A citation that seems to back this up.
Losartan reduces hematocrit in patients with chronic obstructive pulmonary disease and secondary erythrocytosis - PubMed
Ann Intern Med. 2001 Mar 6;134(5):426-7.
Losartan Reduces Hematocrit in Patients With Chronic Obstructive Pulmonary Disease and Secondary Erythrocytosis
For a man not dealing with elevated blood pressure, migraines, or copd, would it be safe? Perhaps others here have a sense of that.
Losartan Reduces Hematocrit in Patients with Chronic Obstructive Pulmonary Disease and Secondary Erythrocytosis
TO THE EDITOR: Many studies suggest a positive correlation be- tween the renin–angiotensin system (RAS) and enhanced erythropoiesis. We recently reported that RAS activation may be pulmonary disease (COPD) (1). Therefore, we investigated whether losartan could normalize hematocrit in such patients.
Our study was a 4-week, open-label trial of losartan in which the daily dose was
increased by 25 mg each week: 25, 50, 75, and 100 mg. Participants were nine chronically hypoxemic patients, all former smokers (six men and three women; mean age [ SD], 62 3 years), who had severe COPD and secondary erythrocytosis (hematocrit was greater than 0.52 and had been stable for more than 3 months) despite long-term oxygen therapy. After discontinuation of losartan therapy, patients were followed for 3 months. As shown in the Figure, hematocrit and hemoglobin levels gradually declined in all patients—from 0.56 0.009 and 1.72 0.05 g/L at baseline to 0.46 0.007 and 1.45 0.04 g/L at the end of therapy (P 0.001). The higher the baseline value, the greater the reduction in hematocrit (r 0.7085; P 0.05). After losartan therapy was discontinued, hematocrit and hemoglobin levels uniformly increased; after 3 months, they averaged 0.50 0.007 and 1.59 0.02 g/L, respectively. No other clinical or laboratory variables were significantly affected.
These results are in accordance with previous observations. For instance, enalapril caused
reversible anemia in renal transplant recipients (2) and was subsequently used to treat kidney recipients who had post-transplantation erythrocytosis (3). The manner in which RAS affects erythropoiesis has not yet been fully understood, but both erythropoietin-related and non– erythropoietin-related mechanisms seem to be involved. In this regard, RAS activation was associated with enhanced erythropoietin secretion in patients undergoing hemodialysis (4), while angiotensin II could directly stimulate erythroidn progenitors in in vitro experiments (5).
In conclusion, losartan can be safely and effectively used to normalize hematocrit in patients with COPD and erythrocytosis, an effect that could obviate the need for therapeutic phlebotomy.
