2000
DOI: 10.1016/s0022-3468(00)90212-4
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Manganese deposits in patients with biliary atresia after hepatic porto-enterostomy

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Cited by 18 publications
(21 citation statements)
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“…In previous investigations, whole blood Mn concentrations were reported to be 1.5±11.1 lg/dl in patients with chronic hepatic encephalopathy [8], and 1.2±9.6 lg/ dl in patients with biliary atresia who had undergone hepatic porto-enterostomy [6]. Because Mn values in our congenital PSVS cases with normal liver function were much less elevated, we believe that in general the degree of Mn elevation is related to severity of hepatic dysfunction.…”
Section: Discussionmentioning
confidence: 48%
“…In previous investigations, whole blood Mn concentrations were reported to be 1.5±11.1 lg/dl in patients with chronic hepatic encephalopathy [8], and 1.2±9.6 lg/ dl in patients with biliary atresia who had undergone hepatic porto-enterostomy [6]. Because Mn values in our congenital PSVS cases with normal liver function were much less elevated, we believe that in general the degree of Mn elevation is related to severity of hepatic dysfunction.…”
Section: Discussionmentioning
confidence: 48%
“…Although ammonia is widely regarded to play a key role in the development of hepatic encephalopathy, 22 studies have shown that the severity of hepatic encephalopathy is not directly linked to ammonia concentrations 23,24 . This finding has lead to the suggestion that other substances and metabolic abnormalities are important in the pathogenesis of hepatic encephalopathy including Mn‐related neurological dysfunction 15,20,25 . A direct relationship among blood Mn concentration, MRI hyperintensity consistent with Mn deposition, and severity of encephalopathic score in humans has been identified 20,26…”
mentioning
confidence: 90%
“…Hypermanganesemia can occur as a result of liver disease and decreased biliary excretion (Ikeda et al, 2000), as bile is the major excretory route for Mn. Patients on long-term PN may develop biliary stasis or obstructive jaundice (Angsten et al, 2012; Fallon et al, 2010; Graham et al, 1984; Jones et al, 1993; Pierro et al, 1989; Sax et al, 1986; Shattuck et al, 1993), resulting in excess tissue Mn accumulation (Alves et al, 1997; Fell et al, 1996; Ikeda et al, 2000; Witzleben et al, 1968).…”
Section: Modulating Factors Of Mn Induced Neurotoxicitymentioning
confidence: 99%
“…Patients on long-term PN may develop biliary stasis or obstructive jaundice (Angsten et al, 2012; Fallon et al, 2010; Graham et al, 1984; Jones et al, 1993; Pierro et al, 1989; Sax et al, 1986; Shattuck et al, 1993), resulting in excess tissue Mn accumulation (Alves et al, 1997; Fell et al, 1996; Ikeda et al, 2000; Witzleben et al, 1968). Elevated Mn levels have also been seen in patients suffering from chronic liver failure (with inability to excrete Mn via the biliary system) and undergoing PN supplementation (McKinney et al, 2004; Mehta and Reilly, 1990).…”
Section: Modulating Factors Of Mn Induced Neurotoxicitymentioning
confidence: 99%