Defining the genetic aetiology of monogenic diabetes can improve treatment.

2.50
Hdl Handle:
http://hdl.handle.net/11287/619234
Title:
Defining the genetic aetiology of monogenic diabetes can improve treatment.
Authors:
Gloyn, A. L.; Ellard, Sian ( 0000-0002-7620-5526 )
Abstract:
A molecular genetic diagnosis is now possible for > 80% of patients with monogenic diabetes. This not only provides accurate information regarding inheritance and prognosis, but can inform treatment decisions and improve clinical outcome. Mild fasting hyperglycaemia caused by heterozygous GCK mutations rarely requires pharmacological intervention, whereas patients with mutations in the genes encoding the transcription factors HNF-1alpha and HNF-4alpha respond well to low doses of sulphonylureas. The recent discovery that mutations in the KCNJ11 gene (encoding the Kir6.2 subunit of the K(ATP) channel) are the most common cause of permanent neonatal diabetes, has enabled children to stop insulin injections and achieve improved glycaemic control with high doses of sulphonylurea tablets. Molecular genetic testing is an essential prerequisite for the pharmacogenetic treatment of monogenic diabetes.
Citation:
Defining the genetic aetiology of monogenic diabetes can improve treatment. 2006, 7 (13):1759-67 Expert Opin Pharmacother
Publisher:
Taylor & Francis
Journal:
Expert opinion on pharmacotherapy
Issue Date:
Sep-2006
URI:
http://hdl.handle.net/11287/619234
DOI:
10.1517/14656566.7.13.1759
PubMed ID:
16925503
Additional Links:
http://www.tandfonline.com/doi/full/10.1517/14656566.7.13.1759?needAccess=true
Type:
Research Support, Non-U.S. Gov't
Language:
en
ISSN:
1744-7666
Appears in Collections:
pre-2014 RD&E publications; Diabetes/Endocrine Services

Full metadata record

DC FieldValue Language
dc.contributor.authorGloyn, A. L.en
dc.contributor.authorEllard, Sianen
dc.date.accessioned2016-09-01T13:12:04Z-
dc.date.available2016-09-01T13:12:04Z-
dc.date.issued2006-09-
dc.identifier.citationDefining the genetic aetiology of monogenic diabetes can improve treatment. 2006, 7 (13):1759-67 Expert Opin Pharmacotheren
dc.identifier.issn1744-7666-
dc.identifier.pmid16925503-
dc.identifier.doi10.1517/14656566.7.13.1759-
dc.identifier.urihttp://hdl.handle.net/11287/619234-
dc.description.abstractA molecular genetic diagnosis is now possible for > 80% of patients with monogenic diabetes. This not only provides accurate information regarding inheritance and prognosis, but can inform treatment decisions and improve clinical outcome. Mild fasting hyperglycaemia caused by heterozygous GCK mutations rarely requires pharmacological intervention, whereas patients with mutations in the genes encoding the transcription factors HNF-1alpha and HNF-4alpha respond well to low doses of sulphonylureas. The recent discovery that mutations in the KCNJ11 gene (encoding the Kir6.2 subunit of the K(ATP) channel) are the most common cause of permanent neonatal diabetes, has enabled children to stop insulin injections and achieve improved glycaemic control with high doses of sulphonylurea tablets. Molecular genetic testing is an essential prerequisite for the pharmacogenetic treatment of monogenic diabetes.en
dc.language.isoenen
dc.publisherTaylor & Francisen
dc.relation.urlhttp://www.tandfonline.com/doi/full/10.1517/14656566.7.13.1759?needAccess=trueen
dc.rightsArchived with thanks to Expert opinion on pharmacotherapyen
dc.subjectWessex Classification Subject Headings::Oncology. Pathology.::Geneticsen
dc.subjectWessex Classification Subject Headings::Endocrinology::Diabetesen
dc.titleDefining the genetic aetiology of monogenic diabetes can improve treatment.en
dc.typeResearch Support, Non-U.S. Gov'ten
dc.identifier.journalExpert opinion on pharmacotherapyen
dc.type.versionPublisheden

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