Last updated:
7/27/2026
Years published: 1986, 1990, 1994, 1995, 1997, 1998, 2005, 2008, 2011, 2013, 2016, 2018, 2023, 2025, 2026
NORD gratefully acknowledges Jerry Spivak, MD, MACP, Emeritus Professor of Medicine, John Hopkins University School of Medicine for assistance in the preparation of this report.
Summary
Polycythemia vera (PV) is a rare, chronic condition in which the bone marrow produces too many blood cells. The bone marrow is the soft tissue inside bones where blood cells are made. In PV, the body makes too many normal red blood cells, white blood cells, and platelets.
When red blood cells are produced in excess, the volume of red blood cells circulating in the bloodstream becomes abnormally high. This slows blood flow and causes the blood to become thicker, a condition called hyperviscosity, which can impair blood circulation.
People with PV can experience a range of symptoms, including migraine-like headaches, fatigue, weakness, dizziness, itching of the skin (especially after warm baths or showers), and an enlarged spleen. Some people may also have digestive problems such as acid reflux, gout from the large turnover of white blood cells, and a condition called erythromelalgia, which causes burning pain in the hands and feet. PV also increases the risk of developing blood clots, since blood becomes thicker as its flow slows down.
About 95% of people with PV have a change (variant) in the JAK2 gene (JAK2 V617F), which is called a driver mutation (driver variant) because it leads to the uncontrolled production of normal red blood cells, white blood cells, and platelets. Most of the remaining patients have variants in exon 12 of the JAK2 gene. These acquired (somatic) variants develop after birth and are not inherited. Although PV is considered a chronic blood cancer, it usually progresses slowly, and with appropriate treatment most people can expect a near-normal life expectancy.
Treatment includes phlebotomy, a procedure that removes excess blood from the body to reduce the number of circulating red blood cells, along with medications like pegylated interferon and inhibitors of the JAK2 enzyme to help control blood cell production and reduce complications. Ongoing research is focused on therapies that directly target the abnormal stem cell clone responsible for the disease and may ultimately modify its natural course.
Introduction
PV was first described in 1892 by French physician Louis Henri Vaquez and was further characterized as a distinct clinical condition in 1903 by Canadian physician William Osler. The term “myeloproliferative disorder” was first used in 1951 by William Dameshek to describe PV and several related conditions in which the bone marrow makes too many normal blood cells.
In 2008, the World Health Organization reclassified these conditions as “myeloproliferative neoplasms” (MPNs) to reflect the understanding that they arise from a single abnormal blood-forming stem cell. MPNs are characterized by the overproduction of one or more of the three main blood cell types, red blood cells (which carry oxygen), white blood cells (which fight infection), and platelets (which help blood clot).
In addition to PV, two companion conditions are also classified as MPNs, essential thrombocythemia (ET), in which there is primarily an increase in platelets, and primary myelofibrosis (PMF), in which there is usually anemia, an increase in white cells and platelets, spleen enlargement, and bone marrow scarring. Like PV, ET and PMF arise from a single blood-forming stem cell and can involve the same JAK2 V617F driver variant, but they can also be caused by variants in the CALR or MPL genes.
Although PV is classified as a type of cancer, its clinical behavior differs substantially from that of most cancers. The abnormal cells remain mature and functional, disease progression is typically slow, and many individuals live for decades with appropriate treatment. Current therapies effectively reduce complications and improve quality of life, while ongoing research seeks treatments capable of eliminating the abnormal stem cell clone that drives the disease.
PV usually develops slowly over many years before causing obvious symptoms. In many people, the condition is first discovered during routine blood work before noticeable symptoms appear. Some people may initially experience vague symptoms such as changes in concentration, fatigue, dizziness, itching after contact with water (aquagenic pruritus), visual disturbances (ocular migraine), or burning pain in the hands or feet (erythromelalgia).
Additional symptoms can include blurred vision, ringing in the ears (tinnitus), and abnormal redness of the skin (erythema), especially on the face.
Over time, some people with PV develop an enlarged spleen (splenomegaly). The spleen is an organ in the upper left side of the abdomen that helps filter aging blood cells and unwanted organisms from the blood. An enlarged spleen can cause a feeling of fullness or bloating in the abdomen and difficulty eating a full meal.
