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<meta name="DC.Title" content="Treatment Monitoring of Brain Creatine Deficiency Syndromes: A 1H- and 31P-MR Spectroscopy Study" />
<meta name="DC.Date" content="2007-03-01" />
<meta name="DC.Publisher" content="American Journal of Neuroradiology" />
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<meta name="DC.Description" content="BACKGROUND AND PURPOSE: Brain creatine (Cr) deficiencies (BCr-d) are rare disorders of creatine biosynthesis and transport. We performed consecutive measures of total Cr (tCr) and of its phosphorylated fraction, phosphocreatine (PCr), in the brains of children affected by Cr synthesis defects during a long period of therapy. The aim was to identify the optimal treatment strategy for these disorders.

MATERIALS AND METHODS: Two patients with guanidinoacetate methyltransferase defect (GAMT-d) were treated with different amounts of Cr and with diet restrictions aimed at reducing endogenous guanidinoacetate (GAA) synthesis. Three patients with arginine:glycine amidinotransferase defect (AGAT-d) were treated with different Cr intakes. The patients’ treatments were monitored by means of 1H- and 31P-MR spectroscopy.

RESULTS: Cr and PCr replenishment was lower in GAMT-d than in AGAT-d even when GAMT-d therapy was carried out with a very high Cr intake. Cr and especially PCr replenishment became more efficient only when GAA blood values were reduced. Adenosine triphosphate (ATP) was increased in the baseline phosphorous spectrum of GAMT-d, and it returned to a normal value with treatment. Brain pH and brain Pi showed no significant change in the AGAT-d syndrome and at any Cr intake. However, 1 of the 2 GAMT-d patients manifested a lower brain pH level while consuming the GAA-lowering diet.

CONCLUSIONS: AGAT-d treatment needs lower Cr intake than GAMT-d. Cr supplementation in GAMT-d treatment should include diet restrictions aimed at reducing GAA concentration in body fluids. 1H- and especially 31P-MR spectroscopy are the ideal tools for monitoring the therapy response to these disorders." />
<meta name="DC.Contributor" content="M.C. Bianchi" />
<meta name="DC.Contributor" content="M. Tosetti" />
<meta name="DC.Contributor" content="R. Battini" />
<meta name="DC.Contributor" content="V. Leuzzi" />
<meta name="DC.Contributor" content="M.G. Alessandri’" />
<meta name="DC.Contributor" content="C. Carducci" />
<meta name="DC.Contributor" content="I. Antonozzi" />
<meta name="DC.Contributor" content="G. Cioni" />
<meta name="article:published_time" content="2007-03-01" />
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<meta name="citation_title" content="Treatment Monitoring of Brain Creatine Deficiency Syndromes: A 1H- and 31P-MR Spectroscopy Study" />
<meta name="citation_abstract" lang="en" content="&lt;p&gt;&lt;b&gt;BACKGROUND AND PURPOSE:&lt;/b&gt; Brain creatine (Cr) deficiencies (BCr-d) are rare disorders of creatine biosynthesis and transport. We performed consecutive measures of total Cr (tCr) and of its phosphorylated fraction, phosphocreatine (PCr), in the brains of children affected by Cr synthesis defects during a long period of therapy. The aim was to identify the optimal treatment strategy for these disorders.&lt;/p&gt;&lt;p&gt;&lt;b&gt;MATERIALS AND METHODS:&lt;/b&gt; Two patients with guanidinoacetate methyltransferase defect (GAMT-d) were treated with different amounts of Cr and with diet restrictions aimed at reducing endogenous guanidinoacetate (GAA) synthesis. Three patients with arginine:glycine amidinotransferase defect (AGAT-d) were treated with different Cr intakes. The patients’ treatments were monitored by means of &lt;sup&gt;1&lt;/sup&gt;H- and &lt;sup&gt;31&lt;/sup&gt;P-MR spectroscopy.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS:&lt;/b&gt; Cr and PCr replenishment was lower in GAMT-d than in AGAT-d even when GAMT-d therapy was carried out with a very high Cr intake. Cr and especially PCr replenishment became more efficient only when GAA blood values were reduced. Adenosine triphosphate (ATP) was increased in the baseline phosphorous spectrum of GAMT-d, and it returned to a normal value with treatment. Brain pH and brain P&lt;sub&gt;i&lt;/sub&gt; showed no significant change in the AGAT-d syndrome and at any Cr intake. However, 1 of the 2 GAMT-d patients manifested a lower brain pH level while consuming the GAA-lowering diet.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS:&lt;/b&gt; AGAT-d treatment needs lower Cr intake than GAMT-d. Cr supplementation in GAMT-d treatment should include diet restrictions aimed at reducing GAA concentration in body fluids. &lt;sup&gt;1&lt;/sup&gt;H- and especially &lt;sup&gt;31&lt;/sup&gt;P-MR spectroscopy are the ideal tools for monitoring the therapy response to these disorders.&lt;/p&gt;" />
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<meta name="citation_reference" content="citation_title=Pediatric Research;citation_journal_abbrev=Pediatr. Res.;citation_title=Creatine deficiency in the brain: a new, treatable inborn error of metabolism;citation_pages=409-413;citation_volume=36;citation_year=1994;citation_issue=3;citation_issn=0031-3998;citation_pmid=7808840;citation_doi=10.1203/00006450-199409000-00023" />
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<meta name="twitter:title" content="Treatment Monitoring of Brain Creatine Deficiency Syndromes: A 1H- and 31P-MR Spectroscopy Study" />
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<meta name="twitter:description" content="BACKGROUND AND PURPOSE: Brain creatine (Cr) deficiencies (BCr-d) are rare disorders of creatine biosynthesis and transport. We performed consecutive measures of total Cr (tCr) and of its phosphorylated fraction, phosphocreatine (PCr), in the brains of children affected by Cr synthesis defects during a long period of therapy. The aim was to identify the optimal treatment strategy for these disorders.

