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Cited by 426Erythropoietin and Anemia TreatmentHormonal and reproductive studiesIron Metabolism and Disorders

Testosterone induces erythrocytosis via increased erythropoietin and suppressed hepcidin: evidence for a new erythropoietin/hemoglobin set point

Open access
Bachman, E., Travison, T. G., Basaria, S., Davda, M. N., Guo, W., Li, M., Connor Westfall, J., Bae, H. +2 more·2014·The Journals of Gerontology Series A: Biological Sciences and Medical Sciences
DOI 10.1093/gerona/glt154PMC PMC4022090
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Abstract

BACKGROUND: The mechanisms by which testosterone increases hemoglobin and hematocrit remain unclear. METHODS: We assessed the hormonal and hematologic responses to testosterone administration in a clinical trial in which older men with mobility limitation were randomized to either placebo or testosterone gel daily for 6 months. RESULTS: The 7%-10% increase in hemoglobin and hematocrit, respectively, with testosterone administration was associated with significantly increased erythropoietin (EPO) levels and decreased ferritin and hepcidin levels at 1 and 3 months. At 6 months, EPO and hepcidin levels returned toward baseline in spite of continued testosterone administration, but EPO levels remained nonsuppressed even though elevated hemoglobin and hematocrit higher than at baseline, suggesting a new set point. Consistent with increased iron utilization, soluble transferrin receptor (sTR) levels and ratio of sTR/log ferritin increased significantly in testosterone-treated men. Hormonal and hematologic responses were similar in anemic participants. The majority of testosterone-treated anemic participants increased their hemoglobin into normal range. CONCLUSIONS: Testosterone-induced increase in hemoglobin and hematocrit is associated with stimulation of EPO and reduced ferritin and hepcidin concentrations. We propose that testosterone stimulates erythropoiesis by stimulating EPO and recalibrating the set point of EPO in relation to hemoglobin and by increasing iron utilization for erythropoiesis.

AI snapshot

Written from the paper’s full text.

TL;DR

In older men with mobility limitation and low testosterone, 6 months of testosterone gel increased hemoglobin/hematocrit and was associated with increased erythropoietin (EPO), suppressed hepcidin/ferritin, and increased soluble transferrin receptor. The authors propose that testosterone induces erythrocytosis by stimulating EPO, resetting the EPO/hemoglobin set point, and increasing iron utilization for erythropoiesis.

Key findings

  • Testosterone increased hemoglobin by a mean 1.1 g/dL and hematocrit by 4.4%, representing 7% and 10% increases from baseline; red blood cell count also increased, and hemoglobin/hematocrit returned to normal 3 months after discontinuation.
  • Serum EPO rose from 13.5 ± 12 to 21.3 ± 17 mIU/mL at 1 month, a 58% increase, and remained significant at 3 months; at 6 months EPO trended toward baseline but remained nonsuppressed despite elevated hemoglobin/hematocrit, with the EPO-hemoglobin relationship shifted right by about 30% higher EPO at each hemoglobin level.
  • Hepcidin was suppressed by 49%, ferritin decreased, and soluble transferrin receptor and the sTR/log ferritin ratio increased in the testosterone group; hepcidin and ferritin rebounded after treatment stopped. IL-6, C-reactive protein, and TNF-α did not differ between groups.
  • In sensitivity analyses, anemic men (n = 33) and nonanemic men (n = 133) had generally similar hematologic responses; 64% of men anemic at baseline were no longer anemic after 6 months of testosterone.

Methods

  • Randomized, double-blind, placebo-controlled trial (Testosterone in Older Men with Mobility Limitation): 209 men randomized, 166 completed 6 months and constituted the analytic sample; participants were ambulatory men aged 65 years and older with mobility limitation and total testosterone 100–350 ng/dL or free testosterone <50 pg/mL, assigned to 10 g testosterone gel daily or placebo for 6 months.
  • Outcomes were assessed at baseline, 1, 3, and 6 months and 3 months after discontinuation; measurements included EPO, hepcidin, ferritin, soluble transferrin receptor, complete blood counts/red cell indices, and hormones.
  • Changes over time were modeled with generalized estimating equations controlling for baseline outcome levels, with treatment contrasts at each visit and Wald tests; generalized additive models assessed EPO-hemoglobin/hematocrit relationships, and sensitivity analyses compared anemic and nonanemic participants.

