Sorted By Test Name - Mayo Medical Laboratories

MNRU
86154
FMNRB
57196
days) should be used.
Reference Values:
4.7-18.3 ng/mL
Clinical References: 1. Jiang Y, Zheng W, Long L, et al: Brain magnetic resonance imaging and
manganese concentrations in red blood cells of smelting workers: search for biomarkers of manganese
exposure. NeuroToxicology 2007;28:126-135 2. Guilarte T, Chen M, McGlothan J, et al: Nigrostriatal
dopamine system dysfunction and subtle motor deficits in manganese-exposed non-human primates. Exp
Neurol 2006;202:381-390 3. Choi Y, Park J, Park N, et al: Whole blood and red blood cell manganese
reflected signal intensities of T1-weighted magnetic resonance images better than plasma manganese in
liver cirrhotics. J Occup Health 2005;47:68-73 4. Sanotsky Y, Lesyk R, Fedoryshyn L, et al: Manganic
encephalopathy due to "Ephedrone" abuse. Mov Disord 2007;22:1337-1343
Manganese, Random, Urine
Clinical Information: Manganese (Mn) is an essential trace element with many industrial uses.
Manganese is the 12th most abundant element in the earth's crust and is used predominantly in the
production of steel. These industrial processes cause elevated environmental exposures to airborne
manganese dust and fumes, which in turn have lead to well-documented cases of neurotoxicity among
exposed workers. Mining and iron and steel production have been implicated as sources of exposure.
Inhalation is the primary source of entry for manganese toxicity. Signs of toxicity may appear quickly or
not at all; neurological symptoms are rarely reversible. Manganese toxicity is generally recognized to
progress through 3 stages. Levy describes these stages. "The first stage is a prodrome of malaise,
somnolence, apathy, emotional lability, sexual dysfunction, weakness, lethargy, anorexia, and headaches.
If there is continued exposure, progression to a second stage may occur, with psychological disturbances,
including impaired memory and judgment, anxiety, and sometimes psychotic manifestations such as
hallucinations. The third stage consists of progressive bradykinesia, dysarthrian axial and extremity
dystonia, paresis, gait disturbances, cogwheel rigidity, intention tremor, impaired coordination, and a
mask-like face. Many of those affected may be permanently and completely disabled."(1) Few cases of
manganese deficiency or toxicity due to ingestion have been documented. Only 1% to 3% manganese is
absorbed via ingestion, while most of the remaining manganese is excreted in the feces. As listed in the
United States National Agriculture Library, manganese adequate intake is 1.6 mg/day to 2.3 mg/day for
adults. This level of intake is easily achieved without supplementation by a diverse diet including fruits
and vegetables, which have higher amounts of manganese than other food types. Patients on a long-term
parenteral nutrition should receive manganese supplementation and should be monitored to ensure that
circulatory levels of manganese are appropriate.
Useful For: Monitoring manganese exposure Nutritional monitoring Clinical trials
Interpretation: Manganese in urine represents the excretion of excess manganese from the body, and
may be used to monitor exposure or excessive nutritional intake. Reference values have not been
established for random urine specimens. Assessment of overexposure may require collection of a blood
specimen or a 24-hour urine specimen.
Reference Values:
0-15 years: not established
> or =16 years: 0.1-0.9 mcg/L
Clinical References: 1. Levy BS, Nassetta WJ: Neurologic effects of Manganese in humans: A
review. Int J Occup Environ Health Apr/Jun 2003;9(2):153-163 2. Paschal DC, Ting BG, Morrow JC, et.
at. Trace metals in urine of United States residents: Reference range concentrations. Environmental
Research 1998;7:53-59.
Manganese, Red Blood Cell
Reference Values:
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