Manganese intoxication during total parenteral nutrition

Ejima, A; Imamura, Toru; Nakamura, Shozo; Saito, Hiroshi; Matsumoto, Kazuya; Momono, Satoshi

doi:10.1016/0140-6736(92)90109-g

Cited by 134 publications

(62 citation statements)

References 7 publications

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“…Furthermore, the characteristic high signals are also frequently observed in asymptomatic workers exposed to Mn 3) . A similar MRI pattern has been observed in patients receiving total parenteral nutrition, because of excessive Mn intake 4,5) . Chronic liver failure is also associated with increased signal intensities in the GP using T1-weighted MRI 6,7) .…”

mentioning

confidence: 52%

Whole Blood and Red Blood Cell Manganese Reflected Signal Intensities of T1‐Weighted Magnetic Resonance Images better than Plasma Manganese in Liver Cirrhotics

Choi¹,

Park²,

Park³

et al. 2005

Journal of Occupational Health

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Whole Blood and Red Blood Cell Manganese Reflected Signal Intensities of T1-Weighted Magnetic Resonance Images better thanPlasma Manganese in Liver Cirrhotics: Younghee CHOI, et al. Department of Occupational and Environmental Medicine, Ulsan University Hospital, South Korea-We examined whole blood (MnB), red blood cell (MnRBC), plasma (MnP) and urinary Mn (MnU) concentrations in 22 liver cirrhotics and 10 healthy controls to evaluate Mn concentration in which a fraction of biological samples best reflects pallidal signal intensities (pallidal index; PI) on T1-weighted magnetic resonance images (MRI) in liver cirrhotics. Increased signal intensity in the globus pallidus was observed in 18 (81.8%) of the 22 patients with liver cirrhosis. In a transplanted patient, increased pallidal signals also resolved as his liver function tests normalized after liver transplantation. There were significant correlations between MnB/MnRBC and PI (ρ=0.529, ρ=0.573, respectively) in liver cirrhotics, although no significant correlation was observed between MnP/MnU and PI. According to a multiple linear regression, MnB and MnRBC reflected the signal intensities of T1-weighted MRI better than MnP or MnU. (J Occup Health 2005; 47: 68-73)

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confidence: 52%

Whole Blood and Red Blood Cell Manganese Reflected Signal Intensities of T1‐Weighted Magnetic Resonance Images better than Plasma Manganese in Liver Cirrhotics

Choi¹,

Park²,

Park³

et al. 2005

Journal of Occupational Health

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“…Regardless of the administration route of MnCl 2 , an increasing signal intensity on MRI is observed in the caudate nucleus, globus pallidus, substantia nigra, ventromedial hypothalamus, and pituitary gland [23]. Even in man, a hyperintense globus pallidus was found in patients receiving long-term total parenteral nutrition therapy that included manganese [24] and in workers exposed to manganese [25][26][27], with these hyperintensities diminishing after cessation of the manganese exposure [25,28,29]. Intravenous administration or inhalation of manganese causes manganese deposition in the brain, but the oral intake of manganese rarely results in manganese deposition.…”

Section: Manganesementioning

confidence: 99%

Contribution of metals to brain MR signal intensity: review articles

et al. 2016

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“…Brain Mn analysis in non-human primates Shinotoh et al 1995) and in patients with chronic liver failure (Klos et al 2006;Krieger et al 1995) has proven that Mn is the cause of the abnormal signal, but the relationship between that signal and onset of symptoms is still unclear. The MRI signal tends to disappear 5 months-1 year after cessation of exposure (Newland et al 1989;Ejima et al 1992;Kim et al 1999;Nelson et al 1993), but symptoms can persist and progress (Huang et al 1993;Nelson et al 1993) in the absence of treatment to remove Mn.…”

Section: Diagnosismentioning

confidence: 99%

Manganese and its Role in Parkinson’s Disease: From Transport to Neuropathology

et al. 2009

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Abstract:The purpose of this review is to highlight recent advances in the neuropathology associated with Mn exposures. We commence with a discussion on occupational manganism and clinical aspects of the disorder. This is followed by novel considerations on Mn transport (see also chapter by Yokel, this volume), advancing new hypotheses on the involvement of several transporters in Mn entry into the brain. This is followed by a brief description of the effects of Mn on neurotransmitter systems that are putative modulators of dopamine (DA) biology (the primary target of Mn neurotoxicity), as well as its effects on mitochondrial dysfunction and disruption of cellular energy metabolism. Next, we discuss inflammatory activation of glia in neuronal injury and how disruption of synaptic transmission and glial-neuronal communication may serve as underlying mechanisms of Mn-induced neurodegeneration commensurate with the cross-talk between glia and neurons. We conclude with a discussion on therapeutic aspects of Mn exposure. Emphasis is directed at treatment modalities and the utility of chelators in attenuating the neurodegenerative sequelae of exposure to Mn. For additional reading on several topics inherent to this review as well as others, the reader may wish to consult Aschner and Dorman (Toxicological Review 25:147-154, 2007) and Bowman et al. (Metals and neurodegeneration, 2009).

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Manganese intoxication during total parenteral nutrition

Cited by 134 publications

References 7 publications

Whole Blood and Red Blood Cell Manganese Reflected Signal Intensities of T1‐Weighted Magnetic Resonance Images better than Plasma Manganese in Liver Cirrhotics

Whole Blood and Red Blood Cell Manganese Reflected Signal Intensities of T1‐Weighted Magnetic Resonance Images better than Plasma Manganese in Liver Cirrhotics

Contribution of metals to brain MR signal intensity: review articles

Manganese and its Role in Parkinson’s Disease: From Transport to Neuropathology

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