Causes, Diagnosis and Treatment of Rickets

• CAUSES OF RICKETS:
• 1. VITAMIN D DISORDERS
• 2. CALCIUM DEFICIENCY
• 3. PHOSPHORUS DEFICIENCY
• 4. RENAL LOSSES
• 5. DISTAL RTA

• 4. RENAL LOSSES
• 5. DISTAL RTA
Nutritional Vit D deficiency
Congenital Vit D deficiency
Secondary Vit D deficiency
-Malabsorption
-Increased degradation
-Decreased liver 25-hydroxylase
Vit D–dependent rickets type 1
Vit D–dependent rickets type 2
Chronic renal failure

• 4. RENAL LOSSES
• 5. DISTAL RTA
Low intake
-Diet
-Premature infants (rickets of
prematurity)
Malabsorption
-Primary disease
-Dietary inhibitors of calcium
absorption

• 4. RENAL LOSSES
• 5. DISTAL RTA
Inadequate intake
-Premature infants (rickets of
prematurity)
-Aluminum-containing
antacids

• 4. RENAL LOSSES
• 5. DISTAL RTA
XL Hypophosphatemic rickets
AD Hypophosphatemic rickets
Hereditary hypophosphatemic
rickets with hypercalciuria
Overproduction of
phosphatonin
-Tumor-induced rickets
-McCune-Albright syndrome
-Epidermal nevus syndrome
-Neurofibromatosis
Fanconi syndrome
Dent disease

• DIAGNOSIS OF RICKETS:
• HISTORY
• PHYSICAL FINDINGS
• RADIOGRAPHICAL CHANGES
• LAB TESTS

• Clinical Evaluation.
• HISTORY REGARDING:
• 1.Diet intake of Vit D, Calcium
• 2.Sun exposure
• 3.Maternal risk factors for vit D deficiency.
• 4.Child's medication history.
• 5.History of liver or intestinal disease – malabsorption of vit D
• 6.History of Renal disease
• 7.Family history of bone disease, short stature, unexplained sibling
death.
• 8.History of dental caries, poor growth, delayed walking, waddling
gait, pneumonia, and hypocalcemic symptoms.

• CLINICAL FEATURES:
• GENERAL
• Failure to thrive
• Listlessness
• Protuding abdomen
• Muscle weakness (especially proximal)
• Fractures

• HEAD
• Craniotabes
• Frontal bossing
• Delayed fontanelle closure
• Delayed dentition; caries
• Craniosynostosis

• CHEST
• Rachitic rosary
• Harrison groove
• Respiratory infections and atelectasis
• BACK
• Scoliosis
• Kyphosis
• Lordosis

• EXTREMITIES
• Enlargement of wrists and ankles
• Valgus or varus deformities
• Anterior bowing of the tibia and femur
• Coxa vara
• Leg pain

• EXTREMITIES
• Valgus or varus deformities
• Windswept deformity
(combination of valgus deformity
of 1 leg with varus deformity of
the other leg)
• Anterior bowing of the tibia and femur
• Coxa vara

• HYPOCALCEMIC SYMPTOMS:
• Tetany
• Seizures
• Stridor due to laryngeal spasm

• Craniotabes:
• Softening of cranial bones.
• Detected by applying pressure at the occiput or parietal bones.

• Craniotabes:
• Craniotabes may also be secondary to
-osteogenesis imperfecta,
-hydrocephalus,
-syphilis.
• May be a normal finding in many newborns, especially near the
suture lines, but disappears within a few months of birth.

• Rachitic Rosary:
• Widening of costochondral junctions  Rachitic rosary.
• Feels like beads of a rosary as the examiner's fingers move along the
costochondral junctions from rib to rib.
• Growth plate widening:
• This is also responsible for the enlargement at wrists and ankles.

• Harrison groove:
• Horizontal depression along lower anterior chest.
• Due to pulling of softened ribs by diaphragm during inspiration.
• Softening of ribs  impairs air movement & predisposes to
atelectasis.
• Risk of pneumonia high in children with rickets

• RADIOLOGY:
• Decreased calcification  Thickening of growth plate.
• FRAYING: Edge of metaphysis loses its sharp border.
• CUPPING: Edge of metaphysis changes from convex or flat to concave
surface. Most easily seen at distal ends of radius, ulna, fibula.
• Widening of distal end of metaphysis  Clinically causes thickened
wrists and ankles, and rachitic rosary.

