Vitamin D deficiency, rickets and osteomalacia

• Vitamin D is made in the skin by sunlight, eaten in a few foods, and must be activated in the liver and kidneys; its job is to let the gut absorb calcium and phosphate so that bone can mineralise.
• In a growing child with open growth plates, failure of mineralisation produces rickets: swollen wrists and ankles, bowed legs, rachitic rosary, delayed motor milestones and, if severe, hypocalcaemic seizures or heart failure.
• In an adult whose growth plates have closed, the same deficiency produces osteomalacia: diffuse bone pain, proximal muscle weakness and susceptibility to insufficiency fractures, often with non-specific symptoms that are mislabelled.
• The sentinel test is serum 25-hydroxyvitamin D (25OHD). Levels, calcium intake and radiographs together tell you whether someone has deficiency, insufficiency or nutritional rickets.
• Treatment is high-dose vitamin D plus oral calcium for a minimum of 12 weeks, followed by a maintenance dose for life in anyone persistently at risk, with the response reassessed at about 3 months. ^[1]

By the end of this page you should be able to:

1. Explain the pathway from sunlight and diet to active vitamin D, and how its failure leads to rickets in children and osteomalacia in adults.
2. Recognise the clinical and radiographic features of nutritional rickets and of osteomalacia, and tell them apart from the other causes of rickets.
3. Order and interpret 25OHD, calcium, phosphate, parathyroid hormone (PTH) and alkaline phosphatase (ALP), and decide when each patient needs a radiograph.
4. Treat nutritional rickets and osteomalacia with the right vitamin D dose, route, calcium dose and duration, including emergency management of hypocalcaemia.
5. Prevent vitamin D deficiency across the lifespan, including infants, pregnant women, older adults and high-risk groups, and say what to do where tests or treatment are limited.

Vitamin D deficiency is not one disease. The same low result on a blood test can be silent, can be rickets, or can be osteomalacia, depending on age, calcium intake, growth velocity and chronicity. The 2016 Global Consensus on Nutritional Rickets defines nutritional rickets as a disorder of defective chondrocyte differentiation and mineralisation of the growth plate together with defective mineralisation of newly formed bone, caused by vitamin D deficiency and/or low calcium intake in a child. Osteomalacia is the same mineralisation defect in already formed bone, and is the term used after growth has finished, although a child with rickets has osteomalacia too.^{[1] [2]}

Two classification axes matter in practice:

• Cause: nutritional (vitamin D and/or calcium lack), against the genetic vitamin D-dependent and vitamin D-resistant rickets, the hypophosphataemic rickets driven by excess fibroblast growth factor 23 (FGF23) or renal phosphate wasting, and the organ-related forms due to malabsorption, liver or kidney failure.
• Age: child with open growth plates (rickets) versus adult (osteomalacia).

A second axis is severity. Vitamin D status is classified differently by different authorities, and the numbers an examination expects depend on which one you quote:

(1 ng per mL equals 2.5 nmol per L.)^[1] The consensus defines deficiency at less than 30 nmol per L because radiographic rickets occurs almost exclusively below that level, especially below 34 nmol per L where parathyroid hormone begins to climb.^[1] A widely quoted alternative, less than 20 ng per mL (less than 50 nmol per L), catches more people but is not the rickets threshold. Where sources disagree, state which you are using rather than pretending one number is universal.^[1][2]

Calcipenic rickets itself should be kept distinct from the other forms. The tables and treatment below are for nutritional, calcipenic disease. Vitamin D-dependent rickets type 1A and 1B arise from failure to activate vitamin D (renal 1-alpha-hydroxylase deficiency or hepatic 25-hydroxylase deficiency); type 2 from resistance to calcitriol; hypophosphataemic rickets from renal phosphate wasting, most often FGF23-driven. They share radiological features but need different treatment, and confusing them leads to prolonged, fruitless vitamin D dosing.^[2]

