Vitamin D in pregnancy and childhood: nutritional rickets, the 30 and 50 thresholds, calcium intake and who to supplement

Speaker

Craig, paediatrician. Introduced with roles linked to the University of Queensland (director of the Child Health Research Centre, as transcribed) and Queensland Children's Hospital, with a clinical and research interest in paediatric bone and endocrine disorders (as we read the garbled introduction). He describes himself as a "57 year old balding paediatric endocrinologist" and a "bone nerd". Other titles in the introduction were garbled and are not repeated. His surname was not captured.

Disclosures and sponsor context

Craig showed a disclosures slide (not read aloud) and asked delegates to complete a short questionnaire, put together with help from a pharmaceutical company (name unclear in the transcript), asking whether Australian guidelines for maternal and childhood vitamin D supplementation should be updated. Keep that context in mind.

Session context

Otter title Vitamin D Supplementation Seminar · id 6yR6lSI3kTNgg78CpZbzvvsac2I · ~26 min. Held in Brisbane at the end of National Reconciliation Week; Craig opened with an Acknowledgement of Country and a reflection on closing the gap through children's health.

Key messages for GPs

• Nutritional rickets is preventable. "Our job is to never see nutritional rickets."
• Prevention plan: all infants 400 units a day for the first 12 months; children at risk 600 units a day after that; all pregnant women 1000 units a day.
• Thresholds in children: 25-hydroxy vitamin D below 30 nmol/L is deficient (rickets risk climbs steeply); aim for above 50. Dietary calcium below 300 mg a day is deficient; aim for about 500 mg (about two glasses of milk).
• Rickets usually needs both low vitamin D and low dietary calcium. Talk about calcium every time you talk about vitamin D.
• Order 25-hydroxy vitamin D, not 1,25-dihydroxy vitamin D. Add calcium, phosphate, alkaline phosphatase, PTH and a wrist X-ray when rickets is suspected.
• Treat with both calcium and vitamin D, in large doses, then maintenance. Everything (bloods and X-rays) should be better by three months; if not, think of rarer genetic rickets.
• Treat and test the mother too. Rickets is "vertically transmitted" through maternal deficiency.
• In pregnancy, correct deficiency with 2000 to 4000 units a day for three months. Avoid high-dose stoss therapy, which has not been shown to be safe in pregnancy.

The case: a three-month-old with fractures

Craig explained the key split when assessing rickets:

• Calcipenic (hypocalcaemic) rickets: driven by a high PTH, as in this case.
• Phosphopenic (normocalcaemic) rickets: PTH normal; usually a genetic problem with kidney phosphate handling or similar.

Vitamin D is a hormone

"It looks like a hormone, it smells like a hormone, it binds to a hormone receptor." We make vitamin D in skin exposed to sun; it is converted in the liver to 25-hydroxy vitamin D (the storage form) and in the kidney to 1,25-dihydroxy vitamin D (the active form), which acts on the vitamin D receptor. Its best-established job is to increase calcium absorption from the gut. Indoor lifestyles are a big reason deficiency is rising ("the first sunny day in Brisbane for how long, and where are we? Inside.").

Pregnancy and lactation

• Pregnancy does not change the vitamin D requirement: the standard supplement is about 1000 units a day, which is what most modern pregnancy supplements contain.
• Old data from an antenatal clinic showed 91% sufficient. Craig suspects GPs see far more deficiency; local GPs had told him figures closer to 40% deficient in some areas. "You know your patients better than I do."
• Classical features of deficiency in pregnancy: worse hypocalcaemia from higher calcium demand; osteomalacia with bone pain; myopathy; problems in labour (the uterus is a muscle). Historically, a rachitic pelvis from childhood rickets caused obstructed labour, which is where caesarean section began.
• What you will actually see: a pregnant woman with a low vitamin D level and no symptoms.
• Treating deficiency in pregnancy: 2000 to 4000 units a day for three months.
• Stoss therapy (for example 600,000 units in one dose), common in the Asia-Pacific region, has not been shown to be safe in pregnancy. Use daily dosing; studies are under way.

Newborns and breastfeeding

• In the womb, the baby's vitamin D tracks the mother's. Unless the mother is hypocalcaemic, fetal skeletal development is normal.
• At birth the baby has about 75% of the mother's level. A mother at 50 nmol/L gives a baby still above the rickets threshold.
• Breast milk is best, but it contains little vitamin D, and babies are rarely outdoors now.
• Craig quoted a vitamin D half-life of about eight weeks (as spoken): an unsupplemented baby's level falls steadily after birth, so the risk of deficiency is high.