Less common symptoms include:
Some people with PV develop very high platelet counts (sometimes called “platelet millionaires”). When platelet counts are extremely high, the main risk is actually bleeding, not blood clots in large vessels. This is because the large number of platelets can break down a protein needed for normal clotting. Moreover, in about 30% of people with PV, platelets can become “sticky” due to excessive activation and cause problems in small blood vessels (microvascular thrombosis).
Blood clots are one of the most serious complications of PV. Clots can lead to stroke, chest pain (angina), heart attack, deep vein thrombosis (DVT), or pulmonary embolism (PE). DVT occurs when a clot forms in the deep veins of the legs, causing pain and swelling. Pulmonary embolism occurs when a clot forms in or travels to the lungs, where it blocks a blood vessel. A PE can cause shortness of breath, sudden chest pain, fainting, or in severe cases, life-threatening complications.
Some people with PV, especially women, may develop the Budd-Chiari syndrome, a serious condition caused by a blood clot in the veins leading out of the liver. Symptoms may include pain in the upper right abdomen, an enlarged liver, yellowing of the skin and eyes (jaundice), and fluid buildup (ascites) in the abdomen.
Some patients, particularly men, may develop portal hypertension due to clotting in the portal vein, which can cause spleen enlargement, liver abnormalities, and gastrointestinal bleeding.
The rapid production of blood cells in PV may also increase the risk of peptic ulcers, gout (a painful form of arthritis caused by high uric acid levels), and uric acid kidney stones.
Rarely, over many years, PV may enter what is sometimes called a “spent phase,” in which the disease appears to stabilize and the need for phlebotomy decreases, but the spleen remains enlarged and the red blood cell mass is masked by an expanded plasma volume. This state appears to occur more often in patients treated primarily with phlebotomy and may reflect the depletion of iron that the disease needs to drive blood cell production.
In rare cases, PV may progress to an aggressive blood cancer called acute myeloid leukemia (AML). This occurs most often in older men and is frequently associated with prior exposure to chemotherapy. AML arising from PV is usually very difficult to treat.
About 10–15% of people with PV develop a condition resembling primary myelofibrosis (PMF), in which inflammation leads to scarring (fibrosis) in the bone marrow and enlargement of the spleen. However, this transition is generally much milder than PMF itself, develops gradually over many years, and carries a longer survival, approximately 8 years after transformation. It is important to understand that bone marrow fibrosis in PV is considered a reactive and potentially reversible process and does not necessarily impair the bone marrow’s ability to produce blood cells.
Polycythemia vera (PV) begins when a single blood-forming stem cell (hematopoietic stem cell) in the bone marrow develops a change (variant) in its genetic material (DNA). Because all the abnormal blood cells arise from this one altered stem cell, PV is considered a clonal disorder. The underlying reason why this first genetic change occurs is unknown. It is an acquired (somatic) variant, meaning it develops after birth during a person’s lifetime and is not inherited from a parent. Although rare familial cases have been reported, these are thought to result from inherited genetic factors that increase susceptibility to developing the disease rather than inheritance of the JAK2 gene variant itself.
Approximately 95% of people with PV carry the JAK2 V617F variant. Most of the remaining patients have variants in exon 12 of the JAK2 gene, which generally produces a similar but often milder form of the disease.
The JAK2 gene encodes Janus kinase 2 (JAK2), an enzyme that is part of the JAK-STAT signaling pathway, which regulates normal blood cell production. Under normal circumstances, JAK2 is activated only when growth factors, such as erythropoietin (EPO), signal the bone marrow to produce new blood cells. In PV, the JAK2 variant causes this signaling pathway to remain continuously active, even when the body does not need additional blood cells. As a result, blood-forming cells continue to grow, divide, and survive longer than normal.
Unlike many cancers, the abnormal cells in PV mature normally and retain their normal functions. However, because the disease originates in a hematopoietic stem cell capable of producing all blood cell types, many patients develop increased numbers of red blood cells, white blood cells, and platelets, although the increase in red blood cells usually predominates.
As the abnormal stem cell reproduces, it gradually expands and competes with normal stem cells in the bone marrow. The proportion of cells carrying the JAK2 variant, known as the variant allele frequency (VAF), generally increases over time. Studies suggest that a higher VAF is associated with greater disease burden and an increased risk of progression to myelofibrosis and venous thrombosis, although it is only one of several factors that influence disease behavior.
