholipid (Hughes) syndrome (APS)” OR “rheumatoid arthritis” OR “Sjögren's syndrome” OR “systemic lupus erythematosus” OR “systemic sclerosis” OR “systemic vasculitis” published between 1991 and 2011 using Medline database. Results. 22 out of 65 found articles were identified as relevant. Lp(a) association was highest in rheumatoid arthritis (RA), followed by systemic lupus erythematosus (SLE), moderate in APS and lowest in systemic sclerosis (SSc). There was no association found between Lp(a) and systemic vasculitis or Sjögren's syndrome. Conclusion. Immune reactions are highly relevant in the pathophysiology of atherosclerosis, and patients with specific autoimmune diseases are at high risk for CVD. Elevated Lp(a) is an important risk factor for premature atherosclerosis and high Lp(a) levels are also associated with autoimmune diseases. Anti-Lp(a)-antibodies might be a possible explanation. Therapeutic approaches thus far include niacin, Lp(a)-apheresis, farnesoid x-receptor-agonists, and CETP-inhibitors being currently under investigation.

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Section: Resultsmentioning

confidence: 99%

A Systematic Literature Review of the Association of Lipoprotein(a) and Autoimmune Diseases and Atherosclerosis

Missala

Kassner

Steinhagen‐Thiessen

2012

International Journal of Rheumatology

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“…Inflammatory conditions including rheumatoid arthritis and systemic lupus are associated with reduced CK levels. 15 Statins reduce systemic inflammation 1 and could increase average CK by decreasing inflammation. We did not measure inflammatory markers in STOMP so cannot evaluate this possible relationship.…”

Section: Discussionmentioning

confidence: 99%

Effect of Statins on Skeletal Muscle Function

et al. 2013

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Background Many clinicians believe that statins cause muscle pain, but this has not been observed in clinical trials and the effect of statins on muscle performance has not been carefully studied. Methods and Results The Effect of STatins On Skeletal Muscle Function and Performance (STOMP) study assessed symptoms and measured creatine kinase (CK), exercise capacity, and muscle strength before and after atorvastatin 80 mg or placebo were administered for 6 months to 420 healthy, statin-naive subjects. No individual CK value exceeded 10 times normal, but average CK increased 20.8 ± 141.1 U/L (p<0.0001) with atorvastatin. There were no significant changes in several measures of muscle strength or exercise capacity with atorvastatin, but more atorvastatin than placebo subjects developed myalgia (19 vs 10; p = 0.05). Myalgic subjects on atorvastatin or placebo decreased muscle strength in 5 of 14 and 4 of 14 variables respectively (p = 0.69). Conclusions These results indicate that high-dose atorvastatin for 6 months does not decrease average muscle strength or exercise performance in healthy, previously untreated subjects. Nevertheless, this blinded, controlled trial confirms the undocumented impression that statins increase muscle complaints. Atorvastatin also increased average CK suggesting that statins produce mild muscle injury even among asymptomatic subjects. This increase in CK should prompt studies examining the effects of more prolonged, high-dose statin treatment on muscular performance. Clinical Trial Registration Information: www.clinicaltrials.gov; Identifier: NCT00609063.

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“…Serum CK has been shown to be lower in patients with RA versus healthy volunteers and to correlate with the level of inflammation [35]. Generally, mean CK tended to plateau after six months of tofacitinib treatment, stayed within the normal reference range and was not associated with clinical myopathy or changes in markers of muscle catabolism (lactate dehydrogenase and myoglobin).…”

Section: Discussionmentioning

confidence: 99%

Changes in serum creatinine in patients with active rheumatoid arthritis treated with tofacitinib: results from clinical trials

et al. 2014

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IntroductionSmall increases in mean serum creatinine (SCr) were observed in studies of rheumatoid arthritis patients during tofacitinib treatment. These SCr changes were investigated and potential mechanisms explored.MethodsSCr values and renal adverse event data were pooled from five Phase 3 and two long-term extension (LTE) studies. Dose-response relationships and association with inflammation (C-reactive protein (CRP)) were explored using Phase 2 data and confirmed with Phase 3 data.ResultsIn Phase 3, least squares mean SCr differences from placebo at Month 3 were 0.02 and 0.04 mg/dl for tofacitinib 5 and 10 mg twice daily (BID) (P <0.05), respectively. During Months 0 to 3, confirmed SCr ≥33% increases over baseline were reported in 17 (1.4%; 5 mg BID) and 23 (1.9%; 10 mg BID) patients. Generally, elevations plateaued and remained within normal limits throughout Phase 3 and LTE studies. Exposure-response modeling demonstrated small, reversible effects of tofacitinib on mean SCr, and significant (P <0.05) effects of CRP on model parameters. Phase 3 data confirmed that patients with higher baseline CRP or greater CRP decreases following tofacitinib treatment had the largest increases in SCr. Across Phase 3 and LTE studies, 22 tofacitinib-treated patients had clinical acute renal failure (ARF), predominantly in the setting of concurrent serious illness.ConclusionsTofacitinib treatment was associated with small, reversible mean increases in SCr that plateaued early. The mechanism behind these SCr changes remains unknown, but may involve effects of tofacitinib on inflammation. ARF occurred infrequently, was associated with concurrent serious illness, and was unrelated to prior SCr increases.Electronic supplementary materialThe online version of this article (doi:10.1186/ar4673) contains supplementary material, which is available to authorized users.

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Serum Creatine Kinase in Patients with Rheumatic Diseases

Cited by 27 publications

References 17 publications

A Systematic Literature Review of the Association of Lipoprotein(a) and Autoimmune Diseases and Atherosclerosis

A Systematic Literature Review of the Association of Lipoprotein(a) and Autoimmune Diseases and Atherosclerosis

Effect of Statins on Skeletal Muscle Function

Changes in serum creatinine in patients with active rheumatoid arthritis treated with tofacitinib: results from clinical trials

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