Evidence map›Paper›PMID 19560866›Full record

Trial reportPain2009

Activation of the prostaglandin system in response to sleep loss in healthy humans: potential mediator of increased spontaneous pain.

Monika Haack, Erin Lee, Daniel A Cohen, Janet M Mullington

Abstract readRandomized Controlled Trial
In one paragraph

Trial report in Pain, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed, 4 pooled it
2.9field-weighted citation impact, top 10% 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

75 citing papers in PubMed, 4 syntheses or guidelines pooled it, 158 citations in OpenAlex.

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15 more citing papers are in PubMed but not listed here.

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

4 authors at 3 institutions in 2 countries.

Monika HaackDepartment of Neurology, Beth Israel Deaconess Medical Center & Harvard Medical School, Boston, MA 02215, USA. mhaack@bidmc.harvard.edu
Erin Lee
Daniel A Cohen
Janet M Mullington
Association pour la Recherche de Thérapeutiques Innovantes en Cancérologie · FRBeth Israel Deaconess Medical Center · USHarvard University · US

Funding

ZINC STATUS AND T CELL DISORDER IN MILD HUMAN ZINC DEFICIENCYM01RR001032 · NCRR · BETH ISRAEL DEACONESS MEDICAL CENTER · PI MANTZOROS, CHRISTOS S · 1985 to 2008
$32.3M
Adiposity, BP &the inflammatory response to sleep lossR01HL075501 · NHLBI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI MULLINGTON, JANET M · 2003 to 2006
$1.6M
NCRR NIH HHS M01 RR001032NCRR NIH HHS RR01032NHLBI NIH HHS HL075501NHLBI NIH HHS R01 HL075501
6 · The paper itself

Abstract

Insufficient duration of sleep is a highly prevalent behavioral pattern in society that has been shown to cause an increase in spontaneous pain and sensitivity to noxious stimuli. Prostaglandins (PGs), in particular PGE2, are key mediators of inflammation and pain, and we investigated whether PGE2 is a potential mediator in sleep-loss-induced changes in nociceptive processing. Twenty-four participants (7 females, age 35.1+/-7.1 years) stayed for 7 days in the Clinical Research Center. After two baseline days, participants were randomly assigned to either 3 days of 88 h of sleep deprivation (TSD, N=15) or 8h of sleep per night (N=9), followed by a night of recovery sleep. Participants rated the intensity of various pain-related symptoms every 2h across waking periods on computerized visual analog scales. PGE2 was measured in 24-h-urine collections during baseline and third sleep deprivation day. Spontaneous pain, including headache, muscle pain, stomach pain, generalized body pain, and physical discomfort significantly increased by 5-14 units on a 100-unit scale during TSD, compared to the sleep condition. Urinary PGE2 metabolite significantly increased by about 30% in TSD over sleep condition. TSD-induced increase in spontaneous pain, in particular headache and muscle pain, was significantly correlated with increase in PGE2 metabolite. Activation of the PGE2 system appears to be a potential mediator of increased spontaneous pain in response to insufficient sleep.

Indexed as

AdultAffectDinoprostoneFemaleHumansLinear ModelsMaleMiddle AgedPain MeasurementPain ThresholdPolysomnographyProstaglandinsSleepSleep DeprivationWakefulnessYoung Adult7-hydroxy-5,11-dioxotetranorprostane-1,16-dioic acidDinoprostoneProstaglandins

Identifiers

PMID19560866
PMCPMC2737342
OpenAlexW2082070599

What OpenQuestion holds

Textmetadata
LicenceTDM
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.