Polycythemia vera and metabolic syndrome: is the relationship between the two diseases more than we think?
Key claim: Oxidative stress is markedly higher in polycythemia vera patients who also have metabolic syndrome than in PV alone, supporting a pathophysiological link between the two conditions.
Abstract
BACKGROUND: Polycythemia vera (PV), the most common myeloproliferative neoplasm, is driven by JAK2 mutations and often coexists with metabolic syndrome (MS), a major cardiovascular risk factor. Few studies have examined oxidative stress as a potential link between PV and MS. RESEARCH DESIGN AND METHODS: This observational case-control study included 36 PV patients (15 with MS) and 40 healthy volunteers between 2017 and 2023. Diagnosis followed 2016 WHO criteria. Patients with abnormal hematologic values, organ dysfunction, elevated CRP, or confounding comorbidities were excluded. Oxidative stress was assessed by spectrophotometric measurement of total antioxidant status (TAS) and total oxidant status (TOS). RESULTS: TOS levels were significantly higher in PV-MS patients compared to PV alone (p < 0.05), and oxidative stress markers overall were elevated versus healthy controls ( < 0.05). No significant differences in TAS or TOS were observed between ELN high- and low-risk groups or among patients receiving hydroxyurea, aspirin, metformin, ACE inhibitors, and untreated patients ( > 0.05). CONCLUSIONS: Oxidative stress is markedly elevated in PV patients with MS, supporting a pathophysiological link between the two conditions. These findings highlight the importance of considering oxidative stress in the clinical evaluation of PV patients with metabolic syndrome.
Why this matters
PV natural history is increasingly framed as more than JAK2-driven erythrocytosis, with cardiovascular and metabolic comorbidities shaping thrombosis risk and progression. Quantifying elevated oxidative stress specifically in PV patients with metabolic syndrome nominates a concrete mechanistic axis — and potential biomarker/intervention target — that could stratify a comorbidity-defined PV subgroup distinct from ET or PMF, where the metabolic-syndrome interaction has been less characterized.