Cases reported "Manganese Poisoning"

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1/7. manganese intoxication during total parenteral nutrition: report of two cases and review of the literature.

    We report two cases of manganese (Mn) intoxication during total parenteral nutrition including manganese (Mn). Both patients showed parkinsonism with psychiatric symptoms and elevated serum Mn levels. T1-weighted magnetic resonance images (MRI) revealed symmetrical high intensity lesions in the globus pallidus. Discontinuation of Mn supplementation and levodopa treatment improved the symptoms and MRI abnormalities in the both patients. Thus, careful attention should be paid to the long-term intravenous administration of Mn.
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2/7. tremor and seizures associated with chronic manganese intoxication.

    tremor and seizures developed in a 2-year-old girl receiving total parenteral nutrition. T1-weighted images on MRI revealed areas of hyperintensity in the basal ganglia, brainstem and cerebellum. blood manganese was elevated. The symptoms and MRI abnormalities disappeared after withdrawal of manganese administration. The recommendation of daily parenteral manganese intake was discussed.
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3/7. manganese intoxication during intermittent parenteral nutrition: report of two cases.

    BACKGROUND AND methods: The administration of trace elements is thought to be needed in patients receiving long-term parenteral nutrition. Recently, manganese intoxication or deposition was documented in such patients. We report two cases of manganese intoxication during intermittent parenteral nutrition including manganese. manganese had been administered for 4 years at a frequency of one or two times per week in one case and for 5 years at a frequency of one or two times per month in the other case. Both cases showed mild symptoms with headache and dizziness. One case had mild hepatic dysfunction and the other did not. The whole-blood manganese level increased in one case, but not in the other case. T1-weighted magnetic resonance images revealed symmetrical high-intensity areas in basal ganglia and thalamus in both cases. After the administration of manganese was stopped, these symptoms all disappeared and the magnetic resonance images abnormalities gradually improved in both patients. Mild long-term manganese intoxication is thus considered to occur regardless of the frequency of using a manganese supplement. CONCLUSIONS: patients should be carefully monitored when receiving long-term parenteral nutrition including manganese, even when the manganese dose is small and the frequency of receiving a manganese supplement is low.
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4/7. manganese levels in a jaundiced long-term total parenteral nutrition patient: potentiation of haloperidol toxicity? Case report and literature review.

    manganese is vital in human nutrition. When oral intake is precluded, the recommended parenteral supplementation is 0.15 to 0.8 mg/day. manganese is excreted primarily in the bile; during cholestasis, serum manganese levels may rise, and manganese toxicity ensue. Neuropsychiatric symptoms are prominent. Phenothiazine-derivative drugs may potentiate manganese toxicity. serum or whole blood manganese levels should guide manganese therapy in jaundiced patients.
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5/7. Determination of manganese in human brain samples.

    A method is presented for the determination of manganese (Mn) in human tissue samples (especially brain) by graphite furnace atomic absorption spectrophometry (GFAAS). After complete digestion by a mixture of concentrated nitric acid (HNO3)/concentrated perchloric acid (HClO4) (50:50, v/v), the samples are assayed on a Perkin-Elmer 5100 PC apparatus, equipped with transversal graphite tubes and a Mn-specific hollow cathode lamp. The furnace conditions are as follows (for each step: temperature (degree C)/ramp (s)/duration (s)) dry 120/1/40; char 1200/5/10; atomization 2250/0/4; pyrolysis 2400/1/1. Zeeman correction is employed. The method is linear over the range 0.05 to 5.00 micrograms/g wet tissue, and the limit of detection for Mn is about 0.01 microgram/g wet tissue. This simple and rapid method may be of value for the post-mortem assessment of Mn accumulation in brain structures due to occupational or iatrogenic exposure. An application is presented in which elevated levels of Mn were determined in the brain samples of a 63-year-old female deceased after long-term total parenteral nutrition involving Mn supplementation.
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6/7. Dyskinesia from manganism in a hepatic dysfunction patient.

    A 14-year-old boy came to the neurological clinic because of involuntary movement. He represented a case of common variable hypogammaglobulinemia, with hepatosplenomegaly noted for 5 years and jaundice for 1 month. Neurological and laboratory examinations revealed choreoathetosis and hyperbilirubinemia, hypoalbuminemia, increased hepatic aminotransferase, and decreased indocyanine green clearance; as well as increased signal change over the globus pallidus, subthalamic area, internal capsule, tegmentum, brain stem and pituitary gland revealed by a brain magnetic resonance (T1-weighted) imaging study. A manganese study confirmed high body manganese loading. trihexyphenidyl administration ameliorated the dyskinesia; however, the patient died from hepatic failure later. Though rare in incidence, manganese intoxication should be considered in cases with dyskinesia and the characteristic brain MRI findings. Even if no environmental exposure is involved, total parenteral nutrition, porto-systemic shunt and chronic hepatic dysfunction could lead to a heavy manganese load resulting in symptomatic manifestation.
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7/7. Neurologic disorders due to brain manganese deposition in a jaundiced patient receiving long-term parenteral nutrition.

    BACKGROUND: Neurologic and radiologic disorders have been reported in patients receiving long-term parenteral nutrition (PN). On the basis of elevated serum manganese levels, some of these abnormalities have been attributed to manganese intoxication. Alterations of the basal ganglia signal intensity on T1-weighted magnetic resonance images (MRIs) have been previously reported, but the precise nature of these alterations remains controversial although the deposition of manganese has been suggested in patients with chronic hepatic encephalopathy due to liver failure. methods: We report the case of a patient who was receiving PN and exhibited a chronic cholestasis. Neurologic disorders appeared after several months of PN, when a hypersignal in the basal ganglia and white matter was found on T1-weighted MRIs of the brain in association with elevated serum and manganese levels. RESULTS: Elevated autopsic concentrations of manganese were found in the radiologic abnormal cerebral areas. CONCLUSIONS: Our observation is the first demonstration of a relationship between high intracerebral manganese levels, radiologic abnormalities, and neurologic disorders during long-term PN. Moreover, serum manganese levels are not a good indicator of cerebral levels. In fact, in our patient, serum manganese levels returned to normal, whereas those of cerebral manganese remained increased.
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