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Vein thrombosis oral contraceptives

Lenalidomide (Revlimid) Possible birth defects (since analogue of thalidomide), neutropenia, thrombocytopenia, deep vein thrombosis, pulmonary embolism, pruritis, fatigue Dose is 10 mg orally taken with water once daily Women of childbearing age must use two forms of contraception Pregnancy test must be taken before and during use... [Pg.1422]

Martinelli I, Sacchi E, Landi G, Taio-li E, Duca F, Mannucci PM. High risk of cerebral-vein thrombosis in carriers of a prothrombin-gene mutation and in users of oral contraceptives. N Engl J Med 1998 338[25] 1793-1797. [Pg.79]

A 25-year-old woman presents to the emergency department complaining of acute onset of shortness of breath and pleuritic pain. She had been in her usual state of health until 2 days prior when she noted that her left leg was swollen and red. Her only medication was oral contraceptives. Family history was significant for a history of "blood clots" in multiple members of the maternal side of her family. Physical examination demonstrates an anxious woman with stable vital signs. The left lower extremity demonstrates erythema and edema and is tender to touch. Ultrasound reveals a deep vein thrombosis in the left lower extremity chest computed tomography scan confirms the presence of pulmonary emboli. What are the likely risk factors in this woman—hereditary, acquired, or both What therapy is indicated acutely What are the long-term therapy options How long should she be treated Should this individual use oral contraceptives ... [Pg.753]

It also appears that the incidence of hepatic adenomas is increased in women taking oral contraceptives. Ischemic bowel disease secondary to thrombosis of the celiac and superior and inferior mesenteric arteries and veins has also been reported in women using these drugs. [Pg.911]

Data from the Leiden Thrombophilia Study have been used to construct a case-control study, based on contraceptive users who had experienced a first episode of objectively proven deep vein thrombosis (100). Patients and controls were considered thrombophilic when they had protein C deficiency, protein S deficiency, antithrombin deficiency, factor V Leiden mutation, or a prothrombin 20210 A mutation. Among healthy women, the risk of developing deep vein thrombosis was trebled in the first 6 months and doubled in the first year of contraceptive use. Among women with thrombophilia, the risk of deep vein thrombosis was increased 19-fold during the first 6 months and 11-fold (95% Cl = 2.1, 57) in the first year of use. Venous thrombosis during the first period of oral contraceptive use might actually point to the presence of an inherited clotting defect. [Pg.229]

Bohler J, Hauenstein KH, Hasler K, Schollmeyer P. Renal vein thrombosis in a dehydrated patient on an oral contraceptive agent. Nephrol Dial Transplant 1989 4(ll) 993-5. [Pg.243]

Bloemenkamp KW, Rosendaal FR, Helmerhorst FM, Buller HR, Vandenbroucke JP. Enhancement by factor V Leiden mutation of risk of deep-vein thrombosis associated with oral contraceptives containing a third-generation progestagen. Lancet 1995 346(8990) 1593-6. [Pg.245]

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. [Pg.341]

Valla and colleagues [17], in a case-control study of 33 women with BCS, identified a relative risk of 2.37 for this complication in users of oral contraceptives, a figure very close to that for other vascular complications of the pill. Current evidence suggests that oral contraceptives lead to hepatic vein thrombosis by exacerbating an underlying throm-bogenic condition [16]. [Pg.282]

Valla D, Le MG, Paynard T, Rueff B, Benhamou JP (1986) Risk of hepatic vein thrombosis in relation to the recent use of oral contraceptives a case control study. Gastroenterology 90 967-972. [Pg.292]

A 39-year-old woman developed idiopathic thrombosis of the posterior tibial vein. Oral contraceptives and resistance to activated protein C were identified as risk factors. After initial treatment with intravenous heparin, she was given phenprocoumon and the oral contraceptive was withdrawn. After 4 months she developed subacute liver failure and phenprocoumon was withdrawn immediately. Autoimmune disease, viral hepatitis, toxic causes, and Budd-Chiari syndrome were excluded. Despite symptomatic treatment, she deteriorated further and orthotopic liver transplantation was performed. Histopathology of the explanted liver further excluded ischemic Uver cell necrosis and Budd-Chiari syndrome. [Pg.985]

A 28-year-old woman took thalidomide 100 mg/day for Behget s disease and after 3 months developed amenorrhea (89). She took an oral contraceptive for 8 months, but then had a deep vein thrombosis in association with a factor V Leiden mutation the oral contraceptive was withdrawn and she was given warfarin. She remained amenorrheic. She had a raised serum concentration of follicle-stimulating hormone but all other laboratory tests were normal. Ultrasonography showed a normal uterus and an endometrial lining of 4 mm. The amenorrhea was attributed to thahdomide, which she decided to continue taking she remained amenorrheic. [Pg.3349]

MartineUi I, Taioli E, Bucciarelli P, Akhavan S, Mannucci PM. Interaction between the G20210A mutation of the prothrombin gene and oral contraceptive use in deep vein thrombosis. Arteriosder Thromb Vase Biol 1999 19 700-3. [Pg.1527]

A client who is obese is at risk for hypertension, hypercholesterolemia, and deep vein thrombosis and should not take oral contraceptives. [Pg.193]

To conclude, the epidemiological studies on oral contraceptives and thromboembolism all point to the same direction, i.e. to an increased risk of thromboembolic disease (deep vein thrombosis, pulmonary embolism, cerebral thrombosis, myocardial infarction) in women using oral contraceptives of the combined type. Support can also be obtained from the studies on changes in the fibrinolytic system (see below). For thrombosis with rare localization, e.g. in the mesenteric vessels, epidemiological data are still lacking. It remains to be seen whether the risk of thrombosis is reduced with the new low-dose combinations. [Pg.298]

Sagar, S., Stamatakis, J. D., Thomas, D. P. and Kakkar, V.V. (1976) Oral contraceptives, anti-thromin-111 activity, and postoperative deep-vein thrombosis. Lancet, I, 509. [Pg.309]


See other pages where Vein thrombosis oral contraceptives is mentioned: [Pg.64]    [Pg.910]    [Pg.210]    [Pg.217]    [Pg.219]    [Pg.453]    [Pg.956]    [Pg.547]    [Pg.676]    [Pg.731]    [Pg.586]    [Pg.1647]    [Pg.1506]    [Pg.1507]    [Pg.1507]    [Pg.83]    [Pg.352]    [Pg.474]    [Pg.162]    [Pg.1140]    [Pg.299]    [Pg.299]   
See also in sourсe #XX -- [ Pg.299 ]




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