Limitations

  • Stated in the paper: analyses were relatively infrequent (monthly), and the study lacked analyses of changes in or response to hypoxia-inducible factor, Von Hippel Lindau, and prolyl hydroxylase levels/activity, limiting mechanistic interpretation.
  • Evident from the text: trial enrollment was halted by the Data and Safety Monitoring Board due to increased cardiovascular events in the testosterone arm, and the analytic sample was restricted to 166 of 209 randomized men who completed 6 months, which may introduce selection or attrition bias.
  • The paper also states that the clinical consequences of testosterone-induced erythrocytosis in men remain to be elucidated.

Model-written summary. Check it against the paper before relying on it.

Integrity signals

Registry

Crossref · 10.1093/gerona/glt154

Cites

48 of 48 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Claims the paper makes

0 of 51 cited sources checked · 0 supported · 0 flagged

  • Findingown data

    The hematologic changes in response to testosterone administration in anemic men were generally similar to those observed in nonanemic men and in the entire cohort.

    “The hematologic changes in response to testosterone administration in anemic men were generally similar to those observed in nonanemic men and in the entire cohort.”
    Quote in the paperNot a substantial claim
  • Findingown data

    The placebo group showed no significant change in serum EPO level.

    “The placebo group showed no significant change in serum EPO level.”
    Quote in the paperSubstantial claim
  • Findingown data

    Testosterone-induced increase in hemoglobin and hematocrit is associated with stimulation of EPO and reduced ferritin and hepcidin concentrations.

    “Testosterone-induced increase in hemoglobin and hematocrit is associated with stimulation of EPO and reduced ferritin and hepcidin concentrations.”
    Quote in the paperSubstantial claim
  • Findingown data

    A difference of 100 ng/dL total testosterone was associated with a mean (95% CI) difference of -2.8 (-5.6, -0.08) ng/mL in 6-month change in hepcidin.

    “A difference of 100 ng/dL total testosterone was associated with a mean (95% CI) difference of -2.8 (-5.6, -0.08) ng/mL in 6-month change in hepcidin.”
    Quote in the paperSubstantial claim
  • Findingown data

    Three months after treatment discontinuation, hepcidin levels had rebounded slightly above baseline.

    “Three months after treatment discontinuation, hepcidin levels had rebounded slightly above baseline.”
    Quote in the paperNot a substantial claim
  • May combine two claims. 29
  • Classified as probably not a substantial claim. 14
  • The quote only partly states this claim. 1

  • May combine two claims.

    Findingown data

    By the sixth month of treatment, hepcidin levels in men assigned to testosterone arm tended to fall back toward baseline and were no longer significantly different from placebo.

    “By the sixth month of treatment, hepcidin levels in men assigned to the testosterone arm tended to fall back toward baseline and were no longer significantly different from those in participants assigned to placebo arm.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingown data

    Serum EPO levels trended toward baseline by 6 months despite continued testosterone administration, but remained nonsuppressed despite elevated hemoglobin and hematocrit in testosterone-treated men.

    “Serum EPO levels trended toward baseline by 6 months in spite of continued testosterone administration, but remained nonsuppressed in spite of elevated levels of hemoglobin and hematocrit in testosterone-treated men.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    Serum sTR levels increased markedly in testosterone group at 1 and 3 months and then returned toward baseline but remained higher than placebo at 6 months.

    “Levels of sTR increased markedly in the testosterone group at 1 and 3 months and then returned toward baseline but remained higher than placebo at 6 months (Figure 4B).”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    The ratio of sTR to log10 ferritin increased significantly in men assigned to testosterone arm but did not change in those assigned to placebo arm.

