A Case Series of HIV-Seropositive Patients and Hypercoagulable State-Is It Difficult to Treat Even with Therapeutic Anticoagulation?
ABSTRACT Patients with human immunodeficiency virus (HIV) are at risk of developing thrombosis and are 8 to 10 times more likely to develop thrombosis than the general population. Moreover, if they have hypercoagulable state they can have severe thrombosis and life-threatening thrombotic events. The purpose of this retrospective study is to analyze hypercoagulable state in HIV-seropositive patients who have been diagnosed with venous thromboembolism (VTE). This study is a subgroup study of a larger cohort group of HIV-seropositive patients with VTE followed up with our vascular medicine outpatient clinic. The patients included for this study were HIV-seropositive patients with hypercoagulable state, analyzed over the past 3 years, and followed prospectively. HIV-seropositive patients with arterial thrombosis were excluded. These patients had minimum, regular follow-up of 3 months, with a Doppler scan in the beginning and last follow-up. All the patients were analyzed for hypercoagulable state and the patients selected in this study were those who were tested positive for hypercoagulable state. All patients were analyzed for age, gender, race, site of thrombosis, coagulation factors, lipid panel, type of antiretroviral treatment, past or present history of infections or malignancy, CD4 absolute and helper cell counts at the beginning of thrombosis, and response to treatment and outcome. Patients with HIV with arterial thrombosis were excluded. The study was approved by the ethics committee. Five patients were included in this study. The mean age was 47.8 years (range 38 to 58 years). All were male patients with lower limb thrombosis. Most common venous thrombosis was popliteal vein thrombosis, followed by common femoral, superficial femoral, and external iliac thrombosis. Two patients had deficiency of protein S, two had high homocysteine levels, one had deficiency of antithrombin 3, and one had increase in anticardiolipin immunoglobulin G antibody. All the patients were taking nucleoside and nonnucleoside inhibitors but only one patient was taking protease inhibitors. There was no history of malignancy but two patients had past history of tuberculosis. The mean absolute CD4 counts were 244 cells/UL (range 103 to 392 cells/UL) and helper CD4 counts were 19.6 cells/UL (range 15 to 30 cells/UL). All were anticoagulated with warfarin or enoxaparin. There was complete resolution of deep vein thrombosis only in one patient on long-term anticoagulation but there was no resolution of thrombosis in the other four patients despite of therapeutic anticoagulation for more than 6 months. All the patients are alive and on regular follow-up. Thrombosis in HIV patients is seen more commonly in middle aged, community ambulant male patients. The most common hypercoagulable state was noted as deficiency of protein S and hyperhomocysteinemia. Eighty percent of the patients did not respond to therapeutic anticoagulation.
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ABSTRACT: Retrospective cohort studies of HIV-infected patients suggest an incidence of venous thromboembolism (VTE) of 1% to 2%, which is 10 times that expected among people without HIV. We investigated the prevalence of established risk factors for VTE in this population and explored novel risk factors. We conducted a case-control study using patients in the Johns Hopkins University AIDS Service cohort. We used conditional logistic regression and paired t tests to test for covariates significantly associated with VTE. We identified 160 patients with VTE diagnosed radiologically or with a clinical course consistent with VTE; 23% of the cases of VTE were diagnosed in hospitalized patients. The incidence of VTE was approximately 0.5% per patient-year. Patients with VTE and control patients did not differ by gender, but black patients were overrepresented among those with VTE (odds ratio [OR]=1.9, 95% confidence interval [CI]: 1.11 to 3.08) and patients with VTE were older than controls (mean: 39 vs. 37 years; P=0.001). Patients with VTE had lower CD4 counts (229 vs. 362 cells/mm; P<0.0001), higher HIV RNA titers (120,254 vs. 71,262 copies/mL; P=0.013), and lower hemoglobin concentrations (11.4 vs. 12.7 g/dL; P<0.0001) preceding the event than those without VTE. The use of highly active antiretroviral therapy was not associated with VTE. In multivariate analyses, independent risks for VTE were age, hospitalization in the past 3 months (OR=13, 95% CI: 6.4 to 27), central venous catheter use in the past 3 months (OR=6.0, 95% CI: 2.3 to 16), and a CD4 count<500 cells/mm (OR=3.0, 95% CI: 1.2 to 7.8). The incidence of VTE in our cohort is similar to that reported in other cohorts of patients with HIV. Recent hospitalization was the risk factor most strongly associated with VTE.JAIDS Journal of Acquired Immune Deficiency Syndromes 07/2008; 48(3):310-4. DOI:10.1097/QAI.0b013e318163bd70 · 4.39 Impact Factor
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ABSTRACT: HIV infection has been recognized as a prothrombotic condition and this association has now been proven by a large number of studies with a reported VTE frequency among HIV-infected patients ranging from 0.19% to 7,63 %/year. HIV infection is associated with a two to tenfold increased risk of venous thrombosis in comparison with a general population of the same age. Some risk factors demonstrated a strongest association with VTE such as, low CD4(+) cell count especially in the presence of clinical AIDS, protein S deficiency, and protein C deficiency. Whereas other risk factors are still controversial like protease inhibitor therapy, presence of active opportunistic infections and presence of antiphospholipid antibodies, including anticardiolipin antibodies and lupus anticoagulant. Physicians caring for HIV positive patients should be able to recognize and treat not only the well-known opportunistic infections and malignancies associated with this chronic disease, but also be alert to the less well-known complications such as thromboses. Pulmonary embolism should be included in the differential diagnosis when patients with HIV/AIDS have unexplained dyspnea or hypoxemia. In younger individuals with VTE, especially men, without other identifiable risk factors for VTE, HIV should be considered. Because interactions between warfarin and antiretrovirals is possible, health care providers should also be alert to the potential of dangerously high or low INRs when they are giving anticoagulants to patients with HIV infection who are undergoing antiretroviral therapy.Mediterranean Journal of Hematology and Infectious Diseases 07/2011; 3(1):e2011030. DOI:10.4084/MJHID.2011.030
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ABSTRACT: Infection with human immunodeficiency virus (HIV) may lead to hemostatic imbalances. Forty-nine consecutive patients with acute opportunistic infections were screened for thrombophilic parameters. A follow-up investigation was performed after 10 +/- 8 weeks in 26 patients. In acutely ill patients, the incidence of protein S deficiency was 67% (33/49) and of protein C deficiency 25% (12/49), while at the follow-up visit the incidences were 54% (14/26) and 8% (2/26), respectively. Protein S and protein C levels increased significantly from initial to follow-up visit (p < 0.05). Lupus anticoagulants were not detected and anticardiolipin IgG antibodies were present in 11.4% (5/44). Three patients presented with deep venous thrombosis on admission; in two, protein S or protein C deficiency was observed. In conclusion, an acquired protein S and protein C deficiency often develop in patients with HIV and acute illness; this may be reversible after treatment for opportunistic infections.Clinical and Applied Thrombosis/Hemostasis 10/2003; 9(4):325-31. DOI:10.1177/107602960300900408 · 1.58 Impact Factor