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Rheumatology Advance Access originally published online on April 7, 2006
Rheumatology 2006 45(6):782-783; doi:10.1093/rheumatology/kel125
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© The Author 2006. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org


LETTER TO THE EDITOR

Re: Obesity and cardiovascular risk factors in rheumatoid arthritis

F. C. Hall1 and N. Dalbeth2

1 University of Cambridge, School of Clinical Medicine, Cambridge, UK and 2 University of Auckland, Department of Medicine, Auckland, New Zealand

Correspondence to: F. C. Hall. E-mail: fch22{at}medschl.cam.ac.uk

SIR, Armstrong and colleagues raise the important issue of optimizing body mass index (BMI) in patients with rheumatoid arthritis (RA), as part of a cardiovascular risk reduction strategy. They include some interesting data from a local RA cohort, which revealed that 68% patients had a BMI >25 and 31% had a BMI >30. They also report positive correlations in this cohort between BMI and both diastolic blood pressure and cholesterol: high-density lipoprotein cholesterol ratio, both of which are established risk factors for cardiovascular disease. Since population data suggest that a modest reduction in BMI is associated with a substantial reduction of cardiovascular morbidity, Armstrong and colleagues advocate that rheumatologists adopt a more aggressive approach to overweight and obesity in RA patients. They suggest that this include prescription of orlistat, which reduces the absorption of dietary fat.

In the general population, obesity is clearly associated with increased mortality [1, 2], and emerging evidence links obesity and inflammation [3]. It is intriguing to speculate that the optimization of BMI may have beneficial effects on disease acitivity in chronic inflammatory diseases, such as RA. We, therefore, have sympathy with the proposal of Armstrong and colleagues and have included in our algorithms the objective of achieving a BMI <25 in patients with RA in all risk groups. A potential problem with this recommendation is the lack of studies on the relationship between BMI and cardiovascular risk, specifically in the rheumatoid population. Indeed, Escalante and co-workers [4] have shown an inverse relationship between mortality in RA and BMI. This relationship disappears when adjustment for RA disease activity is made, and it therefore seems likely that the adverse association with low BMI in RA patients reflects the cachexia associated with severe systemic disease. Furthermore, the adverse effect of a low BMI mainly reflects the effect of having a BMI <20. Based on current evidence, we believe that it is sensible to recommend aiming for a BMI <25, but only in RA patients with well-controlled disease. Similarly, we think that orlistat would be a useful therapeutic adjunct in patients with a BMI ≥30, provided their disease is well-controlled, and we agree with Armstrong and colleagues that it would be worthwhile including controlled RA to the list of comorbidities in the NICE guidelines [5] for the use of orlistat. An additional consideration is that the use of orlistat may reduce the absorbtion of fat-soluble vitamins, including vitamin D. Since patients with RA are at an increased risk of osteoporosis, it is important to ensure that they do not become osteomalacic. Monitoring of vitamin D at 3–6 monthly intervals would therefore be a sensible precaution in RA patients treated with orlistat. If calcium/vitamin D supplements are indicated, the patient should be advised to take them at least 2 h after taking orlistat.

A final comment is that measurements of central obesity (abdominal circumference and waist-to-hip ratio) may prove better predictors than BMI of cardiovascular disease in RA. This has been demonstrated in the general population [6] and seems likely to be the case in chronic inflammatory disease, since these measurements reflect abdominal adiposity rather than the general nutritional status and muscle bulk. Studies in the RA population are required to clarify this.

References

  1. Fontaine KR, Redden DT, Wang C, Westfall AO, Allison DB. Years of life lost due to obesity. JAMA 2003;289:187–93.[Abstract/Free Full Text]
  2. Peeters A, Barendregt JJ, Willekens F et al. Obesity in adulthood and its consequences for life expectancy: a life-table analysis. Ann Intern Med 2003;138:24–32.[Abstract/Free Full Text]
  3. Lehrke M, Lazar MA. Inflamed about obesity. Nat Med 2004;10:126–7.[CrossRef][Web of Science][Medline]
  4. Escalante A, Haas RW, del Rincón I. Paradoxical effect of body mass index on survival in rheumatoid arthritis: role of comorbidity and systemic inflammation. Arch Intern Med 2005;165:1624–9.[Abstract/Free Full Text]
  5. National Institute for Clinical Excellence. Technology Appraisal Guidance – No. 22 Guidance on the Use of Orlistat for the Treatment of Obesity in Adults. March 2001 (http://www.nice.org.uk/pageaspx?0=15716).
  6. Dagenais GR, Yi Q, Mann JF, Bosch J, Pogue J, Yusuf S. Prognostic impact of body weight and abdominal obesity in women and men with cardiovascular disease. Am Heart J 2005;149:54–60.[CrossRef][Web of Science][Medline]
Accepted 15 March 2006


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This Article
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