    “The ratio of sTR to log 10 ferritin, which has been described as an index of iron-dependent erythropoietic activity, increased significantly in men assigned to the testosterone arm but did not change in those assigned to the placebo arm (Figure 4D).”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    Changes in hemoglobin and hematocrit during testosterone administration did not differ significantly from those in the entire cohort (n = 166) as well as in nonanemic participants.

    “The changes in hemoglobin and hematocrit during testosterone administration did not differ significantly from those in the entire cohort (n = 166) as well as in nonanemic participants (Figure 5).”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingown data

    Testosterone administration increased hemoglobin and hematocrit by average 1.1 g/dL and 4.4%, respectively, representing 7% and 10% increase from baseline.

    “As expected, hemoglobin and hematocrit increased in men assigned to testosterone group by an average 1.1 g/dL and 4.4%, respectively (Table 2), representing 7% and 10% increase, respectively, from baseline.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    Serum ferritin levels decreased in testosterone group in parallel with hepcidin but remained unchanged in placebo group.

    “Serum ferritin levels decreased in the testosterone group in parallel with hepcidin but remained unchanged in the placebo group (Figure 4C).”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    Testosterone administration significantly increased serum EPO level into high normal range (13.5 ± 12 to 21.3 ± 17 mIU/mL) at 1 month; this 58% increase from baseline was statistically significant and remained significant at 3 months.

    “Testosterone administration significantly increased serum EPO level into the high normal range (13.5 ± 12 to 21.3 ± 17 mIU/mL) at 1 month; this 58% increase from baseline was statistically significant and remained significant at 3 months (Figure 3A).”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    After controlling for testosterone changes, 1 pg/mL differences in change in E2 or E1 were associated with -0.93 (-1.37, -0.48) and -1.04 (-1.47, -0.61) differences in change in hepcidin, respectively.

    “After controlling for testosterone changes, 1 pg/mL differences in change in E2 or E1 were associated with -0.93 (-1.37, -0.48) and -1.04 (-1.47, -0.61) differences in change in hepcidin, respectively.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingown data

    Hemoglobin and hematocrit levels in testosterone-treated men peaked at month 3 in most participants and remained elevated for remainder of intervention.

    “Hemoglobin and hematocrit levels in testosterone-treated men peaked at month 3 in most participants and remained at these elevated levels for the remainder of the intervention period.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    Serum interleukin-6 levels were similar between groups at baseline and did not change significantly in either group.

    “However, serum interleukin-6 levels were similar between groups at baseline and did not change significantly in either group (Figure 4E).”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingown data

    The linear-log relationship between hemoglobin levels and serum EPO levels was shifted to the right after 6 months of testosterone administration; at each level of hemoglobin, serum EPO levels were greater by about 30% after testosterone administration than at baseline.

    “However, this linear-log relationship between hemoglobin levels and serum EPO levels was shifted to the right after 6 months of testosterone administration (Figure 3B); at each level of hemoglobin, serum EPO levels were greater by about 30% after testosterone administration than they had been at baseline.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    Testosterone administration increased mean testosterone levels from low baseline (252 ± 56 ng/dL) into mid-normal range at 3 months (708 ± 327 ng/dL) and 6 months (633 ± 419 ng/dL), whereas placebo remained unchanged.

    “Testosterone administration increased mean testosterone levels (Figure 2) from low levels at baseline (252 ± 56 ng/dL) into the mid-normal range (reference range 300-1000 ng/dL) for healthy young men at 3 months (708 ± 327 ng/dL) and 6 months (633 ± 419 ng/dL), whereas testosterone levels remained unchanged in the placebo group (236 ± 63, 282 ± 126, and 290 ± 157 ng/dL at baseline, 3 months, and 6”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    During testosterone treatment, testosterone and estradiol levels increased, and both correlated negatively and similarly with change in serum hepcidin levels.

    “In our studies, testosterone and estradiol levels increased during treatment, both correlated negatively and similarly with change in serum hepcidin levels, although there was direct concordance between the temporal relationship of testosterone increase and hepcidin suppression.”
    Quote in the paperNot a substantial claim

  • Classified as probably not a substantial claim. May combine two claims.

