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	<title>Translations:Riboflavin/40/en - Revision history</title>
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	<updated>2026-11-12T22:55:26Z</updated>
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		<title>FuzzyBot: Importing a new version from external source</title>
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		<updated>2024-02-19T07:27:21Z</updated>

		<summary type="html">&lt;p&gt;Importing a new version from external source&lt;/p&gt;
&lt;p&gt;&lt;b&gt;New page&lt;/b&gt;&lt;/p&gt;&lt;div&gt;There are rare genetic defects that compromise riboflavin absorption, transport, metabolism or use by flavoproteins. One of these is riboflavin transporter deficiency, previously known as [[Brown–Vialetto–Van Laere syndrome]]. Variants of the genes SLC52A2 and [[SLC52A3]] which code for [[Transport protein|transporter proteins]] RDVT2 and RDVT3, respectively, are defective. Infants and young children present with muscle weakness, [[cranial nerve]] deficits including hearing loss, sensory symptoms including sensory [[ataxia]], feeding difficulties, and respiratory distress caused by a [[Sensorimotor network|sensorimotor]] [[axon]]al [[neuropathy]] and cranial nerve pathology. When untreated, infants with riboflavin transporter deficiency  have labored breathing and are at risk of dying in the first decade of life. Treatment with oral supplementation of high amounts of riboflavin is lifesaving.&lt;/div&gt;</summary>
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