Genetic thrombophilia in patients with retinal vascular occlusion

ISSN:
1573-2630
Keywords:
central retinal vein occlusion ; resistance to activated protein C ; thrombophilia
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Abstract Background: This study was carried out to determine the prevalence of genetic thrombophilia in patients with retinal vascular occlusion.Methods: We investigated 116 consecutive patients with central retinal vein occlusion (CRVO, n = 48), branch retinal vein occlusion (BRVO, n = 33), central retinal artery occlusion (CRAO, n = 21), branch retinal artery occlusion (BRAO, n = 14). All patients underwent comprehensive tests for coagulation disorders including determinations of protein C, protein S, lupus anticoagulants, prothrombin gene mutation (G20210A), resistance to activated protein C (APCR), and were screened for vascular disease risk factors. APC resistance was confirmed by a PCR method to detect the factor V R506Q mutation. A PCR method was also used to detect the G20210A mutation. For comparative purposes, we screened 209 consecutive patients with deep vein thrombosis (DVT) and 581 patients with coronary heart disease (control group) for APC resistance.Results: 13 (27%) of 48 patients with CRVO had the factor V R506Q mutation. The factor V R506Q mutation was detected in six (18%) of 33 patients with BRVO, but in only one patient with CRAO and in two patients with BRAO. Other thrombophilic defects were not detected. The APCR prevalence within the CRVO group was significantly increased when compared to the control group (8%). There was no significant difference in the factor V R506Q mutation prevalence between the CRVO group and the DVT group (19%).Conclusion: The factor V R506Q mutation is the most commoncause of genetic thrombophilia in patients with CRVO and has a similar prevalence as in DVT patients.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1023/A:1010639332737
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autor Greiner, Kathrin
Peetz, Dirk
Winkgen, Andrea
Prellwitz, Winfried
Pfeiffer, Norbert
Hafner, Gerd
autorsonst Greiner, Kathrin
Peetz, Dirk
Winkgen, Andrea
Prellwitz, Winfried
Pfeiffer, Norbert
Hafner, Gerd
book_url http://dx.doi.org/10.1023/A:1010639332737
datenlieferant nat_lic_papers
hauptsatz hsatz_simple
identnr NLM194449483
issn 1573-2630
journal_name International ophthalmology
materialart 1
notes Abstract Background: This study was carried out to determine the prevalence of genetic thrombophilia in patients with retinal vascular occlusion.Methods: We investigated 116 consecutive patients with central retinal vein occlusion (CRVO, n = 48), branch retinal vein occlusion (BRVO, n = 33), central retinal artery occlusion (CRAO, n = 21), branch retinal artery occlusion (BRAO, n = 14). All patients underwent comprehensive tests for coagulation disorders including determinations of protein C, protein S, lupus anticoagulants, prothrombin gene mutation (G20210A), resistance to activated protein C (APCR), and were screened for vascular disease risk factors. APC resistance was confirmed by a PCR method to detect the factor V R506Q mutation. A PCR method was also used to detect the G20210A mutation. For comparative purposes, we screened 209 consecutive patients with deep vein thrombosis (DVT) and 581 patients with coronary heart disease (control group) for APC resistance.Results: 13 (27%) of 48 patients with CRVO had the factor V R506Q mutation. The factor V R506Q mutation was detected in six (18%) of 33 patients with BRVO, but in only one patient with CRAO and in two patients with BRAO. Other thrombophilic defects were not detected. The APCR prevalence within the CRVO group was significantly increased when compared to the control group (8%). There was no significant difference in the factor V R506Q mutation prevalence between the CRVO group and the DVT group (19%).Conclusion: The factor V R506Q mutation is the most commoncause of genetic thrombophilia in patients with CRVO and has a similar prevalence as in DVT patients.
