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Normal arterial stiffness in familial Mediterranean fever. Evidence for a possible cardiovascular protective role of colchicine


1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12

 

  1. Heller Institute of Medical Research; and Institute of Nephrology and Hypertension, Sheba Medical Center, Tel Hashomer, Israel.
  2. Heller Institute of Medical Research; Rheumatology Unit; and Department of Medicine F, Sheba Medical Center, Tel Hashomer; and Sackler Faculty of Medicine, Tel Aviv University, Israel. alivneh@post.tau.ac.il
  3. Omnistat Statistical Counseling, Tel Aviv, Israel.
  4. Institute of Nephrology and Hypertension, Sheba Medical Center, Tel Hashomer; and Sackler Faculty of Medicine, Tel Aviv University, Israel.
  5. Rheumatology Unit, Sheba Medical Center, Tel Hashomer, Israel.
  6. Heller Institute of Medical Research, Sheba Medical Center, Tel Hashomer, Israel.
  7. Heller Institute of Medical Research; and Department of Medicine F, Sheba Medical Center, Tel Hashomer, Israel.
  8. Heller Institute of Medical Research; and Department of Medicine F, Sheba Medical Center, Tel Hashomer, Israel.
  9. Sackler Faculty of Medicine, Tel Aviv University; Rheumatology Unit; and Department of Medicine F, Sheba Medical Center, Tel Hashomer, Israel.
  10. Sackler Faculty of Medicine, Tel Aviv University; and Rheumatology Unit, Sheba Medical Center, Tel Hashomer, Israel.
  11. Institute of Nephrology and Hypertension, Sheba Medical Center, Tel Hashomer; and Sackler Faculty of Medicine, Tel Aviv University, Israel.
  12. Institute of Nephrology and Hypertension, Sheba Medical Center, Tel Hashomer; and Sackler Faculty of Medicine, Tel Aviv University, Israel.

CER9580
2017 Vol.35, N°6 ,Suppl.108
PI 0032, PF 0037
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PMID: 28229824 [PubMed]

Received: 13/05/2016
Accepted : 27/10/2016
In Press: 09/02/2017
Published: 27/11/2017

Abstract

OBJECTIVES:
Familial Mediterranean fever (FMF) is an autoinflammatory disorder with episodic and persistent inflammation, which is only partially suppressed by continuous colchicine treatment. While chronic inflammation is considered an important cardiovascular risk factor in many inflammatory disorders, its impact in FMF is still disputed. We measured arterial stiffness, a marker of atherosclerotic cardiovascular disease, in a group of FMF patients, in order to evaluate the cardiovascular consequences of inflammation in FMF and the role of colchicine in their development.
METHODS:
Eighty colchicine treated FMF patients, without known traditional cardiovascular risk factors, were randomly enrolled in the study. Demographic, genetic, clinical and laboratory data were retrieved from patient files and examinations. Arterial stiffness was measured using pulse wave velocity (PWV). The recorded values of PWV were compared with those of an age and blood pressure adjusted normal population, using internationally endorsed values.
RESULTS:
FMF patients displayed normal PWV values, with an even smaller than expected proportion of patients deviating from the 90th percentile of the reference population (5% vs. 10%, p=0.02). The lowest PWV values were recorded in patients receiving the highest dose of colchicine (≥2 mg vs. 0-1 mg, p=0.038), and in patients of North African Jewish origin, whose disease was typically more severe than that of patients of other ethnicities; both observations supporting an ameliorating colchicine effect (p=0.043).
CONCLUSIONS:
Though subjected to chronic inflammation, colchicine treated FMF patients have normal PWV. Our findings provide direct evidence for a cardiovascular protective role of colchicine in FMF.

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