Vitamin D deficiency is common worldwide. Reviews open with the estimate that it affects more than one billion people worldwide, and it is more prevalent in winter, at higher latitudes, in people with dark skin, and wherever clothing, disability or indoor living remove sun exposure.^[2] Risk of rickets reappears in immigrant groups, in breast-fed infants without supplementation, and wherever diets are low in calcium, but daily infant supplementation has been associated with the absence of new radiographic rickets in monitored populations. Population migration, poverty and sun-avoiding lifestyles keep incidence rising even in wealthy countries.^[1][2]

Risk is concentrated where synthesis fails: darker skin pigmentation, full body covering, high latitude in winter and spring, indoor living, disability, pollution and cloud cover, together with low vitamin D or low calcium diets and poverty.^[1]

Age patterns are bimodal. In one national series of Turkish children, rickets peaked at 0 to 2 years and at 12 to 15 years, reflecting first the reliance of infants on maternal stores and then the growth spurt of adolescence.^[3] Infants are the most vulnerable because breast milk is a poor source of vitamin D and neonatal stores depend entirely on the mother's status.

The causes split into four groups.

1. Failure to make enough vitamin D. The skin produces pre-vitamin D3 from 7-dehydrocholesterol only when ultraviolet B (UVB) reaches it. Anything that reduces UVB dose or skin exposure (winter, high latitude, dark skin, indoor life, full body covering, cloud and pollution) produces deficiency.^[1]
2. Failure to take enough in. Vitamin D is scarce in food. It occurs in oily fish, egg yolk and fortified foods, and is added to infant formula. Vegans without fortified foods, people on restricted diets and families in poverty are at risk.^[1]
3. Failure to absorb or process it. Conditions that impair fat absorption or vitamin D handling, such as malabsorptive bowel disease, liver disease and chronic kidney disease, interrupt the pathway. Some chronic diseases and medications alter vitamin D metabolism.^[1][2]
4. Increased requirements or stores lost. Obesity sequesters vitamin D in adipose tissue; chronic inflammation, pregnancy and adolescence raise demand.^[2]

Maternal factors are the starting point in the perinatal chain: maternal vitamin D deficiency, dark skin, full body covering, winter or spring pregnancy at high latitude, low sun exposure, pollution, low vitamin D diet, low calcium diet, poverty, malnutrition and special diets all predict deficiency in the infant. Infant factors add to this: neonatal deficiency from the mother, failure to give the standard infant supplement, and prolonged breast-feeding without appropriate complementary feeding from 6 months of age.^[1]

The same risk factors cause osteomalacia in adults; the additional adult pattern is long-standing, low-grade deficiency unmasked by a fracture, bone pain or proximal weakness, particularly in older adults whose skin synthesis has faded.

The mineralisation of bone requires calcium and phosphate in extracellular fluid at sufficient concentration for hydroxyapatite to crystallise. Vitamin D is the hormone that makes this possible.

1. Skin. UVB converts 7-dehydrocholesterol in keratinocyte membranes to pre-vitamin D3, which isomerises to cholecalciferol (vitamin D3) and moves into the circulation. Dietary vitamin D2 (ergocalciferol, from fungi and yeast) and D3 enter the same pool.^[2]
2. Liver. The liver hydroxylates vitamin D to 25-hydroxyvitamin D (25OHD, calcifediol) through cytochrome P450 2R1 (CYP2R1). This is the storage and measurement form.^[2]
3. Kidney. The kidney performs a second hydroxylation, by CYP27B1, to 1,25-dihydroxyvitamin D (calcitriol), the active form. Renal 1-alpha-hydroxylase is induced by parathyroid hormone and inhibited by calcitriol itself and by FGF23.^[2]
4. Action. Calcitriol binds the vitamin D receptor (VDR), partners with the retinoid X receptor and alters gene transcription in enterocytes, raising calcium and phosphate absorption from the gut. It also helps regulate bone mineral homeostasis alongside PTH and phosphate.^[2]

When vitamin D is lacking, calcitriol falls, gut absorption of calcium drops and serum calcium edges downward. The parathyroid glands sense this and secrete PTH. PTH releases calcium from bone by osteoclast activation and protects the serum calcium at the expense of phosphate, increasing urinary phosphate loss. Bone disease appears once PTH-driven phosphaturia has lowered serum phosphate enough to stop hydroxyapatite from crystallising: the result is a calcium-phosphate product too low for mineralisation.^[1]

