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dc.contributor.authorTerzi M.
dc.contributor.authorCengiz N.
dc.contributor.authorOnar M.K.
dc.date.accessioned2020-06-21T09:23:51Z
dc.date.available2020-06-21T09:23:51Z
dc.date.issued2004
dc.identifier.issn1300-2996
dc.identifier.urihttps://hdl.handle.net/20.500.12712/3676
dc.description.abstractDiabetic neuropathy is a common and debilitating complication of diabetes mellitus associated with high health costs. The major pathogenetic hypotheses that have been invoked in diabetic neuropathy include activation of the polyol pathway, increased nonenzymatic glycation, vascular dysfunction, perturbed lipid metabolism and impaired neurotrophism. New neurotrophins and other growth factors or inflammatory mediators that influence neurons and axons have been recently identified. The diagnosis of diabetic neuropathy by neurologic history and examination, supplemented by neurophysiologic and quantitative sensory testing, is efficient and reliable. The increasing availability of additional putative treatments for diabetic neuropathy, such as islet or whole pancreas transplantation, aldose reductase inhibitors, myoinositol and trophic substances accentuates the need to search for additional means to demonstrate patient benefit related to treatment.en_US
dc.language.isoturen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectDiabetesen_US
dc.subjectNeuropathyen_US
dc.subjectNeurotrophismen_US
dc.titleDiabetic neuropathyen_US
dc.title.alternativeDiyabetik nöropatien_US
dc.typearticleen_US
dc.contributor.departmentOMÜen_US
dc.identifier.volume21en_US
dc.identifier.issue1en_US
dc.identifier.startpage39en_US
dc.identifier.endpage49en_US
dc.relation.journalOndokuz Mayis Universitesi Tip Dergisien_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US


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