Post-mortem ABCB1 genotyping reveals an elevated toxicity for female digoxin users

Neuvonen, Anu M.; Palo, Jukka U.; Sajantila, Antti

doi:10.1007/s00414-011-0550-0

Cited by 24 publications

(16 citation statements)

References 34 publications

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“…This study’s results are consistent with the notion that ABCB1 3435T confers higher SDC [67], but adds to the existing data by suggesting that the interactions with C3435T may be gender-specific. There was a relationship between the frequency of 3435T allele and post-mortem SDC, but surprisingly the results were driven by females.…”

Section: Digoxin Pharmacogenetics: Recent Advances (Publication Year supporting

confidence: 90%

Pharmacogenetics in Chronic Heart Failure: New Developments and Current Challenges

Talameh

Lanfear

2011

Curr Heart Fail Rep

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The individual patient responses to chronic heart failure (HF) pharmacotherapies are highly variable. This variability cannot be entirely explained by clinical characteristics, and genetic variation may play a role. Therefore the purpose of this review is to 1) summarize the background pharmacogenetic literature for major HF pharmacotherapy classes (i.e. beta-blockers, angiotensin converting enzyme inhibitors, digoxin, and loop diuretics), 2) evaluate recent advances in the HF pharmacogenetic literature in the context of previous findings, and 3) discuss the challenges and conclusions for HF pharmacogenetic data and its clinical application.

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Section: Digoxin Pharmacogenetics: Recent Advances (Publication Year supporting

confidence: 90%

Pharmacogenetics in Chronic Heart Failure: New Developments and Current Challenges

Talameh

Lanfear

2011

Curr Heart Fail Rep

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“…This genetic difference may have arisen from an ancient border between two different immigration waves that arrived at different times and could represent two different modes of subsistence, i.e., hunter-gathering (east) and animal husbandry/farming (west) 9 . A similar but less dramatic border has been observed with the autosomal data 8 and even in genes with pharmacogenetic relevance 10, 11 .…”

Section: Introductionsupporting

confidence: 75%

Identification and analysis of mtDNA genomes attributed to Finns reveal long-stagnant demographic trends obscured in the total diversity

Översti

Onkamo

Stoljarova

et al. 2017

Sci Rep

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In Europe, modern mitochondrial diversity is relatively homogeneous and suggests an ubiquitous rapid population growth since the Neolithic revolution. Similar patterns also have been observed in mitochondrial control region data in Finland, which contrasts with the distinctive autosomal and Y-chromosomal diversity among Finns. A different picture emerges from the 843 whole mitochondrial genomes from modern Finns analyzed here. Up to one third of the subhaplogroups can be considered as Finn-characteristic, i.e. rather common in Finland but virtually absent or rare elsewhere in Europe. Bayesian phylogenetic analyses suggest that most of these attributed Finnish lineages date back to around 3,000–5,000 years, coinciding with the arrival of Corded Ware culture and agriculture into Finland. Bayesian estimation of past effective population sizes reveals two differing demographic histories: 1) the ‘local’ Finnish mtDNA haplotypes yielding small and dwindling size estimates for most of the past; and 2) the ‘immigrant’ haplotypes showing growth typical of most European populations. The results based on the local diversity are more in line with that known about Finns from other studies, e.g., Y-chromosome analyses and archaeology findings. The mitochondrial gene pool thus may contain signals of local population history that cannot be readily deduced from the total diversity.

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“…This area continues to be investigated; a recent study confirms that the ABCB1 TTT haplotype may be predictive of elevated digoxin concentrations in patients receiving this medication, especially in females. 75 However, similar to the 2008 digoxin report mentioned, this 2012 study did not include a population of exclusively heart failure patients. The negative finding in heart failure patients hint that perhaps clinical or other factors related to the disease state may override any genetic association altering digoxin response.…”

Section: Other Heart Failure Therapiesmentioning

confidence: 95%

Pharmacogenomics in Heart Failure

Oni‐Orisan

Lanfear

2014

Cardiology in Review

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Heart failure is becoming increasingly prevalent in the United States and is a significant cause of morbidity and mortality. Several therapies are currently available to treat this chronic illness; however, clinical response to these treatment options exhibit significant interpatient variation. It is now clearly understood that genetics is a key contributor to diversity in therapeutic response, and evidence that genetic polymorphisms alter the pharmacokinetics, pharmacodynamics, and clinical response of heart failure drugs continues to accumulate. This suggests that pharmacogenomics has the potential to help clinicians improve the management of heart failure by choosing the safest and most effective medications and doses. Unfortunately, despite much supportive data, pharmacogenetic optimization of heart failure treatment regimens is not yet a reality. In order to attenuate the rising burden of heart failure, particularly in the context of the recent paucity of new effective interventions, there is an urgent need to extend pharmacogenetic knowledge and leverage these associations in order to enhance the effectiveness of existing heart failure therapies. The present review focuses on the current state of pharmacogenomics in heart failure and provides a glimpse of the aforementioned future needs.

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Post-mortem ABCB1 genotyping reveals an elevated toxicity for female digoxin users

Cited by 24 publications

References 34 publications

Pharmacogenetics in Chronic Heart Failure: New Developments and Current Challenges

Pharmacogenetics in Chronic Heart Failure: New Developments and Current Challenges

Identification and analysis of mtDNA genomes attributed to Finns reveal long-stagnant demographic trends obscured in the total diversity

Pharmacogenomics in Heart Failure

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