Can rickets be cured?

Written by Li Jiao Yan
Neonatology
Updated on April 15, 2025
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Can rickets be cured? Rickets is a type of nutritional disease caused by a deficiency of vitamin D, which disrupts the body's calcium and phosphorus metabolism and leads to abnormal bone development. The common form is nutritional vitamin D deficiency rickets. This type of disease is self-limiting and can be cured. Once children engage in sufficient outdoor activities and supplement their vitamin D levels, they can be completely cured. There are also some special cases, such as severe liver and kidney diseases caused by vitamin D deficiency, and some genetic diseases. These diseases require treatment to promote the absorption of vitamin D. However, for genetic diseases, treating rickets with vitamin D is ineffective, and these cases are more difficult to treat. For liver and kidney diseases, if the condition can be effectively controlled, they can also be cured.

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Written by Li Jiao Yan
Neonatology
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Why does rickets cause sweating?

Rickets is a chronic, nutritional disease characterized by skeletal lesions due to a deficiency of vitamin D in the body, leading to disturbances in calcium and phosphorus metabolism. It is primarily caused by a lack of vitamin D, which can increase neural excitability. Research shows that the vitamin D metabolite, 1,25-dihydroxyvitamin D3, is not only an essential nutrient but also a precursor to hormones. It is potentially related to various cells including those in the thyroid, pancreas, stomach, brain, and those involved with calcium balance, as well as the immune, endocrine, reproductive systems, skin, and tumors. A deficiency in vitamin D can increase myocardial excitability and lead to symptoms like excessive sweating.

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Written by Li Jiao Yan
Neonatology
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Rickets lacks what element

Rickets, also known as Vitamin D deficiency rickets, is caused by a deficiency in Vitamin D, which leads to abnormal calcium and phosphorus metabolism in the body. Calcium salts cannot deposit normally in the growing parts of bones, resulting in incomplete mineralization of bone tissue during growth phases and ultimately leading to skeletal abnormalities. This condition is characterized by a chronic nutritional disease closely related to lifestyle. The main symptoms are a deficiency of Vitamin D levels in the blood, followed by low levels of calcium and phosphorus, meaning that the levels of these elements significantly drop. The primary treatment for rickets involves supplementing Vitamin D, thus the main cause of rickets is due to a deficiency of this vitamin.

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Written by Li Jiao Yan
Neonatology
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Rickets symptoms

Rickets, also known as nutritional vitamin D deficiency rickets, is a chronic nutritional disease in children caused by inadequate vitamin D in their bodies, leading to disorders in calcium and phosphorus metabolism and characterized by changes in the growth plates. Its manifestation varies with different ages. In infants under six months, especially those under three months, symptoms often include increased nervous excitability, such as being easily irritable, restless, sweating, and shaking their heads due to scalp irritation. As the condition progresses in children under six months, the primary changes are seen in the skull; the edges of the anterior fontanelle are softer, and the skull is thinner. After six months, the softening of the skull disappears, but there can be ping-pong ball-like changes around the skull, leading to a box-shaped head from seven to eight months. Gradually, beading changes form, most notably around the 7th to 10th ribs. Around the age of one, children can develop a pigeon chest deformity, and in severe cases of rickets, a horizontal depression forms at the lower edge of the thoracic cage, known as the costal groove or Harrison's groove. Due to bone softening and muscle and joint laxity, when the child begins to stand and walk, the legs may become bow-legged or X-shaped, and in severe cases, can develop into 'K'-shaped leg deformities. Once the child starts to sit and stand, general ligament laxity can cause spinal deformities. Severe hypophosphatemia leads to muscle carbohydrate metabolism disorder, resulting in overall muscle laxity, decreased muscle tone, and subsequently reduced muscle strength.

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Written by Li Jiao Yan
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How should children with rickets supplement calcium?

Rickets is a nutritional disease caused by a deficiency in vitamin D, leading to disturbances in calcium and phosphorus metabolism in the body, which results in abnormal bone development. It is mainly due to a lack of vitamin D, so the primary treatment is supplementing with vitamin D. Dairy is a reliable source of calcium nutrition for infants, and generally, it is not necessary to supplement calcium for the treatment of rickets; attention should be paid to supplementing with vitamin D according to the severity of the condition, and spending more time in the sun. For children who have started eating complementary foods, or older children, it is generally recommended to fully supplement vitamin D levels, spend more time in the sun during summer, and consume high-protein nutrients. Additionally, eating more vegetables and appropriately supplementing with calcium supplements in the winter is advised. The dosage should be based on the child's internal levels of calcium and phosphorus, with calcium supplementation adjusted accordingly.

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Written by Li Jiao Yan
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How is rickets diagnosed?

Rickets is a chronic nutritional disease caused by a deficiency in vitamin D, which leads to a disruption in calcium and phosphorus metabolism, resulting in abnormal bone development. Typically, the initial symptoms of rickets are most commonly seen 2-3 months after birth. At this stage, affected children often show neurological symptoms such as excessive sweating unrelated to the season, irritability, particularly in infants under three months old who can become easily agitated, and exhibit straining as if constipated, but these are not specific symptoms of rickets. Early diagnosis generally requires specific tests such as blood biochemistry to check the levels of 125 dihydroxy vitamin D3, as well as calcium and phosphorus levels in the blood, and to see if there is any change in serum alkaline phosphatase. The active phase is mainly characterized by skeletal changes, such as early signs of enlarged fontanelles or delayed closure, late teething, and sometimes a softening of the skull resembling a ping-pong ball, gradually leading to a square skull. Subsequently, changes like pigeon chest or noticeable deformities in the lower limbs such as X-shaped legs, O-shaped legs, or K-shaped legs may appear. Sometimes, there may also be curvature of the spine, with occasional scoliosis. These obvious skeletal changes make the condition more recognizable, though the initial presentations are not very typical, necessitating related biochemical blood tests.