Evidence map›Paper›PMID 22020825›Full record

ArticleHepatology international2012

Comparison between acetylator phenotype and genotype polymorphism of n-acetyltransferase-2 in tuberculosis patients.

S V Rana, R P Ola, Sanjeev K Sharma, S K Arora, S K Sinha, P Pandhi, K Singh

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In one paragraph

Article in Hepatology international, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 6 pooled it
3.2field-weighted citation impact, top 9% 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

13 citing papers in PubMed, 6 syntheses or guidelines pooled it, 25 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. The international journal of tuberculosis and lung disease : the official journal of the International Union against Tuberculosis and Lung Disease · 2019
    Pooled it
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  6. Pooled it
  7. Article
  8. Genotype-Guided Hydralazine Therapy.American journal of nephrology · 2020
    Review
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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 1 institution in 1 country.

S V RanaDepartment of Gastroenterology, Postgraduate Institute of Medical Education and Research, Chandigarh, India. svrana25@hotmail.com.
R P OlaDepartment of Gastroenterology, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
Sanjeev K SharmaDepartment of Gastroenterology, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
S K AroraDepartment of Immunopathology, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
S K SinhaDepartment of Gastroenterology, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
P PandhiDepartment of Pharmacology, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
K SinghDepartment of Gastroenterology, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
Post Graduate Institute of Medical Education and Research · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIsoniazid (INH) is one of the most important drugs of antitubercular treatment regime, and in some cases it causes hepatotoxicity. It is metabolized by hepatic N-acetyltransferase-2 (NAT2).

aimTo compare whether both methods, i.e., genotype NAT2 and phenotype test of measuring serum INH levels, are useful to identify acetylator status of patients on antitubercular treatment (ATT).

methodsA total of 251 tuberculosis (TB) patients on standard treatment were followed up to 6 months for this study. NAT2 genotype was assessed by PCR with restriction fragment length polymorphism (RFLP) whereas serum INH levels were measured by fluorometry.

resultsOf the 251 patients, 50 (19.9%) developed ATT-induced hepatotoxicity. By phenotypic estimation, in the hepatotoxicity group, 17/50 (34%) were slow acetylators whereas 33/50 (66%) were fast acetylators. Genotypically, 19/50 (38%) were slow acetylators and 31/50 (62%) fast acetylators. By phenotypic analysis, in non-hepatotoxicity group, 46/201 (22.9%) were slow acetylators and 155/201 (77.1%) fast acetylators. By genotypic analysis, 30/201 (14.9%) were slow acetylators and 171/201 (85%) fast acetylators. Overall, slow acetylators (25.1%) measured phenotypically were not significantly different from slow acetylators (19.5%) measured genotypically.

conclusionThis study suggests that the acetylator status of TB patients can be detected by phenotypic method as efficaciously as by genotypic method. Therefore, phenotypic method can replace genotypic method to determine acetylating status as phenotypic method is simple and inexpensive.

Indexed as

HepatotoxicityIsoniazidN-acetyltransferase-2Slow and fast acetylator

Identifiers

PMID22020825
OpenAlexW2018024247

What OpenQuestion holds

Textmetadata
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Registered trials

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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.