Liver, Pancreas, and Biliary TractManganese deposition in basal ganglia structures results from both portal-systemic shunting and liver dysfunction☆,☆☆
Section snippets
Human studies
Brain samples were obtained from 12 cirrhotic patients who died in hepatic coma and 12 control subjects who had no hepatic, neurological, or psychiatric disorders at the time of death and were matched for age, sex, and autopsy delay times. In no cases had patients or control subjects received total parenteral nutrition before death. Brain dissection was performed using a ceramic knife according to a standardized dissection protocol.10 Brain samples were frozen at −80°C until time of assay.
Human studies
Patient characteristics (cirrhotics and controls) are summarized in Table 1.
Empty Cell Controls (n = 12) Empty Cell Cirrhotics (n = 12) Empty Cell Age (yr) 64.3 ± 3.7 60.6 ± 2.5 Sex (M/F) 10/2 9/3 Diagnosis Respiratory failure 3 Alcoholic cirrhosis 7 Myocardial infarction 3 B viral cirrhosis 3 Septic shock 2 C viral cirrhosis 1 Cryptogenic cirrhosis 1 Lung cancer 2 Aortic aneurysm 1 Multiorgan failure 1 Delay between death and autopsy (h) 13 ± 2 13 ± 4
Discussion
This study confirms and extends previous reports of increased pallidal manganese concentrations in cirrhotic patients.17, 18 The results also show that increased manganese in brain is a region-selective phenomenon with concentrations being highest in globus pallidus > putamen > caudate nucleus >> cerebral cortex in these patients.
It has been suggested that selective manganese deposition in the pallidum could be the cause of the high signal intensity in T1-weighted images that has been
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Address requests for reprints to: Gilles Pomier-Layrargues, M.D., Centre de recherche, Centre Hospitalier de l'Université de Montréal, Campus Saint-Luc 264, East René-Lévesque Boulevard, Montréal, Québec, Canada H2X 1P1. Fax: (514) 281-2492.
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Supported by grant MT 12392 from the Medical Research Council of Canada.