A pro thrombotic state in TB can be attributed to elevated plasma fibrinogen, impaired fibrinolysis, decreased levels of
anti-thrombin III and reactive thrombocytosis (7, 8).
Further laboratory work-up for autoimmune and coagulation disorders, such as anti-phospholipid syndrome, protein-S, protein-C and
anti-thrombin III deficiency was negative.
Thrombophilia screening including protein C, protein S, lupus anticoagulant, anticardiolipin antibody, anti-[beta] glycoprotein-I antibody, and
anti-thrombin III were all normal.
Antinuclear antibodies were negative and protein C, protein S,
anti-thrombin III and antiphospholipid antibodies profile which were carried out 4 weeks afterwards were within normal limits, hence ruling out any coagulopathy.
At one side estrogen is found to be thrombogenic by cohorts of the patients using contraceptive pills or receiving hormonal replacement therapy1,2 which is also supported by the fact that a number of pathways are altered by estrogen that effect the cardiovascular system14,15 and many changes in factors influencing coagulation have been reported including increased circulating levels of factors II, VII, IX and X and decreased
anti-thrombin III pathway due to hepatic effects16.
Fibrinogen degradation products tend to be raised and concentrations of proteins C, S, and
anti-thrombin III reduced (9).
D-dimer was 5.42 pg [mL.sup.-1] (normal range: 0-0.48 pg [mL.sup.-1]),
anti-thrombin III activity was 101% (normal range: 80%-120%), plasma protein C and protein S levels were 84% (normal range: 70%-130%) and 92% (normal range: 60%-130%), respectively, and the plasma factor VIII level was 126% (normal range: 53%-170%).
Anti-thrombin III activity was measured with a chromogenic substrate (cat.