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Explain me the VITAMIN D , metabolism , formation , functions from HARRISONS internal medicine latest edition . Everything relating to VITAMIN D , the disorders relatinh to it . As i am a PG resident pursuing MD Biochemistry .

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"vitamin D" deficiency metabolism

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This is a complete, research-grade breakdown sourced directly from Harrison's Principles of Internal Medicine, 22nd Edition (2025). Here's a quick orientation to the material above:
What's covered and where to focus for MD Biochemistry:
  1. Synthesis & Metabolism (Section 2-3) - The three-step activation (skin → liver → kidney), the enzymes (CYP2R1, CYP27B1, CYP24A1), their genes, regulation by PTH/FGF23/calcium, and protein binding via DBP. This is pure biochemistry and is exam-critical.
  2. Mechanism of Action (Section 4) - VDR-RXR heterodimer, VDREs, ligand-independent VDR action in hair follicles - these are molecular biochemistry concepts.
  3. Functions (Section 5) - Classical (mineral ion homeostasis) and pleiotropic effects, with the important caveat that RCTs have not confirmed non-skeletal benefits of supplementation.
  4. Disorders (Section 7) - All disorders organized by pathomechanism:
    • VDDR Type I (CYP27B1 mutation) vs. Type II (VDR mutation)
    • FGF23-mediated phosphopenic rickets (XLH, ADHR, oncogenic osteomalacia)
    • Drug-induced deficiency (phenytoin, barbiturates, rifampin - via CYP induction)
    • CYP24A1 loss-of-function → hypercalcemia
    • Sarcoidosis hypercalcemia - the unregulated extra-renal 1α-hydroxylase mechanism
  5. Clinical preparations (Section 9) - Helps understand which diseases need active calcitriol vs. standard vitamin D.
The biochemistry exam highlight: CYP27B1 (1α-hydroxylase) is the rate-limiting, tightly regulated step, and CYP2R1 (25-hydroxylase) is substrate-driven and not tightly regulated - this distinction explains why 25(OH)D is the best clinical marker and why 1,25(OH)₂D can be paradoxically elevated even in deficiency.
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