Evidence map›Paper›PMID 27300575›Full record

Trial reportThe Journal of clinical endocrinology and metabolism2016

Effects of Testosterone and Estradiol Deficiency on Vasomotor Symptoms in Hypogonadal Men.

Alexander P Taylor, Hang Lee, Matthew L Webb, Hadine Joffe, Joel S Finkelstein

Open access · bronzeAbstract readComparative StudyRandomized Controlled Trial
PubMed Full text at PMC Publisher
In one paragraph

Trial report in The Journal of clinical endocrinology and metabolism, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.5field-weighted citation impact, top 17% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 1 country.

Alexander P TaylorFeinberg School of Medicine (A.P.T.), Northwestern University, Chicago, Illinois 60611; Endocrine Unit (J.S.F.), Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114; Biostatistics Center (H.L.) and Department of Psychiatry (H.J.), Brigham and Women's Hospital, and Department of Psychosocial Oncology and Palliative Care (M.L.W.), Dana Farber Cancer Institute, Yale School of Medicine, New Haven, Connecticut 06510.
Hang LeeFeinberg School of Medicine (A.P.T.), Northwestern University, Chicago, Illinois 60611; Endocrine Unit (J.S.F.), Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114; Biostatistics Center (H.L.) and Department of Psychiatry (H.J.), Brigham and Women's Hospital, and Department of Psychosocial Oncology and Palliative Care (M.L.W.), Dana Farber Cancer Institute, Yale School of Medicine, New Haven, Connecticut 06510.
Matthew L WebbFeinberg School of Medicine (A.P.T.), Northwestern University, Chicago, Illinois 60611; Endocrine Unit (J.S.F.), Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114; Biostatistics Center (H.L.) and Department of Psychiatry (H.J.), Brigham and Women's Hospital, and Department of Psychosocial Oncology and Palliative Care (M.L.W.), Dana Farber Cancer Institute, Yale School of Medicine, New Haven, Connecticut 06510.
Hadine JoffeFeinberg School of Medicine (A.P.T.), Northwestern University, Chicago, Illinois 60611; Endocrine Unit (J.S.F.), Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114; Biostatistics Center (H.L.) and Department of Psychiatry (H.J.), Brigham and Women's Hospital, and Department of Psychosocial Oncology and Palliative Care (M.L.W.), Dana Farber Cancer Institute, Yale School of Medicine, New Haven, Connecticut 06510.
Joel S FinkelsteinFeinberg School of Medicine (A.P.T.), Northwestern University, Chicago, Illinois 60611; Endocrine Unit (J.S.F.), Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114; Biostatistics Center (H.L.) and Department of Psychiatry (H.J.), Brigham and Women's Hospital, and Department of Psychosocial Oncology and Palliative Care (M.L.W.), Dana Farber Cancer Institute, Yale School of Medicine, New Haven, Connecticut 06510.
Dana-Farber Brigham Cancer Center · USMassachusetts General Hospital · USNorthwestern University · US

Funding

ZD6416 Analgesic--Painful Distal Symmetrical PolyneuropaM01RR001066 · NCRR · MASSACHUSETTS GENERAL HOSPITAL · PI BROWN, EMERY N · 1985 to 2008
$37.4M
Physiologic effects of androgen and estrogen deficiency in young and old menR01AG030545 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI FINKELSTEIN, JOEL S · 2007 to 2011
$3.1M
Defining the Mechanisms of Menopause-Associated Sleep and Mood DisturbancesR01MH082922 · NIMH · MASSACHUSETTS GENERAL HOSPITAL · PI JOFFE, HADINE · 2009 to 2013
$2.0M
EFFECTS OF ANDROGENS, ESTROGENS, AND PTH ON BONEK24DK002759 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI FINKELSTEIN, JOEL S · 1999 to 2008
$1.2M
NCRR NIH HHS M01 RR001066NIA NIH HHS R01 AG030545NIDDK NIH HHS K24 DK002759NIMH NIH HHS R01 MH082922
6 · The paper itself

Abstract

contextThe hormonal basis of vasomotor symptoms (VMS) in hypogonadal men is incompletely understood.

objectiveTo determine the contributions of testosterone and estradiol deficiency to VMS in hypogonadal men.

designTwo randomized trials were conducted sequentially between September 2004 and April 2011. Controls were recruited separately.

settingA single-site academic medical center.

participantsHealthy men ages 20-50, with normal serum testosterone levels.

interventionCohort 1 (n = 198, 81% completion) received goserelin acetate every 4 weeks to suppress gonadal steroids and were randomized to placebo or 1.25, 2.5, 5, or 10 g of testosterone gel daily for 16 weeks. Cohort 2 (n = 202, 78% completion) received the same regimen as cohort 1 plus anastrozole to block aromatization of testosterone. Controls (n = 37, 89% completion) received placebos for goserelin acetate and testosterone.

main outcome measuresIncidence of visits with VMS. This was a preplanned secondary analysis.

resultsVMS were reported at 26% of visits in cohort 1, and 35% of visits in cohort 2 (P = .02), demonstrating an effect of estradiol deficiency. When adjacent estradiol level groups in cohort 1 were compared, the largest difference in VMS incidence was observed between the 5-9.9 and 10-14.9 pg/mL groups (38% vs 16%, P < .001). In cohort 2, the 10-g testosterone group differed significantly from placebo (16% vs 43%, P = .048) after adjustment for small differences in estradiol levels, indicating that high testosterone levels may suppress VMS.

conclusionsEstradiol deficiency is the key mediator of VMS in hypogonadal men. At high levels, testosterone may have a suppressive effect.

Indexed as

AdultAgedBiomarkersBlood GlucoseCase-Control StudiesDiabetes Mellitus, Type 1Diabetes Mellitus, Type 2EstradiolFemaleFollow-Up StudiesGlycated HemoglobinHumansHypoglycemic AgentsHypogonadismMaleMiddle AgedBiomarkersBlood GlucoseEstradiolGlycated Hemoglobinhemoglobin A1c protein, humanHypoglycemic AgentsTestosterone

Identifiers

PMID27300575
PMCPMC5010571
OpenAlexW2434509691

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.