MATERIALS AND METHODS: Two patients with guanidinoacetate methyltransferase defect (GAMT-d) were treated with different amounts of Cr and with diet restrictions aimed at reducing endogenous guanidinoacetate (GAA) synthesis. Three patients with arginine:glycine amidinotransferase defect (AGAT-d) were treated with different Cr intakes. The patients’ treatments were monitored by means of 1H- and 31P-MR spectroscopy.

RESULTS: Cr and PCr replenishment was lower in GAMT-d than in AGAT-d even when GAMT-d therapy was carried out with a very high Cr intake. Cr and especially PCr replenishment became more efficient only when GAA blood values were reduced. Adenosine triphosphate (ATP) was increased in the baseline phosphorous spectrum of GAMT-d, and it returned to a normal value with treatment. Brain pH and brain Pi showed no significant change in the AGAT-d syndrome and at any Cr intake. However, 1 of the 2 GAMT-d patients manifested a lower brain pH level while consuming the GAA-lowering diet.

CONCLUSIONS: AGAT-d treatment needs lower Cr intake than GAMT-d. Cr supplementation in GAMT-d treatment should include diet restrictions aimed at reducing GAA concentration in body fluids. 1H- and especially 31P-MR spectroscopy are the ideal tools for monitoring the therapy response to these disorders." />
<meta name="og-title" property="og:title" content="Treatment Monitoring of Brain Creatine Deficiency Syndromes: A 1H- and 31P-MR Spectroscopy Study" />
<meta name="og-url" property="og:url" content="http://ajnr-stage2.stage.highwire.org/content/28/3/548" />
<meta name="og-site-name" property="og:site_name" content="American Journal of Neuroradiology" />
<meta name="og-description" property="og:description" content="BACKGROUND AND PURPOSE: Brain creatine (Cr) deficiencies (BCr-d) are rare disorders of creatine biosynthesis and transport. We performed consecutive measures of total Cr (tCr) and of its phosphorylated fraction, phosphocreatine (PCr), in the brains of children affected by Cr synthesis defects during a long period of therapy. The aim was to identify the optimal treatment strategy for these disorders.

