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Gut microbiota differences in MPN

By Oscar Williams

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Feb 7, 2024

Learning objective: After reading this article, learners will be able to cite a new clinical development in myeloproliferative neoplasms.


Changes in gut microbiota composition are associated with a wide range of inflammatory conditions. It is therefore likely that gut changes are involved in the development of myeloproliferative neoplasms (MPN).

Here, we summarize a study by Eickhardt-Dalbøge et al.1 in European Journal of Hematology investigating the overall association of gut microbiota across MPN subtypes and somatic mutations.

Study design1

  • Overall, 227 patients with MPN aged ≥18 years were enrolled between November 2018 and August 2021; 42 healthy controls (HC) were also included
  • Patients had a confirmed diagnosis of essential thrombocythemia (ET), polycythemia vera (PV), preprimary myelofibrosis (MF), MF or post PV/ET-MF, and were grouped according to sub-diagnoses and Janus kinase (JAK)2V617F/calreticulin mutation status.
  • Gut microbiota was analyzed using next-generation sequencing

Key findings1

The median observed bacterial richness of gut microbiota was higher in patients with MPN vs HC (Figure 1).

Figure 1. Median observed significant differences in the richness of gut microbiota* 

CALR, calreticulin; ET, essential thrombocythemia; HC, healthy control; JAK, Janus kinase; MPN, myeloproliferative neoplasia.
*Adapted from Eickhardt-Dalbøge, et al.1

  • The alpha diversity (as measured by the median Inverse Simpson index) did not differ between patients with MPN and HC
    • Patients with MPN and JAK2V617F positive had a significantly lower median Inverse Simpson index vs calreticulin positive patients and HC (21.8 vs 26.3, and 29, respectively, p < 0.05)
  • The bacterial composition in patients with ET resembled that of HC the most, compared with those from patients with PV, preprimary MF, MF, or post PV/ET-MF
  • Patients with MPN had a significantly lower abundance of Firmicutes vs HC (52% vs 59%, p = 0.01) but higher Actinobacteriota (4% vs 2%, p < 0.001)
  • Patients with a high JAK2V617F allele burden had a higher relative abundance of Akkermansia vs patients with a lower allele burden (5% vs 1%, p < 0.01)

Key learnings

  • The gut microbiota in patients with MPN compared with HCs is characterized by a higher observed richness
  • The difference in gut microbiota in patients with MPN vs HC is driven by JAK2V617F; the gut microbiota in calreticulin positive patients with MPN is more similar to HC

References

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