TY - JOUR
T1 - Systemic iron deficiency in a nonhuman primate model of endometriosis
AU - Atkins, Hannah M.
AU - Appt, Susan E.
AU - Taylor, Robert N.
AU - Torres-Mendoza, Yaritbel
AU - Lenk, Emily E.
AU - Rosenthal, Nancy S.
AU - Caudell, David L.
N1 - Funding Information:
This work was supported in part by the NCI Cancer Center Support Grant (P30CA012197) to the Comprehensive Cancer Center of Wake Forest Baptist Medical Center; NIH grants T32OD010957-37, T35OD010946, and P30CA012197; and the North Carolina Biotechnology Center (2015-IDG-1006). This project also was funded by the Wake Forest School of Medicine Pathology Department Mature Pilot Grant (120-100400-00000-700066-ENDO23). We acknowledge the support of the Comparative Pathology Laboratory Shared Resources (Jean Gardin, Cathy Mathis, and Lisa O’Donnell) of the Wake Forest Baptist Medical Center Comprehensive Cancer Center. We also thank Drs Michael Nader, Thomas Register, Janice Wagner, Jay Kaplan, and J Mark Cline (Wake Forest School of Medicine) for their contribution of NHP tissues. We acknowledge the editorial assistance of Karen Klein, MA, through the Wake Forest Clinical and Translational Science Institute (UL1TR001420, PI: McClain). Finally, we thank the anonymous reviewers for their constructive critiques.
Publisher Copyright:
Copyright 2018 by the American Association for Laboratory Animal Science.
PY - 2018/8
Y1 - 2018/8
N2 - Endometriosis is characterized by endometrial tissue development outside the uterus. Anemia and iron depletion do not commonly accompany endometriosis in women, despite chronic abdominal inflammation and heavy menstrual bleeding. The objective of this study was to examine iron kinetics associated with endometriosis by using a NHP model, to better understand the underlying mechanism of abnormal hematogram values in women with endometriosis. Hematologic data from 46 macaques with endometriosis were examined for signs of iron depletion. Bone marrow, liver, and serum were used to elucidate whether iron loss or inflammation best explained the hematologic findings. Additional serum markers and intestinal biopsies from NHP with and without endometriosis were evaluated for patterns in iron kinetics across the menstrual cycle and for relative dietary iron-absorbing capacity. Almost half of the NHP with endometriosis were anemic. Overall, NHP had decreased RBC counts, increased MCV, increased percentage of reticulocytes, decreased serum hepcidin, and decreased hepatic and bone marrow iron. Intestinal expression of ferroportin 1, a mediator of iron absorption, was increased, indicating that despite high dietary iron, intestinal iron absorption did not compensate for iron losses. We concluded that use of oral iron supplementation alone does not replenish iron stores in endometriosis. Consequently, iron stores should be evaluated in women with endometriosis, even without overt clinical signs of anemia.
AB - Endometriosis is characterized by endometrial tissue development outside the uterus. Anemia and iron depletion do not commonly accompany endometriosis in women, despite chronic abdominal inflammation and heavy menstrual bleeding. The objective of this study was to examine iron kinetics associated with endometriosis by using a NHP model, to better understand the underlying mechanism of abnormal hematogram values in women with endometriosis. Hematologic data from 46 macaques with endometriosis were examined for signs of iron depletion. Bone marrow, liver, and serum were used to elucidate whether iron loss or inflammation best explained the hematologic findings. Additional serum markers and intestinal biopsies from NHP with and without endometriosis were evaluated for patterns in iron kinetics across the menstrual cycle and for relative dietary iron-absorbing capacity. Almost half of the NHP with endometriosis were anemic. Overall, NHP had decreased RBC counts, increased MCV, increased percentage of reticulocytes, decreased serum hepcidin, and decreased hepatic and bone marrow iron. Intestinal expression of ferroportin 1, a mediator of iron absorption, was increased, indicating that despite high dietary iron, intestinal iron absorption did not compensate for iron losses. We concluded that use of oral iron supplementation alone does not replenish iron stores in endometriosis. Consequently, iron stores should be evaluated in women with endometriosis, even without overt clinical signs of anemia.
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U2 - 10.30802/AALAS-CM-17-000082
DO - 10.30802/AALAS-CM-17-000082
M3 - Article
C2 - 29871715
AN - SCOPUS:85060828448
SN - 1532-0820
VL - 68
SP - 298
EP - 307
JO - Comparative Medicine
JF - Comparative Medicine
IS - 4
ER -