    Study design and conductcitation

    Serum hepcidin was measured by ELISA with sensitivity 5 ng/mL, interassay CV 12%, and range 29-254 ng/mL in men.

    “Serum hepcidin was measured by enzyme-linked immunosorbent assay (Intrinsic Life Sciences) with sensitivity of 5 ng/mL, interassay coefficient of variation 12%, and range 29-254 ng/ mL in men (12,15).”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [12] source

      Not checked in the free run.

    • cites [15] source

      Not checked in the free run.

  • Classified as probably not a substantial claim.

    Premisecitation

    Interleukin-6 is a known positive regulator of hepcidin.

    “To explain the observed suppression of hepcidin, we considered the possibility that testosterone suppresses the cytokine interleukin-6, a known positive regulator of hepcidin (23).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [23] source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Administration of graded doses of testosterone to healthy young and older men, whose endogenous testosterone production was suppressed, dose dependently increased hemoglobin and hematocrit but did not change EPO levels consistently after 20 weeks even at supraphysiologic doses.

    “For example, administration of graded doses of testosterone to healthy young and older men, whose endogenous testosterone production was suppressed by administration of a long-acting gonadotropin releasing hormone agonist, dose dependently increased hemoglobin and hematocrit but did not change EPO levels consistently after 20 weeks even at supraphysiologic doses of testosterone (4).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [4] source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Serum sTR concentration reflects total erythroid activity and iron status and reflects plasma iron turnover and erythroid transferrin uptake if iron deficiency is not present.

    “Serum sTR concentration reflects total erythroid activity and iron status and has been shown to reflect plasma iron turnover and erythroid transferrin uptake if iron deficiency is not present (22,25).”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [22] source

      Not checked in the free run.

    • cites [25] source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Study design and conductcitation

    The trial was randomized, double-blind, placebo-controlled.

    “The Testosterone in Older Men with Mobility Limitation trial was a randomized, double-blind, placebo-controlled trial whose design and primary results have been published (13).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [13] source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductcitation

    Testosterone levels were measured by a radioimmunoassay validated against liquid chromatography tandem mass spectrometry.

    “Testosterone levels were measured by a radioimmunoassay that has been validated against liquid chromatography tandem mass spectrometry (13) and has a sensitivity of 10 ng/dL.”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [13] source

      Not checked in the free run.

  • Classified as probably not a substantial claim. May combine two claims.

    Premisecitation

    Serum sTR concentration reflects total erythroid activity in rats and humans and reflects plasma iron turnover and erythroid transferrin uptake very closely if iron deficiency is not present.

    “Serum sTR concentration reflects total erythroid activity in rats and humans and has been shown to reflect plasma iron turnover and erythroid transferrin uptake very closely if iron deficiency is not present (22).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [22] source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductreasoning

    Study personnel and participants were unaware of intervention assignment.

    “Study personnel and participants were unaware of intervention assignment.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Study design and conductcitation

    Randomization was concealed and computer-generated with block size 6, stratified by age.

    “Eligible participants were randomized to placebo or testosterone gel based on concealed, computer-generated randomization tables, using a block size of 6. Randomization was stratified by age: (a) 65-74 and (b) 75 and older.”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [13] source

      Not checked in the free run.

  • The quote only partly states this claim.

    Premisecitation

    Testosterone stimulates the incorporation of intravenously administered transferrin-bound diferric 58Fe into red blood cells in mice.

    “Our studies in mice indicate that testosterone stimulates the incorporation”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [26] source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Study design and conductcitation

    Serum hepcidin and ferritin levels were within reference ranges and similar between groups at baseline.

    “Serum hepcidin and ferritin levels were within the reported reference ranges for men and similar between groups (15).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [15] source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Administration of supraphysiologic doses of testosterone in healthy men suppresses hepcidin while EPO levels remained unchanged after 20 weeks.