The excessive production of red blood cells increases the total red blood cell mass, making the blood thicker (hyperviscous) and slowing its flow through small blood vessels. This contributes to many of the symptoms of PV and substantially increases the risk of blood clots. Chronic activation of the abnormal stem cells also promotes inflammation through the release of cytokines, including interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α), which contribute to symptoms such as fatigue, itching, and night sweats and may play a role in the development of bone marrow fibrosis over time.
The estimated prevalence of PV is about 44 to 60 per 100,000 people in the United States. It is most often diagnosed in people over 60 years old but can affect individuals of any age, especially young women. It is extremely rare in people under age 20. Overall, PV affects slightly more males than females.
Polycythemia vera (PV) is diagnosed using a combination of a detailed medical history, physical examination, and specialized laboratory testing, including genetic molecular testing.
In many people, PV is first suspected after routine blood work reveals abnormal blood counts. A complete blood count (CBC) typically shows an increased red blood cell count and may also reveal elevated white blood cell and platelet counts.
Doctors also evaluate several laboratory findings, including:
Molecular testing for JAK2 variants is a key part of the diagnostic evaluation. Approximately 95% of people with PV have the JAK2 V617F variant, while most of the remainder have variants in JAK2 exon 12.
Some laboratories also report the JAK2 variant allele frequency (VAF), which indicates the proportion of blood-forming cells carrying the variant. A very low VAF (generally below about 5%) may represent clonal hematopoiesis of indeterminate potential (CHIP) rather than PV. The VAF is also important for understanding how the disease may behave over time. When the VAF is 50% or below, meaning that at least half of the blood-forming stem cells still carry normal JAK2 genes, the disease tends to be more indolent (milder). When the VAF rises above 50%, the abnormal cells may become dominant in the bone marrow, and the disease may behave more aggressively. For this reason, doctors may monitor the VAF over time as part of ongoing care. Studies have shown that a JAK2 V617F VAF of 50% or higher is associated with an increased risk of venous blood clots and progression to myelofibrosis.
A bone marrow biopsy may also be performed, usually when the diagnosis is uncertain or to help distinguish PV from other myeloproliferative neoplasms. A small sample of bone marrow, typically obtained from the pelvic bone, is examined under a microscope to evaluate blood cell production. Depending on how long a person has had PV, bone marrow findings may or may not help confirm the diagnosis, and they do not always reliably distinguish among the different myeloproliferative neoplasms.
The World Health Organization (WHO) has established threshold values that suggest erythrocytosis:
However, these thresholds have important limitations. Unlike other causes of erythrocytosis, PV is often associated with an expansion of the plasma volume, which can dilute the blood and make the hematocrit appear lower than the actual increase in red blood cell mass. As a result, some people with PV may have hematocrit values below the standard diagnostic thresholds despite having true erythrocytosis. In the past, separate measurements of red blood cell mass and plasma volume could help clarify these cases, but these tests are no longer widely available.
For this reason, diagnosis should never rely on a single laboratory value. Instead, physicians interpret the blood counts together with the clinical findings, serum EPO level, JAK2 testing, and, when appropriate, bone marrow examination.
PV is diagnosed using a combination of a detailed medical history, physical examination, and specialized laboratory testing including genetic testing.
In many people, PV is first suspected after routine blood work shows abnormalities. A complete blood count (CBC) may reveal increased red blood cells, along with elevated white blood cells and/or platelets.
Doctors also evaluate:
Some people may also undergo a bone marrow biopsy. During this procedure, a small sample of bone marrow is removed, usually from the pelvic bone, and examined under a microscope. This helps doctors evaluate how the bone marrow is functioning. Depending on how long a person has had PV, a bone marrow biopsy may or may not help confirm the diagnosis and it may not always reliably distinguish between different MPNs. Clinical features, genetic testing, and laboratory results may provide more consistent diagnostic information.
Doctors strongly suspect PV when:
For this reason, controlling the hematocrit is critical for preventing blood clots. Experts recommend maintaining the hematocrit at or below 42% in women and below 45% in men. If symptoms continue despite reaching these targets, further lowering the hematocrit may be necessary. The thrombosis risk in PV is driven by hyperviscosity from the expanded red cell mass rather than by the VAF per se.
