Are all types of polycythemias, regardless of their aetiology, predispose to thromboembolic disease (such as pulmonary embolism and deep vein thrombosis)?
Primary polycythemia (PRV) is a risk factor for thromboembolic disease. However, it seems that secondary polycythemia (due to COPD or smoking) is a less significant or less independent risk factor for DVT and PE. Is it correct to assume t hat not all polycythemias are equally significant for this matter?
If this observation is correct, what are the basis of such differences?
I think that your question, is the answer of the question. Primary Polycythemia (PRV) is a disease with many different festures compared with others secondary polycythemia.
I agree, because it is one of the simptoms of this myeloproligferative disease
Polycythaemia vera (PV) is an MPN that is associated with an increased risk of both arterial and venous thrombosis. Secondary thrombocytosis is often a physiological response to tissue hypoxia and there is less evidence to suggest an increased risk of venous thrombosis. For example, in a recent case control study of patients with COPD (PMID 23007895), secondary polycythaemia was not associated with an increased risk of VTE. This uncertainty is also true of apparent polycythaemia (PMID 8405326). The decision to treat polycythaemia that is not primary (PV) will be influenced by other factors includng the absolute haematocrit value, symptoms of hyperviscosity, additional risk factors for thrombosis and cause of polycythaemia. Although written in 2005, the current UK BCSH guidelines on management of polycythaemia is a useful document.
In the case of secondary polycythemia due to COPD or smoking, the increase in red blood cell production is supposed to counterbalance the decrease in SpO2, so that Oxygen Delivery(and thus, consumption) remains stable. In cases like these, when polycythemia constitutes a physiological response, I believe an example can be drawn from other physiological responses, such as sinus tachycardia, a condition that may alarm the patient, yet seldom does it have a serious impact or consequences itself. Therefore, although I think such cases merit consideration and follow-up, no additional burden on thrombotic risk is usually carried with them. Of course, every patient is unique and given a heavy-burden history of thrombotic risk, measures might be necessary. Secondary polycythemia due to other causes(erratic EPO production, for example) is a different story.
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