MATERIALS AND METHODS: Two patients with guanidinoacetate methyltransferase defect (GAMT-d) were treated with different amounts of Cr and with diet restrictions aimed at reducing endogenous guanidinoacetate (GAA) synthesis. Three patients with arginine:glycine amidinotransferase defect (AGAT-d) were treated with different Cr intakes. The patients’ treatments were monitored by means of 1H- and 31P-MR spectroscopy.

RESULTS: Cr and PCr replenishment was lower in GAMT-d than in AGAT-d even when GAMT-d therapy was carried out with a very high Cr intake. Cr and especially PCr replenishment became more efficient only when GAA blood values were reduced. Adenosine triphosphate (ATP) was increased in the baseline phosphorous spectrum of GAMT-d, and it returned to a normal value with treatment. Brain pH and brain Pi showed no significant change in the AGAT-d syndrome and at any Cr intake. However, 1 of the 2 GAMT-d patients manifested a lower brain pH level while consuming the GAA-lowering diet.

CONCLUSIONS: AGAT-d treatment needs lower Cr intake than GAMT-d. Cr supplementation in GAMT-d treatment should include diet restrictions aimed at reducing GAA concentration in body fluids. 1H- and especially 31P-MR spectroscopy are the ideal tools for monitoring the therapy response to these disorders." />
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      <h1 class="highwire-cite-title" id="page-title">Treatment Monitoring of Brain Creatine Deficiency Syndromes: A <sup>1</sup>H- and <sup>31</sup>P-MR Spectroscopy Study</h1>  
    	<div class="highwire-cite-authors"><span  class="highwire-citation-authors"><span class="highwire-citation-author first" data-delta="0">M.C. Bianchi</span>, <span class="highwire-citation-author" data-delta="1">M. Tosetti</span>, <span class="highwire-citation-author" data-delta="2">R. Battini</span>, <span class="highwire-citation-author" data-delta="3">V. Leuzzi</span>, <span class="highwire-citation-author" data-delta="4">M.G. Alessandri’</span>, <span class="highwire-citation-author" data-delta="5">C. Carducci</span>, <span class="highwire-citation-author" data-delta="6">I. Antonozzi</span> and <span class="highwire-citation-author" data-delta="7">G. Cioni</span></span></div>
  
    	<div class="highwire-cite-metadata"><span  class="highwire-cite-metadata-journal highwire-cite-metadata">American Journal of Neuroradiology </span><span  class="highwire-cite-metadata-date highwire-cite-metadata">March 2007,  </span><span  class="highwire-cite-metadata-volume highwire-cite-metadata">28 </span><span  class="highwire-cite-metadata-issue highwire-cite-metadata">(3) </span><span  class="highwire-cite-metadata-pages highwire-cite-metadata">548-554; </span></div>
  
  
  
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<div id="hw-article-author-popups-top-node-6823--61774411792" style="display: none;"><div class="author-tooltip-0"><div class="author-tooltip-name">M.C. Bianchi </div><ul class="author-tooltip-find-more"><li class="author-tooltip-gs-link first"><a href="/lookup/google-scholar?link_type=googlescholar&amp;gs_type=author&amp;author%5B0%5D=M.C.%2BBianchi%2B" target="_blank" class="" data-icon-position="" data-hide-link-title="0">Find this author on Google Scholar</a></li><li class="author-tooltip-pubmed-link"><a href="/lookup/external-ref?access_num=Bianchi%20M&amp;link_type=AUTHORSEARCH" target="_blank" class="" data-icon-position="" data-hide-link-title="0">Find this author on PubMed</a></li><li class="author-site-search-link last"><a href="/search/author1%3AM.C.%2BBianchi%2B" rel="nofollow" class="" data-icon-position="" data-hide-link-title="0">Search for this author on this site</a></li></ul></div><div class="author-tooltip-1"><div class="author-tooltip-name">M. 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      <div class="highwire-cite-title">Treatment Monitoring of Brain Creatine Deficiency Syndromes: A <sup>1</sup>H- and <sup>31</sup>P-MR Spectroscopy Study</div>  
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