• RADIOLOGY:
• Especially on PA view of wrist. Also in other growth plates.
• Other radiologic features:
-Coarse trabeculation of diaphysis -Generalized rarefaction.

• LAB TESTS:
• Initial laboratory tests in Rickets should include:
• Serum calcium;
• Phosphorus;
• Alkaline phosphatase;
• Parathyroid hormone (PTH);
• 25-hydroxyvitamin D;
• 1,25-dihydroxyvitamin D3;
• Creatinine; and
• Electrolytes.

• Urinalysis: Useful for detecting glycosuria and aminoaciduria
(positive dipstick for protein) in Fanconi syndrome.
• Evaluation of urinary excretion of calcium (24 hr collection for
calcium or calcium-creatinine ratio) : If hereditary hypophosphatemic
rickets with hypercalciuria or Fanconi syndrome is suspected.
• Direct measurement of other fat-soluble vitamins (A, E, and K) or
indirect assessment of deficiency (prothrombin time for vitamin K
deficiency) : if malabsorption is a consideration.

• Laboratory Findings in Disorders Causing Rickets:

• VITAMIN D:
7-DEHYDROCHOLESTEROL
UV radiation in sunlight Inhibited by melanin
VITAMIN D3
Bound to Vit D binding protein Transported to liver
25-Hydroxylase
25-D
1 α Hydroxylase Kidney
1,25 D
Binds to intracellular receptor
and forms a COMPLEX
CALCIUM PHOSPHORUS BONE PTH secrn Inhibits its own
absorption absorption resorption synthesis in kidney

• NOTE:
• PTH  Increased Calcium, Decreased Phosphate
• 1,25 D  Increased Calcium, Increased Phosphate
• Calcitonin  Decreased Calcium

• NUTRITIONAL VIT D DEFICIENCY:
• Most common cause of rickets globally.
• Etiology:
• Most common in infancy: Due to poor intake + inadequate cutaneous
synthesis.
• Transplacental transport of vitamin D, mostly 25-D,provides vitamin D
for 1st 2 mo of life unless there is severe maternal vitamin D
deficiency.
• Breast-fed infants, because of low vitamin D content of breast milk,
rely on cutaneous synthesis or vitamin supplements.
• Infants who receive formula receive adequate vitamin D, even
without cutaneous synthesis.

• Most common cause of rickets globally.
• Etiology:
• Cutaneous synthesis is limited by ineffective winter sun; and by
increased skin pigmentation.
• Mothers may have same risk factors  decreased maternal vitamin D
 reduced vitamin D in breast milk + less transplacental delivery of
vitamin D.
• Unconventional dietary practices, such as vegan diets that use
unfortified soy milk or rice milk.

• Laboratory Findings.
• Elevated PTH Hypophosphatemia
• Variable hypocalcemia
• Hypophosphatemia & hyperparathyroidism  Upregulation of renal
1α-hydroxylase  Wide variation in 1,25-D levels (low, normal, or
high)
• 1,25-D is only low when there is severe vitamin D deficiency.
• Some have metabolic acidosis secondary to PTH-induced renal
bicarbonate-wasting.
• There may be generalized aminoaciduria.

• DIAGNOSIS:
• History of poor vitamin D intake & risk factors for decreased
cutaneous synthesis.
• Radiographic changes consistent with rickets, and
• Laboratory findings.
• Normal PTH level almost never occurs with vitamin D deficiency and
suggests a primary phosphate disorder.
• Calcium deficiency may occur with or without vitamin D deficiency.
• A normal level of 25-D and a dietary history of poor calcium intake
support a diagnosis of isolated calcium deficiency.