Treatment
The main goal of treatment is to lower the number of red blood cells to prevent blood clots, which are the most serious complication of PV. Blood clots can block blood flow and lead to problems such as arteriole or venous thrombosis, stroke or heart attack. Treatment also aims to relieve symptoms and manage other complications. PV cannot be cured, but with proper management, most people with PV can expect a near-normal life span.
Doctors classify patients with PV as lower risk or higher risk for thrombosis. In general, people younger than 60 years of age who have never had a blood clot are considered lower risk, whereas those 60 years of age or older and/or with a history of thrombosis are considered higher risk. Studies have also shown that the amount of the JAK2 variant present in blood cells, expressed as the variant allele frequency (VAF), provides additional information about disease behavior. Patients with a VAF greater than 50% appear more likely to have a more proliferative form of the disease and are at increased risk of progression to myelofibrosis and venous thrombosis. Although VAF is not currently incorporated into standard risk stratification, it is increasingly recognized as an important marker of disease burden and may become more useful in guiding treatment decisions as evidence evolves.
For nearly all people with PV, the first and most important treatment is phlebotomy, a procedure in which blood is removed from the body, similar to donating blood. This reduces the number of circulating red blood cells, lowers blood viscosity, and helps prevent thrombosis. Initially, phlebotomy may be required every few weeks until the hematocrit reaches the target range. Over time, treatment is usually needed only every one to three months.
Current guidelines recommend maintaining the hematocrit at 45% or below. Some experts recommend a lower target (approximately 42%) in women because they normally have a lower red blood cell mass. If symptoms persist despite reaching these targets, further lowering of the hematocrit may be beneficial in selected patients.
Repeated phlebotomy gradually removes iron from the body, which slows the production of red blood cells over time. However, phlebotomy does not control elevated white blood cell or platelet counts, reduce spleen enlargement, or adequately treat symptoms such as severe itching, constitutional symptoms, or gout. For many patients with lower-risk disease, however, phlebotomy alone provides effective long-term management.
Unless contraindicated, most people with PV are treated with low-dose aspirin (81–100 mg daily). Aspirin reduces platelet activation and lowers the risk of thrombosis. It is also particularly effective for relieving microvascular symptoms such as headaches, visual disturbances, and erythromelalgia. However, aspirin should be used with caution in patients with extremely elevated platelet counts because acquired von Willebrand syndrome, a bleeding disorder caused by depletion of von Willebrand factor, may increase the risk of bleeding. The decision to use aspirin should always balance the risk of thrombosis against the risk of bleeding.
The ECLAP trial demonstrated that low-dose aspirin significantly reduced cardiovascular complications in patients with PV. However, aspirin should be used cautiously in patients with extremely high platelet counts because they may develop acquired von Willebrand syndrome, a bleeding disorder caused by depletion of von Willebrand factor.
When phlebotomy alone is not sufficient, or when additional control of blood cell production is needed, cytoreductive therapy is recommended.
Peginterferon alfa-2a and ropeginterferon alfa-2b-njft (Besremi) differ from other cytoreductive therapies because they target the abnormal hematopoietic stem cell rather than simply lowering blood counts. Over time, interferon therapy reduces the number of abnormal stem cells carrying the JAK2 variant and lowers the JAK2 VAF. In some patients, complete molecular remissions have been reported, in which the disease-causing variant becomes undetectable.
Interferons effectively control red blood cell production, reduce elevated white blood cell and platelet counts, relieve aquagenic pruritus, reduce splenomegaly, and improve constitutional symptoms. For lower-risk patients who require medication beyond phlebotomy, current NCCN guidelines list ropeginterferon alfa-2b-njft (Besremi) as a preferred first-line treatment. For higher-risk patients, both interferon therapy and hydroxyurea are recommended first-line treatment options.
Hydroxyurea has been used for decades and remains one of the most commonly prescribed cytoreductive therapies for PV. It effectively lowers red blood cell, white blood cell, and platelet counts by suppressing bone marrow activity. However, unlike interferon therapy, hydroxyurea has not been shown to reduce the underlying abnormal hematopoietic stem cell clone, consistently lower the JAK2 VAF, or produce molecular remissions.
About one-quarter of patients either do not respond adequately or cannot tolerate hydroxyurea. Side effects may include mouth ulcers, skin changes, fatigue, leg ulcers, and suppression of normal blood cell production. Hydroxyurea is a cytotoxic drug, and concerns have been raised that prolonged exposure may contribute to additional genetic abnormalities and leukemic transformation, although separating treatment-related risk from the natural history of PV remains difficult. Because PV is generally associated with a near-normal life expectancy, even small potential long-term treatment risks are worth considering.