The same hormonal cascade produces different anatomy at different ages:

• In children the growth plate is open and cartilage is being laid down rapidly. Unmineralised osteoid accumulates there, producing the widening, cupping and fraying of the metaphysis that define rickets.^[1]
• In adults the growth plate is gone, so failure of mineralisation accumulates as thick seams of unmineralised osteoid on the surfaces of existing bone. That is osteomalacia. The child has both at once; after growth ends only osteomalacia remains.^[1]

Calcium matters as much as vitamin D. Where calcium intake is under 300 mg per day in children over 12 months, rickets occurs even with 25OHD above 30 nmol per L, because the gut has nothing to absorb. Vitamin D and calcium are therefore partners, and treating one without the other is a common reason for poor response.^{[1] [2]}

(This section deepens the cascade above; the short version is that PTH defends blood calcium at the price of phosphate and bone.)

Bone formation and resorption are coupled. Calcitriol supports mineralisation by keeping both minerals available; PTH, in low but chronic excess, strips mineral out of bone to keep the blood level normal. The blood calcium is therefore normal in many deficient patients until the disease is advanced, which is why symptoms can be absent for years. In children the growth plate is the first place to fail because it mineralises fastest. In adults it is the sites of high turnover (ribs, pelvis, femoral necks) that hurt first. These mechanisms explain the clinical patterns that follow.

Histologically and radiologically, rickets and osteomalacia are problems of hypo-mineralisation, not of lack of bone matrix. The matrix (osteoid) is laid down in normal or increased quantity but never hardens.

In rickets the growth plate becomes:

• widened, because cartilage keeps being produced but not replaced by mineralised bone;
• cupped and frayed at its metaphyseal edge, because the soft cartilage splays under load;
• osteopenic, with coarse trabecular patterning;
• deformed, so long bones bow, the thorax develops its rachitic rosary, the pelvis deforms and the spine curves.

In osteomalacia the unmineralised seams widen throughout cortical and trabecular bone, bone becomes soft and painful, and repeated normal loading produces insufficiency fractures. Severe pelvic deformity in a woman who had rickets or osteomalacia in childhood can cause cephalopelvic disproportion years later.^[1]

Most vitamin-D-deficient children have no symptoms at all; rickets is uncommon relative to deficiency, and it is more likely when deficiency has been sustained.^[1] When rickets develops it produces a recognisable picture, best remembered from its causes.

Osseous features (Munns 2016 clinical list). Swelling of wrists and ankles; delayed closure of the anterior fontanelle (normally closed by 2 years); delayed tooth eruption (no incisors by 10 months, no molars by 18 months); leg deformity (genu varum, genu valgum or windswept deformity); rachitic rosary (enlarged costochondral joints, felt just anterior to the nipple line); frontal bossing; craniotabes (softening of the skull bones, palpable along the sutures in the first 3 months); bone pain, restlessness and irritability.^[1] In infants with severe radiographic rickets, fracture occurred in 7 of 45 (about 17.5%) aged 2 to 14 months, only after they were mobile; in a Canadian national survey 11 of 108 cases had fractures.^[1]

Non-osseous features. Hypocalcaemic seizures and tetany; hypocalcaemic dilated cardiomyopathy that can present as heart failure, arrhythmia, cardiac arrest and death; failure to thrive and poor linear growth; delayed gross motor development with muscle weakness; raised intracranial pressure.^[1] Severe nutritional rickets can kill, including from cardiomyopathy, even in affluent settings, and in adolescents the narrowed pelvis can obstruct labour years later.^[1]

Biasucci's review adds the mechanism-linked signs worth knowing for an exam: muscle hypotonia, increased frequency of respiratory infections, hypochromic anaemia, hypocalcaemia that may be asymptomatic, latent (positive Chvostek and Trousseau signs) or symptomatic with seizures, and dilated cardiomyopathy leading to heart failure or death.^[2] Delayed dental eruption and enamel hypoplasia raise caries risk into the permanent dentition.^[2]