• Treatment:
• Vitamin D + Calcium + Phosphorus.
• 2 strategies for vitamin D admn:
• Stoss therapy: 300,000–600,000 IU of vitamin D oral or IM as 2–4
doses over 1 day.
• Because doses are observed, stoss therapy is ideal where adherence to therapy is questionable.
• Alternative: Daily, high-dose vitamin D, with doses ranging from
2,000–5,000 IU/day over 4–6 wk.
• Either strategy should be followed by daily vitamin D intake of 400
IU/day, typically given as a multivitamin.
• Ensure adequate dietary calcium & phosphorus;
(milk, formula, and other dairy products)

• Treatment:
• Symptomatic hypocalcemia: IV Calcium acutely, followed by oral
calcium supplements, tapered over 2–6 wk in children who receive
adequate dietary calcium.
• Transient use of intravenous or oral 1,25-D (calcitriol) to reverse
hypocalcemia in acute phase.
(by providing active vitamin D during the delay as supplemental vitamin D is converted to
active vitamin D. )

• Prognosis.
• Most: Excellent response to treatment.
• Radiologic healing within a few months.
• Laboratory tests normalize rapidly.
• Many of the bone malformations improve dramatically, but children
with severe disease may have permanent deformities.
• Short stature does not resolve in some children.
• Prevention.
• Universal administration of daily multivitamin containing 200–400 IU
of vitamin D to children who are breast-fed.
• For other children, diet should have sources of vitamin D.

• CONGENITAL VIT D DEFICIENCY:
• Occurs if severe maternal vitamin D deficiency during pregnancy.
• Maternal risk factors:
-Poor dietary intake of vitamin D,
-Lack of adequate sun exposure, and
-Closely spaced pregnancies.

• Newborns may have:
-symptomatic hypocalcemia,
-intrauterine growth retardation,
-decreased bone ossification, and
-classic rachitic changes.
• Subtler maternal vitamin D deficiency:
-adverse effect on neonatal bone density
-adverse effect on birthweight,
-defect in dental enamel, and
-predispose to neonatal hypocalcemic tetany.

• Treatment of congenital rickets:
-Vitamin D supplementation
-Adequate intake of Calcium and Phosphorus.
• Prevention:
-Use of prenatal vitamins containing vitamin D.

• SECONDARY VIT D DEFICIENCY:
• Etiology.
-inadequate intake,
-inadequate absorption,
-decreased hydroxylation in liver, and
-increased degradation.

• Etiology.
-inadequate intake,
-decreased hydroxylation in liver &
Liver & gastrointestinal
diseases:
-Cholestatic liver disease,
-Defects in bile acid metabolism
-Cystic fibrosis
-Other causes of pancreatic
dysfunction,
-Celiac disease,
-Crohn disease.
-Intestinal lymphangiectasia
-After intestinal resection.

• Etiology.
-inadequate intake,
-decreased hydroxylation in liver
Severe Liver disease:
-Insufficient enzyme axn
(25 hydroxylase)

• Etiology.
-inadequate intake,
-decreased hydroxylation in liver &
-Drugs by inducing P450
-Anticonvulsants: Phenobarb,
Phenytoin.
-ATT : Isoniazid,
Rifampin

• Treatment.
• 1. Malabsorption:
• Requires high doses of vitamin D.
• 25-D (25–50 μmg/day or 5–7 μmg/kg/day)-Better absorption - superior to vitamin D3.
• Alternatively:
• 1,25-D (also better absorbed in presence of fat malabsorption) or
• Parenteral vitamin D.
• 2. In rickets due to increased degradation of Vit D by P450 system:
Require same acute therapy as for nutritional deficiency,
followed by
Long-term administration of high doses of Vit D (e.g., 1,000 IU/day),
(With dosing titrated based on serum levels of 25-D)
Some patients require as much as 4,000 IU/day.

• VITAMIN D–DEPENDENT RICKETS, TYPE 1.
• Autosomal Recessive.
• Mutations in gene encoding renal 1α-hydroxylase.
• Prevent conversion of 25-D into 1,25-D.
• Normally present during 1st 2 yr of life.
• Can have any features of rickets, including symptomatic
hypocalcemia.

