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The Journal of the American Board of Family Practice 18:328a-328 (2005)
© 2005 American Board of Family Practice


Letter to the Editor

Author’s Reply

Robert S. Bobrow, MD

Department of Family Medicine
Stony Brook University
Stony Brook, NY

To the Editor: In her critique of our article, Dr Hoffman states that factor V Leiden and the prothrombin gene mutation were not evaluated in the three patients. They were. The "NP" in the table means "not present" (see key under table).

That factor VIII can be an acute phase reactant seems to be common knowledge. However, I listed 3 references13 that specifically examined this in patients with venous thromboembolism (VTE) and concluded that the increase in factor VIII was "persistent and independent of the acute phase response." O’Donnell et al1 use that specific phrase in their title and find 94% of 35 VTE patients with elevated FVIII to have a persistent increase, independent of CRP and fibrinogen. O’Donnell et al2 found elevated FVIII to be the single most common risk factor in 260 VTE patients and also stated that it did not correlate with CRP or fibrinogen. Kamphuisen et al3 reached the same conclusion. ("Increased levels of FVIII and fibrinogen in patients with VTE are not caused by acute phase reactions.")

I would have liked to have had CRP and fibrinogen levels on my patients, but this was a retrospective study and none were done.

References

  1. O’Donnell J, Mumford AD, Manning RA, Laffan M. Elevation of FVIII: C in venous thromboembolism is persistent and independent of the acute phase reaction. Thromb Haemost 2000; 83: 10–3.[Medline]

  2. O’Donnell J, Tuddenham EG, Manning R, Kemball-Cook G, Johnson D, Laffan M. High prevalence of elevated factor VIII levels in patients referred for thrombophilia screening: role of increased synthesis and relationship to the acute phase reaction. Thromb Haemost 1997; 77: 825–8.[Medline]

  3. Kamphuisen PW, Eikenboom JC, Vos HL, et al. Increased levels of factor VIII and fibrinogen in patients with venous thromboembolism are not caused by acute phase reactions. Thromb Haemost 1999; 81: 680–3.[Medline]





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