    “We have reported that administration of supraphysiologic doses of testosterone in healthy men suppresses the iron regulatory peptide hepcidin while EPO levels remained unchanged after 20 weeks of treatment (12).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [12] source

      Not checked in the free run.

  • Classified as probably not a substantial claim.

    Premisecitation

    Chuvash polycythemia due to homozygosity for VHL R200W has EPO levels often in normal range but inappropriately increased in context of polycythemia.

    “These observations are similar to those reported in Chuvash polycythemia due to homozygosity for VhL R200W , in which EPO levels are often in the normal range but inappropriately increased in the context of polycythemia (24).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [24] source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    Estradiol regulates hepcidin transcription and systemic levels of hepcidin in vitro and in vivo.

    “Recent studies have demonstrated that estradiol, which is the product of aromatasecatalyzed testosterone metabolism, regulates hepcidin transcription and systemic levels of hepcidin in vitro and in vivo, respectively (35)(36)(37).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites (35)(36)(37)

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S4 (based). May combine two claims.

    Interpretationown data

    Testosterone stimulates renal secretion of EPO through unknown mechanisms that stimulate erythropoiesis, which could suppress hepcidin.

    “testosterone stimulates renal secretion of EPO through unknown mechanisms that stimu- lates erythropoiesis, which could suppress hepcidin (this manuscript)”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites (this manuscript)

      Not checked in the free run.

  • May combine two claims.

    Interpretationreasoning

    Increased EPO levels lead to increased erythropoiesis and increased iron utilization to support the increase in hemoglobin levels.

    “Therefore, it is likely that increased EPO levels lead to increased erythropoiesis and increased iron utilization to support the increase in hemoglobin levels.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Interpretationnone given

    Many adaptations induced by testosterone-increased hemoglobin and hematocrit, increased red cell 2,3-bisphosphoglycerate, and increased muscle capillarity-would be expected to increase net oxygen delivery to tissue.

    “However, many of the adaptations induced by testosterone-increased hemoglobin and hematocrit, increased red cell 2,3-bisphosphoglycerate, and increased muscle capillarity-would be expected to increase net oxygen delivery to the tissue.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    Testosterone upregulates the expression of GATA-1-and GATA-dependent genes, which could increase EPO sensitivity and stimulate stress erythropoiesis.

    “testosterone upregulates the expression of GATA-1-and GATA-dependent genes, which could increase EPO sensitivity and stimulate stress erythropoiesis (38)”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [38] source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Men and women have different hemoglobin reference ranges yet similar EPO levels.

    “This new equilibrium set point for EPO/hemoglobin has precedent in the observation that men and women have different hemoglobin reference ranges yet similar EPO levels (42).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [42] source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Testosterone is converted to estradiol (E2), which can regulate hepcidin transcription.

    “testosterone is converted to estradiol (E2), which can regulate hepcidin transcription (35-37).”
    Quote in the paperNot a substantial claim0 of 3 sources checked
    • cites [35] source

      Not checked in the free run.

    • cites [36] source

      Not checked in the free run.

    • cites [37] source

      Not checked in the free run.

  • May combine two claims.

    Interpretationown data

    A model for testosterone-induced erythrocytosis involves both EPO secretion and increased iron bioavailability (suppressed hepcidin).

    “A model for testosteroneinduced erythrocytosis is proposed (Figure 6) that involves both EPO secretion and increased iron bioavailability (suppressed hepcidin) and that has experimental support from our work and that of others.”
    Quote in the paperSubstantial claim
    • Rests on an assumption: Suppressed hepcidin increases iron bioavailability.

  • Classified as probably not a substantial claim.

    Premisecitation

    Increased hematocrit levels are associated with increased risk of adverse cardiovascular events.

    “Large epidemiologic studies show that increased hematocrit levels are associated with increased risk of adverse cardiovascular events (39).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [39] source

      Not checked in the free run.

36 of 36

  • The paper relies on this without support.

    Suppressed hepcidin increases iron bioavailability.

