A 68-year-old man with chronic malabsorption due to celiac disease presents with a 6-month history of progressive muscle weakness, ataxia, and loss of vibration sense in the lower limbs. He reports easy bruising and epistaxis for the past 2 months. Laboratory investigations reveal: INR 2.8 (normal: 0.8–1.1), aPTT 45 seconds (normal: 25–35 seconds), serum α-tocopherol 2.1 mg/L (normal: 5.4–17.2 mg/L). Prothrombin time corrects with fresh frozen plasma but not with vitamin K injection. Which vitamin deficiency best explains the neurological findings?

Explanation

## Clinical Presentation Analysis **Key Point:** This patient has two distinct deficiency syndromes: 1. **Coagulation defect** (INR ↑, aPTT ↑) — corrects with FFP but NOT vitamin K 2. **Neurological syndrome** (ataxia, vibration sense loss, muscle weakness) — characteristic of vitamin E deficiency ## Why Vitamin K Deficiency Does NOT Explain Neurological Findings | Feature | Vitamin K Deficiency | Vitamin E Deficiency | |---------|----------------------|----------------------| | **Coagulation defect** | Yes (corrects with vitamin K) | No | | **INR/aPTT correction** | Corrects with vitamin K | Does NOT correct with vitamin K | | **Neurological signs** | Absent | Present (ataxia, neuropathy) | | **Mechanism** | Impaired synthesis of factors II, VII, IX, X | Impaired antioxidant protection of myelin | **Clinical Pearl:** The fact that coagulation defect does NOT correct with vitamin K injection indicates a **dual deficiency**: vitamin K deficiency (explaining coagulopathy) PLUS vitamin E deficiency (explaining neurological findings). Both are common in celiac disease due to fat malabsorption. ## Pathophysiology of Vitamin E Deficiency Neuropathy **High-Yield:** Vitamin E (α-tocopherol) is a lipophilic antioxidant essential for: - Protection of polyunsaturated fatty acids in myelin sheaths - Prevention of lipid peroxidation in nervous tissue - Maintenance of axonal integrity Deficiency causes **spinocerebellar degeneration** characterized by: 1. **Ataxia** (cerebellar involvement) — most prominent feature 2. **Loss of vibration and proprioception** (dorsal column degeneration) 3. **Muscle weakness** (motor neuron involvement) 4. **Ophthalmoplegia** (in severe cases) ## Why This Is Vitamin E, Not Vitamin K **Mnemonic: "VITE" — Vitamin E causes Neurological disease** - **V**itamin E - **I**ncreases oxidative stress in neurons - **T**ouches spinocerebellar tracts - **E**arly sign: ataxia **Serum α-tocopherol 2.1 mg/L** (normal >5.4) confirms vitamin E deficiency biochemically. ## Malabsorption Context Celiac disease damages small intestinal mucosa → impaired absorption of fat-soluble vitamins (A, D, E, K). Vitamin E deficiency is particularly common because it requires intact enterohepatic circulation and normal bile salt-dependent micelle formation. **Warning:** Vitamin E deficiency is often overlooked in malabsorption because coagulopathy (vitamin K deficiency) is more obvious. The neurological syndrome is the distinguishing clue.