Vitamin D deficiency is a widespread problem globally and in India. It can cause rickets in children and bone problems in adults. The document discusses the causes, presentation, diagnosis, and treatment of vitamin D deficiency. Key points include that it is caused by low dietary intake and sun exposure, symptoms range from bone pain to rickets, screening involves vitamin D and calcium levels as well as imaging, and treatment consists of high dose vitamin D supplements and calcium for several weeks.

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Vitamin-D DeficiencyVitamin-D Deficiency
Dr. M. S. PrasadDr. M. S. Prasad
Retired Consultant & Head
Department of Pediatrics
VM Medical College & Safdarjung Hospital
New Delhi

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S Balasubramanian, K Dhanalakshmi and Sumanth Amperavani:
Vitamin-D Deficiency in Childhood – A Review of Current
Guidelines on Diagnosis and Management.
Indian Pediatrics, Vol. 50 – July 15, 2013 pp 669 – 675.
Indian Pediatrics, Volume 51, April 15, 2014.

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IntroductionIntroduction
• Most common nutritional deficiency,
• One of the most common undiagnosed
medical conditions in the world.
• Vitamin-D has evolved into a hormone.

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FunctionsFunctions
• Regulates calcium and bone metabolism,
• Reduce the risk of chronic diseases:
– Auto-immune diseases,
– Malignancies,
– Cardiovascular, and
– Infectious diseases.

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Facts!!Facts!!
• It has been estimated that 1 billion people
worldwide have vitamin-D deficiency or
insufficiency.
• Though majority of population in India lives in
areas with ample sunlight throughout the year,
vitamin-D deficiency is very common in all the
age groups and both the sexes across the
country.

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Facts!!!Facts!!!
• Nutritional Rickets has recently re-
emerged as a problem in many countries
where it was thought to have been
eradicated.
• Hospitalization rates for rickets in England
are now the highest in 5 decades.

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EtiologyEtiology
• Prevalence: 50-90% in India,
• Low dietary intake of calcium, skin color and
changing life-style.
• Deficiency of dietary calcium is more
responsible for rickets than deficiency of vitamin-
D.

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EtiologyEtiology (continued)
• Vitamin-D insufficiency + decreased
calcium intake or high phytate intake
combine to induce rickets.
• Common in infancy:
– Decreased dietary intake,
– Decreased cutaneous synthesis,
– Increased rate of exclusive breastfeeding, and
– Low maternal vitamin-D.

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EtiologyEtiology (continued)
• Decreased vitamin-D synthesis,
• Decreased nutritional intake of vitamin-D,
• Age & Physiology related,
• Decreased maternal vitamin-D stores,

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EtiologyEtiology (continued)
• Malabsorption,
• Decreased metabolic conversion to
active form,
• Increased degradation of 25(OH)D.

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Decreased vitamin-D synthesisDecreased vitamin-D synthesis
• Skin pigmentation,
• Physical agents blocking
UVR exposure,
• Clothing,
• Latitude,
• Season,
• Air-pollution,
• Cloud cover,
• Altitude.

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MalabsorptionMalabsorption
• Celiac disease,
• Pancreatic insufficiency (cystic fibrosis),
• Biliary obstruction (Biliary Atresia)

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Decreased metabolic conversionDecreased metabolic conversion
• Chronic Liver Disease,
• Chronic Renal Failure.

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Increased degradation of 25(OH)DIncreased degradation of 25(OH)D
• Drugs such as:
– Rifampicin,
– Isoniazid,
– Anticonvulsants,
– Glucocorticocoids.

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OthersOthers
• Decreased nutritional intake:
– Strict Vegan Diet.
• Age & Physiology related:
– Elderly,
– Obese,
– Institutionalized.
• Decreased maternal vitamin-D stores:
– Exclusive Breastfeeding.

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Definition of vitamin-D statusDefinition of vitamin-D status
• Debated by clinicians and researchers,
• Defined as serum level of 25(OH)D less
than 20 ng/dL.
• Less than 15 ng/dl: Definite Deficiency.
• Less than 5 ng/dL: Severe Deficiency.

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Serum vitamin-D levelsSerum vitamin-D levels
• Sufficient data are not available to define the
upper level of normal or dose levels above
which toxicity occurs.
• Previous thought: intoxication does not occur
until serum levels of 25(OH)D reach 100 to 200
ng/dL.
• Recently, risks identified at higher levels above
50 ng/dL.