• Normal levels of 25-D, but low levels of 1,25-D.
• Occasionally, 1,25-D levels may be low normal.
• High PTH.
• Low serum phosphorus levels.
• Metabolic acidosis & generalized aminoaciduria.
(Due to renal tubular dysfunction)

• VITAMIN D:
7-DEHYDROCHOLESTEROL
UV radiation in sunlight Inhibited by melanin
VITAMIN D3
Bound to Vit D binding protein Transported to liver
25-Hydroxylase
25-D
1 α Hydroxylase Kidney
1,25 D
Binds to intracellular receptor
and forms a COMPLEX
CALCIUM PHOSPHORUS BONE PTH secrn
absorption absorption resorption

• Normal levels of 25-D, but low levels of 1,25-D.
• Occasionally, 1,25-D levels may be at the lower limit of normal, but
this is inappropriate, given the high PTH and low serum phosphorus
levels, both of which should increase the activity of renal 1α-
hydroxylase and cause elevated levels of 1,25-D.
• As in nutritional vitamin D deficiency, renal tubular dysfunction may
cause a metabolic acidosis and generalized aminoaciduria.

• TREATMENT:
• Long-term treatment with 1,25-D (calcitriol).
• Initial: 0.25–2 μmg/day, with lower doses used once the rickets has
healed.
• During initial therapy, ensure adequate intake of calcium.
• Periodic monitoring of urinary calcium excretion,
with target of <4 mg/kg/day.

• Autosomal Recessive.
• Mutations in gene encoding the vitamin D receptor.
• Prevents a normal physiologic response to 1,25-D.
• Levels of 1,25-D are extremely elevated.
• Less severe disease is associated with a partially functional vitamin
D receptor.

• Most patients present during infancy.
• Less severely affected patients may not be diagnosed until
adulthood.
• 50–70% of children have alopecia.

• Treatment.
• Some patients, especially those without alopecia, respond to
extremely high doses of vitamin D2, 25-D, or 1,25-D.
• Due to partially functional vitamin D receptor.
• 3–6 month trial of high-dose vitamin D and oral calcium.

• Treatment.
• The initial dose of 1,25-D should be 2 μmg/day, but some patients
require doses as high as 50–60 μmg/day.
• Calcium doses range from 1,000–3,000 mg/day.

• CHRONIC RENAL FAILURE:
• Decreased activity of 1α-hydroxylase in kidney  diminished
production of 1,25-D.
• In chronic renal failure, unlike the other causes of vitamin D
deficiency, patients have hyperphosphatemia as a result of
decreased renal excretion.
• Along with inadequate calcium absorption and secondary
hyperparathyroidism, the rickets may be worsened by the
metabolic acidosis of chronic renal failure.

• CHRONIC RENAL FAILURE:
• Treatment.
• A form of vitamin D which can act without 1-hydroxylation by
kidney should be used for therapy (Calcitriol).
• Calcitriol permits both adequate absorption of calcium and directly
suppresses the parathyroid gland.
• Dietary phosphorus restriction & Oral phosphate binders.
(Because hyperphosphatemia is a stimulus for PTH secretion)
• Chronic metabolic acidosis should be corrected with alkali.

• CALCIUM DEFICIENCY:
• CAUSES:
• After weaning / early weaning.
• Low calcium content in diet. (<200 mg/day)
• Grains & green leafy vegetables high in phytate, oxalate, and
phosphate  decrease absorption of dietary calcium.
• In children getting IV nutrition without adequate calcium.
• Malabsorption of calcium:
-in celiac disease,
-intestinal abetalipoproteinemia, and
-after small bowel resection.

• Clinical Manifestations.
• Classic signs and symptoms of rickets.
• Presentation: infancy or early childhood, although some are
diagnosed in teenagers.
• Because calcium deficiency occurs after cessation of breast-feeding,
it tends to occur LATER than nutritional vitamin D deficiency that is
associated with breast-feeding.

• Diagnosis.
• Laboratory findings:
• Increased levels of Alkaline phosphatase, PTH, and 1,25-D.
• Calcium levels may be normal or low, although symptomatic
hypocalcemia is uncommon.
• Decreased urinary excretion of calcium.
• Secondary hyperparathyroidism  Low Serum phosphorus levels.
• In some children, there is coexisting nutritional vitamin D deficiency
 Low 25-D.

• Treatment.
• Calcium supplement (350–1,000 mg/day of elemental calcium).
• Vitamin D supplementation if concurrent vitamin D deficiency.
• Prevention:
-Discourage early cessation of breast-feeding.
-Increase dietary sources of calcium.

