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10.1186/s13023-015-0342-6 http://scihub22266oqcxt.onion/10.1186/s13023-015-0342-6 C4581011!4581011 !26399329     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26399329 &cmd=llinks): Failed to open stream: HTTP request failed! 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Ketogenic diet in a patient with congenital hyperinsulinism: a novel approach to prevent brain damage |pdf=|usr=}}{{26399329 }} gab.com Text Ketogenic diet in a patient with congenital hyperinsulinism: a novel approach to prevent brain damage JO: Orphanet J Rare Dis http://www.kidney.de/pget.php?&tw=1&pmid=26399329 #FOAvip BACKGROUND: Congenital hyperinsulinism (CHI) is the most frequent cause of hypoglycemia in children. In addition to increased peripheral glucose utilization, dysregulated insulin secretion induces profound hypoglycemia and neuroglycopenia by inhibiting glycogenolysis, gluconeogenesis and lipolysis. This results in the shortage of all cerebral energy substrates (glucose, lactate and ketones), and can lead to severe neurological sequelae. Patients with CHI unresponsive to medical treatment can be subjected to near-total pancreatectomy with increased risk of secondary diabetes. Ketogenic diet (KD), by reproducing a fasting-like condition in which body fuel mainly derives from beta-oxidation, is intended to provide alternative cerebral substrates such ketone bodies. We took advantage of known protective effect of KD on neuronal damage associated with GLUT1 deficiency, a disorder of impaired glucose transport across the blood-brain barrier, and administered KD in a patient with drug-unresponsive CHI, with the aim of providing to neurons an energy source alternative to glucose. METHODS: A child with drug-resistant, long-standing CHI caused by a spontaneous GCK activating mutation (p.Val455Met) suffered from epilepsy and showed neurodevelopmental abnormalities. After attempting various therapeutic regimes without success, near-total pancreatectomy was suggested to parents, who asked for other options. Therefore, we proposed KD in combination with insulin-suppressing drugs. RESULTS: We administered KD for 2 years. Soon after the first six months, the patient was free of epileptic crises, presented normalization of EEG, and showed a marked recover in psychological development and quality of life. CONCLUSIONS: KD could represent an effective treatment to support brain function in selected cases of CHI. Twit Text FOAVip Ketogenic diet in a patient with congenital hyperinsulinism: a novel approach to prevent brain damage ????Orphanet J Rare Dis http://www.kidney.de/pget.php?&tw=1&pmid=26399329 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26399329 #FOAvip English Wikipedia <ref>{{Cite pmid|26399329 }}</ref> Ketogenic diet in a patient with congenital hyperinsulinism: a novel approach to prevent brain damage #MMPMID26399329 Maiorana A ; Manganozzi L ; Barbetti F ; Bernabei S ; Gallo G ; Cusmai R ; Caviglia S ; Dionisi-Vici C Orphanet J Rare Dis 2015[Sep]; 10 (ä): 120 PMID26399329 show ga BACKGROUND: Congenital hyperinsulinism (CHI) is the most frequent cause of hypoglycemia in children. In addition to increased peripheral glucose utilization, dysregulated insulin secretion induces profound hypoglycemia and neuroglycopenia by inhibiting glycogenolysis, gluconeogenesis and lipolysis. This results in the shortage of all cerebral energy substrates (glucose, lactate and ketones), and can lead to severe neurological sequelae. Patients with CHI unresponsive to medical treatment can be subjected to near-total pancreatectomy with increased risk of secondary diabetes. Ketogenic diet (KD), by reproducing a fasting-like condition in which body fuel mainly derives from beta-oxidation, is intended to provide alternative cerebral substrates such ketone bodies. We took advantage of known protective effect of KD on neuronal damage associated with GLUT1 deficiency, a disorder of impaired glucose transport across the blood-brain barrier, and administered KD in a patient with drug-unresponsive CHI, with the aim of providing to neurons an energy source alternative to glucose. METHODS: A child with drug-resistant, long-standing CHI caused by a spontaneous GCK activating mutation (p.Val455Met) suffered from epilepsy and showed neurodevelopmental abnormalities. After attempting various therapeutic regimes without success, near-total pancreatectomy was suggested to parents, who asked for other options. Therefore, we proposed KD in combination with insulin-suppressing drugs. RESULTS: We administered KD for 2 years. Soon after the first six months, the patient was free of epileptic crises, presented normalization of EEG, and showed a marked recover in psychological development and quality of life. CONCLUSIONS: KD could represent an effective treatment to support brain function in selected cases of CHI. |Brain Injuries/*diet therapy/etiology/*prevention & control [MESH] |Child [MESH] |Congenital Hyperinsulinism/complications/*diagnosis/*diet therapy [MESH] |Diet, Ketogenic/*methods [MESH] |Female [MESH] |Humans [MESH]Ketogenic diet in a patient with congenital hyperinsulinism: a novel a(epmc).pdf DeepDyve Pubget Overpricing