Erythropoiesis in hypothyroidism

R. M. Donati, James Fletcher, M. A. Warnecke, N. I. Gallagher

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

The purpose of the study was to clarify the role which disordered iron metabolism and alterations in the homeostatic regulation of red cell production play in hypothyroid anemia. Following the measurement of the oxygen consumption, rats were thyroidectomized and given an ablative dose of sodium 131iodine. Hypothyroid rats demonstrated a decreased red cell radioiron incorporation and a diminished GI iron absorption. The diminution in erythropoiesis was reverted toward normal by the administration of erythropoietin, D triiodothyronine, L triiodothyronine or exposure to hypobarbaric hypoxia. Erythropoietin, which completely corrected the erythropoietic depression in the hypothyroid rats, did not correct the decreased GI radioiron absorption whereas L triiodothyronine restored both to normal. Urinary erythropoietin was decreased in the hypothyroid rat and reverted to normal following L triiodothyronine administration. These data suggest that the mechanism producing the erythropoietic decompensation in hypothyroid states is complex and involves the lack of erythropoietic stimulation by erythropoietin. Acute erythropoietic compensation appears possible by the administration of nonspecific erythropoietic stimulants; however, the defect in gastrointestinal iron absorption can only be repaired by the administration of thyroid hormones.

Original languageEnglish (US)
Pages (from-to)78-82
Number of pages5
JournalProceedings of the Society for Experimental Biology and Medicine
Volume144
Issue number1
StatePublished - 1973
Externally publishedYes

Fingerprint

Erythropoiesis
Triiodothyronine
Erythropoietin
Hypothyroidism
Rats
Iron
Cells
Thyroid Hormones
Metabolism
Oxygen Consumption
Anemia
Sodium
Oxygen
Defects

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Donati, R. M., Fletcher, J., Warnecke, M. A., & Gallagher, N. I. (1973). Erythropoiesis in hypothyroidism. Proceedings of the Society for Experimental Biology and Medicine, 144(1), 78-82.

Erythropoiesis in hypothyroidism. / Donati, R. M.; Fletcher, James; Warnecke, M. A.; Gallagher, N. I.

In: Proceedings of the Society for Experimental Biology and Medicine, Vol. 144, No. 1, 1973, p. 78-82.

Research output: Contribution to journalArticle

Donati, RM, Fletcher, J, Warnecke, MA & Gallagher, NI 1973, 'Erythropoiesis in hypothyroidism', Proceedings of the Society for Experimental Biology and Medicine, vol. 144, no. 1, pp. 78-82.
Donati, R. M. ; Fletcher, James ; Warnecke, M. A. ; Gallagher, N. I. / Erythropoiesis in hypothyroidism. In: Proceedings of the Society for Experimental Biology and Medicine. 1973 ; Vol. 144, No. 1. pp. 78-82.
@article{85e7a74e5dab41649209fad5544ec08b,
title = "Erythropoiesis in hypothyroidism",
abstract = "The purpose of the study was to clarify the role which disordered iron metabolism and alterations in the homeostatic regulation of red cell production play in hypothyroid anemia. Following the measurement of the oxygen consumption, rats were thyroidectomized and given an ablative dose of sodium 131iodine. Hypothyroid rats demonstrated a decreased red cell radioiron incorporation and a diminished GI iron absorption. The diminution in erythropoiesis was reverted toward normal by the administration of erythropoietin, D triiodothyronine, L triiodothyronine or exposure to hypobarbaric hypoxia. Erythropoietin, which completely corrected the erythropoietic depression in the hypothyroid rats, did not correct the decreased GI radioiron absorption whereas L triiodothyronine restored both to normal. Urinary erythropoietin was decreased in the hypothyroid rat and reverted to normal following L triiodothyronine administration. These data suggest that the mechanism producing the erythropoietic decompensation in hypothyroid states is complex and involves the lack of erythropoietic stimulation by erythropoietin. Acute erythropoietic compensation appears possible by the administration of nonspecific erythropoietic stimulants; however, the defect in gastrointestinal iron absorption can only be repaired by the administration of thyroid hormones.",
author = "Donati, {R. M.} and James Fletcher and Warnecke, {M. A.} and Gallagher, {N. I.}",
year = "1973",
language = "English (US)",
volume = "144",
pages = "78--82",
journal = "Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N. Y.)",
issn = "1535-3702",
publisher = "SAGE Publications Ltd",
number = "1",

}

TY - JOUR

T1 - Erythropoiesis in hypothyroidism

AU - Donati, R. M.

AU - Fletcher, James

AU - Warnecke, M. A.

AU - Gallagher, N. I.

PY - 1973

Y1 - 1973

N2 - The purpose of the study was to clarify the role which disordered iron metabolism and alterations in the homeostatic regulation of red cell production play in hypothyroid anemia. Following the measurement of the oxygen consumption, rats were thyroidectomized and given an ablative dose of sodium 131iodine. Hypothyroid rats demonstrated a decreased red cell radioiron incorporation and a diminished GI iron absorption. The diminution in erythropoiesis was reverted toward normal by the administration of erythropoietin, D triiodothyronine, L triiodothyronine or exposure to hypobarbaric hypoxia. Erythropoietin, which completely corrected the erythropoietic depression in the hypothyroid rats, did not correct the decreased GI radioiron absorption whereas L triiodothyronine restored both to normal. Urinary erythropoietin was decreased in the hypothyroid rat and reverted to normal following L triiodothyronine administration. These data suggest that the mechanism producing the erythropoietic decompensation in hypothyroid states is complex and involves the lack of erythropoietic stimulation by erythropoietin. Acute erythropoietic compensation appears possible by the administration of nonspecific erythropoietic stimulants; however, the defect in gastrointestinal iron absorption can only be repaired by the administration of thyroid hormones.

AB - The purpose of the study was to clarify the role which disordered iron metabolism and alterations in the homeostatic regulation of red cell production play in hypothyroid anemia. Following the measurement of the oxygen consumption, rats were thyroidectomized and given an ablative dose of sodium 131iodine. Hypothyroid rats demonstrated a decreased red cell radioiron incorporation and a diminished GI iron absorption. The diminution in erythropoiesis was reverted toward normal by the administration of erythropoietin, D triiodothyronine, L triiodothyronine or exposure to hypobarbaric hypoxia. Erythropoietin, which completely corrected the erythropoietic depression in the hypothyroid rats, did not correct the decreased GI radioiron absorption whereas L triiodothyronine restored both to normal. Urinary erythropoietin was decreased in the hypothyroid rat and reverted to normal following L triiodothyronine administration. These data suggest that the mechanism producing the erythropoietic decompensation in hypothyroid states is complex and involves the lack of erythropoietic stimulation by erythropoietin. Acute erythropoietic compensation appears possible by the administration of nonspecific erythropoietic stimulants; however, the defect in gastrointestinal iron absorption can only be repaired by the administration of thyroid hormones.

UR - http://www.scopus.com/inward/record.url?scp=0015820149&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0015820149&partnerID=8YFLogxK

M3 - Article

VL - 144

SP - 78

EP - 82

JO - Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N. Y.)

JF - Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N. Y.)

SN - 1535-3702

IS - 1

ER -