Approach

Evidence suggests children and adults should have a level of serum 25-hydroxyvitamin D of >75 nanomoles/L (>30 nanograms/mL) to obtain the maximum benefit of vitamin D for overall health and wellbeing.[2] The amount of vitamin D required to achieve this depends on a wide variety of factors, including age, baseline 25-hydroxyvitamin D, body mass index, sun-exposure history, and the use of medications that can affect vitamin D metabolism and intestinal absorption.

Correction of vitamin D deficiency and insufficiency in children will promote growth and deposition of calcium into the skeleton. Children with skeletal manifestations of rickets should be aggressively treated. The earlier the intervention, the more likely a favourable prognosis, with resolution of many of the associated skeletal deformities. This is especially true for deformities in the legs. Correction of vitamin D deficiency in adults improves bone mineral density and stimulates mineralisation of the collagen matrix, resulting in resolution of bone pain associated with osteomalacia.

Vitamin D replacement

The mainstay of treatment is the provision of vitamin D to correct the causative deficiency. The goal is to reach and maintain a serum 25-hydroxyvitamin D level in both children and adults of between 75-250 nanomoles/L (30-100 nanograms/mL).[1][2][73][88]​​​ A child or adult is considered vitamin D-insufficient if serum 25-hydroxyvitamin D level is between 52-72 nanomoles/L (21-29 nanograms/mL) or if history suggests lack of adequate daily vitamin D from supplements (400 IU for children <1 year of age; 600 IU for children ≥1 year of age; and 1500-2000 IU for adults), diet, and/or adequate sun exposure.[2] These patients should be treated with vitamin D replacement as for those with true deficiency.

Vitamin D deficiency in adults and children is corrected by treatment with vitamin D2 (ergocalciferol) or vitamin D3 (colecalciferol) given orally for 6-8 weeks, followed by a lower maintenance dose continued throughout childhood and adulthood.[2][89][90]

Patients with intestinal or fat malabsorption syndromes (including liver failure and obesity), or who have a history of gastric bypass surgery, usually do not respond to small doses of vitamin D replacement. Therefore, higher daily oral doses are often required.[2]​ Patients taking antiepileptic medications, glucocorticoids, or other drugs that activate the steroid and xenobiotic receptors (e.g., highly active antiretroviral therapy, rifampicin, St John's wort) may also require higher doses of vitamin D. Data on the optimal dose for vitamin D deficiency in pregnancy is lacking.[91]​ Seek specialist advice before starting treatment if a woman is pregnant.

Sensible sun or ultraviolet B (UV-B) radiation exposure

Adequate sensible sun exposure is an excellent source of vitamin D and should be recommended to all patients for both the treatment and prevention of vitamin D deficiency.[58][71]​ Usually, exposure of the arms and legs (with sun protection on the face) for about 5-30 minutes (depends on degree of skin pigmentation, time of day, season, latitude, and age of patient) between 10 a.m. and 3 p.m. twice a week is sufficient to stimulate cutaneous vitamin D production. There are smartphone apps available that can provide advice about sensible sun exposure, give information about how much vitamin D is being made in the skin during current sun exposure, and alert the user when to stop the exposure to prevent sunburn.

Patients with fat malabsorption who are unable to absorb vitamin D when taken orally can benefit from exposure to UV-B radiation.[1] This is usually achieved by using a tanning bed for 30% to 50% of the time recommended for tanning (sunscreen should be applied to the face).[1] Tanning beds may also be considered in climates with limited sunlight.

Calcium and phosphate replacement

Because inadequate calcium intake may contribute to vitamin D deficiency and many patients do not meet daily calcium requirements from dietary sources alone, all patients at risk of calcium deficiency should be given calcium supplementation.[78][92]​ Calcium supplements, with or without vitamin D, are considered safe from a cardiovascular standpoint.[93]

Phosphate supplementation is not usually necessary unless there is an acquired or inherited disorder causing phosphate wasting in the kidneys, such as hypophosphataemic rickets or oncogenic osteomalacia.​[4][5] These patients require phosphate supplementation in addition to vitamin D replacement and vitamin D metabolite. Caution should be exercised when giving phosphate supplements, because high-dose phosphate multiple times a day causes a reduction in ionised calcium, resulting in an increase in parathyroid hormone production and tertiary hyperparathyroidism. Therefore, smaller doses of phosphate should be taken more frequently throughout the day to maintain a normal serum phosphate level without causing significant hyperparathyroidism.

Disorders of vitamin D metabolism

Patients with acquired and inherited disorders of metabolism of 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D, or a defective recognition of 1,25-dihydroxyvitamin D, should receive vitamin D along with either 1,25-dihydroxyvitamin D3 (calcitriol) or one of its active analogues (e.g., paricalcitol or doxercalciferol), depending on the cause of the abnormality.[1]

Patients with chronic kidney disease have high-normal or elevated serum phosphate levels and a decreased capacity to produce 1,25-dihydroxyvitamin D, which causes secondary hyperparathyroidism. Therefore, they need to maintain a serum 25-hydroxyvitamin D of between 75-250 nanomoles/L (30-100 nanograms/mL) and control their serum phosphate level by using a phosphate binder (e.g., calcium carbonate). In addition, if the estimated GFR is <50% of normal, they may also require 1,25-dihydroxyvitamin D3 or one of its active analogues (to treat and prevent secondary hyperparathyroidism).[1][10]

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