Anabolic/androgenic steroids can induce various changes in the hematologic system that affect blood clotting. However, these effects are highly variable. These drugs are known for their therapeutic use in increasing fibrinolysin, antithrombin III, and protein levels, stimulating fibrinolysis (clot breakdown), and inhibiting clotting factors II, V, VII, and X. These changes help reduce clotting ability. Prescription guidelines for anabolic/androgenic steroids warn about the potential for increased prothrombin time, which is the time it takes for a blood clot to form.

If the prothrombin time is increased too much, healing may be impaired. The impact of anabolic/androgenic steroids on prothrombin time is usually not clinically significant for healthy individuals using therapeutic doses of these drugs. However, patients taking anticoagulants (blood thinners) may be adversely affected by their use. Conversely, the abuse of anabolic/androgenic steroids has been associated with increased blood clotting ability. These drugs can elevate thromboxane and C-reactive protein levels and thromboxane A2 receptor density, which can promote platelet aggregation and clot formation.

Studies on steroid users have shown statistically significant increases in platelet aggregation values. There are also numerous case reports of thromboembolic events (sometimes fatal) occurring in steroid abusers, including blood clots and strokes. Although it is challenging to directly link these events to steroid abuse, the adverse effects of anabolic steroids on clotting system components are well understood. These severe adverse effects are now recognized as a known risk of many anabolic steroid hormones studied.

At therapeutic levels, the antithrombotic effects of anabolic/androgenic steroids seem to dominate physiology, leading to reduced blood clotting ability. However, at some supra-therapeutic dose point, prothrombotic changes appear to outweigh antithrombotic changes, favoring rapid abnormal clot formation (hypercoagulable state). The exact dose threshold or conditions needed to increase blood clotting are not yet determined, and some studies on users of supraphysiological doses of steroids have failed to demonstrate enhanced clotting function. Nevertheless, warnings about the increased risk of thrombosis caused by anabolic/androgenic steroid hormones are warranted.

The tendency for blood clotting should return to pre-treatment status after discontinuing anabolic/androgenic steroids. Until the hematocrit issue is resolved, a slight elevation in hematocrit can be addressed with phlebotomy. For this, one pint of blood may be regularly removed, usually every two months, during steroid use. Proper hydration is also essential, as dehydration can temporarily elevate hematocrit levels, resulting in a false positive for polycythemia.

If hematocrit exceeds normal values, aspirin intake is typically increased to reduce platelet aggregation, or the tendency for platelets to stick together and form clots. Individuals must remain vigilant about the potential cardiovascular risks associated with high hematocrit levels from anabolic/androgenic steroid use.