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OBESITY AND MYELOPROLIFERATIVE NEOPLASMS: A SYSTEMATIC REVIEW

Article  in  Journal of Hypertension · June 2022

DOI: 10.1097/01.hjh.0000836480.33984.57

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the result of renal dysfunction in some of the previous studies. The present study
was designed to explore the different responses of blood pressure and kidney in
the apatinib-induced hypertensive rat model.
Design and method: 30 Wistar-Kyoto rat were randomly divided into 3 groups,
each group was administered with 2 mL 0.9% saline, 30 mg/d of apatinib or 15
mg/d of apatinib by oral gavage for 2 weeks. Blood pressure was monitored at
the baseline and during the treatment. Level of creatinine, urea nitrogen, sodium,
albumin and protein in blood and urine were tested both at baseline and at the
end of the treatment. Urinary sodium excretion and glomerular filtration rate was
calculated. Specific mRNA and proteins were detected at the end of the treatment.
Results: Average mean blood pressure (MBP) in the high dose apatinib group was
105 mmHg at the 9th day and 113 mmHg at the 15th day, average MBP in the low
dose apatinib was 98 mmHg at the 9th day and 108 mmHg at the 15th day. MBP
were significantly high in apatinib group, no matter in the high dose or low dose
(p < 0.01). Compared with the control group, the level of endothelin 1(ET-1) and
college-1 were significantly high in both apatinib group (p < 0.01). There was no
significant differences of urinary sodium excretion, glomerular filtration rate and
microalbuminuria between the control group and the low dose apatinib group,
while that in the high dose apatinib group were significantly high (p < 0.01).
Conclusions: There are differences in the response to different doses of apatinib
between blood pressure and kidney, blood pressure was elevated even at a rel-
evantly lower dose of apatinib, which was accompanied with the elevation of ET-1
level and vascular emodelling, while the kidney injury occurred only at higher
dose of apatinib. The hypertension induced by apatinib was independent with kid-
ney injury caused by the drug, not the consequence of it.
OBESITY AND MYELOPROLIFERATIVE NEOPLASMS:
A SYSTEMATIC REVIEW
Mihnea -Alexandr Gaman1, Mirela Elena Epingeac2, Amelia Maria Gaman2,
Camelia Cristina Diaconu1. 1Faculty of Medicine, Carol Davila University of
Medicine and Pharmacy, Bucharest, ROMANIA, 2Department of Pathophysiol-
ogy, University of Medicine and Pharmacy of Craiova, Craiova, ROMANIA
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Copyright © 2022 Wolters Kluwer Health, Inc. All rights reserved.
Abstracts e121
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 incep-
tion 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 ex-
clusion 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 dur-
ing 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 oc-
currence 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.