X-linked (familial) and other rickets add their own: in X-linked hypophosphataemic rickets, dental abscesses with gingival fistulae occur in over half of patients despite no trauma or caries.^[2]

Adults do not have bruised growth plates, so the presentation is subtler and is often missed for years. The defining features are bone pain (classically the spine, pelvis, femora and ribs, worse with weight-bearing), proximal muscle weakness (difficulty climbing stairs or rising from a chair, a waddling gait) and a tendency to insufficiency fractures. Biochemical and radiographic abnormalities or, historically, a bone biopsy are needed to separate osteomalacia from osteoporosis. The Munns consensus groups the severe outcomes of rickets and osteomalacia together: hypocalcaemic seizures and tetany; hypocalcaemic cardiomyopathy; bone pain and muscle weakness; limb and pelvic deformities; failure to thrive and developmental delay in the young; dental anomalies; and death in severe cases.^[1]

Vitamin D deficiency is one of several causes of rickets. A comparison of the main calcipenic and phosphopenic forms on the laboratory pattern tested avoids treating the wrong condition.^[2]

In children the greatest practical mimic is non-accidental injury. Rickets can produce rib fractures; 7 of 45 infants with radiographic rickets in one series fractured, and a child with rickets is not protected from abuse. The converse misconception, that vitamin D deficiency explains any fracture, is equally dangerous: simple vitamin D deficiency without biochemical or radiological evidence of rickets has not been associated with increased fracture risk in infants and children.^[1]

• Serum 25OHD is the single test of vitamin D status. 25OHD2 plus 25OHD3 is what is reported as total 25OHD, and circulating concentrations are many-fold higher than those of the active hormone. Total 25OHD is the appropriate assay because it represents body stores better than calcitriol. Assays have improved but variability remains, particularly at the extremes, so borderline values should be interpreted with the clinical picture.^[1]

• Serum calcium may be normal even in severe deficiency, because PTH defends it. Ionised calcium is preferable when it is available and the patient is acutely unwell.^[1][2]

• Serum phosphate falls when PTH-driven renal phosphate wasting is significant. Low phosphate is more marked in osteomalacia and in hypophosphataemic rickets; in pure calcium deficiency phosphate may be less affected.^[2]

• Parathyroid hormone is raised in calcipenic rickets, and PTH begins to climb as 25OHD falls, an intersection that depends on the prevailing calcium intake and sits around 30 to 34 nmol per L. PTH is normal or only mildly raised in hypophosphataemic rickets, which helps separate them.^[1][2]

• Alkaline phosphatase is raised in all forms of rickets and osteomalacia, a feature described as peculiar though not pathognomonic, and is higher in calcipenic than phosphopenic disease. A low alkaline phosphatase points to hypophosphatasia, which mimics rickets on imaging.^[2]

• Renal and liver function and magnesium when the presentation is atypical or resistance to vitamin D is suspected.

Radiographs confirm rickets; they are not needed to diagnose simple deficiency. In a child with suspected rickets, posteroanterior views of the wrist and knee are standard because these are the fastest-growing sites. Typical findings are widening and fraying of the metaphysis, cupping, cortical thinning and delayed appearance of ossification centres; generalised osteopenia and, in severe cases, greenstick or metaphyseal fractures. The Rickets Severity Score, applied to bilateral wrist and knee radiographs, grades the degree of metaphyseal fraying and concavity and the proportion of growth plate affected, and is useful for research and for following a case.^[2]

In adults with suspected osteomalacia, plain films may show osteopenia and minimal-trauma fractures; dual-energy X-ray absorptiometry is normal or low and does not separate osteomalacia from osteoporosis. Bone biopsy with tetracycline labelling remains the historical gold standard where the diagnosis is uncertain, but is rarely needed today.