Ruxolitinib (Jakafi) is an oral inhibitor of JAK1 and JAK2 approved by the U.S. Food and Drug Administration (FDA) for adults with PV who are resistant to or intolerant of hydroxyurea. By blocking abnormal JAK signaling, ruxolitinib helps control blood counts, reduce splenomegaly, relieve itching and constitutional symptoms, and decrease inflammatory cytokine production. Unlike hydroxyurea, ruxolitinib has also been shown to reduce the JAK2 VAF, although the long-term clinical significance of this effect continues to be studied.
Allopurinol is commonly prescribed to lower uric acid levels and prevent gout or uric acid kidney stones. Although severe itching was previously managed with antihistamines or ultraviolet light therapy, pegylated interferon has largely replaced these approaches because it addresses both the symptoms and the underlying disease.
Rusfertide is a hepcidin mimetic that has received Breakthrough Therapy designation from the FDA. By limiting iron availability, it reduces red blood cell production and has shown promising results in reducing the need for repeated phlebotomy. However, it does not replace the need for initial phlebotomy to lower the hematocrit to a safe level.
Givinostat is a histone deacetylase inhibitor that has received Fast Track designation from the FDA. Early studies suggest that it may help control abnormal blood cell production and reduce symptoms, particularly in patients whose disease is not adequately controlled with currently available therapies.
Older treatments, including busulfan, chlorambucil, and radioactive phosphorus, are now rarely recommended because they are associated with decreased survival and an increased risk of leukemia.
As discussed earlier, PV appears to exist along a spectrum ranging from a relatively indolent form, in which phlebotomy alone may provide long-term disease control, to a more proliferative form affecting approximately 10–15% of patients, who eventually develop progressive bone marrow fibrosis and significant splenomegaly. This progression typically occurs over many years and is generally less aggressive than primary myelofibrosis.
An area of active investigation involves the MPL receptor on hematopoietic stem cells and its interaction with thrombopoietin (TPO). In PV, impaired MPL expression may alter TPO metabolism, resulting in elevated plasma TPO levels and increased production of growth factors such as TGF-β1 and PDGF, which contribute to bone marrow fibrosis. This evolving understanding suggests that PV may be, in part, a disorder of abnormal hormone signaling and may identify new therapeutic targets in the future.
Pregnancy
Women with PV can become pregnant and have successful pregnancies. There is an increased risk of miscarriage, especially during the first trimester, and complications such as poor fetal growth or stillbirth may also occur, although serious complications for the mother are less common. Platelet counts often decrease during pregnancy but may rise again after delivery.
Low-dose aspirin is recommended to help reduce the risk of early miscarriage. Phlebotomy management during pregnancy is especially important because the body’s plasma volume naturally increases during pregnancy, which can further mask the true hematocrit level. Current guidelines recommend keeping the hematocrit below the normal pregnancy range, 41% in the first trimester, 38% in the second trimester, and 39% in the third trimester, however, some experts recommend even lower targets (around 35%), during pregnancy. Concerns that phlebotomy may deprive the baby of iron are generally not supported, because iron absorption naturally increases during pregnancy. Preventing blood clots remains the higher priority.
Hydroxyurea should be stopped before conception or as soon as pregnancy is confirmed because it may harm the developing baby. Peginterferon alfa-2a can be used during pregnancy if medication is needed to control blood counts or spleen size. Besremi (ropeginterferon alfa-2b-njft) should not be used during pregnancy due to insufficient safety data.
Blood-thinning injections (low-molecular-weight heparin) may be recommended after delivery. Current guidelines recommend preventive blood-thinning injections for the first 6 weeks after delivery. However, some experts believe that blood thinners may not always be necessary in women without a history of blood clots. The care team will determine the best approach based on the individual situation.
Information on current clinical trials is posted on the Internet at https://clinicaltrials.gov/ . All studies receiving U.S. Government funding, and some supported by private industry, are posted on this government web site.
