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OBESITY AND MYELOPROLIFERATIVE NEOPLASMS: A SYSTEMATIC REVIEW
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Objective:
Obesity is a known trigger for carcinogenesis and its involvement is proven in the development of solid and blood cancers. However, the involvement of obesity in myeloproliferative neoplasms (MPNs), namely polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF), has not been assessed so far.
Design and method:
Systematic review in PubMed/MEDLINE from its inception to March 13th, 2022. The database was searched using specific keywords/word combinations to identify relevant papers which were further evaluated if they were original articles and investigated the role of obesity in MPNs. Reviews, case reports, meeting abstracts, letters to the editor, in vivo/in vitro studies were excluded.
Results:
The initial search yielded 88 results of which 62 remained after the exclusion of reviews/case reports (n = 26). After screening of titles/abstracts, 25 full-texts were assessed of which 18 were entered into the qualitative analysis. Most conclusions were drawn from singular studies. Two papers pointed out that obesity affects the evaluation of red cell mass in PV due to the hypovascular nature of the adipose tissue, arguing for new reference ranges in obese subjects. Adults with obesity during adolescence had an increased risk of MPNs development during adulthood. Obesity was particularly linked to the development of ET. Obese MPNs adults had an elevated number of bone marrow adipocytes, higher total symptom burden (U-shaped association with BMI), higher rate of cerebrovascular accidents (ET) and venous thrombosis, lower risk of post-PV myelofibrosis and stroke, higher survival rates. Obesity did not influence anxiety in MPNs or the occurrence of thrombosis (ET). However, lower survival rates and thrombosis-free survival were noted in MPNs patients with multiple cardiovascular risk factors. PMF patients treated with ruxolitinib who had higher BMI values registered better outcomes. Ruxolitinib-treated subjects exhibited an increase in BMI. Obesity did not influence the outcome of allogeneic bone marrow transplantation in PMF, nor did it influence the outcome of this procedure in elderly patients transplanted for myeloid malignancies.
Conclusions:
Obesity can influence the development and evolution of MPNs and should be carefully monitored. Further studies should assess the obesity paradox in MPNs.
Ovid Technologies (Wolters Kluwer Health)
Title: OBESITY AND MYELOPROLIFERATIVE NEOPLASMS: A SYSTEMATIC REVIEW
Description:
Objective:
Obesity is a known trigger for carcinogenesis and its involvement is proven in the development of solid and blood cancers.
However, the involvement of obesity in myeloproliferative neoplasms (MPNs), namely polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF), has not been assessed so far.
Design and method:
Systematic review in PubMed/MEDLINE from its inception to March 13th, 2022.
The database was searched using specific keywords/word combinations to identify relevant papers which were further evaluated if they were original articles and investigated the role of obesity in MPNs.
Reviews, case reports, meeting abstracts, letters to the editor, in vivo/in vitro studies were excluded.
Results:
The initial search yielded 88 results of which 62 remained after the exclusion of reviews/case reports (n = 26).
After screening of titles/abstracts, 25 full-texts were assessed of which 18 were entered into the qualitative analysis.
Most conclusions were drawn from singular studies.
Two papers pointed out that obesity affects the evaluation of red cell mass in PV due to the hypovascular nature of the adipose tissue, arguing for new reference ranges in obese subjects.
Adults with obesity during adolescence had an increased risk of MPNs development during adulthood.
Obesity was particularly linked to the development of ET.
Obese MPNs adults had an elevated number of bone marrow adipocytes, higher total symptom burden (U-shaped association with BMI), higher rate of cerebrovascular accidents (ET) and venous thrombosis, lower risk of post-PV myelofibrosis and stroke, higher survival rates.
Obesity did not influence anxiety in MPNs or the occurrence of thrombosis (ET).
However, lower survival rates and thrombosis-free survival were noted in MPNs patients with multiple cardiovascular risk factors.
PMF patients treated with ruxolitinib who had higher BMI values registered better outcomes.
Ruxolitinib-treated subjects exhibited an increase in BMI.
Obesity did not influence the outcome of allogeneic bone marrow transplantation in PMF, nor did it influence the outcome of this procedure in elderly patients transplanted for myeloid malignancies.
Conclusions:
Obesity can influence the development and evolution of MPNs and should be carefully monitored.
Further studies should assess the obesity paradox in MPNs.
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