Routine 25OHD screening of healthy children is not recommended, and population-based screening with serum 25OHD, serum ALP or radiographs is not indicated. Test when there are clinical features of rickets or osteomalacia, symptoms of deficiency, very low sun exposure, or a clinical reason such as a fall in an older adult. High-risk groups who should be considered for testing include those with malabsorption, chronic kidney or liver disease, and women with dark skin or covering in pregnancy.^[1]

Nutritional rickets is diagnosed on history, physical examination and biochemistry, and confirmed by radiograph. The vitamin D status cut-offs, calcium intake limits and toxicity threshold are those in the comparison at the start. The treatment and dietary reference intakes are:

• 400 IU per day of vitamin D for all infants from birth to 12 months, independent of feeding mode.^[1]
• At least 600 IU per day from diet and/or supplements beyond 12 months of age, as recommended by the Institute of Medicine (IOM, now the National Academy of Medicine).^[1][3]
• 200 mg per day calcium for infants 0 to 6 months and 260 mg per day for 6 to 12 months.^[1]
• Under 300 mg per day of dietary calcium raises rickets risk in children over 12 months; over 500 mg per day is sufficient and 300 to 500 mg per day is insufficient.^{[1] [2]}

Toxicity is defined as hypercalcaemia with serum 25OHD above 250 nmol per L, hypercalciuria and suppressed PTH. Intoxication is reported in infants and young children after vitamin D exposures in the 240,000 to 4,500,000 IU range.^[1]

Symptomatic hypocalcaemia (seizures, tetany, laryngospasm, heart failure) is a medical emergency. Give intravenous calcium gluconate 10% in an age-appropriate bolus, with careful electrocardiographic monitoring: 100 to 200 mg per kg in a neonate, 29 to 60 mg per kg in a child over one month, and 1 to 2 g in an adult, repeated every 6 hours and rechecked, infused no faster than 100 mg per minute in a child or 200 mg per minute in an adult; then 8 to 13 or 5.4 to 21.5 mg per kg per hour as a continuous infusion where needed, with serum calcium measured every 4 to 6 hours, while starting oral vitamin D and calcium. Treat the cause as well as the biochemical abnormality.^[2]

Daily oral treatment is the recommended first line; compared with intramuscular treatment it restores 25OHD more quickly. For daily treatment, vitamin D2 and vitamin D3 are equally effective, but when large single (stoss) doses are used vitamin D3 is preferable because its half-life is longer. Daily dosing also improves compliance and avoids the hypercalcaemia risk of bolus therapy. Treatment should last a minimum of 12 weeks, and some children need longer. ^[1]

The minimum recommended dose for treatment is 2000 IU per day (50 microgram) for at least 3 months, and oral calcium 500 mg per day with it, either as food or a supplement, regardless of age or weight. In calcium-deficient rickets, calcium alone (500 mg per day in the consensus; in practice 30 to 75 mg per kg per day in divided doses in some reviews) heals about as well as combined therapy and better than vitamin D alone; the exact dose string should match the guideline your unit follows. Where the local approach uses stoss therapy, single doses of 150,000, 300,000 or 600,000 IU have been studied in Turkish and Indian children, with hypercalcaemia in a small minority receiving the larger doses; daily dosing remains first line. Stoss doses are converted from IU to microgram by dividing by 40. ^[1]

Biochemical improvement precedes radiological healing. Reassess at about 3 months, looking for normalisation of calcium and phosphate, falling PTH and a declining alkaline phosphatase. If the patient is not improving, consider poor adherence, ongoing malabsorption, a calcium-deficient diet, or a different form of rickets. Maintenance doses then follow: 400 IU per day under 12 months and 600 IU per day thereafter, with higher or lifelong dosing for anyone with continued risk factors.

Oral calcium 500 mg per day should accompany vitamin D whatever the age. In the practical formulation used by many paediatric units this is given as 30 to 75 mg per kg per day divided in 2 to 3 doses for children with symptomatic hypocalcaemia, using calcium gluconate or carbonate by mouth once the emergency is controlled. Combined therapy heals more reliably than vitamin D alone in calcium-deficient rickets: in one Nigerian study the combined endpoint of alkaline phosphatase under 350 U per L plus radiographic near-complete healing occurred in 58% with combined calcium and vitamin D versus 19% with vitamin D alone, and 61% with calcium alone. Combined treatment is therefore justified, because the diets of children and adolescents with nutritional rickets are generally low in both vitamin D and calcium. Withdrawal of calcium before vitamin D can allow biochemical relapse.^[1][2]

Preventing rickets is simpler than treating it and is the public-health core of this topic.

