Does rickets cause dry skin and an absence of sweating?

Written by Tong Peng
Pediatrics
Updated on April 05, 2025
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Rickets does not cause dry skin or an absence of sweat. Rickets is a disorder of calcium and phosphorus metabolism caused by a deficiency in vitamin D, and it may also be associated with bone deformities. In infants, it often presents with neurological symptoms such as being easily startled during sleep, increased night sweats, and a variety of symptoms including bald patches on the back of the head. However, an absence of sweating is often a symptom of sweat gland disorders and is not necessarily related to rickets. In some cases, babies sweat less because their sweat glands are underdeveloped, so if a child with rickets has symptoms of dry skin, they are not particularly prominent. If rickets is confirmed, it is crucial to actively supplement vitamin D, spend more time in the sun, and engage in outdoor exercise to facilitate the body's natural synthesis of vitamin D. Severe cases require oral or injected high doses of vitamin D to prevent the condition from worsening and causing bone deformities.

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Written by Li Jiao Yan
Neonatology
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Rickets Causes

Rickets, fully termed as nutritional vitamin D deficiency rickets, is a chronic systemic nutritional disease characterized by epiphyseal lesions, caused by insufficient vitamin D in children, leading to disordered calcium and phosphate metabolism. The main causes of the disease include insufficient perinatal vitamin D, particularly during the prenatal and postnatal periods, as well as factors like severe maternal malnutrition, liver and kidney diseases, chronic diarrhea, prematurity, and having twins, which may lead to inadequate levels of vitamin D storage in the body. Additionally, insufficient sunlight exposure, such as children spending prolonged periods indoors, blocks sunlight, as ultraviolet rays cannot pass through glass. Ultraviolet light aids in the synthesis of endogenous vitamin D; lack of exposure can also reduce vitamin D levels. Another factor is rapid growth rates, and fourthly, insufficient dietary supplementation of vitamin D along with some diseases that affect the absorption of vitamin D, like gastrointestinal or liver and biliary diseases.

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Written by Li Jiao Yan
Neonatology
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Which department should I go to for rickets?

Rickets, known as nutritional vitamin D deficiency rickets, is a chronic nutritional disease characterized by skeletal lesions, caused by a deficiency of vitamin D in the body leading to disturbed calcium and phosphate metabolism. In the early stages of rickets, it is primarily due to insufficient levels of vitamin D, which then leads to abnormal calcium and phosphate metabolism; at this stage, it is necessary to consult the endocrinology department to correct it timely. If rickets has already caused developmental deformities of the bones, orthopedic consultation is required for corrective treatment. For instance, if children exhibit pigeon chest, or noticeable bow legs or knock knees, they need to see an orthopedic specialist.

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Written by Zeng Hai Jiang
Pediatrics
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Is a square skull definitely rickets?

Square skull is not necessarily rickets; square skull can be seen in rickets and congenital syphilis, especially common in rickets. It is often seen in children with rickets older than 8-9 months, due to a lack of calcium in the bones which leads to inadequate bone deposition and calcification. Under the periosteum of the child's frontal bone, parietal bone, and occipital bone, a large amount of osteoid deposition forms the square skull. Therefore, while square skull is not necessarily indicative of rickets, it is a common manifestation in rickets.

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Written by Li Jiao Yan
Neonatology
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Can rickets be cured?

The rickets we commonly talk about is nutritional Vitamin D deficiency rickets, which is due to a deficiency of Vitamin D in the body leading to a disorder of calcium and phosphorus metabolism. This results in a systemic nutritional disease characterized by skeletal lesions. If rickets is caused by insufficient intake, it can be self-healing and is a self-limiting disease. Once infants and young children spend enough time outdoors and receive physiological doses of Vitamin D treatment, rickets can be treated. However, treatment becomes significantly challenging in cases of congenital developmental abnormalities causing skeletal lesions, or any genetic diseases that lead to Vitamin D absorption disorders. Such cases often result in severe complications, including prominent kidney dysfunction leading to further disturbances in calcium and phosphorus metabolism, as well as liver function abnormalities causing Vitamin D synthesis disorders. Therefore, it is important to understand the specific causes of Vitamin D deficiency in children, and if the deficiency is due to common reasons that can be promptly controlled, then supplementation with Vitamin D and trace elements like calcium can effectively treat the condition.

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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.