For information about clinical trials being conducted at the NIH Clinical Center in Bethesda, MD, contact the NIH Patient Recruitment Office:
Toll-free: (800) 411-1222
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Email: [email protected]
Some current clinical trials also are posted on the following page on the NORD website:
https://rarediseases.org/for-patients-and-families/information-resources/info-clinical-trials-and-research-studies/
For information about clinical trials sponsored by private sources, contact:
https://www.centerwatch.com/
For information about clinical trials conducted in Europe, contact:
https://www.clinicaltrialsregister.eu/
TEXTBOOKS
Longo DL. et al., Harrison’s Principles of Internal Medicine. 22nd Edition: 2025, Chapter 108:815-825.
Porter RS., ed. The Merck Manual of Diagnosis and Therapy: Professional Edition. 20th ed.: 2018, Chapter151:1163-1169.
JOURNAL ARTICLES
Spivak, JL. Myeloproliferative Neoplasms. N Engl J Med. 2017;376:2168-2181
Moliterno AR, Kaizer H, Reeves BN. JAK2 V617F allele burden in polycythemia vera: burden of proof. Blood. 2023, 141: 1934-1942.
Scott LM, Tong W, Levine RL, et al. JAK2 Exon 12 mutations in polycythemia vera and essential thrombocythemia. N Engl J Med. 2007;356:459-468.
Spivak JL, Silver RT. The revised World Health Organization diagnostic criteria for polycythemia vera, essential thrombocytosis, and primary myelofibrosis: an alternative proposal. Blood 2008;112:231-9
Cassinat B, Laguillier C, Gardin C, et al. Classification of myeloproliferative disorders in the JAK2 era: is there a role for red cell mass? Leukemia 2008;22:452-3.
Lamy T, Devillers A, Bernard M, et al. Inapparent polycythemia vera: an unrecognized diagnosis. Am J Med 1997;102:14-20.
Hasselbalch HC. Time for revival of the red blood cell count and red cell mass in the differential diagnosis between essential thrombocythemia and polycythemia vera? Haematologica 2019;104:2119-25.
Ruggeri M, Tosetto A, Frezzato M, Rodeghiero F. The rate of progression to polycythemia vera or essential thrombocythemia in patients with erythrocytosis or thrombocytosis. Ann Intern Med 2003;139:470-5.
Spivak, JL. How I treat patients with polycythemia vera. Blood. 2019;134: 341-352.
Stein BL, Williams DM, Wang NY, et al. Sex differences in the JAK2 V617F allele burden in chronic myeloproliferative disorders. Haematologica 2010;95:1090-7.
Abu-Zeinah G, Silver RT, Abu-Zeinah K, Scandura JM. Normal life expectancy for polycythemia vera (PV) patients is possible. Leukemia 2022;36:569-72.
Wouters H, Mulder R, van Zeventer IA, et al. Erythrocytosis in the general population: clinical characteristics and association with clonal hematopoiesis. Blood Adv 2020;4:6353-63.
McNeil JJ, Wolfe R, Woods RL, et al. Effect of Aspirin on Cardiovascular Events and Bleeding in the Healthy Elderly. N Engl J Med 2018;379:1509-18.
Kiladjian JJ, Klade C, Georgiev P, et al. Long-term outcomes of polycythemia vera patients treated with ropeginterferon Alfa-2b. Leukemia 2022;36:1408-11.
Tremblay D, Kremyanskaya M, Mascarenhas J, Hoffman R. Diagnosis and treatment of polycythemia vera: a review. JAMA. 2025.
Kremyanskaya M, Kuykendall AT, Pemmaraju N, et al. Rusfertide, a hepcidin mimetic, for control of erythrocytosis in polycythemia vera. N Engl J Med. 2024.
Spivak, JL and Moliterno AR. The Thrombopoietin Receptor, MPL, Is a Therapeutic Target of Opportunity in the MPN. Front Oncol, 11:641613, 2021
INTERNET
Cortese T. FDA Gives Fast Track Designation to Givinostat for Polycythemia Vera. Cancer Network. May 6, 2025. Available at: https://www.cancernetwork.com/view/fda-gives-fast-track-designation-to-givinostat-for-polycythemia-vera Accessed on 3/9/2026.
Spindler S. Rusfertide Nearly Eliminates Need for Phlebotomies to Treat Polycythemia Vera. National Cancer Institute. March 28, 2024. Available at: https://www.cancer.gov/news-events/cancer-currents-blog/2024/rusfertide-polycythemia-vera-fewer-phlebotomies Accessed on 3/9/2026.
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