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PubMed1993

The hypercoagulable states.

In most cases, acute venous thrombosis has a straightforward etiology--for example, the patient who has had prolonged bed rest with a broken leg and received no heparin. A significant minority of patients, however, have an inherited biochemical deficiency or an acquired disorder that increases the risk of thrombosis. Some general guidelines suggest when to suspect such defects and what tests to apply.

Adolescent↗
PubMed1997

Both sides of the hypercoagulable state.

Thrombosis can occur on the venous or the arterial side of the circulation. Each has different causes, requires a different diagnostic workup, and responds to different therapies. Venous thrombosis may be situational, but may also reflect inherited or acquired anticoagulation defects. Arterial thrombosis usually results from abnormalities in the blood vessel wall--most often atherosclerosis.

Adult↗
PubMed1996

Haemodilution induces a hypercoagulable state.

It has been suggested that haemodilution with saline may increase whole blood coagulation. This study was conducted in two parts. First, we investigated the effect of in vitro dilution of blood with saline on whole blood coagulation as measured by the thrombelastogram (TEG). Blood (4 ml) was diluted with 0.9% saline 1 ml and coagulation compared with that of an undiluted control specimen obtained concurrently from the same subject. In the second part, the study was repeated using a modified gelatin colloidal solution (Haemaccel) as the diluent. The r time, k time and r + k time were decreased relative to control in both diluent groups. The alpha angles were increased compared with control in both groups while maximum amplitude was unchanged in the Haemaccel diluted group. We conclude that haemodilution per se increases the coagulability of whole blood in vitro, but that saline haemodilution has a more marked effect on final clot strength.

Blood Coagulation↗
PubMed1997

Environmental and genetic determinants of the hypercoagulable state and cardiovascular disease in renal transplant recipients.

BACKGROUND: Fibrinogen and factor VII coagulant activity (VIIc), risk factors for cardiovascular disease (CVD) in the general population, could contribute to CVD risk in renal transplant recipients (RTR). METHODS: We measured fibrinogen and VIIc in 38 RTR and 31 controls, along with prothrombin fragment F1 + 2 and D-Dimer (markers of coagulation and fibrinolytic activation), plasma lipids and the acute phase response cytokine, interleukin 6. The effect of genetic polymorphisms of beta-fibrinogen (G/A-455) and factor VII (Arg/Gln353) was explored. RESULTS: F1 + 2, D-Dimer, and fibrinogen were increased in all RTR, indicating a chronic prothrombotic state. Fibrinogen correlated with age. F1 + 2, and trough cyclosporin A (CsA). RTR carriers of the A-455 allele had a greater increment in plasma fibrinogen concentration and correlation with CsA than homozygotes for the G-455 allele. Interleukin 6 was increased in RTR confirming that a persistent lowgrade acute-phase response could contribute to increased fibrinogen. Differences in plasma VIIc were associated with factor VII genotype, disease status, and blood lipids. Carriers of the Gln353 allele had 30% lower VIIc when compared with Arg353 homozygotes, which could confer a reduced thrombotic risk. The 12 RTR with CVD or metabolic complications (RTR+) were more hyperlipidaemic and had higher fibrinogen and VIIc than the 26 RTR free of disease complications (RTR-), or the controls. CONCLUSIONS: Long-term RTR manifest features of a chronic prothrombotic and persistent inflammatory state. Alterations in fibrinogen and VIIc in RTR arise in part as a result of interactions between common genetic and environmental factors, and these changes could contribute to the increased risk of CVD in RTR.

Adult↗
PubMed1990

Rheumatoid arthritis and hypercoagulable state.

Rheumatoid arthritis is not considered to be associated with recurrent thrombosis. We report a patient, who while receiving anticoagulants had repeated life-threatening episodes of thrombosis. She later developed severe rheumatoid arthritis. After receiving successful antiarthritic therapy and withdrawal of anticoagulants, she had no further episodes of thrombosis.

Arthritis, Rheumatoid↗
PubMed1994

The hypercoagulable state in cancer patients: evidence for impaired thrombin inhibitions.

Activation of prothrombin and the subsequent reactions of thrombin with its substrates and its major inhibitors, antithrombin III (AT III) and heparin cofactor II (HC II), likely reflect both intravascular and extravascular coagulation. Several studies have reported increased in vivo coagulation in cancer. Whether the increased thrombin production in malignancy is accompanied by a corresponding increase in thrombin inhibition is unknown. This study quantified prothrombin fragment 1 + 2 (F1 + 2), thrombin-AT III (TAT), thrombin-AT III-vitronectin (TAT.V), and thrombin-HC II-vitronectin (THCII.V) in the plasmas of healthy volunteers (n = 37); patients with localized solid tumours before treatment was initiated (n = 39); and five patients with non-Hodgkin's lymphoma, both before and during weekly chemotherapy. Two of the five non-Hodgkin's lymphoma patients developed deep venous thrombosis (DVT) during chemotherapy. In normal plasma, where the concentrations of the four parameters likely reflect haemostasis, the sum of TAT, TAT.V and THCII.V was 61% that of F1 + 2, compared with 30% in cancer plasmas. In addition, the mean +/- SEM of F1 + 2 in the plasmas of cancer patients (1.56 +/- 0.09 nM) was significantly elevated (P < 0.001) when compared with healthy volunteers (0.89 +/- 0.06 nM). Eight weeks of chemotherapy increased the F1 + 2 and the binary TAT in plasmas of the non-Hodgkin's lymphoma patients by approximately 1.5- and 2.9-fold, respectively. Thus, increased prothrombin activation in cancer patients, without corresponding increases in concentrations of thrombin-inhibitor complexes, raise the possibility that a significant portion of the thrombin generated in vivo escapes inhibition in cancer and contributes to the high risk of DVT in malignancy.

Adult↗
PubMed2003

Hypercoagulable states and central retinal vein occlusion.

Central retinal vein occlusion is a common cause of permanent visual loss. Work up and laboratory evaluation of patients requires the clinician to rule out hypertension, diabetes, hyperlipidemia, and glaucoma. Patients without an identifiable risk factor are often subject to extensive testing for primary and secondary thrombophilias. The purpose this paper is to review the literature to determine which of these tests is associated with central retinal vein occlusion. Antiphospholipid antibodies and elevated plasma homocysteine levels appear to be the tests associated most commonly in patients with central retinal vein occlusion in most controlled studies. Primary thrombophilias are found rarely when screening patients with central retinal vein occlusion. Extensive testing for thrombophilias is not warranted in the vast majority of patients with central retinal vein occlusion. Older patients with any of the common vascular risk factors do not require thrombophilic screening. By carefully selecting the patients who are evaluated for thrombophilias, the likelihood of finding true-positive tests is increased.

Biomarkers↗