• INADEQUATE INTAKE.
• Only in starvation or severe anorexia.
• Malabsorption of phosphorus.(celiac disease, cystic
fibrosis, cholestatic liver disease); But rickets is primarily
due to malabsorption of vitamin D and/or calcium.
• Isolated malabsorption of phosphorus: in long-term use of
aluminum-containing antacids.

• PHOSPHATONIN.
Phosphatonin (a humoral mediator)
Decreases renal tubular reabsorption Decreases activity of renal
of phosphate 1α-hydroxylase
Increased excretion of Phosphorus Decrease in production of 1,25-D.
Decreases S.phosphorus
• Fibroblast growth factor-23 (FGF-23) is the most well characterized phosphatonin.

• X-LINKED HYPOPHOSPHATEMIC RICKETS.
• X-linked hypophosphatemic rickets (XLH) is the most common
genetic cause of Rickets.
• Defective gene is on X chromosome.
• Female carriers are affected, so it is X-linked dominant.
• Pathophysiology.
• Defective gene: ‘PHEX’ (PHosphate-regulating gene with homology
to Endopeptidases on X chromosome)

PHEX GENE
Product of this gene
inactivates phosphatonin
Increased Phosphatonin
Decreased Phosphorus

• Rickets.
• Abnormalities of lower extremities and poor growth are the
dominant features.
• Short stature
• Delayed dentition, tooth abscesses.

• High renal excretion of phosphate,
• Hypophosphatemia,
• Increased alkaline phosphatase,
• PTH and serum calcium levels are normal.
• Hypophosphatemia normally upregulates renal 1α-
hydroxylase, and should lead to an increase in 1,25-D, but
these patients have low or inappropriately normal levels.

• Treatment.
• Patients respond well to combination of oral phosphorus
and 1,25-D (calcitriol).
• Daily : 1–3 g of elemental phosphorus divided into 4–5
doses.
• Frequent dosing helps to prevent prolonged decrements in
serum phosphorus because there is a rapid decline after
each dose.
• In addition, frequent dosing decreases diarrhea, a
complication of high-dose oral phosphorus.
• Calcitrol : 30–70 ng/kg/day divided into 2 doses.

• Complications of treatment occur when there is no balance
between phosphorus supplementation and calcitriol.
• Excess phosphorus  decrease enteral calcium absorption 
secondary hyperparathyroidism  worsening of bone lesions.
• Excess calcitriol  hypercalciuria and nephrocalcinosis; it may
even cause hypercalcemia.
• Hence, laboratory monitoring of treatment includes :
Serum calcium, phosphorus, alkaline phosphatase, PTH, and
urinary calcium; Periodic renal ultrasounds to evaluate
nephrocalcinosis.

• Normalization of alkaline phosphatase levels is a more
useful method of assessing therapeutic response than
measuring serum phosphorus.
• For children with significant short stature, growth hormone
is an effective option.
• Children with severe deformities may need osteotomies,
but done only when treatment has led to resolution of the
bone disease.

• AUTOSOMAL DOMINANT HYPOPHOSPHATEMIC
RICKETS.
• Less common than XLH.
• Incomplete penetrance and variable age of onset.
• Mutation in gene encoding FGF-23.
• Mutation prevents degradation of FGF-23 by proteases, leading to
increased levels of this phosphatonin.
• In ADHR, as in XLH, abnormal laboratory findings are
hypophosphatemia, an elevated alkaline phosphatase level, and a low
or inappropriately normal 1,25-D level .
• Treatment is similar as in XLH.

• Rickets Associated with Renal Tubular Acidosis :
• Rickets may be present in RTA, particularly in type II or proximal RTA.
• Hypophosphatemia and phosphaturia are common.
(Also characterized by hyperchloremic metabolic acidosis, various
degrees of bicarbonaturia, and frequently, hypercalciuria and
hyperkaluria. )
• Proximal RTA is treated with both bicarbonate and oral phosphate
supplements to heal rickets.
• Vitamin D given to offset the secondary hyperparathyroidism that
complicates oral phosphate therapy.

