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EX-000080·DNB Ortho·2023·Rickets — Orthopaedic Sequelae

Describe the regulation of mineral metabolism by 1,25-(OH)₂ vitamin D. Discuss the classification of rickets. Management of a child with severe genu valgum deformity in both lower limbs.

Wiki topic: Rickets — Orthopaedic Sequelae
Answer

Vitamin D Regulation, Classification of Rickets and Management of Severe Genu Valgum

DNB Orthopaedics • October 2023 • Paper I • Question 4 • 10 Marks [3+3+4]

Introduction

1,25-dihydroxy vitamin D [1,25-(OH)₂D; calcitriol] is the active hormonal form of vitamin D and is a major regulator of calcium and phosphate homeostasis. Deficiency of mineral availability at the growing physis results in rickets, characterized by defective mineralization of growth plate cartilage and newly formed osteoid.

Severe rickets may produce progressive angular deformity such as bilateral genu valgum. Management requires correction of the underlying metabolic disorder before definitive deformity correction.

Key orthopaedic principle: Do not correct a rachitic deformity surgically until the metabolic disease has been treated and the child is biochemically healing.

A. Regulation of Mineral Metabolism by 1,25-(OH)₂ Vitamin D [3 Marks]

Vitamin D Metabolism

Skin / Diet
   ↓
Vitamin D3 / D2
   ↓
LIVER
25-hydroxylase
   ↓
25-hydroxy vitamin D
[25(OH)D]
   ↓
KIDNEY
1α-hydroxylase
   ↓
1,25-(OH)₂ vitamin D
CALCITRIOL

25(OH)D is the major circulating storage form and is the preferred test for assessing vitamin D status. The kidney converts it to the active hormone 1,25-(OH)₂D.

Regulation of Renal 1α-Hydroxylase

Stimulates Calcitriol Formation Inhibits Calcitriol Formation
Parathyroid hormone

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