ArticleEuropean journal of clinical pharmacology2009
Genetic polymorphisms of CYP2D6 oxidation in patients with systemic sclerosis.
Article in European journal of clinical pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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.
Who cites it
1 citing paper in PubMed, 6 citations in OpenAlex.
- Genetic polymorphisms of CYP2D6 oxidation in patients with autoimmune bullous diseases.Postepy dermatologii i alergologii · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundInvolvement of genetic and environmental factors in the pathogenesis of scleroderma has contributed to a number of studies whose aim is to elucidate the way in which xenobiotics exert effects on the occurrence of autoimmune processes resulting in development of systemic sclerosis (SSc).
objectiveThe study dealt with the evaluation of the genetically determined polymorphism of CYP2D6, one of the phase I drug metabolizing isoenzymes, in patients suffering from SSc. Usefulness of the CYP2D6 genotype examination and prevalence of CYP2D6 gene mutation in light of susceptibility to SSc development were assessed.
methodsForty-three patients with SSc and 129 healthy volunteers were included in the study. Of the 43 patients with SSc, 17 fulfilled the criteria of diffuse SSc (dSSc) and 26 of limited SSc (lSSc). The determination of the CYP2D6 oxidative polymorphism was performed with the PCR-RFLP method.
resultsRelative risk of SSc development for particular genotype carriers expressed by the odds ratio (OR) was statistically significantly higher for subjects with CYP2D6*1/CYP2D6*4 (OR = 4.8; P < 0.001). A statistically significant correlation between the CYP2D6*4 allele prevalence and the risk for developing SSc was found (OR = 2.6; P = 0.0002).
conclusionHigher prevalence of the CYP2D6*4 mutated alleles in patients with SSc and the obtained OR values suggest that this mutation has the effect of increasing SSc morbidity rate.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.