• All infants from birth to 12 months should receive 400 IU per day, independent of whether they are breast or formula fed.^[1]
• Beyond 12 months all children and adults should meet a vitamin D intake of at least 600 IU per day through diet, fortification and/or supplements.^[1]
• Pregnant women should receive 600 IU per day, ideally combined with iron and folic acid. Women of childbearing age and pregnant women should keep intake at or above 600 IU per day so that the fetus is not born deficient.^[1]
• Lactating women should meet their own requirement of 600 IU per day but should not take pharmacological doses to supplement the baby indirectly; the infant needs its own 400 IU per day.^[1]
• High-risk groups beyond 12 months (history of symptomatic deficiency, restricted sun exposure, dark skin, covering, indoor living, malabsorption, chronic disease, poverty) should receive supplements in the absence of fortification.^[1]
• Sunlight remains a source but an unreliable one: UVB availability varies by latitude, season, cloud cover and pollution, and skin synthesis depends on time spent outdoors, pigmentation, clothing and age. No threshold of sun exposure guarantees sufficiency without raising skin cancer risk, so behaviour-based public health messages must be nuanced.^[1]
• Food fortification of staples (infant formula, milk, flour, oil) is the most scalable prevention, and indigenous calcium sources should be promoted or subsidised where dairy is scarce.^[1]

Vitamin D deficiency in pregnancy has been associated with elevated cord alkaline phosphatase, larger fontanelle size, neonatal hypocalcaemia and congenital rickets; supplementing the mother at 600 IU per day, where needed together with calcium, is the protective measure. Neither calcium intakes above the non-pregnant recommendation nor high-dose vitamin D have shown convincing effects on birth anthropometry or bone mass beyond these.^[1]

Infants and children. The 400 IU per day infant dose is effective and safe; 400 IU per day maintained 25OHD above 50 nmol per L in 97% of infants after 12 months, whereas higher doses (800 to 1200 IU per day) added no bone mineral density benefit and 1600 IU per day raised toxicity concerns. Intermittent bolus dosing (50,000 to 100,000 IU every 3 months) holds promise for infants and toddlers in whom daily dosing is impractical. In children, simple vitamin D deficiency without rickets does not raise fracture risk. Surgical, dental and (in familial cases) endocrine review are needed for inherited vitamin D-dependent rickets.^[1]

Adolescents. The second rickets peak is 12 to 15 years, when growth velocity is high and diets are often poor. Prevention here means diet, fortification and supplements during the growth spurt.^[3]

Adults and older adults. From age 65, skin synthesis declines and year-round rather than seasonal supplementation is recommended. The Institute of Medicine reference nutrient intake is 600 IU per day for ages 1 to 74 (including pregnancy and lactation) and 800 IU per day for those 75 and over. The 2024 Endocrine Society guideline suggests empiric vitamin D supplementation (that is, intake above the dietary reference intakes without 25OHD testing) for adults aged 75 and over, and suggests daily rather than intermittent high-dose therapy where treatment is indicated. For adults with established osteomalacia, replacement follows the over-12-years schedule (6000 IU per day for 90 days or 300,000 IU once, then maintenance 600 IU per day) alongside at least 500 mg per day of calcium, with attention to underlying malabsorption. Adults with prediabetes are another group in which the 2024 guideline suggested supplementation.^{[3] [1][2]}

