Thromboembolic disorders venous

Spitzer WO, Lewis MA, Heinemann LA, Thorogood M, MacRae KD. Third generation oral contraceptives and risk of venous thromboembolic disorders an international case-control study. Transnational Research Group on Oral Contraceptives and the Health of Young Women. BMJ 1996 312(7023) 83-8. 

Venous thromboembolism (VTE) is one of the most common cardiovascular disorders in the United States. VTE is manifested as deep vein thrombosis (DVT) and pulmonary embolism (PE) resulting from thrombus formation in the venous circulation (Fig. 7-1).1 It is often provoked by prolonged immobility and vascular injury and is most frequently seen in patients who have been hospitalized for a serious medical illness, trauma, or major surgery. VTE can also occur with little or no provocation in patients who have an underlying hypercoagulable disorder. 

Cardiovascular disorders Estrogen and estrogen/progestin therapy have been associated with an increased risk of cardiovascular events (eg, Ml and stroke, venous thrombosis, PE [venous thromboembolism]). Manage risk factors for cardiovascular disease appropriately. 

Thrombosis in the dural sinuses or cerebral veins is much less common than cerebral arterial thromboembolism. It causes a variety of clinical syndromes, which often do not resemble stroke (Bousser and Ross Russell 1997). While ischemic arterial stroke and cerebral venous thrombosis share some causes (Southwick et al. 1986), others are specific to cerebral venous thrombosis (Table 29.1). A particularly high index of suspicion is required in women on the oral contraceptive pill (Saadatnia and Tajmirriahi 2007) and in the puerperium. In the past, cerebral venous thrombosis was strongly associated with otitis media and mastoiditis, lateral sinus thrombosis or otitic hydrocephalus, but the most common causes are now pregnancy and the puerperium, which cause 5-20% of the cerebral venous thrombosis in the developed world, the oral contraceptive pill, malignancy, dehydration, inflammatory disorders and hereditary coagulation disorders. No cause is found in around 20% of cases. 

Deficiencies of methionine adenosyltransferase, cystathionine 8-synthase, and cystathionine )/-lyase have been described. The first leads to hypermethioninemia but no other clinical abnormality. The second leads to hypermethioninemia, hyperhomocysteinemia, and homo-cystinuria. The disorder is transmitted as an autosomal recessive trait. Its clinical manifestations may include skeletal abnormalities, mental retardation, ectopia lentis (lens dislocation), malar flush, and susceptibility to arterial and venous thromboembolism. Some patients show reduction in plasma methionine and homocysteine concentrations and in urinary homocysteine excretion after large doses of pyridoxine. Homocystinuria can also result from a deficiency of cobalamin (vitamin B12) or folate metabolism. The third, an autosomal recessive trait, leads to cystathioninuria and no other characteristic clinical abnormality. 

Strodium ranelate is restricted to second-line treatment of severe osteoporosis in postmenopausal women at high risk of fracture, and in men at increased risk of fracture. A review of available safety data for strodixun ranelate has raised concern about its cardiovascular safety beyond the already recognised risk of venous thromboembolism. An analysis of randomised controlled trial data has identified an increased risk of serious cardiac disorders, including myocardial infarction [65 ]. 

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