Evidence map›Paper›PMID 25971875›Full record

ArticlePsychopharmacology2016

Norepinephrine-enhancing antidepressant exposure associated with reduced antiviral effect of interferon alpha on hepatitis C.

Renata Fialho, Alison Burridge, Marco Pereira, Majella Keller, Alexandra File, Jeremy Tibble, Richard Whale

Abstract read
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In one paragraph

Article in Psychopharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.2field-weighted citation impact, top 51% 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

3 citing papers in PubMed, 7 citations in OpenAlex.

  1. Modifiable contributing factors to COVID-19: A comprehensive review.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2023
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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

7 authors at 4 institutions in 2 countries.

Renata FialhoSussex Partnership NHS Foundation Trust, Brighton, UK.
Alison BurridgeBrighton and Sussex Medical School, Falmer, Brighton, Sussex, BN1 9PH, UK.
Marco PereiraFaculty of Psychology and Educational Sciences, University of Coimbra, Coimbra, Portugal.
Majella KellerDigestive Diseases Centre, Brighton and Sussex University Hospitals NHS Trust, Brighton, UK.
Alexandra FileDigestive Diseases Centre, Brighton and Sussex University Hospitals NHS Trust, Brighton, UK.
Jeremy TibbleDigestive Diseases Centre, Brighton and Sussex University Hospitals NHS Trust, Brighton, UK.
Richard WhaleSussex Partnership NHS Foundation Trust, Brighton, UK. Richard.whale@brighton.ac.uk.
University Hospitals Sussex NHS Foundation Trust · GBBrighton and Sussex Medical School · GBSussex Partnership NHS Foundation Trust · GBUniversity of Coimbra · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

rationaleMajor depressive disorder is a common consequence of exposure to the pro-inflammatory cytokine interferon alpha, which is treated effectively with antidepressant medication. Antidepressant mode of action may conflict with interferon alpha's mechanism in treating hepatitis C however.

objectivesThe purpose of this study is to prospectively explore, in a large naturalistic cohort, whether antidepressant exposure influenced end of treatment response of hepatitis C to interferon alpha.

methodsTwo hundred thirty-nine patients infected with chronic hepatitis C and due to receive treatment were recruited. All participants initiated peg-interferon-2-alpha 180 μg weekly sub-cutaneously plus oral ribavirin 800-1200 mg daily. Participants were assessed for DSM-IV major depression at baseline and four weekly during treatment.

results32.6 % of the cohort was exposed to an antidepressant (serotonin-reuptake inhibitor: other categorised antidepressants 49:29). At baseline, 3.8 % had major depression and 55.2 % developed major depression during interferon alpha treatment. Exposure to an antidepressant not classified as a serotonin-reuptake inhibitor, of which all were norepinephrine-enhancing (OR 0.15, 95 % CI 0.04-0.60) and having a past history of psychiatric disorder (OR 4.41, 95 % CI 1.39-13.96) independently reduced the likelihood of end of treatment response. Serotonin-reuptake inhibitor exposure did not influence end of treatment response (OR 1.21, 95 % CI 0.35-4.19), neither did major depression at baseline (OR 2.31, 95 % CI 0.55-9.60) or during treatment (OR 0.69, 95 % CI 0.36-1.33).

conclusionsOur findings support a lack of conflict of therapeutic mechanism of serotonin-reuptake inhibitor antidepressants with interferon alpha in treating hepatitis C, which may include inflammatory influence. This appears not to be true for norepinephrine-enhancing antidepressant types and warrants investigation using more direct methods.

Indexed as

AdolescentAdultAgedAntidepressive AgentsAntiviral AgentsCohort StudiesDrug InteractionsFemaleHepatitis C, ChronicHumansInterferon-alphaMajor Depressive DisorderMaleMiddle AgedNorepinephrineProspective StudiesAntidepressive AgentsAntiviral AgentsInterferon-alphaNorepinephrineRibavirinSelective Serotonin Reuptake InhibitorsAntidepressantCohort studiesDepressionHepatitis CInflammationInterferon alphaNorepinephrineS-RISSRI

Identifiers

PMID25971875
OpenAlexW1902121722

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.