package_name Springer
publikationsjahr_anzeige 1999
publikationsjahr_facette 1999
publikationsjahr_intervall 8004:1995-1999
publikationsjahr_sort 1999
publisher Springer
reference 23 (1999), S. 155-160
schlagwort central retinal vein occlusion
resistance to activated protein C
thrombophilia
search_space articles
shingle_author_1 Greiner, Kathrin
Peetz, Dirk
Winkgen, Andrea
Prellwitz, Winfried
Pfeiffer, Norbert
Hafner, Gerd
shingle_author_2 Greiner, Kathrin
Peetz, Dirk
Winkgen, Andrea
Prellwitz, Winfried
Pfeiffer, Norbert
Hafner, Gerd
shingle_author_3 Greiner, Kathrin
Peetz, Dirk
Winkgen, Andrea
Prellwitz, Winfried
Pfeiffer, Norbert
Hafner, Gerd
shingle_author_4 Greiner, Kathrin
Peetz, Dirk
Winkgen, Andrea
Prellwitz, Winfried
Pfeiffer, Norbert
Hafner, Gerd
shingle_catch_all_1 Greiner, Kathrin
Peetz, Dirk
Winkgen, Andrea
Prellwitz, Winfried
Pfeiffer, Norbert
Hafner, Gerd
Genetic thrombophilia in patients with retinal vascular occlusion
central retinal vein occlusion
resistance to activated protein C
thrombophilia
central retinal vein occlusion
resistance to activated protein C
thrombophilia
Abstract Background: This study was carried out to determine the prevalence of genetic thrombophilia in patients with retinal vascular occlusion.Methods: We investigated 116 consecutive patients with central retinal vein occlusion (CRVO, n = 48), branch retinal vein occlusion (BRVO, n = 33), central retinal artery occlusion (CRAO, n = 21), branch retinal artery occlusion (BRAO, n = 14). All patients underwent comprehensive tests for coagulation disorders including determinations of protein C, protein S, lupus anticoagulants, prothrombin gene mutation (G20210A), resistance to activated protein C (APCR), and were screened for vascular disease risk factors. APC resistance was confirmed by a PCR method to detect the factor V R506Q mutation. A PCR method was also used to detect the G20210A mutation. For comparative purposes, we screened 209 consecutive patients with deep vein thrombosis (DVT) and 581 patients with coronary heart disease (control group) for APC resistance.Results: 13 (27%) of 48 patients with CRVO had the factor V R506Q mutation. The factor V R506Q mutation was detected in six (18%) of 33 patients with BRVO, but in only one patient with CRAO and in two patients with BRAO. Other thrombophilic defects were not detected. The APCR prevalence within the CRVO group was significantly increased when compared to the control group (8%). There was no significant difference in the factor V R506Q mutation prevalence between the CRVO group and the DVT group (19%).Conclusion: The factor V R506Q mutation is the most commoncause of genetic thrombophilia in patients with CRVO and has a similar prevalence as in DVT patients.
1573-2630
15732630
Springer
shingle_catch_all_2 Greiner, Kathrin
Peetz, Dirk
Winkgen, Andrea
Prellwitz, Winfried
Pfeiffer, Norbert
Hafner, Gerd
Genetic thrombophilia in patients with retinal vascular occlusion
central retinal vein occlusion
resistance to activated protein C
thrombophilia
central retinal vein occlusion
resistance to activated protein C
thrombophilia
Abstract Background: This study was carried out to determine the prevalence of genetic thrombophilia in patients with retinal vascular occlusion.Methods: We investigated 116 consecutive patients with central retinal vein occlusion (CRVO, n = 48), branch retinal vein occlusion (BRVO, n = 33), central retinal artery occlusion (CRAO, n = 21), branch retinal artery occlusion (BRAO, n = 14). All patients underwent comprehensive tests for coagulation disorders including determinations of protein C, protein S, lupus anticoagulants, prothrombin gene mutation (G20210A), resistance to activated protein C (APCR), and were screened for vascular disease risk factors. APC resistance was confirmed by a PCR method to detect the factor V R506Q mutation. A PCR method was also used to detect the G20210A mutation. For comparative purposes, we screened 209 consecutive patients with deep vein thrombosis (DVT) and 581 patients with coronary heart disease (control group) for APC resistance.Results: 13 (27%) of 48 patients with CRVO had the factor V R506Q mutation. The factor V R506Q mutation was detected in six (18%) of 33 patients with BRVO, but in only one patient with CRAO and in two patients with BRAO. Other thrombophilic defects were not detected. The APCR prevalence within the CRVO group was significantly increased when compared to the control group (8%). There was no significant difference in the factor V R506Q mutation prevalence between the CRVO group and the DVT group (19%).Conclusion: The factor V R506Q mutation is the most commoncause of genetic thrombophilia in patients with CRVO and has a similar prevalence as in DVT patients.
