Maternal and paternal thrombophilia: risk factors for perinatal mortality.
BACKGROUND
Although some paternal components to the predisposition to pre-eclampsia have been demonstrated recently, it is not known whether such paternal factors play a role to thrombophilia-related perinatal mortality.


OBJECTIVE
To compare the paternal and maternal contribution to perinatal mortality.


METHODS
Data from a prospective registry of perinatal mortality in a Dutch healthcare region were used. Between December 1999 and May 2000, the prevalence of thrombophilia was studied in 74 women with a history of perinatal mortality (female cases) and 54 of their male partners (male cases). Seventy-one healthy unrelated women after uneventful pregnancies only and 66 of their male partners were used as controls.


METHODS
Obstetric outpatient clinic in a regional hospital (Remierde Graaf Group, Deflt).


METHODS
Presence of various coagulation abnormalities, hyperhomocysteinaemia and anticardiolipins was investigated.


RESULTS
The frequency of antithrombin deficiency (12% vs 0%), increased activated protein C (APC) resistance (32% vs 6%), total protein S deficiency (11% vs 1%) and elevated factor VIII:C activity (43% vs 17%) was significantly higher in female cases compared with controls. In male cases, the frequency of increased APC resistance was significantly higher compared with controls (22% vs 0%). In 30 of the 54 couples with a history of perinatal mortality, more than one thrombophilic abnormality was found (55%) compared with 10 of the 62 control couples (17%).


CONCLUSIONS
The risk of having thrombophilia is doubled in men who have fathered pregnancies which ended in perinatal death as well as in the mothers of such pregnancies.
de Galan-Roosen
Agnes E M
AE
Department of Obstetrics and Gynaecology, TweeSteden Hospital, 5000 LA Tilburg, The Netherlands.
Kuijpers
Johan C
JC
Rosendaal
Frits R
FR
Steegers
Eric A
EA
van Beers
Wil A
WA
Ponjee
Gabriëlle A
GA
Merkus
Hans M
HM
D000328:Adult; D017153:Antibodies, Anticardiolipin / Q000097:blood; D000991:Antithrombins / Q000172:deficiency; D004812:Epidemiologic Methods; D005165:Factor V / Q000235:genetics; D005169:Factor VIII / Q000032:analysis; D005220:Fathers / Q000706:statistics & numerical data*; D005260:Female; D006579:Heterozygote; D006720:Homozygote; D006801:Humans; D020138:Hyperhomocysteinemia / Q000235:genetics / Q000401:mortality; D007223:Infant; D007226:Infant Mortality; D007231:Infant, Newborn; D008297:Male; D042965:Methylenetetrahydrofolate Reductase (NADPH2) / Q000235:genetics; D008875:Middle Aged; D009035:Mothers / Q000706:statistics & numerical data*; D009154:Mutation / Q000235:genetics; D009426:Netherlands / Q000453:epidemiology; D010375:Pedigree; D011247:Pregnancy; D019851:Thrombophilia / Q000235:genetics* / Q000401:mortality
D017153:Antibodies, Anticardiolipin; D000991:Antithrombins; C095381:factor V Leiden; D005165:Factor V; D005169:Factor VIII; D042965:Methylenetetrahydrofolate Reductase (NADPH2)