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Brief Reports: Robert S. Bobrow Excess Factor VIII: A Common Cause of Hypercoagulability J Am Board Fam Pract 2005; 18: 147-149 [Abstract] [Full text] [PDF]

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Author's response to "FVIII is an Acute Phase Reactant"

Robert S. Bobrow   (11 April 2005)

FVIII IS an Acture Phase Reactant

Maureane Hoffman   (8 April 2005)

Author's response to "FVIII is an Acute Phase Reactant" 11 April 2005
Robert S. Bobrow, physician Stony Brook University Send response to journal: Re: Author's response to "FVIII is an Acute Phase Reactant" rbobrow{at}notes.cc.sunysb.edu Robert S. Bobrow	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 list 3 references (6,7,8) that specifically looked at this in venous thromboembolism (VTE) patients and concluded the increase in Factor VIII was "persistent and independent of the acute phase response". O'Donnell and Mumford (6) 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 and Tuddenham (7) found elevated FVIII to be the single most common risk factor in 260 VTE patients, and also state that it did not correlate with CRP or fibrinogen. Kamphuisen (8) reaches the same conclusion ("Increased levels of FVIII and fibrinogen in patients with VTE are not caused by acute phase reactions"). I would liked to have had CRP and fibrinogen levels on my patients, but this was a retrospective study and none were done.
FVIII IS an Acture Phase Reactant 8 April 2005
Maureane Hoffman, Pathologist Durham VA Medical Center Send response to journal: Re: FVIII IS an Acture Phase Reactant maureane.hoffman{at}med.va.gov Maureane Hoffman	The author of this article states that "This is a report of 3 cases of thromboembolism not associated with conventional risk factors (trauma, cancer, or immobility). The patients were found to have elevated factor VIII activity without other evidence of a hypercoagulable state." I would respectfully disagree that they show no evidence of any other hypercoagulable state. The ATIII level was low in all three patients and the known thrombotic risk factors, FV Leiden and the Prothrombin gene mutation, were not evaluated. The author also quotes sources to support the contention that "Elevated factor VIII levels have been found to persist over time and to be independent of the acute phase response." This statement is a little misleading in the context of the current report. Previous studies found that even though FVIII is an acute phase reactant, elevated FVIII levels persisted in some patients with thrombosis. Also, those authors compared FVIII levels with other acute phase reactants fibrinogen and CRP. The current study did not verify with CRP or fibrinogen levels that the patients did not suffer from an inflammatory state that could have elevated FVIII levels. Thus, it would have been very useful to know the CRP and fibrinogen levels for the patients reviewed in this report. This would allow firm conclusions to be drawn about whether the FVIII elevation was or was not related to a concurrent inflammatory state. The presence of an inflammatory state might suggest other factors predisposing to thrombosis instead of or in addition to the elevated FVIII level.