ACP-ASIM Information:
  Change of Address
  Residency Database
  Career Resource Center
  Where we stand
  Discussion Groups
  Committees [M]
  IM Bookmarks
Missouri Chapter
Missouri Resident Poster Competition 1999

Mary M. Klix M.D.              St. John's Medical Center
Thrombophilia in women on oral contraceptives: 
we should not just blame the pill


A 31-year-old female with a 2-day history of a throbbing, occipital headache, presented to the emergency room. She developed nausea and vomiting several hours after the headache began. Her medical history included irritable bowel syndrome and polycystic ovary disease. Her only medication was oral contraceptives which she’d been taking for 3 years. Family history was negative for thrombophilia or related disorders. Physical exam was unremarkable, as was the neuro exam. The PT & PTT were normal. Cranial CT scan revealed a right transverse and sigmoid sinus thrombosis.

The patient was started on heparin, decadron and phenytoin and admitted to the hospital. On day 3, she became unresponsive with fixed, dilated pupils. She was intubated and repeat CT revealed acute cerebral edema obliterating all ventricles. The interventional radiologist was able to use intracranial urokinase to lyse the superior sagittal sinus and bilateral transverse sinus thromboses. Venous flow markedly improved. On hospital day eight, she was extubated, was able to speak and follow simple commands.

Lab investigation of the patient’s hypercoagulable state revealed: Normal, nonfasting homocysteine levels; low Protein C & S Activity, (she’d received one dose of warfarin on day 2); heterozygosity for the Factor V Leiden mutation; negative lupus anticoagulant and negative prothrombin promoter gene mutation.

There are many known predisposing factors for thrombophilia. In young women who wish to begin OCP therapy, a careful medical and family history should be obtained. If they later present with unusually located thromboses, underlying risk factors should be sought. Congenital heparin cofactor 2, Protein C & S deficiencies; activated protein C resistance, (some due to Factor V Leiden); prothrombin promoter gene mutation; antiphospholipid syndrome: lupus anticoagulant: sticky platelet syndrome; tissue plasminogen activator defects and others can cause patients to be more susceptible to thrombophilia. We can evaluate for many of these factors, but some values are altered by anticoagulants. Protein C and S are among these, and they are significantly reduced within 48 hours of beginning warfarin therapy. Factor V Leiden, conversely, is detected by DNA analysis, and is unchanged by drug therapies. Patients who are heterozygous for this mutation, which is believed to be part of the most common known risk factor for venous thrombosis, (present in as much s 15% of the population), increase their risk of a significant event by 5 to 10 times that of the general population.

[ Chapter Home | Home | Search | Site Map ]
Contact Missouri ACP-ASIM