Abstract
Activated protein C resistance (APCR) may occur in up to one fourth of patients with venous leg ulcers and has recently emerged as the most frequent cause of venous thrombosis. Deep venous thrombosis often precedes deep venous insufficiency and is of major importance in the pathogenesis of venous leg ulcers. APCR is most frequently caused by a point mutation in the factor V gene (fV R506Q), resulting in reduced inactivation of activated factor V and imbalance of the hemostatic system. Recent data suggest that APCR/fV R506Q may be common in patients with venous leg ulcers. We review APCR as a genetically determined risk factor that may contribute to the development of venous leg ulcers. New diagnostic developments are discussed, and therapeutic guidelines specifically directed toward the prevention of thrombosis are suggested.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 616-620 |
| Number of pages | 5 |
| Journal | Journal of the American Academy of Dermatology |
| Volume | 36 |
| Issue number | 4 |
| DOIs | |
| State | Published - 1997 |
Fingerprint
ASJC Scopus subject areas
- Dermatology
Cite this
Activated protein C resistance caused by factor V gene mutation : Common coagulation defect in chronic venous leg ulcers? / Peus, D.; Heit, J. A.; Pittelkow, M. R.
In: Journal of the American Academy of Dermatology, Vol. 36, No. 4, 1997, p. 616-620.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Activated protein C resistance caused by factor V gene mutation
T2 - Common coagulation defect in chronic venous leg ulcers?
AU - Peus, D.
AU - Heit, J. A.
AU - Pittelkow, M. R.
PY - 1997
Y1 - 1997
N2 - Activated protein C resistance (APCR) may occur in up to one fourth of patients with venous leg ulcers and has recently emerged as the most frequent cause of venous thrombosis. Deep venous thrombosis often precedes deep venous insufficiency and is of major importance in the pathogenesis of venous leg ulcers. APCR is most frequently caused by a point mutation in the factor V gene (fV R506Q), resulting in reduced inactivation of activated factor V and imbalance of the hemostatic system. Recent data suggest that APCR/fV R506Q may be common in patients with venous leg ulcers. We review APCR as a genetically determined risk factor that may contribute to the development of venous leg ulcers. New diagnostic developments are discussed, and therapeutic guidelines specifically directed toward the prevention of thrombosis are suggested.
AB - Activated protein C resistance (APCR) may occur in up to one fourth of patients with venous leg ulcers and has recently emerged as the most frequent cause of venous thrombosis. Deep venous thrombosis often precedes deep venous insufficiency and is of major importance in the pathogenesis of venous leg ulcers. APCR is most frequently caused by a point mutation in the factor V gene (fV R506Q), resulting in reduced inactivation of activated factor V and imbalance of the hemostatic system. Recent data suggest that APCR/fV R506Q may be common in patients with venous leg ulcers. We review APCR as a genetically determined risk factor that may contribute to the development of venous leg ulcers. New diagnostic developments are discussed, and therapeutic guidelines specifically directed toward the prevention of thrombosis are suggested.
UR - http://www.scopus.com/inward/record.url?scp=0030899025&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0030899025&partnerID=8YFLogxK
U2 - 10.1016/S0190-9622(97)70251-2
DO - 10.1016/S0190-9622(97)70251-2
M3 - Article
C2 - 9092749
AN - SCOPUS:0030899025
VL - 36
SP - 616
EP - 620
JO - Journal of the American Academy of Dermatology
JF - Journal of the American Academy of Dermatology
SN - 0190-9622
IS - 4
ER -