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<pubDate>Thu, 21 Aug 2008 07:19:00 BST</pubDate>


	<title>CiteULike: omalbams Patti</title>
	<description>CiteULike: omalbams Patti</description>


	<link>http://www.citeulike.org/user/omalbam/author/Patti</link>
	<dc:publisher>CiteULike.org</dc:publisher>
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<item rdf:about="http://www.citeulike.org/user/omalbam/article/2675329">
    <title>Usefulness of statin pretreatment to prevent contrast-induced nephropathy and to improve long-term outcome in patients undergoing percutaneous coronary intervention.</title>
    <link>http://www.citeulike.org/user/omalbam/article/2675329</link>
    <description>&lt;i&gt;The American journal of cardiology, Vol. 101, No. 3. (1 February 2008), pp. 279-285.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Contrast-induced nephropathy (CIN) is an important cause of mortality and morbidity in patients undergoing angiography. This study investigated whether statins decrease incidence of CIN in the setting of percutaneous coronary intervention (PCI) and evaluated the influence of such potential benefit on long-term outcome. Four-hundred thirty-four patients undergoing PCI were prospectively enrolled and followed up to 4 years. Patients were stratified according to preprocedural statin therapy (260 statin treated, 174 statin naive). CIN was defined as a postprocedural increase in serum creatinine of &#62;or=0.5 mg/dl or&#62;25% from baseline. Follow-up assessment included 4-year occurrence of major adverse cardiac events. Statin-treated patients had a significantly lower incidence of CIN (3% vs 27%, p&#60;0.0001; 90% risk decrease) and had better postprocedural creatinine clearance (80+/-20 vs 65+/-16 ml/min, p&#60;0.0001). Benefit of statin before treatment was observed in all subgroups, except in patients with a pre-existing creatinine clearance&#60;40 ml/min. During follow-up, CIN was a predictor of poorer outcome; 4-year survival free of major adverse cardiac events was highest in statin-treated patients without CIN (95%, p&#60;or=0.015) and lowest in statin-naive patients with CIN (53%, p&#60;or=0.018). In conclusion, patients receiving statins before PCI have a significant decrease of CIN; this early protective effect translates into better long-term event-free survival. These results may lend further support to utilization of statins as adjuvant pharmacologic therapy before PCI.</description>
    <dc:title>Usefulness of statin pretreatment to prevent contrast-induced nephropathy and to improve long-term outcome in patients undergoing percutaneous coronary intervention.</dc:title>

    <dc:creator>G Patti</dc:creator>
    <dc:creator>A Nusca</dc:creator>
    <dc:creator>M Chello</dc:creator>
    <dc:creator>V Pasceri</dc:creator>
    <dc:creator>A D'Ambrosio</dc:creator>
    <dc:creator>GW Vetrovec</dc:creator>
    <dc:creator>G Di Sciascio</dc:creator>
    <dc:identifier>doi:10.1016/j.amjcard.2007.08.030</dc:identifier>
    <dc:source>The American journal of cardiology, Vol. 101, No. 3. (1 February 2008), pp. 279-285.</dc:source>
    <dc:date>2008-04-15T20:33:19-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>The American journal of cardiology</prism:publicationName>
    <prism:issn>0002-9149</prism:issn>
    <prism:volume>101</prism:volume>
    <prism:number>3</prism:number>
    <prism:startingPage>279</prism:startingPage>
    <prism:endingPage>285</prism:endingPage>
    <prism:category>cardiovascular</prism:category>
    <prism:category>hplp</prism:category>
    <prism:category>nephropathy</prism:category>
    <prism:category>prevention</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/omalbam/article/2223114">
    <title>Patients with Neuroglycopenia after Gastric Bypass Surgery Have Exaggerated Incretin and Insulin Secretory Responses to a Mixed Meal</title>
    <link>http://www.citeulike.org/user/omalbam/article/2223114</link>
    <description>&lt;i&gt;J Clin Endocrinol Metab, Vol. 92, No. 12. (1 December 2007), pp. 4678-4685.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Context and Objective: Hyperinsulinemic hypoglycemia is newly recognized as a rare but important complication after Roux-en-Y gastric bypass (GB). The etiology of the syndrome and metabolic characteristics remain incompletely understood. Recent studies suggest that levels of incretin hormones are increased after GB and may promote excessive -cell function and/or growth. Patients and Methods: We performed a cross-sectional analysis of metabolic variables, in both the fasting state and after a liquid mixed-meal challenge, in four subject groups: 1) with clinically significant hypoglycemia [neuroglycopenia (NG)] after GB surgery, 2) with no symptoms of hypoglycemia at similar duration after GB surgery, 3) without GB similar to preoperative body mass index of the surgical cohorts, and 4) without GB similar to current body mass index of the surgical cohorts. Results: Insulin and C-peptide after the liquid mixed meal were both higher relative to the glucose level achieved in persons after GB with NG compared with asymptomatic individuals. Glucagon, glucagon-like peptide 1, and glucose-dependent insulinotropic peptide levels were higher in both post-GB surgical groups compared with both overweight and morbidly obese persons, and glucagon-like peptide 1 was markedly higher in the group with NG. Insulin resistance, assessed by homeostasis model assessment of insulin resistance, the composite insulin sensitivity index, or adiponectin, was similar in both post-GB groups. Dumping score was also higher in both GB groups but did not discriminate between asymptomatic and symptomatic patients. Notably, the frequency of asymptomatic hypoglycemia after a liquid mixed meal was high in post-GB patients. Conclusion: A robust insulin secretory response was associated with postprandial hypoglycemia in patients after GB presenting with NG. Increased incretin levels may contribute to the increased insulin secretory response. 10.1210/jc.2007-0918</description>
    <dc:title>Patients with Neuroglycopenia after Gastric Bypass Surgery Have Exaggerated Incretin and Insulin Secretory Responses to a Mixed Meal</dc:title>

    <dc:creator>AB Goldfine</dc:creator>
    <dc:creator>EC Mun</dc:creator>
    <dc:creator>E Devine</dc:creator>
    <dc:creator>R Bernier</dc:creator>
    <dc:creator>M Baz-Hecht</dc:creator>
    <dc:creator>DB Jones</dc:creator>
    <dc:creator>BE Schneider</dc:creator>
    <dc:creator>JJ Holst</dc:creator>
    <dc:creator>ME Patti</dc:creator>
    <dc:identifier>doi:10.1210/jc.2007-0918</dc:identifier>
    <dc:source>J Clin Endocrinol Metab, Vol. 92, No. 12. (1 December 2007), pp. 4678-4685.</dc:source>
    <dc:date>2008-01-12T18:34:40-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>J Clin Endocrinol Metab</prism:publicationName>
    <prism:volume>92</prism:volume>
    <prism:number>12</prism:number>
    <prism:startingPage>4678</prism:startingPage>
    <prism:endingPage>4685</prism:endingPage>
    <prism:category>bariatric</prism:category>
    <prism:category>hypoglycemia</prism:category>
    <prism:category>incretin</prism:category>
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