Evidence map›Paper›PMID 27262302›Full record

Trial reportEuropean journal of clinical pharmacology2016

Influence of ACE gene on differential response to sertraline versus fluoxetine in patients with major depression: a randomized controlled trial.

Ehsan Bahramali, Negar Firouzabadi, Ilnaz Yavarian, Mohammad Reza Hooshangi Shayesteh, Nasrallah Erfani, Ali Alavi Shoushtari, Roja Asadpour

Abstract readRandomized Controlled Trial
PubMed Publisher
In one paragraph

Trial report in European journal of clinical pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.1field-weighted citation impact, top 19% 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

11 citing papers in PubMed, 23 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. The pharmacogenetics ofFrontiers in pharmacology · 2023
    Article
  8. Review
  9. PharmGKB summary: sertraline pathway, pharmacokinetics.Pharmacogenetics and genomics · 2020
    Article
  10. Article
  11. Review
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 2 institutions in 1 country.

Ehsan BahramaliNoncommunicable Diseases Research Center, Fasa University of Medical Sciences, Fasa, Iran.
Negar FirouzabadiNoncommunicable Diseases Research Center, Fasa University of Medical Sciences, Fasa, Iran. firouzabadi@sums.ac.ir.
Ilnaz YavarianSchool of Pharmacy, Shiraz University of Medical Sciences, International Branch, Shiraz, Iran.
Mohammad Reza Hooshangi ShayestehDepartment of Pharmacology & Toxicology, School of Pharmacy, Shiraz University of Medical Sciences, Shiraz, Iran.
Nasrallah ErfaniCancer Immunology Group, Shiraz Institute for Cancer Research, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran.
Ali Alavi ShoushtariDepartment of Psychiatry, School of Medicine, Hafez Hospital, Shiraz University of Medical Sciences, Shiraz, Iran.
Roja AsadpourSchool of Pharmacy, Shiraz University of Medical Sciences, International Branch, Shiraz, Iran.
Shiraz University of Medical Sciences · IRFasa University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundExtensive distribution of the different components of renin angiotensin system (RAS) in the brain, along with their roles in promoting anxiety, depression and brain inflammation, opposes RAS as a potential therapeutic target in major depression. Actions of angiotensin II, the main product of RAS, are reduced by antidepressants and this signifies the complex interplay of different mechanisms involved in response to therapy. Here, we hypothesized that genetic polymorphisms of RAS may affect the outcome of therapy in depressed patients.

methodsThe frequencies of variants of genes encoding for angiotensin-converting enzyme (ACE) insertion/deletion (I/D), rs4291 and rs4343 polymorphisms were determined in extracted DNAs of 200 newly diagnosed depressed patients. Patients were randomly divided into two groups, one treated with fluoxetine and the other treated with sertraline for 12 weeks. Responsive patients were determined by psychiatrist using Hamilton questionnaire and were compared with regard to their genetic variants.

resultsCarriers of the D allele and patients with DD genotype responded significantly better to sertraline than to fluoxetine (P = 0.0006, odds ratio (OR) = 3.0, 95 % confidence interval (CI) = 1.80-5.08; P = 0.006, OR = 3.7, 95 % CI = 1.66-8.29, respectively). Mutant genotypes (GG and TT) of rs4343 and rs4291 polymorphisms were also more frequent in patients responding to sertraline, though not achieving the significance level (P = 0.162 and P = 0.256, respectively).

conclusionThese findings suggest that special genetic variants of RAS may influence or be an indicator for better response to sertraline.

Indexed as

AdolescentAdultAgedAllelesAntidepressive AgentsFemaleFluoxetineGenotypeHumansMajor Depressive DisorderMaleMiddle AgedPeptidyl-Dipeptidase APolymorphism, GeneticSertralineYoung AdultACE protein, humanAntidepressive AgentsFluoxetinePeptidyl-Dipeptidase ASertralineAngiotensin-converting enzymeFluoxetineGenetic polymorphismMajor depressive disorderSertraline

Identifiers

PMID27262302
OpenAlexW2413836758

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.