• Rickets Associated with Renal Tubular Acidosis
• Bone demineralization without overt rickets: in type I or distal RTA.
• Bone pain, growth retardation, osteopenia, and, occasionally,
pathologic fractures.
• Bone demineralization in distal RTA probably due to dissolution of
bone because calcium carbonate in bone serves as a buffer against
metabolic acidosis due to hydrogen ions retained in RTA.
• Administration of sufficient bicarbonate to reverse acidosis stops
bone dissolution and the hypercalciuria that is common in distal RTA.
• Following therapy, growth in patients with type II (proximal) RTA is
greater than in patients with primary Fanconi syndrome.

• RICKETS OF PREMATURITY :
• Pathogenesis.
• Transfer of calcium and phosphorus from mother to fetus occurs
throughout pregnancy, but 80% occurs during the 3rd trimester.
• Premature birth interrupts this process  rickets develop.
• Most cases of rickets of prematurity occur in birthweight <1,000 g.
• More likely to develop in infants with lower birthweight and younger
gestational age.
• Rickets occurs because unsupplemented breast milk and standard
infant formula do not contain enough calcium and phosphorus to
supply the needs of the premature infant.

• RICKETS OF PREMATURITY
• Rickets of prematurity presents 1–4 mo after birth.
• Infants may have nontraumatic fractures.
• Fractures & softening of ribs  decreased chest compliance 
respiratory distress due to atelectasis & poor ventilation.
• Rachitic respiratory distress usually develops >5 weeks after birth,
distinguishing it from the early-onset respiratory disease of
premature infants.

• Poor linear growth.
• Enamel hypoplasia.
• Poor bone mineralization  dolichocephaly.
• Classic rachitic findings MAY be present.
• Most infants with rickets of prematurity have no clinical
manifestations, and diagnosis is based on radiographic & lab
findings.

• Due to inadequate intake: serum phosphorus level is low or low-
normal.
• Renal conservation of phosphate : Low urine phosphate level;
• Most patients have normal levels of 25-D, unless there has been
inadequate intake or poor absorption .
• Hypophosphatemia stimulates renal 1α-hydroxylase  1,25-D is
high or high-normal. These high levels may contribute to bone
demineralization because 1,25-D stimulates bone resorption.

• Serum calcium is low, normal, or high, and patients often have
hypercalciuria.
• Elevated serum calcium levels and hypercalciuria are secondary to:
-increased intestinal absorption and bone dissolution due to
elevation of 1,25-D levels and
-the inability to deposit calcium in bone because of an
inadequate phosphorus supply.
• There is an inadequate supply of calcium and phosphorus, but the
deficiency in phosphorus is greater.

• Alkaline phosphatase often elevated, but some have normal levels.
• No single blood test is 100% sensitive for the diagnosis of rickets.
• The diagnosis should be suspected in infants with :
-alkaline phosphatase level more than 5–6 times the upper
limit of normal for adults (unless there is concomitant liver
disease)
or
-phosphorus level <5.6 mg/dL.

• Confirmed by radiologic evidence of rickets- best seen on films of1
wrists and ankles.
• Rachitic rosary may be visible on chest x-ray.
• Unfortunately, x-rays are not able to detect early demineralization
of bone because changes are not evident until there is >20–30%
reduction in bone mineral content.

• Diagnosis.
• Screening tests are recommended.
• Weekly measurements of calcium, phosphorus, and alkaline
phosphatase.
• Periodic measurement of serum bicarbonate is important because
metabolic acidosis causes dissolution of bone.
• At least 1 screening x-ray for rickets at 6–8 wk of age; additional
films in very high-risk infants.

• Prevention.
• Adequate amounts of calcium, phosphorus & vitamin D decreases
the risk of rickets of prematurity.
• Parenteral nutrition is often necessary initially in very premature
infants. Current amino acid preparations allow for higher
concentrations of calcium and phosphate.
• Early transition to enteral feedings is also helpful.
• Soy formula should be avoided because there is decreased
bioavailability of calcium and phosphorus.

• Prevention.
• Human milk fortified with calcium & phosphorus or preterm infant
formula, which has higher concentrations of calcium and
phosphorus than standard formula.
• Increased mineral feedings should continue until the infant weighs
3–3.5 kg.
• These infants should also receive approximately 400 IU/day of
vitamin D via formula and vitamin supplements.
• Treatment.
• Ensure adequate calcium, phosphorus, and vitamin D.

Causes, Diagnosis and Treatment of Rickets

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Causes, Diagnosis and Treatment of Rickets

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