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Vitamin-D levelsVitamin-D levels (continued)
• 25(OH)D:
– Major circulating vitamin-D,
– Half-life 2-3 weeks,
– Best available indicators of vitamin-D status.
• 1,25(OH)2D (calcitriol):
– Active form,
– Half-life only 4 hours.

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When to treat?When to treat?
• Symptomatic:
– Signs & symptoms of hypocalcaemia,
– Signs & symptoms of Rickets.
• Asymptomatic:
– When vitamin-D levels are in the
deficient range even if asymptomatic.

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Treatment RegimenTreatment Regimen
• D3: 2000 IU daily or D2: 50000 IU weekly.
• Stoss Therapy: 6 lakh units once, or
• D3: 1000 – 5000 IU/day for weeks, or
• D2: 50000 units/wk for 8 weeks.

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TreatmentTreatment
Group
Daily regimen
(8-12 weeks)
Weekly
regimen
(8-12 weeks)
Stoss Therapy
(Oral or IM)
Maintenance
<1 mo old 1000 IU 50000 IU 400-1000 IU
1-12 mo 1000-5000 IU 50000 IU
1 – 6 lakh units
over 1-5 days
400-1000 IU
1-18 y old 5000 IU 50000 IU
3-6 lakh units
over 1-5 days
600-1000 IU
>18 y old 6000 IU 50000 IU
3-6 lakh units
over 1-5 days
1500-2000 IU
Obese,
Malabsorption
6000-10000 IU 3000-6000 IU

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TreatmentTreatment (continued)
• A single dose of 300, 000 IU is not inferior to
double of this dose (600, 000 IU).
• The dose is effective orally.
• Intramuscular dose is painful and unnecessary.
• I. M. reserved for cases with malabsorption only.

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DiscussionDiscussion
• Lack of compliance  lack of response.
• Solution: Administer high dose of 100000 to 600000 IU
over 1-5 days (Stoss Therapy).
• Advantage of Stoss therapy: Vitamin-D is efficiently
stored in adipose tissue and muscle and is continuously
converted into active form.
• Shah and Finberg successfully administered 1 lakh IU
every 12 hours over 12 hour period.

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MaintenanceMaintenance
• After completion of treatment, continue
vitamin-D at 800-1000 IU/day till serum
alkaline phosphatase returns to normal.
• D3 is 3 times more potent than D2.
• Provide Calcium supplement throughout
treatment and maintenance.
(elemental calcium 30-75 mg/kg/day in 3 divided doses).

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Indian Pediatrics: Volume 51, April 15, 2014Indian Pediatrics: Volume 51, April 15, 2014
• Both 3 lakh and 6 lakh IU vitamin D3 as
single day doses are equally effective in
treating children between 6 months and 5
years of age with vitamin D deficiency
rickets.
• Neither dose is able to normalize the
vitamin D status of the children 3 months
after the administered dose.

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How to screen?
SAP
Normal ElevatedElevated
1. 25(OH)D
2. Calcium
3. Phosphorus
4. PTH and
5. Radiology.SAP =Serum Alkaline Phosphatase

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Whom to screen?Whom to screen?
• Dark skinned infants who live at higher
altitude and infants born to vitamin-D
deficient mothers.
• In the presence of non-specific symptoms
like poor growth, gross motor
developmental delay and unusual
irritability.

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Whom to screen?
• Children with suspected rickets, those with
osteopenia.
• Chronic Kidney Disease.
• Hepatic Failure.
• Hyperparathyroidism.

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Whom to screen?
• Malabsorption syndrome:
– Cystic Fibrosis,
– IBD (Inflammatory Bowel Disease),
– Crohn’s Disease
• Medications:
– Anticonvulsants,
– Glucocorticosteroids,
– AIDS medication,
– Antifungal (ketoconazole).

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Whom to screen?
• Obese children and adults (BMI>30 kg/M2
)
• Granuloma forming disorders:
– Sarcoidosis,
– Tuberculosis,
– Histoplasmosis.

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PreventionPrevention
• Improve maternal vitamin-D status,
• Administration of high dose of vitamin-D (400-
6400 IU) daily to breastfeeding mothers
increases anti-rachitic activity of breastmilk
without causing hypervitaminosis in the mother.
• Vitamin-D supplementation to preterm babies
since birth (400-800 IU/day)

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Sources of vitamin-DSources of vitamin-D
• Sunlight,
• Diet:
– Oily fish (salmon, mackerel and sardine),
– Cod liver oil,
– Liver and organ meat.

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