1573-2630
15732630
Springer
shingle_catch_all_3 Greiner, Kathrin
Peetz, Dirk
Winkgen, Andrea
Prellwitz, Winfried
Pfeiffer, Norbert
Hafner, Gerd
Genetic thrombophilia in patients with retinal vascular occlusion
central retinal vein occlusion
resistance to activated protein C
thrombophilia
central retinal vein occlusion
resistance to activated protein C
thrombophilia
Abstract Background: This study was carried out to determine the prevalence of genetic thrombophilia in patients with retinal vascular occlusion.Methods: We investigated 116 consecutive patients with central retinal vein occlusion (CRVO, n = 48), branch retinal vein occlusion (BRVO, n = 33), central retinal artery occlusion (CRAO, n = 21), branch retinal artery occlusion (BRAO, n = 14). All patients underwent comprehensive tests for coagulation disorders including determinations of protein C, protein S, lupus anticoagulants, prothrombin gene mutation (G20210A), resistance to activated protein C (APCR), and were screened for vascular disease risk factors. APC resistance was confirmed by a PCR method to detect the factor V R506Q mutation. A PCR method was also used to detect the G20210A mutation. For comparative purposes, we screened 209 consecutive patients with deep vein thrombosis (DVT) and 581 patients with coronary heart disease (control group) for APC resistance.Results: 13 (27%) of 48 patients with CRVO had the factor V R506Q mutation. The factor V R506Q mutation was detected in six (18%) of 33 patients with BRVO, but in only one patient with CRAO and in two patients with BRAO. Other thrombophilic defects were not detected. The APCR prevalence within the CRVO group was significantly increased when compared to the control group (8%). There was no significant difference in the factor V R506Q mutation prevalence between the CRVO group and the DVT group (19%).Conclusion: The factor V R506Q mutation is the most commoncause of genetic thrombophilia in patients with CRVO and has a similar prevalence as in DVT patients.
1573-2630
15732630
Springer
shingle_catch_all_4 Greiner, Kathrin
Peetz, Dirk
Winkgen, Andrea
Prellwitz, Winfried
Pfeiffer, Norbert
Hafner, Gerd
Genetic thrombophilia in patients with retinal vascular occlusion
central retinal vein occlusion
resistance to activated protein C
thrombophilia
central retinal vein occlusion
resistance to activated protein C
thrombophilia
Abstract Background: This study was carried out to determine the prevalence of genetic thrombophilia in patients with retinal vascular occlusion.Methods: We investigated 116 consecutive patients with central retinal vein occlusion (CRVO, n = 48), branch retinal vein occlusion (BRVO, n = 33), central retinal artery occlusion (CRAO, n = 21), branch retinal artery occlusion (BRAO, n = 14). All patients underwent comprehensive tests for coagulation disorders including determinations of protein C, protein S, lupus anticoagulants, prothrombin gene mutation (G20210A), resistance to activated protein C (APCR), and were screened for vascular disease risk factors. APC resistance was confirmed by a PCR method to detect the factor V R506Q mutation. A PCR method was also used to detect the G20210A mutation. For comparative purposes, we screened 209 consecutive patients with deep vein thrombosis (DVT) and 581 patients with coronary heart disease (control group) for APC resistance.Results: 13 (27%) of 48 patients with CRVO had the factor V R506Q mutation. The factor V R506Q mutation was detected in six (18%) of 33 patients with BRVO, but in only one patient with CRAO and in two patients with BRAO. Other thrombophilic defects were not detected. The APCR prevalence within the CRVO group was significantly increased when compared to the control group (8%). There was no significant difference in the factor V R506Q mutation prevalence between the CRVO group and the DVT group (19%).Conclusion: The factor V R506Q mutation is the most commoncause of genetic thrombophilia in patients with CRVO and has a similar prevalence as in DVT patients.
1573-2630
15732630
Springer
shingle_title_1 Genetic thrombophilia in patients with retinal vascular occlusion
shingle_title_2 Genetic thrombophilia in patients with retinal vascular occlusion
shingle_title_3 Genetic thrombophilia in patients with retinal vascular occlusion
shingle_title_4 Genetic thrombophilia in patients with retinal vascular occlusion
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source_archive Springer Online Journal Archives 1860-2000
timestamp 2024-05-06T09:55:33.145Z
titel Genetic thrombophilia in patients with retinal vascular occlusion
titel_suche Genetic thrombophilia in patients with retinal vascular occlusion
topic WW-YZ
uid nat_lic_papers_NLM194449483