Treatment for rickets focuses on replacing the missing vitamin or mineral in the body. This will eliminate most of the symptoms associated with rickets. If your child has a vitamin D deficiency, your doctor will likely want them to increase their exposure to sunlight, if possible.
They will also encourage them to consume food products high in vitamin D, such as fish, liver, milk, and eggs. Calcium and vitamin D supplements can also be used to treat rickets. Ask your doctor about the correct dosage, as it can vary based on the size of your child.
Too much vitamin D or calcium can be unsafe. If skeletal deformities are present, your child may need braces to position their bones correctly as they grow.
In severe cases, your child may need corrective surgery. For hereditary rickets, a combination of phosphate supplements and high levels of a special form of vitamin D are required to treat the disease.
Increasing vitamin D, calcium, and phosphate levels will help correct the disorder. Most children with rickets see improvements in about one week. Skeletal deformities will often improve or disappear over time if rickets is corrected while the child is still young. The best way to prevent rickets is to eat a diet that includes adequate amounts of calcium, phosphorous, and vitamin D. People with kidney disorders should have their calcium and phosphate levels monitored on a regular basis by their doctors.
Rickets can also be prevented with moderate sun exposure. According to the National Health Service of England NHS , you only need to expose your hands and face to sunlight a few times a week during the spring and summer months to prevent rickets.
Clinical signs of nutritional rickets. This Nigerian child has severe leg deformities, wrist enlargement, and enlarged costochondral junctions of the ribs.
We participated in the Global Consensus Conference on the Prevention and Management of Nutritional Rickets and conducted a systematic review and grading of the evidence in the English language literature.
The search strategy has been described in the recently published consensus recommendations [ 3 , 4 ]. Recent evidence indicates that the prevalence of nutritional rickets is increasing in high-income countries, with a significant factor being changes in the ethnic composition of the childhood population which is partly related to an increased influx of immigrant populations.
Representative incidence and prevalence data are shown in Table 1. The risk of nutritional rickets will likely continue to increase as the proportion of dark-skinned immigrant and refugee children increases in industrialized countries. In a study of children with nutritional rickets in Australia, the overall annual incidence in children 15 years of age or less was 4. Other cases were identified through general hospitals inpatient or outpatient settings or non-refugee clinic settings.
However, the prevalence in immigrant children was much greater. Approximately two-thirds were born in Africa [ 5 ]. An earlier study found that the increase in the number of cases of rickets in Australia mirrored immigration trends [ 6 ].
An increasing incidence of children with rickets has also been documented in the USA. In a population-based study over 40 years in Olmsted County, Minnesota, the incidence of nutritional rickets in children younger than 3 years was 0, 2.
Most children with rickets were black. The rising incidence of rickets was temporally associated with an increase in dark-skinned predominantly Somali immigrants who have settled in Minnesota since [ 8 ]. The incidence of rickets in black children was estimated as per , In a national survey of pediatricians in Canada, the annual incidence of nutritional rickets was estimated at 9 to 12 cases per , in children younger than 3 years [ 10 ].
Nutritional rickets was associated with breast-feeding in the absence of appropriate vitamin D supplementation. In the UK, a survey of pediatricians identified 24 cases of symptomatic vitamin D deficiency in children less than 5 years of age. The overall annual incidence was 7.
An analysis of historical trends of hospital admissions for rickets in England from to found that hospitalization rates for rickets are now the highest in five decades [ 13 ].
Changes in the population structure with a larger proportion of children from ethnic minorities likely accounts for a large part of the increased incidence. The incidence of hypocalcemic seizures, another manifestation of severe vitamin D deficiency, was greater in children of South Asian or Black ethnicity compared with children from white ethnic backgrounds in the UK [ 14 ].
Data from Glasgow, Scotland document a quadrupling of symptomatic vitamin D deficiency mostly rickets between and , with the greatest increase in patients with an ethnic background of the Sub-Saharan region of Africa, North Africa or the Middle East [ 15 ]. Dark skinned races consistently have a higher risk of rickets.
The greater the number of people at risk, the greater the number of children with nutritional rickets. In Germany, for example, between and , the number of immigrants from Asia has increased 1. The greatest increases were observed in immigrants from India 4-fold and China 3-fold. The overall incidence of nutritional rickets in children aged under 15 years was 2.
The incidence of nutritional rickets declined in ethnic Danish children from 5. During the same interval, the overall incidence of nutritional rickets increased from 1. A report from Spain described nutritional rickets in three teenagers of Pakistani origin [ 21 ]. Nutritional rickets has been reported in infants immigrating to Israel from Ethiopia [ 22 ]. Immigrant and refugee children typically come from countries with a high incidence of nutritional rickets. Many of these countries are in the tropics with abundant sunshine.
