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Diagnosing anemia, a serious and common complication of patients with myelofibrosis, could be made easier with the use of red cell distribution width assessment.
According to the results of a single-center, observational, retrospective study, red blood cell distribution width (RDW) in patients with primary or secondary myelofibrosis (MF) treated with ruxolitinib (Jakavi; Incyte Corporation, Novartis) could predict the presence of drug-induced anemia, which may assist with the detection of patients with poor prognosis.1
RDW is routinely reported as part of full blood count (FBC) values and has been recognized as a marker of clinical inflammation. Because it is used as a quantitative measure of anisocytosis, it is useful for pharmacists and members of a patient care team in the differential diagnosis of anemia pathogenesis, according to the investigators. Anemia is a major feature of MF and is often associated with dismal outcomes.1,4
Severe anemia presents itself in approximately 35% to 54% of patients with primary MF, playing a significant role in reducing overall survival (OS) rates. Studies have indicated that ruxolitinib, a Janus kinase (JAK) inhibitor approved by the FDA for treatment in patients with MF and is effective at both reducing symptoms and slowing fibrotic progression, also carries a risk of dose-dependent anemia and thrombocytopenia, typically occurring in the first 12 weeks of therapy.2,3,4
The study authors sought to investigate the association of RDW values prior to ruxolitinib treatment with baseline clinical characteristics, disease features, prognosis, and drug-related anemia rate in patients with MF who were treated with ruxolitinib. Determining whether RDW are useful in diagnosing anemia could allow for more timely detection and a change in treatment, if necessary.1
A total of 200 ruxolitinib-treated patients were part of the analysis. In patients with higher grade of bone marrow (BM)-fibrosis, baseline RDW was higher, indicating that overt cases of MF had greater RDW values than early MF cases, the investigators found. Investigators observed a statistically significant lower baseline RDW in patients who had a spleen response during ruxolitinib treatment, which occurred in 91 (45.5%) cases.1
In this population, a significant number of patients (74/181; 40.9%) died during follow-up. Major reported causes of death were progression to acute myeloid leukemia (AML) and infections; median OS was 65.7 months (95% CI, 48.7-82.7). Patient prognosis was influenced by anemia, with patients harboring hemoglobin (Hb) levels of less than 10 g/dL having worse median OS than those with Hb levels of 10 g/dL or higher. In both groups, RDW was able to predict adverse outcomes, the investigators found.1
Regarding patients with drug-related anemia, this population at 3 months had significantly higher median baseline RDW compared with those without anemia, in addition to patients who developed drug-related anemia at 6 months. Ultimately, the investigators found that baseline RDW greater than or equal to 20.5% was the threshold that indicated both higher odds of drug-induced anemia at 3 months and 6 months in addition to lower OS rates and poor outcomes.1
Patients with MF often are faced with a diagnosis of anemia, and dose-dependent ruxolitinib treatment may necessitate anemia management. One study of transfusion-dependent patients with MF found that 92.6% of those patients received anemia supportive care following initiation of ruxolitinib. With the results of this current study, the gaps in the limited data surrounding RDW as a prognostic factor for anemia can begin to be filled, though more research is necessary with a larger population and more diverse samples, the researchers wrote.1,5
“RDW could be used as an additional parameter alongside existing prognostic models, molecular mutational data, and emerging biomarkers to assist clinicians in more accurately identifying high-risk patients,” the study authors wrote in their conclusion. “This could ultimately support decisions regarding alternative or novel therapeutic strategies.1