Manganese in urine

Introduction The upper limit of normal urine manganese does not exceed 0.54 mol/L (0.03 mg/L), and the manure manganese generally has 40 mg/kg as the upper limit of normal. Determination of urine and manure manganese can reflect the extent of manganese absorption in the near future. Urine manganese manure manganese is often used for the inspection of manganese poisoning. Acute manganese poisoning may cause acute corrosive gastroenteritis or irritative bronchitis or pneumonia due to oral potassium permanganate or inhalation of high concentrations of manganese oxide. Chronic manganese poisoning is mainly seen in workers who smoke long-term inhalation of manganese. The clinical manifestations are mainly extrapyramidal nervous system symptoms and neurobehavioral dysfunction and mental disorders. More opportunities to contact manganese include manganese mining and smelting, manganese electrode manufacturing, welding and wind-cutting manganese alloys, and industrial workers who manufacture and apply manganese dioxide, permanganate and other manganese compounds.

Cause

Manganese is mainly absorbed through the respiratory tract and the gastrointestinal tract, and the skin is absorbed very little. In the blood, manganese binds to 1 globulin in the blood in a bivalent form into a weak conjugate, which is distributed throughout the body, especially in the cells of the liver, kidney, pancreas, heart, lung, and brain rich in mitochondria. With the extension of time, the accumulated manganese in the body can be redistributed, and the manganese in the brain, hair and bone gradually increases accordingly; the manganese content in the brain can even exceed the stock of the liver, mostly in the lenticular nucleus and cerebellum. Most of the manganese is secreted by the gallbladder, and is slowly discharged with the feces. A small amount is excreted in the urine, and saliva, milk, and sweat glands are excreted in a small amount.

Manganese selectively acts on the thalamus, striatum, globus pallidus, substantia nigra, cerebral cortex and other brain regions. After manganese is applied to animals, manganese in the hypothalamus and striatum can be increased by about 5 times, and in other brain regions by about 1 to 2 times. In the striatum, thalamus, midbrain, there is a decrease in dopamine, an increase in high vanillic acid, an increase in Na-k-ATPase and cholinesterase activity, a change in Mg-ATPase activity, and a decrease in monoamine oxidase activity. Pathological changes can be seen in neuronal degeneration and demyelination of nerve fibers, local blood vessels congestion, thickening of the wall, thrombosis and surrounding tissue edema and lymphocyte infiltration. Vascular lesions further aggravate the damage of nerve cells and nerve fibers. Severe manganese poisoning can cause degeneration of renal tubular epithelial cells, hepatic steatosis, edema and degeneration of myocardium and muscle fibers, adrenal ischemia and partial necrosis.

The pathogenesis of chronic manganese poisoning has not yet been fully elucidated, but with neuronal degeneration, denervation of nerve fibers and decreased dopamine synthesis, and relatively enhanced excitatory effects of the acetylcholine transmitter system, neuropsychiatric symptoms and paralysis syndrome.

an examination

Related inspection

Urine routine renal function test

The diagnosis of acute manganese poisoning is not difficult. The diagnosis of chronic manganese poisoning should be based on the close history of manganese exposure and the neurological and psychiatric clinical manifestations of extrapyramidal lesions, with reference to the determination of manganese concentration in the air and the results of urinary manganese and fecal manganese. It should be differentiated from other diseases caused by tremor palsy, hepatolenticular degeneration and other diseases.

Acute manganese poisoning is common in oral administration of 1% potassium permanganate solution, causing oral mucosal erosion, nausea, vomiting, and stomach pain; 3% to 5% solution occurs in gastrointestinal mucosal necrosis, causing abdominal pain, blood in the stool, and even shock; 5 to 19 g of manganese can be fatal. Electric welding under poor ventilation conditions, inhalation of a large number of new manganese oxide fumes, sore throat, cough, shortness of breath, and sudden chills and high fever (metal smoke).

Chronic manganese poisoning usually occurs after exposure to manganese smoke and dust for 3 to 5 years or more. Early symptoms include dizziness, headache, sore limbs, weakness and heavyness of the lower extremities, excessive sweating, palpitations, and mood changes. As the disease progresses, there is an increase in muscle tone, finger tremors, hyperreflexia, lack of interest in surrounding things and emotional instability. In the later stage, typical tremor paralysis syndrome, limb muscle tension and static tremor, speech disorder, gait difficulty, etc., as well as mental symptoms such as involuntary crying, obsessive attitude and impulsive behavior.

Manganese smoke can cause pneumonia, pneumoconiosis, and conjunctivitis, rhinitis and dermatitis can still occur.

Differential diagnosis

Increased urinary phosphate excretion: Vitamin D rickets, mainly due to the renal transport mechanism of phosphorus in the distal convoluted tubules, increased urinary excretion of phosphate, decreased oleate and affects bone calcification, patients with short stature, treated with vitamin D invalid.

Pyrrolidine and acridine urine: Pyrrolidine and acridine are characteristic of pediatric renal amino aciduria. Hyperaminoaciduria is a type of metabolic disease characterized by excessive amino acid excretion in the urine, which can be divided into pre-renal, renal and mixed. The treatment effects of various types of high amino aciduria vary widely. Some can achieve good results by strictly controlling the intake of the corresponding amino acids in the diet or supplementing certain vitamins. Some even take various measures to make the plasma amino acid level close to normal. It also does not improve clinical symptoms. Renal amino aciduria is a proximal tubular reabsorption of amino acid disorders that causes large amounts of amino acids to be excreted from the urine. The amino acids excreted from the urine are mainly glycine, taurine, methyl histidine and the like. In addition, serine, threonine, leucine, phenylalanine and the like may also be discharged in a small amount.

High amino aciduria: A type of metabolic disease characterized by excessive amino acid excretion in the urine, which can be divided into pre-renal, renal and mixed. The treatment effects of various types of high amino aciduria vary widely. Some can achieve good results by strictly controlling the intake of the corresponding amino acids in the diet or supplementing certain vitamins. Some even take various measures to make the plasma amino acid level close to normal. It also does not improve clinical symptoms. Renal amino aciduria is a proximal tubular reabsorption of amino acid disorders that causes large amounts of amino acids to be excreted from the urine. The amino acids excreted from the urine are mainly glycine, taurine, methyl histidine and the like. In addition, serine, threonine, leucine, phenylalanine and the like may also be discharged in a small amount.

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