The highest prevalence of nutritional rickets is found in children in the Middle East, Africa, and South Asia, corresponding to the sites of origin for many immigrants Table 1. Vitamin D deficiency is highly prevalent in the Middle East and North Africa, in part related to covering by clothing [ 23 ].
For example, reports from Yemen [ 24 ], Jordan [ 25 ], Qatar [ 26 ], Saudi Arabia [ 27 , 28 ], and Turkey [ 29 ] all indicate that nutritional rickets is an important condition in children from the Middle East. Nutritional rickets is prevalent in sub-Saharan African countries, like Nigeria [ 30 ], Ethiopia [ 31 ], and The Gambia [ 32 ], and in South Asian countries, like India [ 33 ] and Bangladesh [ 34 , 35 ].
However, nutritional rickets in children is not limited to these countries [ 36 ]. The burden of vitamin D and dietary calcium deficiency is not limited to children. The lack of mineral supply to the growth plate in children creates rickets and bone deformities, whereas the same lack of mineral supply in adults causes osteomalacia in mature bone.
Both rickets and osteomalacia are associated with muscle weakness and hypocalcemic complications. While the diagnosis of rickets is easily made, diagnostic criteria for osteomalacia in adults are not well established, and there is a huge dark figure of unrecognized osteomalacia in adults. Vitamin D is produced in the skin by ultraviolet radiation from sunlight, and this is the principal source of vitamin D for most populations.
Dark skin pigmentation reduces the quantity of vitamin D produced for a given amount of solar ultraviolet radiation, predisposing children with dark skin to vitamin D deficiency.
Compared with the sunny tropical countries of origin of many immigrants and refugees, most high income countries are at higher latitudes and only receive sufficient ultraviolet light during summer months.
Colder climates lead to greater covering of the skin with clothing, which prevents production of vitamin D in covered skin. Relocating to high latitude countries from sunny tropical regions puts high risk children at even greater risk of nutritional rickets. Australia is an exception to this, having a temperate and tropical climate.
Here too, nutritional rickets is seen amongst the refugee population [ 5 ]. Very few foods are naturally rich in vitamin D, so in the absence of adequate sun exposure, children must rely on oral intake of vitamin D- fortified foods or vitamin D supplements to prevent vitamin D deficiency.
However, immigrant and refugee children may not consume commonly fortified staple foods, due to dietary preferences, or they may migrate to countries that do not practice food fortification. The risk of nutritional rickets is a function of both vitamin D status and calcium intake. Although rickets can result from vitamin D deficiency or calcium deficiency, more commonly these two conditions interact to increase the risk of developing rickets Fig. The combination of low vitamin D status and inadequate calcium intakes poses a very high risk for rickets in growing children and osteomalacia when growth has ceased.
If their diet does not include milk and dairy products, individuals will not likely meet their dietary calcium requirements. Vitamin D and calcium interaction. The risk of nutritional rickets is a function of both calcium intake and vitamin D status. Clinical rickets develops when the threshold is crossed where bone mineralization is impaired in growing bones. Vitamin D status is measured by the serum hydroxyvitamin D [25 OH D] concentration, which has a half-life of 15 days [ 40 ].
Low vitamin D status in immigrants can result from reduced sun exposure during the winter, modest clothing for cultural and religious reasons, reduced cutaneous vitamin D synthesis due to dark skin, a low intake of vitamin D- fortified foods, and infrequent use of vitamin D supplements [ 41 ]. Because the concentration of vitamin D in breast milk is low, prolonged breast feeding without vitamin D supplementation increases the risk of vitamin D deficiency and rickets, which has been described in immigrant children [ 42 ].
Vitamin D deficiency was also common among Pakistani immigrant children in Denmark, where no food fortification with vitamin D is mandated [ 44 ]. Women who are vitamin D deficient during pregnancy give birth to infants who are vitamin D deficient and at risk for nutritional rickets and hypocalcemic seizures early in infancy [ 46 ]. The authors recommended that migrants at high risk be educated, screened, and monitored for vitamin D deficiency. Journal of Clinical Investigation ; : — Clothing prevents ultraviolet-B radiation-dependent photosynthesis of vitamin D3.
Journal of Clinical Endocrinology and Metabolism ; 75 : — Webb AR. Who, what, where and when-influences on cutaneous vitamin D synthesis. Progress in Biophysics and Molecular Biology ; 92 : 17 — Increased skin pigment reduces the capacity of skin to synthesise vitamin D3. Lancet ; 1 : 74 — Sanholi Danskernes kostvaner — Dentin alteration of deciduous teeth in human hypophosphatemic rickets.
Calcified Tissue International ; 79 : — Reviews in Endocrine and Metabolic Disorders ; 2 : — The role of DMP1 in autosomal recessive hypophosphatemic rickets. Journal of Musculoskeletal and Neuronal Interactions ; 7 : — Garg RK , Tandon N. Hypophosphatemic rickets: easy to diagnose, difficult to treat.