    “increased iron bioavailability (suppressed hepcidin)”
1 of 1

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Testosterone increases secretion of and sensitivity to erythropoietin and suppresses hepcidin.

    “Testosterone increases secretion of and sensitivity to erythropoietin, the main trophic hormone for erythrocyte production and thereby hemoglobin synthesis, as well as suppressing hepcidin (122), a crucial iron regulatory protein that governs the body’s iron economy.”

    From Circulating Testosterone as the Hormonal Basis of Sex Differences in Athletic Performance (2018) · cites this paper as [122]

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

Each contradiction between two passages listed here was confirmed by an independent check.

  • Reported hematocrit increase does not match Table 2

    Major

    The text attributes an average 4.4% hematocrit increase to Table 2, but the table lists testosterone-group changes of 3.18, 3.59, and 2.96 percentage points at 1, 3, and 6 months. None matches the reported increase.

  • Trial citation points to a different study

    Minor

    The text cites reference 13 for the trial's design and primary results, but reference 13 is a paper on hepcidin suppression. The trial-related paper is listed as reference 14, indicating a mismatch between the citation and reference list.

2 of 2

Cites

Flagged first, then by citations

Research works printed but not linked: 3

  1. Shahani, 2009, Journal of endocrinological investigation, 32, 704, 10.3275/6149 · DOI
  2. Jockenh  vel, 1997, European journal of medical research, 2, 293
  3. Malgor, 1998, Acta physiologica, pharmacologica et therapeutica latinoamericana : &#x00A0;&#x00A0;rgano de la Asociaci&#x00A0;&#x00A0;n Latinoamericana de Ciencias Fisiol&#x00A0;&#x00A0;gicas y [de] la Asociaci&#x00A0;&#x00A0;n Latinoamericana de Farmacolog&#x00A0;&#x00A0;a, 48, 99

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Related

Authors
Bachman, E., Travison, T. G., Basaria, S., Davda, M. N., Guo, W., Li, M., Connor Westfall, J., Bae, H., Gordeuk, V., & Bhasin, S.
Affiliations
  • Boston University (US)
  • University of Illinois Chicago (US)
  • Brigham and Women's Hospital (US)
ORCID
Venue
The Journals of Gerontology Series A: Biological Sciences and Medical Sciences
Publisher
Oxford University Press (OUP)
Published
2013-10-24
Volume
69
Issue
6
Pages
725-735
ISSN
  • 1079-5006 (ISSN-L)
  • 1758-535X
DOI
10.1093/gerona/glt154
PMC
PMC4022090
OpenAlex
W2108872913
Semantic Scholar
992fd0ad845ed3dfaa094de44dcb3a2d56e4c702
Cited by
426
References
48
Citations by year
2026: 41 · 2025: 56 · 2024: 27 · 2023: 58 · 2022: 27 · 2021: 28 · 2020: 44 · 2019: 31 · 2018: 28 · 2017: 38 · 2016: 18 · 2015: 22 · 2014: 4 · 2013: 2
FWCI
10.99
Type
journal article
Language
en
Open access
Locations
  • The Journals of Gerontology Series A (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5p30ag031679-15)
  • National Institute on Aging (U01AG014369, P30-AG031679, 1UO1AG14369)
  • National Institute of General Medical Sciences (T32GM074905)
Topics
  • Health Sciences › Medicine › Hematology › Erythropoietin and Anemia Treatment
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Hormonal and reproductive studies
  • Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
Keywords
testosterone, erythrocytosis, erythropoietin, hepcidin, hemoglobin, hematocrit, erythropoiesis, iron utilization, soluble transferrin receptor, ferritin, anemia, older men, testosterone gel, mobility limitations
MeSH terms
Aged, Androgens, Dose-Response Relationship, Drug, Double-Blind Method, Erythropoiesis, Erythropoietin, Follow-Up Studies, Hemoglobins, Humans, Male, Middle Aged, Polycythemia, Radioimmunoassay, Testosterone, Treatment Outcome, Mobility Limitation, Hepcidins

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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

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