Seizure Associated With Total Parenteral Nutrition–Related Hypermanganesemia

Hsieh, Chin-Tung; Liang, Jao‐Shwann; Peng, Steven Shinn-Forng; Lee, Wang-Tso

doi:10.1016/j.pediatrneurol.2006.10.005

Cited by 35 publications

(18 citation statements)

References 13 publications

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“…It also could provide a definite marker to analyze the effect of manganism. The rise of Mn levels in the basal ganglia is found in humans, primates, and rodents in manganism [8,12,25] which is consistent with the results of our model. In the striatum studied herein, the dose-dependent accumulation of Mn had been found in the three dosage of MnCl 2 .…”

Section: Discussionsupporting

confidence: 92%

“…It has been hypothesized that manganism is associated with Glu-induced excitotoxicity. Particularly in 2007, a case report attracted us greatly, which was a 10-year-old female who had received total parenteral nutrition including Mn for 3 months because of short bowel syndrome presented with seizure [8]. It might be clinically approved that Mn neurotoxicity might be due to an excitotoxic event caused by altered Glu transportation and metabolism [9].…”

Section: Introductionmentioning

confidence: 99%

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Excitotoxicity in Rat’s Brain Induced by Exposure of Manganese and Neuroprotective Effects of Pinacidil and Nimodipine

Deng

et al. 2009

Biol Trace Elem Res

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Manganese (Mn) is an essential trace element for humans. However, manganism would be caused by excessive Mn. The mechanisms underlying excitotoxicity induced by manganism are poorly understood. As it is known to us, glutamate (Glu) is the most prevalent excitatory neurotransmitter. To determine the possible role of dysfunction of Glu transportation and metabolism in Mn-induced excitotoxicity, the rats were ip injected with different dose of MnCl(2) (0, 50, 100, and 200 micromol/kg), the levels of Mn and activities of GS, PAG, Na(+)-K(+)-ATPase, and Ca(2+)-ATPase in striatum were investigated. In addition, effect of 20.38 micromol/kg pinacidil (K(+) channel opener) or 2.4 micromol/kg nimodipine (Ca(2+) channel blocker) were studied at 200 micromol/kg MnCl(2). With dose-dependent inhibition of GS, Na(+)-K(+)-ATPase, and Ca(2+)-ATPase activities, increase of Mn levels and PAG activity were observed. Further investigation indicated that pre-treatment of pinacidil or nimodipine reversed toxic effect of MnCl(2) significantly. These results suggested that MnCl(2) could induce dysfunction of Glu transportation and metabolism by augmenting the excitotoxicity dose-dependently; pinacidil and nimodipine might antagonize manganese neurotoxicity.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Excitotoxicity in Rat’s Brain Induced by Exposure of Manganese and Neuroprotective Effects of Pinacidil and Nimodipine

Deng

et al. 2009

Biol Trace Elem Res

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“…Whilst none of the studies in which the activity of AChE was measured in the brain of rats exposed acutely or chronically to Mn developed hypercholinergic signs, there are several reports of seizures in patients receiving parenteral nutrition with hypermanganesemia (Fitzgerald et al, 1999; Komaki et al, 1999; Hsieh et al, 2007). Although cases of convulsions associated with Mn intoxication are a rare presentation of Mn intoxication, there is no satisfactory explanation for these symptoms.…”

Section: Discussionmentioning

confidence: 99%

The inhibitory effect of manganese on acetylcholinesterase activity enhances oxidative stress and neuroinflammation in the rat brain

et al. 2012

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Background Manganese (Mn) is a naturally occurring element and an essential nutrient for humans and animals. However, exposure to high levels of Mn may cause neurotoxic effects. The pathological mechanisms associated with Mn neurotoxicity are poorly understood, but several reports have established it is mediated, at least in part, by oxidative stress. Objectives The present study was undertaken to test the hypothesis that a decrease in acetylcholinesterase (AChE) activity mediates Mn-induced neurotoxicity. Methods Groups of 6 rats received 4 or 8 intraperitoneal (i.p.) injections of 25 mg MnCl2/kg/day, every 48 hours. Twenty-four hours after the last injection, brain AChE activity and the levels of F2-isoprostanes (F2-IsoPs) and F4-neuroprostanes (F4-NPs) (biomarkers of oxidative stress), as well as prostaglandin E2 (PGE2) (biomarker of neuroinflammation) were analyzed. Results The results showed that after either 4 or 8 Mn doses, brain AChE activity was significantly decreased (p<0.05), to 60 ± 16 % and 55 ± 13 % of control levels, respectively. Both treated groups exhibited clear signs of neurobehavioral toxicity, characterized by a significant (p<0.001) decrease in ambulation and rearings in open-field. Furthermore, Mn treatment caused a significant increase (p<0.05) in brain F2-IsoPs and PGE2 levels, but only after 8 doses. In rats treated with 4 Mn doses, a significant increase (p<0.05) in brain F4-NPs levels was found. To evaluate cellular responses to oxidative stress, we assessed brain nuclear factor-erythroid 2 p45-related factor 2 (Nrf2) and Mn-superoxide dismutase (Mn-SOD, SOD2) protein expression levels. A significant increase in Mn-SOD protein expression (p<0.05) and a trend towards increased Nrf2 protein expression was noted in rat brains after 4 Mn doses vs. the control group, but the expression of these proteins was decreased after 8 Mn doses. Taken together, these results suggest that the inhibitory effect of Mn on AChE activity promotes increased neuronal oxidative stress and neuroinflammatory biomarkers.

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“…Although increased whole blood or plasma Mn levels are fairly common in parenteral nutrition, overt clinical signs and symptoms are, however, not observed in all patients with hypermanganesemia. Although chronic overexposure to Mn in parenteral nutrition patients has been recognized as a problem for some time now, there have been further reports of elevated Mn levels since Dickerson's review [4,7,11 ,[16][17][18][19][20][21]22 ,23 ] (Table 1). High Mn levels are particularly problematic in the paediatric setting [16,17,19,24] and in long-term HPN patients [18,[25][26][27]; however, hypermanganesemia has also been reported in acute care [7,20].…”

Section: Reports Of Elevated Manganese Levels and Toxicity In Parentementioning

confidence: 99%

Is manganese an essential supplement for parenteral nutrition?

Hardy

Gillanders

Hardy

2008

Current Opinion in Clinical Nutrition and Metabolic Care

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Seizure Associated With Total Parenteral Nutrition–Related Hypermanganesemia

Cited by 35 publications

References 13 publications

Excitotoxicity in Rat’s Brain Induced by Exposure of Manganese and Neuroprotective Effects of Pinacidil and Nimodipine

Excitotoxicity in Rat’s Brain Induced by Exposure of Manganese and Neuroprotective Effects of Pinacidil and Nimodipine

The inhibitory effect of manganese on acetylcholinesterase activity enhances oxidative stress and neuroinflammation in the rat brain

Is manganese an essential supplement for parenteral nutrition?

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