An unusual complication after placement of an inferior vena cava filter via right internal jugular vein access.

INTRODUCTION:: Totally implantable venous access devices are used extensively worldwide in cancer patients for administration of venotoxic agents, blood sampling, and nutrition. Their tip is usually positioned at the junction of superior vena cava and right atrium. Inferior vena cava filters are usually used for deep venous thrombosis in cases where anticoagulation is contraindicated; they can be inserted either via internal jugular or femoral access depending on patient conditions and preference. CASE DESCRIPTION:: We are describing here a case of totally implantable venous access device fracture following a right internal jugular approach for inferior vena cava filter placement as the patient had inferior vena cava thrombus below the renal veins, extending into the right common iliac vein prohibiting femoral approach. CONCLUSION:: Iatrogenic fracture of totally implantable venous access device is a potential complication of accessing the internal jugular vein for other procedures such as insertion of inferior vena cava filter.

Testosterone, thrombophilia, and thrombosis.

We describe thrombosis, deep venous thrombosis (DVT) pulmonary embolism (PE; n = 9) and hip-knee osteonecrosis (n = 5) that developed after testosterone therapy (median 11 months) in 14 previously healthy patients (13 men and 1 woman; 13 Caucasian and 1 African American), with no antecedent thrombosis and previously undiagnosed thrombophilia-hypofibrinolysis. Of the 14 patients, 3 were found to be factor V Leiden heterozygotes, 3 had high factor VIII, 3 had plasminogen activator inhibitor 1 4G4G homozygosity, 2 had high factor XI, 2 had high homocysteine, 1 had low antithrombin III, 1 had the lupus anticoagulant, 1 had high anticardiolipin antibody Immunoglobulin G, and 1 had no clotting abnormalities. In 4 men with thrombophilia, DVT-PE recurred when testosterone was continued despite therapeutic international normalized ratio on warfarin. In 60 men on testosterone, 20 (33%) had high estradiol (E2 >42.6 pg/mL). When exogenous testosterone is aromatized to E2, and E2-induced thrombophilia is superimposed on thrombophilia-hypofibrinolysis, thrombosis occurs. The DVT-PE and osteonecrosis after starting testosterone are associated with previously undiagnosed thrombophilia-hypofibrinolysis. Thrombophilia should be ruled out before administration of exogenous testosterone.

Testosterone therapy, thrombophilia-hypofibrinolysis, and hospitalization for deep venous thrombosis-pulmonary embolus: an exploratory, hypothesis-generating study.

In our study of 596 men hospitalized in the last 3 years for deep venous thrombosis-pulmonary emboli (DVT-PE), we determined the prevalence of exogenous testosterone (T) use with subsequent development of DVT-PE. Of the 596 men, 110 were now dead, 97 had cancer thought to cause DVT-PE, 250 could not be contacted, leaving 139, of whom 7 had taken T before and at the time of their admissions, 1.2% of the total cohort, a conservative estimate of the prevalence of T-associated DVT-PE. In all, 5 of the 7 DVT-PE events occurred within 3 months of initiation of T, with mean and median intervals between initiation of T and hospitalization with DVT-PE 6.7 and 2 months. Of the 7 men treated with exogenous T, all 5 men who had evaluation of thrombophilia-hypofibrinolysis were found to have previously undiagnosed familial or acquired thrombophilia or hypofibrinolysis, suggesting a thrombotic interaction between exogenous T and thrombophilia-hypofibrinolysis.

Thrombosis in three postmenopausal women receiving testosterone therapy for low libido.

Our hypothesis was that thrombosis occurring in postmenopausal women given testosterone (T) or testosterone-estradiol (TE) to improve libido was associated with a prothrombotic interaction between T or TE with underlying inherited procoagulants. In three previously healthy, postmenopausal, Caucasian women with no antecedent thrombosis and previously undiagnosed G20210A prothrombin gene heterozygosity, hyperhomocysteinemia and 4G4G homozygosity of the PAI-1 gene, we describe central retinal vein thrombosis and osteonecrosis that developed at 16 days, 2 months and 11 months in the three cases, respectively, after T or TE therapy was started. Exogenous T or TE in postmenopausal women may be associated with thrombosis, speculatively when it is superimposed on underlying procoagulants. This small observational case series can serve as a starting point for a larger observational study with greater detail on patient history, serum T and estradiol levels, and detailed PCR and serologic assessment of thrombophilia and hypofibrinolysis.

The endothelial nitric oxide synthase T-786c mutation, a treatable etiology of Prinzmetal's angina.

We assessed to what degree the endothelial nitric oxide synthase (eNOS) T-786C polymorphism, leading to reduced nitric oxide (NO) production-coronary artery spasm, was reversibly associated with Prinzmetal's variant angina (PVA). ENOS T-786C PCR analyses were done in 19 women, 8 men, 26 Caucasian, 1 African-American, median age 53, with well-documented PVA and in 72 healthy controls who did not differ by race or gender. Of the 27 cases, 7 (26%) were homozygous for wild-type normal eNOS (CC), 13 (48%) were T-786C heterozygotes (CT), and 7 (26%) were T-786C homozygotes (TT) vs controls, 44 (61%) CC, 27 (38%) TC, and 1 (1%) TT, P < 0.0001. The mutant eNOS T-786C allele frequency in PVA patients was 27/54 (50%) vs 29/144 (20%) in controls, P < 0.0001. On oral L-arginine (9.2 g/d) to increase production of NO for a median of 4.7 months in 16 PVA patients with symptomatic angina despite conventional nitrate-calcium channel blockers, using the Seattle Angina Questionnaire, satisfaction with symptom remission rose (median) from 50% to 100% (P = 0.004), satisfaction with angina frequency reduction rose from 65% to 80% (P = 0.02), satisfaction with treatment for symptoms rose from 38% to 88% (P = 0.001), and perception of overall life status rose from 25 to 71% (P = 0.0002). On L-arginine (median 4.7 months), in 20 patients, none had worsening of angina, and of 7 patients whose angina totally resolved, eNOS T-786C homozygosity was over-represented, P = 0 .04. The eNOS T-786C mutation appears to be a reversible etiology of PVA in patients whose angina may be ameliorated by L-arginine.