• Hypocalcaemic seizures and tetany, from acutely low ionised calcium; possible laryngospasm.
• Hypocalcaemic dilated cardiomyopathy, which can present as heart failure, arrhythmia, cardiac arrest or death, including in developed countries.
• Skeletal deformity: bowed legs, windswept deformity, scoliosis, kyphosis, pectus carinatum, narrowed pelvic outlet. Severe deformity may persist despite biochemical healing.
• Fractures: minimal-trauma (insufficiency) fractures and pseudofractures in adults; metaphyseal fractures around the ankle in mobile toddlers with severe rickets (about 17.5% in one series). Fracture does not by itself prove neglect.
• Failure to thrive and delayed motor development from hypotonia.
• Dental anomalies: delayed eruption, enamel hypoplasia and caries.
• Obstructed labour in women whose pelvis was deformed by rickets in childhood.
• Treatment toxicity: hypercalcaemia, hypercalciuria, nephrocalcinosis and renal failure after excessive dosing, especially with single doses in the 300,000 to 600,000 IU range. Recovery from iatrogenic toxicity is slow. ^[1]

Untreated infantile rickets is life-threatening; treated disease usually heals biochemically within weeks and radiographically over the following months. Long-standing deformity, particularly of the legs and pelvis, may need orthopaedic or (later) obstetric planning. Osteomalacia in adults is fully reversible when the cause is corrected, although insufficiency fractures cause prolonged morbidity. Adults treated for osteomalacia should be reassessed to ensure the 25OHD has risen and symptoms have settled. The recurrence risk for anyone at continued high risk is high unless maintenance and prevention are arranged.

Where testing is limited:

• Diagnose clinically and radiographically. Nutritional rickets is confirmed by history, physical examination and biochemistry where available, and by radiograph. Do not spend scarce laboratory resources on screening healthy infants; target children with features and those at high risk.
• Treat empirically when clinical features are clear with the standard oral vitamin D and calcium regimen, provided no contraindication, and recheck as soon as laboratory capacity allows.
• Use local calcium sources where dairy is scarce: the 500 mg per day target can be met from green leaves, fish bones, legumes or, where available, fortified staples.
• Promote infant supplementation through existing health programmes (immunisation, well-child clinics, antenatal care) rather than building parallel structures, and support food fortification and legislative monitoring.
• Teach families safe sun exposure that balances vitamin D synthesis with skin cancer risk, and remember that at tropical latitudes and in children who are outdoors regularly, deficiency is still possible with covering or malabsorption.
• Refer early for children with severe deformity, cardiomyopathy, resistant hypocalcaemia, or suspected non-nutritional rickets, and for anyone not responding to 3 months of treatment, where a specialist is within reach.

• Vitamin D is activated in the liver and kidney; it enables intestinal calcium and phosphate absorption and thereby bone mineralisation.
• Nutritional rickets affects infants (peak 0 to 2 years) and a second peak in adolescence (12 to 15 years); most deficient people are asymptomatic.
• Osteomalacia is the same deficiency in adults: bone pain, proximal weakness, pseudofractures, easily confused with osteoporosis.
• The sentinel test is serum 25OHD; total 25OHD is the appropriate assay. Typical deficiency below 30 nmol per L on the consensus view, below 20 to 50 nmol per L on other definitions; know which your source uses.
• Radiographs of wrist and knee confirm rickets; sequencing serum PTH, phosphate and alkaline phosphatase separates calcipenic from phosphopenic disease.
• Treat symptomatic hypocalcaemia first with intravenous calcium gluconate under ECG monitoring.
• Then treat with daily oral vitamin D (minimally 2000 IU per day for 3 months) plus at least 500 mg per day of calcium; vitamin D2 and D3 are equivalent daily, but vitamin D3 is preferred for stoss dosing, which is not first line.
• Maintenance doses are 400 IU per day under 12 months and 600 IU per day thereafter; treat adults with the over-12-years schedule.
• Prevention: 400 IU per day for every infant, at least 600 IU per day beyond 12 months, 600 IU per day in pregnancy, sun plus fortification for populations.
• Under 300 mg per day of dietary calcium causes rickets at any 25OHD level; over 500 mg per day is sufficient.
• Vitamin D above 250 nmol per L with hypercalcaemia is toxic; iatrogenic excess is largely avoidable by preferring daily dosing.
• Population-based screening is not indicated; target clinical features and high-risk groups.

Calcium and phosphate homeostasis, hypophosphataemic rickets, vitamin D-dependent genetic rickets, bone mineralization and osteoporosis, maternal and child nutrition, endocrine emergencies: hypocalcaemia.