Indian Journal of Pediatrics ; 66 : — Inadequate bone response to phosphate and vitamin D in familial hypophosphatemic rickets FHR. Advances in Experimental Medicine and Biology ; : — Renal hypophosphatemic rickets. Current Therapy in Endocrinology and Metabolism ; 6 : — Author guidelines Reasons to publish Ethical policy Open-access policy Publication charges Author resource centre.
Advanced Search Help. Incidence and prevalence of nutritional and hereditary rickets in southern Denmark in European Journal of Endocrinology. Free access. Download PDF. Check for updates. Get Permissions. Objective To estimate the incidence of nutritional rickets and the incidence and prevalence of hereditary rickets. Design Population-based retrospective cohort study based on a review of medical records. Methods Patients aged 0— Conclusions Nutritional rickets is rare in southern Denmark and largely restricted to immigrants, but the incidence among ethnic Danish children was unexpectedly high.
Abstract Objective To estimate the incidence of nutritional rickets and the incidence and prevalence of hereditary rickets. Introduction Rickets is characterized by defect mineralization of bones and growth zones. Patients and methods Register study In Denmark, all citizens have a unique personal identification number CPR number making it possible to link personal information from different registers and hospital records, and to link children to parents.
Questionnaire survey In order to identify patients with rickets treated exclusively in the primary health care sector, questionnaires were sent to all general practioners GPs and pediatricians working in primary care in the study region. Statistical analysis The incidence of nutritional rickets was calculated in two study periods — and — , before and after the registration of outpatients in the DNPR. Results A total of medical records from children with a potential diagnosis of rickets were identified.
Figure 1 Flow diagram of patient inclusion. Table 1 Average yearly incidence of nutritional and hereditary rickets in southern Denmark. Hereditary rickets A total of 16 cases presented with hereditary rickets during the study period. Table 2 Prevalence of hereditary rickets in children younger than 15 years, living in southern Denmark on the 1st of January Discussion The average incidence of nutritional rickets among children aged 0— Declaration of interest There is no conflict of interest that could be perceived as prejudicing the impartiality of the research reported.
Davies M Stanbury SW. European Journal of Pediatrics false. Garg RK Tandon N. Your current browser may not support copying via this button. Related Articles. Export Figures View in gallery Flow diagram of patient inclusion. Close View raw image Flow diagram of patient inclusion. Export References.
Follow us on: Share Share. Sign in to annotate. Actions for this page Listen Print. Summary Read the full fact sheet. On this page. A range of causes Some of the contributing factors and causes of rickets include: Not enough exposure of the skin to sunlight Skin colour — the skin pigment in children with naturally dark skin tends to absorb less sunlight than fair skin Lack of vitamin D or calcium in the diet Exclusive breastfeeding without vitamin D supplements of infants whose mothers have vitamin D deficiency Disorders of the intestine, liver or kidneys that prevent the body from absorbing vitamin D or converting it into its active form Disorders that reduce digestion or absorption of fats, as vitamin D is a fat-soluble vitamin.
The role of vitamin D Our body needs vitamin D to help it absorb calcium and phosphorus. High-risk groups Children who may be at increased risk of rickets due to vitamin D deficiency include children who: Are born to women with a vitamin D deficiency Cover most of their body for religious or cultural reasons Are sick, disabled or unable to spend time outdoors for other reasons Never go outside without sunscreen Have naturally very dark skin Have some medical conditions such as certain bowel diseases Are on vegetarian, dairy-free or lactose-free diets.
Diagnosis Rickets may be diagnosed using a number of tests including: Physical examination Blood tests Long bone x-rays Bone scans. Long-term outlook Bones that are poorly mineralised respond very quickly to dietary supplementation with calcium and vitamin D.
Prevention You can help protect your child from the effects of rickets by understanding their risk factors for vitamin D deficiency and taking steps to prevent it. Suggestions include: Sunlight — a sensible balance of sun exposure and sun protection can protect against vitamin D deficiency without putting your child at risk of skin cancer. The recommended amount of sunlight each day is a few minutes of sunlight exposure before 10am and after 3pm each day from September to April and two to three hours of sunlight exposure over the week from May to August.
Foods naturally containing vitamin D include oily fish especially sardines, salmon, herring and mackerel , liver and egg yolks. Be SunSmart UV radiation levels vary depending on location, time of year, time of day, cloud coverage and the environment. Rickets is caused by a lack of vitamin D, calcium or phosphorus.
Vitamin D deficiency can occur as a result of having dark skin, lack of exposure of the skin to sunlight, nutritional deficiencies and disorders of the liver, kidney or small intestine.
Treatment options include improved sunlight exposure, diet, vitamin D and mineral supplements. Prevention and treatment of infant and childhood vitamin D deficiency in Australia and New Zealand: A consensus statement [online], Medical Journal of Australia, vol. More information here.
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