Vitamin B6 (pyridoxine) deficiency is a nutritional disorder caused by inadequate levels of pyridoxine or its active metabolite pyridoxal-5-phosphate (PLP) — an essential coenzyme in amino-acid metabolism, neurotransmitter synthesis, hemoglobin formation, and immune function.

Deficiency primarily affects tissues with high metabolic demand such as:

• Peripheral nerves

• Skin

• Brain

• Bone marrow

Clinically, it commonly presents with neurological and hematological manifestations, especially peripheral neuropathy and sideroblastic anemia.

2. Physiology and Pathophysiology

Normal Functions of Vitamin B6

Pyridoxine acts as a cofactor in:

Mechanism of Disease

Deficiency leads to:

1. ↓ Neurotransmitter synthesis → neuropathy, seizures

2. ↓ Heme synthesis → sideroblastic anemia

3. ↑ Homocysteine → vascular risk

4. Impaired tryptophan metabolism → dermatitis & glossitis

Isoniazid toxicity mechanism:Isoniazid binds pyridoxine → inactive hydrazone complex → functional deficiency.

3. Risk Factors

Nutritional

• Severe malnutrition

• Elderly with poor diet

• Chronic illness

• Pregnancy

• Exclusive polished-rice diets

Drug-Induced

• Isoniazid (most common cause worldwide)

• Penicillamine

• Cycloserine

• Oral contraceptives

• Levodopa without carbidopa

Disease-Associated

• Chronic alcoholism

• Chronic kidney disease

• HIV infection

• Malabsorption syndromes

• Post-bariatric surgery

4. Clinical Features

Early Symptoms

• Irritability

• Fatigue

• Cheilosis

• Glossitis

• Seborrheic dermatitis

Neurological Manifestations

• Tingling sensation

• Burning pain in feet

• Numbness

• Peripheral neuropathy

• Seizures (infants)

• Depression

• Confusion

Hematological Manifestations

• Microcytic sideroblastic anemia

• Pallor

• Weakness

Dermatological Manifestations

• Angular stomatitis

• Glossitis

• Dermatitis (seborrheic type)

Severe Deficiency

• Encephalopathy

• Optic neuropathy

• Ataxia

5. Diagnostic Criteria

Diagnosis is based on clinical suspicion + laboratory confirmation.

Suggestive when patient has:

• Peripheral neuropathy AND

• Risk factor (especially TB therapy) AND

• Response to pyridoxine treatment

6. Investigations

Laboratory Tests

Differential Diagnoses

• Vitamin B12 deficiency

• Diabetic neuropathy

• Alcoholic neuropathy

• Hypothyroidism

• Heavy metal poisoning

7. Management

A. Non-Pharmacological

Lifestyle

• Stop alcohol use

• Nutritional rehabilitation

• Manage malabsorption disorders

Dietary Advice

Increase intake of pyridoxine-rich foods:

• Liver, meat, fish and offal

• Wholegrain cereals and fortified breakfast cereals

• Peanuts and bananas

• Raw vegetables

• Walnuts and seeds

• Avocados and dried fruits

• Potatoes and baked beans

B. Pharmacological Treatment

i. Treatment of Deficiency

Children

• Pyridoxine 12.5 mg PO daily × 3 weeks

Adults

• Pyridoxine 25 mg PO daily × 3 weeks

ii. Drug-Induced Neuropathy (e.g., Isoniazid)

Children

• Pyridoxine 50 mg PO daily × 3 weeks

Adults

• Pyridoxine 200 mg PO daily × 3 weeks

iii. Maintenance (for TB therapy)

• Pyridoxine 25 mg PO daily

4. Acute Neurotoxicity or Seizures (Emergency)

• Pyridoxine IV 50–100 mg immediately(especially in INH overdose)

8. Monitoring and Follow-Up

Improvement usually begins within 1–2 weeks, but neuropathy may take months to recover.

9. Complications if Untreated

• Permanent neuropathy

• Chronic pain syndrome

• Seizure disorder in infants

• Severe anemia

• Cognitive impairment

10. Prevention

High-Risk Groups (MUST receive prophylaxis)

• All TB patients on isoniazid

• Alcohol use disorder

• Malnourished patients

• HIV patients

• Pregnant women on TB therapy

Recommended prophylaxis dose

• Pyridoxine 10–25 mg daily

11. Prognosis

• Excellent if treated early

• Neuropathy reversible in early stages

• Late treatment → permanent nerve damage