Question:hard
A child with this deformity. He has recurrent tooth abscesses. Calcium normal, Phosphorus low, PTH normal, ALP high. Diagnosis is?
A child with this deformity. He has recurrent tooth abscesses. Calcium normal, Phosphorus low, PTH normal, ALP high. Diagnosis is?
Show Hint
Normal calcium with normal PTH but low phosphate — plus recurrent dental abscesses — is a renal phosphate-wasting rickets, not a calcium/vitamin-D problem.
Updated On: Jun 22, 2026
- Nutritional rickets
- VDDR1
- VDDR2
- Hypophosphatemic rickets
Show Solution
The Correct Option is D
Solution and Explanation
Use PTH and phosphate as the discriminators.
All four options can bow a child's legs and raise ALP, so the deformity and ALP alone cannot separate them. The work is done by two values: PTH and phosphate.
Branch 1 - is PTH high or normal? Any rickets driven by calcium deficiency (nutritional, VDDR1, VDDR2) lowers serum calcium, which switches on the parathyroids, so PTH is $high$. Here PTH is normal - this single fact eliminates A, B and C together, because none of them can keep PTH normal.
Branch 2 - what is the phosphate? With calcium and PTH normal, the only way to get rickets is to lose phosphate. The reported phosphate is low. A primary renal phosphate leak (FGF23-driven) gives precisely this: normal Ca, normal PTH, low PO₄, high ALP. That disorder is hypophosphatemic rickets.
The dental clue seals it. Hypophosphatemic rickets is famous for spontaneous recurrent dental abscesses from poorly mineralised dentine and large pulp horns that reach close to the tooth surface, letting bacteria seed the pulp - the "recurrent tooth abscesses" in the stem is a textbook pointer to this condition and to no other option.
One more mechanistic note. The underlying driver is usually excess FGF23, a hormone that tells the proximal renal tubule to dump phosphate into the urine and also suppresses calcitriol activation. Because calcium handling is left essentially intact, the parathyroid axis is never triggered, which is why PTH stays normal - the very finding that separates this from the three calcium-deficiency rickets.
Conclusion: normal Ca + normal PTH + low PO₄ + recurrent dental abscesses = Hypophosphatemic rickets (Option D).
All four options can bow a child's legs and raise ALP, so the deformity and ALP alone cannot separate them. The work is done by two values: PTH and phosphate.
Branch 1 - is PTH high or normal? Any rickets driven by calcium deficiency (nutritional, VDDR1, VDDR2) lowers serum calcium, which switches on the parathyroids, so PTH is $high$. Here PTH is normal - this single fact eliminates A, B and C together, because none of them can keep PTH normal.
Branch 2 - what is the phosphate? With calcium and PTH normal, the only way to get rickets is to lose phosphate. The reported phosphate is low. A primary renal phosphate leak (FGF23-driven) gives precisely this: normal Ca, normal PTH, low PO₄, high ALP. That disorder is hypophosphatemic rickets.
The dental clue seals it. Hypophosphatemic rickets is famous for spontaneous recurrent dental abscesses from poorly mineralised dentine and large pulp horns that reach close to the tooth surface, letting bacteria seed the pulp - the "recurrent tooth abscesses" in the stem is a textbook pointer to this condition and to no other option.
One more mechanistic note. The underlying driver is usually excess FGF23, a hormone that tells the proximal renal tubule to dump phosphate into the urine and also suppresses calcitriol activation. Because calcium handling is left essentially intact, the parathyroid axis is never triggered, which is why PTH stays normal - the very finding that separates this from the three calcium-deficiency rickets.
Conclusion: normal Ca + normal PTH + low PO₄ + recurrent dental abscesses = Hypophosphatemic rickets (Option D).
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