Zinc is one of the essential trace elements in the body, with its content second only to iron. Zinc is present in all tissues, with particularly high concentrations in the iris, retina, choroid, and prostate. The majority of zinc in the blood is intracellular, with white blood cells containing 25 times more zinc than red blood cells, and a small portion is found in plasma. Almost all plant and animal foods contain zinc, but the absorption rate of zinc from plant-based foods is lower than that from animal-based foods. The dietary absorption rate of zinc is generally 20–30%. Zinc is absorbed in the small intestine and primarily excreted through the intestines, with a small amount excreted through urine and sweat. The main physiological functions of zinc include:

1. Participation in the composition of various metalloenzymes in the human body. Among the six major enzyme classes in the body, each contains zinc-dependent enzymes, which play important roles in tissue respiration and the metabolism of proteins, fats, sugars, and nucleic acids;
2. Promotion of growth, development, and tissue regeneration. Zinc-deficient animals may exhibit growth retardation or dwarfism, fetal malformations, or impaired wound healing;
3. Enhancement of appetite. Gustin, which contains zinc, maintains taste perception and promotes appetite;
4. Maintenance of dark adaptation. Zinc is involved in the function of retinol reductase and the synthesis of retinol-binding protein. Zinc deficiency can affect the synthesis of photosensitive substances and the mobilization of vitamin A in the liver, leading to night blindness;
5. Promotion of the development of sexual organs and functions;
6. Maintenance of skin health;
7. Participation in immune function. Zinc deficiency affects the replication of immune response cells and weakens immune function. The daily dietary zinc requirements are: 3–5 mg for infants, 10–15 mg for children and adolescents, and 20 mg for pregnant and lactating women.

bubble_chart Clinical Manifestations

1. Slowed growth rate or growth cessation is the primary manifestation of zinc deficiency in children. In severe cases, it may present as zinc-deficient dwarfism.
2. Delayed sexual maturation, underdeveloped reproductive organs, and incomplete development of secondary sexual characteristics. Zinc deficiency in pregnant women can lead to fetal malformations.
3. Reduced taste sensitivity, loss of appetite, and the occurrence of pica.
4. Impaired dark adaptation, which can occur even when vitamin A reserves are present.
5. Skin lesions are characteristically distributed, primarily around the mouth and anus, but can also occur on other parts of the body. The lesions often manifest as erythema, cystic bullae, or hyperkeratotic patches. Additionally, skin wound healing is slow.
6. Increased susceptibility to bacterial and candida infections due to reduced immunity caused by zinc deficiency.
7. Other severe zinc deficiencies can affect brain function, presenting as irritability, drowsiness, depression, or poor learning ability. It may also lead to gingivitis, glossitis, conjunctivitis, alopecia areata, nail dystrophy, and other eye injuries such as photophobia and keratopathy.

bubble_chart Auxiliary Examination

1. Serum zinc levels decrease (the normal lower limit is 9.83–12.03 μmol/L), and plasma zinc levels also decrease (normal values are 5–15% lower than serum zinc). However, low blood zinc does not absolutely indicate zinc deficiency. For example, the low blood zinc observed during infection primarily reflects changes in zinc distribution within the body rather than the body's zinc nutritional status. Additionally, blood zinc concentrations vary diurnally and postprandially, making the interpretation of normal values somewhat challenging.
2. Whether low hair zinc concentration (normal value: 125–250 μg/g) can serve as an indicator of zinc deficiency has long been debated, so it is only used as a reference indicator.
3. Taste tests can be conducted using solutions of varying concentrations of sucrose (sweet), hydrochloric acid (sour), urea (bitter), and salt (salty). In zinc deficiency, taste acuity decreases and can return to normal after treatment, though the recovery of bitter taste perception is relatively poor.
4. A decline in zinc-dependent enzyme activity, such as serum alkaline phosphatase and erythrocyte carbonic anhydrase, can aid in diagnosis. Reduced retinol (vitamin A) binding protein levels also support the diagnosis. However, the specificity of these diagnostic indicators is not strong unless the effects of zinc supplementation are observed under controlled conditions.
5. Other findings: Erythrocyte zinc levels generally remain unchanged in zinc deficiency. Using leukocyte zinc as a routine indicator is still challenging. Salivary zinc and urinary zinc concentrations are also not ideal indicators.

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bubble_chart Diagnosis

Medical History

1. History of inadequate dietary zinc intake. Such as insufficient animal-based foods, low zinc content in infant formula, long-term use of synthetic diets or intravenous nutrition without zinc supplementation.
2. History of zinc malabsorption. For example, high-cereal diets reduce zinc absorption; intestinal diseases such as enteritis, steatorrhea, and disaccharide intolerance leading to zinc malabsorption; excessive iron intake inhibiting zinc absorption.
3. History of excessive zinc excretion. Such as increased zinc excretion due to chronic bleeding, excessive sweating in high temperatures, intestinal stoma outflow, burn exudates, liver disease, or chronic kidney disease.
4. History of increased zinc requirements. Such as rapid growth, wound healing, pregnancy, lactation, etc.
5. History of congenital disorders of zinc metabolism. For example, acrodermatitis enteropathica, a lethal zinc deficiency caused by partial congenital intestinal zinc absorption blockage.
6. History of using chelating agents like penicillamine or histidine.
7. Premature infants, due to multiple factors such as immature zinc absorption function, higher urinary zinc loss, and rapid growth, often struggle to achieve zinc balance shortly after birth.

bubble_chart Treatment Measures

1. Oral zinc salts: Generally, elemental zinc can be administered orally at 1mg/(kg·d), with a maximum dose of 20–30mg/d. If there is excessive zinc loss or malabsorption, the dose may be appropriately increased. Commonly used zinc salts include zinc sulfate, zinc gluconate, and zinc acetate. One milligram of elemental zinc is equivalent to 4.4mg of zinc sulfate, 7mg of zinc gluconate, or 2.8mg of zinc acetate.
2. Intravenous zinc: The recommended maintenance dose of zinc in intravenous nutrition is 50–100μg/(kg·d), and premature infants may be given 400μg/(kg·d). If there is excessive zinc loss, the dose can be increased. The commonly used intravenous zinc preparation is zinc chloride, where 1mg of elemental zinc is equivalent to 2.1mg of zinc chloride.
3. Topical zinc: Zinc can be absorbed through the skin. Zinc preparations are used for burns, chronic ulcers, and open wounds, serving both to supplement zinc and provide local antibacterial and anti-inflammatory effects.
4. Dietary zinc supplementation: In addition to medicinal zinc supplementation, long-term dietary zinc supplementation should be adopted to prevent recurrence after recovery. Foods with the highest zinc content include oysters and herring, followed by meat, liver, eggs, mussels, cuttlefish, Rhubarb Rhizoma fish, and cheese.
5. Preventing zinc toxicity: Medicinal zinc should not be overdosed, as excessive intake can lead to acute zinc poisoning, manifesting as diarrhea, vomiting, and drowsiness. Long-term overdose may cause anemia due to copper deficiency and a decrease in plasma high-density lipoprotein cholesterol levels. Excessive intravenous zinc administration can result in oliguria, hypotension, diarrhea, vomiting, jaundice, and pulmonary edema. Autopsy findings may reveal pathological changes of acute tubular necrosis.