scholarly journals Gene-Drug Interaction in Stroke

2011 ◽  
Vol 2011 ◽  
pp. 1-14 ◽  
Author(s):  
Serena Amici ◽  
Maurizio Paciaroni ◽  
Giancarlo Agnelli ◽  
Valeria Caso

Stroke is the third cause of mortality and one of most frequent causes of long-term neurological disability, as well as a complex disease that results from the interaction of environmental and genetic factors. The focus on genetics has produced a large number of studies with the objective of revealing the genetic basis of cerebrovascular diseases. Furthermore, pharmacogenetic research has investigated the relation between genetic variability and drug effectiveness/toxicity. This review will examine the implications of pharmacogenetics of stroke; data on antihypertensives, statins, antiplatelets, anticoagulants, and recombinant tissue plasminogen activator will be illustrated. Several polymorphisms have been studied and some have been associated with positive drug-gene interaction on stroke, but the superiority of the genotype-guided approach over the clinical approach has not been proved yet; for this reason, it is not routinely recommended.

2021 ◽  
Author(s):  
Laia Llucià-Carol ◽  
Elena Muiño ◽  
Cristina Gallego-Fabrega ◽  
Jara Cárcel-Márquez ◽  
Jesus Martín-Campos ◽  
...  

Recombinant tissue-plasminogen activator (rtPA) is the only drug used during the acute phase of stroke. Despite its important benefits, a percentage of patients suffer symptomatic hemorrhagic transformations or a lack of early recanalization rates. These undesirable effects are associated with acute neurological and long-term functional deterioration. For the past 20 years, pharmacogenetic studies have tried to find the genetic risk factors associated with rtPA response. Most of these studies have used a gene-candidate strategy; however, recent genome-wide association studies have emerged indicating that genetic predisposition could modulate rtPA response. This review summarizes the most interesting findings in this field, including which genes and genetic variations are associated with hemorrhagic transformations and recanalization rates after thrombolytic therapy.


2008 ◽  
Vol 12 (2) ◽  
pp. 10-22
Author(s):  
Samuel Chew ◽  
Shahid A Kausar ◽  
Steve Sturman

Thrombolysis of appropriate and selected patients presenting with an acute ischaemic stroke within 3 h of onset with recombinant Tissue Plasminogen Activator (alteplase, r-TPA) can be implemented safely, reduce long-term disability, and is recommended by the National Institute of Health and Clinical Excellence and the Department of Health's National Stroke Strategy. We have developed an integrated and comprehensive pathway in order to achieve the above aims, which also provide guidelines for nursing in the peri-acute period and management of complications arising from the ischaemic stroke itself, from thrombolysis or from concomitant hyperglycaemia.


2001 ◽  
Vol 59 (4) ◽  
pp. 936-938 ◽  
Author(s):  
Osama O. Zaidat ◽  
Jose Americo M. Fernandes Filho ◽  
Gurwant Singh ◽  
Jose I. Suarez

Extra-cranial arterial dissection accounts for 10% of strokes in young people. Information on safety of thrombolytic administration in this group is limited. The literature, however, does not favor use of thrombolytics for myocardial ischemia when peripheral arterial dissection coexists. Based on the clinical and radiological features, two patients who presented with acute stroke secondary to arterial dissection were considered for thrombolysis. One of them received intra-venous recombinant tissue plasminogen activator (rtPA), and the other patient received intra-arterial rtPA. There were no post thrombolysis complications. This report supports feasibility of administering thrombolytics in acute ischemic strokes resulting from extra-cranial arterial dissection. Future larger studies are necessary to determine the efficacy, safety and long-term outcome in this patient population.


1997 ◽  
Vol 31 (5) ◽  
pp. 704-713 ◽  
Author(s):  
Bryan J. Mowry ◽  
Derek J. Nancarrow ◽  
Douglas F. Levinson

Objective: This paper aims to summarise the latest molecular genetic findings in schizophrenia, while providing background information on a number of relevant methodological issues. Method: Accumulative genetic data indicate that schizophrenia is a genetically complex disease with an unclear mode of transmission. The development and rapid progression of molecular genetics have provided a wide variety of methods to search for genes predisposing to human disease. The genetic basis for a number of the simpler diseases has been identified and characterised using these methods. More recently, progress has been made in identifying genes predisposing to the genetically more complex diseases such as diabetes mellitus, multiple sclerosis, bipolar disorder and schizophrenia. Results: The latest findings on chromosomes 3, 6, 8, 13, 18 and 22 and on the chromosome are reviewed. Conclusions: There is now suggestive support for three susceptibility loci (6p24–22, 8p22–21 and 22q12-q13.1) for schizophrenia, and it is likely that other regions will emerge from studies now in progress. Finding and then characterising genes within these loci will require long-term commitment and systematic efforts in clinical, laboratory and analytical fields.


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