PEDBASE.org - The Pediatric Database - Detailed information of HYPERVITAMINOSIS D

HYPERVITAMINOSIS D

DEFINITION:

A disorder due to the excessive ingestion of Vitamin D resulting in neurologic, gastrointestinal, and renal manifestations.

EPIDEMIOLOGY:

incidence: ?
age of onset:
- any
risk factors:
- patients on vitamin D for chronic hyperphosphatemic states

PATHOGENESIS:

1. Background

1. Food Sources of Vitamin D (Calciferol)

dairy - fortified milk (10 ug/quart) & margarine, egg yolk
meats - fish-liver oils

2. Intestinal Absorption

in the presence of bile -> calciferol is absorbed by the intestinal mucosa and transported by chylomicrons to the liver and then the kidney (hydroxylated in both) -> 1,25(OH)2D3 (active form) is activated by:
- hypocalcemia
- hypophosphatemia
- parathyroid hormone
and acts at:
- intestines- promotes calcium and phosphate absorption
- bone - promotes bone dissolution & mineralization
- kidneys - promotes renal tubular calcium reabsorption

2. Pathogenesis

1. Chronic Hypervitaminosis

may occur after the ingestion of excessive amounts of vitamin D over weeks (>500 ug/d) or months (>45 ug/d)
may lead to (malignant) calcification of soft tissues:
- heart - aortic valvular stenosis
- blood vessels - hypertension
- renal tubules - nephrocalcinosis -> secondary nephrogenic DI -> polyuria, polydipsia;
- Fanconi Syndrome
- stomach - anorexia, nausea and vomiting, etc
- bronchi

CLINICAL FEATURES:

1. Chronic Hypervitaminosis D

1. Neurological Manifestations

hypotonia
irritability

2. Gastrointestinal Manifestations

anorexia with weight loss
constipation or diarrhea
nausea and vomiting

3. Renal Manifestations

polydipsia
polyuria/nocturia +/- dehydration

4. Ocular Manifestations

conjunctiva - clouding
cornea - clouding and calcific degeneration
retinopathy

5. Other Manifestations

aortic valvular stenosis
hypertension
pallor

2. Fanconi Syndrome

episodes of vomiting, dehydration, weakness, and unexplained fever; anorexia, constipation; polydipsia, polyuria; failure to thrive; growth failure; rickets

INVESTIGATIONS:

1. Hypervitaminosis D

1. Serum

hypercalcemia
evidence of dehydration - elevated BUN, creatinine

2. Urine

hypercalciuria
proteinuria

3. Imaging Studies

1. Renal Ultrasound

nephrocalcinosis +/- metastatic calcification

2. Skeletal X-Rays

metastatic calcification of long bones
generalized osteoporosis

3. 2D Echo

aortic valve stenosis

4. EKG

evidence of hypercalcemia
- short QT interval
- prolonged PR interval
- prolonged QRS duration +/- AV block

2. Fanconi Syndrome

1. Serum

normal anion gap hyperchloremic metabolic acidosis (with low serum bicarbonate)
normal or low amino acids
normal glucose
hypophosphatemia, hypokalemia, hypouricemia
elevated alkaline phosphatase

2. Urine

generalized (non-specific) hyperaminoaciduria
glycosuria, phosphaturia
pH < 5.5 with low specific gravity (hyposthenuria)
bicarbonaturia, hyperkaliuria, uricosuria, tubular protein-uria, carnitinuria, low urinary ammonia

3. Imaging Studies

1. Skeletal X-Rays

rickets, osteopenia, or osteoporosis

MANAGEMENT:

1. Diet

discontinue Vitamin D intake
decrease calcium intake

2. Medical

1. Vitamin D toxicity in infants

aluminum hydroxide po
cortisone
sodium versenate

2. Toxic Hypercalcemia

induce diuresis
- IV fluids
- lasix - 1-2 mg/kg IV

Pediatric Database - HYPERVITAMINOSIS D

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