Selenium deficiency
Introduction
Introduction Selenium is one of the essential trace elements in the human body. It is a strong antioxidant and its effect is similar to that of vitamin E, but it is more effective. Selenium can be used to regulate the rate of redox reactions in the body, affect the metabolism and activity of certain important enzymes, and regulate the absorption and consumption of vitamins A, C, E, and K in the body. Selenium is an important component of glutathione peroxidase in the body, which has a protective effect on the structure of the cell membrane and promotes the immunity of the body. Selenium deficiency is an important cause of Keshan disease. Selenium deficiency can induce liver necrosis, and selenium deficiency can induce cardiovascular disease. People with mild or moderate selenium deficiency, signs and symptoms are not obvious.
Cause
Cause
Selenium is an important trace element that maintains the normal physiological functions of the human body. Selenium is absorbed by the human body and absorbed by the intestines. It is distributed in organs such as liver, spleen, kidney and heart. Selenium is combined with protein and transported to tissues through blood. Selenium participates in glutathione peroxidase and can be catalyzed. Reduced glutathione is converted to oxidized glutathione to prevent damage to cells by hydrogen peroxide and oxidized lipids.
Examine
an examination
Related inspection
Determination of trace elements in trace elements in humans
Selenium deficiency can cause white muscle disease in animals, and selenium and human selenium load levels in human environment have a certain correlation with the incidence of Keshan disease. Supplementing a certain amount of selenium to the ward can reduce the incidence of Keshan disease. In addition, selenium has been shown to have anti-multiple carcinogens in animal experiments. However, excessive selenium can cause selenium poisoning, hair loss, dislocation and the like.
Diagnosis
Differential diagnosis
Acute type needs to be differentiated from acute myocarditis, acute myocardial infarction, acute gastritis, and biliary ascariasis.
The slow type needs to be differentiated from dilated cardiomyopathy (DCM), peripartum cardiomyopathy, coronary heart disease, pericarditis (chronic) and rheumatic heart disease.
Sub-acute type need to be the same, chronic glomerulonephritis or nephropathy, bronchial pneumonia (combined heart failure), endocardial fibroelastosis, pericarditis.
Potential type needs to be associated with focal myocarditis, hypertrophic non-obstructive cardiomyopathy, and differentiation of cardiac neurosis.