Nutritional rickets: thresholds and mechanism

Rickets is a growth plate disease, which is why only children get it. Outside the newborn period, nutritional rickets is most often caused by a combination of low vitamin D and low dietary calcium.

The mechanism Craig stressed: low vitamin D and low calcium trigger secondary hyperparathyroidism. The body is desperate to keep serum calcium normal ("you die if your serum calcium gets low"), and the price is phosphate wasting in the urine. Low phosphate causes rickets and osteomalacia. "Every form of rickets is due to low phosphate."

Clinical features

Craig showed follow-up films of another child: at six months after treatment the rickets had healed but the deformity had not, and at 30 months, despite ongoing supplementation and orthopaedic surgery, long-term lower limb deformity remained. Prevention matters because damage is not always reversible.

Investigations

• Do: serum calcium, phosphate, alkaline phosphatase, PTH, 25-hydroxy vitamin D, and a wrist X-ray (you need to know whether there are radiological changes; rickets is a radiological diagnosis).
• Don't: 1,25-dihydroxy vitamin D. It can be high, low or normal in nutritional rickets. "Only bone nerds like me really need to be ordering" it.
• Test the mother as well when an infant has rickets.

Incidence as spoken: about 5 per 100,000 in Australia, roughly twice Canada's rate (Canada supplements routinely), with the United States highest among the countries shown. Hypocalcaemic seizures are much rarer, though Craig has seen "too much of that".

Who is at risk

• Reduced skin synthesis (the biggest factor): little time outdoors, covering clothing.
• Maternal vitamin D deficiency (passed to the baby).
• Prolonged exclusive breastfeeding without supplementation. Breast is still best.
• Darker skin: Craig said a darker-skinned person may need about seven times longer in the sun to make the same amount of vitamin D. Be culturally sensitive, but do not shy away from the conversation.
• Reduced gut function (malabsorption) and obesity, which is rising.

Treatment and follow-up

Craig's petrol bowser analogy: if the tank is empty you fill it up first ("$500 later"), then top it up a little each day. For nutritional rickets that means large treatment doses of vitamin D together with calcium, then daily maintenance. The detailed regimen was on his slides and not read out.

• The optimal treatment is calcium plus cholecalciferol, not vitamin D alone.
• Check at three months: bloods and X-rays should all be better.
• If not, consider a rarer genetic form of rickets that happens to coexist with vitamin D deficiency. Craig has been "fooled" by this.

Prevention: the plan

"Prevention is everyone's responsibility. This is all I really want you to take away from today."

Beyond bone

Bone health in later life

A recent trial in about 1100 pregnant women (roughly 550 vitamin D, 550 placebo) followed the children's bone density to seven years. It showed a modest increase in whole-body bone mineral density and, as spoken, a 2% reduction in childhood fractures. Craig's framing: "adult osteoporosis is a childhood disorder that manifests in adult life." Building bone in childhood may reduce hip fractures decades later.

Immune and allergic disease

• Immune cells carry the vitamin D receptor and make active vitamin D locally. Associations have been described with multiple sclerosis, type 1 diabetes and rheumatoid arthritis.
• One systematic review (7 studies, about 4000 mother-child pairs) found no benefit of maternal supplementation for allergic and respiratory outcomes, including eczema.
• Another systematic review found higher cord blood vitamin D was linked with less eczema at 12 months. "The data is confusing."

Type 1 diabetes

• The TEDDY study: maternal supplementation did not reduce type 1 diabetes in the child.
• A EURODIAB study (as we read the ASR) supplementing at-risk children during childhood showed a modest reduction in islet autoimmunity. Timing of supplementation may matter.
• Craig thinks diabetes is where the non-bone evidence is strongest, but overall the data are limited and conflicting.

GP clinic checklist

1. Check every pregnant woman is taking a supplement with about 1000 units of vitamin D a day.
2. Pregnant and deficient: 2000 to 4000 units daily for three months; no stoss dosing.
3. Advise 400 units a day for all infants for the first year, especially if exclusively breastfed.
4. Ask about dietary calcium as well as vitamin D (two glasses of milk a day or equivalent for children).
5. Identify at-risk children (darker skin, covering clothing, little outdoor time, maternal deficiency, malabsorption, obesity) and supplement 600 units a day.
6. Suspected rickets: calcium, phosphate, ALP, PTH, 25-OH vitamin D and wrist X-ray. Test the mother.
7. Treat with calcium plus cholecalciferol; recall at three months; refer if not resolving.

Transcript caveats

allcpd.drkotha.com · directory