Vitamin B2 (Riboflavin) Deficiency

Overview

Plain-Language Overview

Vitamin B2, also known as riboflavin, is an important nutrient that helps the body convert food into energy. A deficiency in this vitamin can cause symptoms like sore throat, redness and swelling of the lining of the mouth and throat, cracks or sores on the outside of the lips, and inflammation of the tongue. People with this deficiency may also experience dry and scaly skin. It is often caused by poor diet, certain medical conditions, or increased need during pregnancy or illness. Early recognition and treatment are important to prevent complications.

Clinical Definition

Vitamin B2 (riboflavin) deficiency is a clinical condition characterized by insufficient levels of riboflavin, a water-soluble vitamin essential for cellular energy production and metabolism of fats, drugs, and steroids. It plays a critical role as a precursor for flavin adenine dinucleotide (FAD) and flavin mononucleotide (FMN), cofactors in redox reactions. Deficiency typically results from inadequate dietary intake, malabsorption syndromes, or increased metabolic demands. Clinically, it presents with angular stomatitis, cheilitis, glossitis, seborrheic dermatitis, and ocular symptoms such as photophobia and corneal vascularization. Biochemically, deficiency is confirmed by decreased erythrocyte glutathione reductase activity or elevated urinary excretion of riboflavin metabolites. Riboflavin deficiency often coexists with other B vitamin deficiencies and may contribute to anemia due to impaired iron metabolism. Early diagnosis is essential to prevent progression to neurological symptoms and to restore normal metabolic function through supplementation.

Inciting Event

Prolonged inadequate dietary intake of riboflavin.
Onset or exacerbation of malabsorptive conditions.
Increased physiological demand such as pregnancy.
Chronic alcohol abuse leading to poor nutrition and absorption.

Latency Period

Symptoms typically develop after several months of inadequate riboflavin intake.

Diagnostic Delay

Non-specific symptoms such as fatigue and oral discomfort may be attributed to other causes.
Lack of routine screening and low clinical suspicion in developed countries.
Overlap with other nutritional deficiencies complicates diagnosis.

Clinical Presentation

Signs & Symptoms

Painful angular stomatitis with fissures at the mouth corners.
Glossitis presenting as a smooth, magenta-colored tongue.
Cheilitis with dry, cracked, and inflamed lips.
Photophobia and eye irritation due to corneal vascularization in severe cases.
Possible peripheral neuropathy with numbness and paresthesias.

History of Present Illness

Complaints of sore throat, burning sensation of the mouth, and angular stomatitis.
Development of cheilitis with fissuring at the corners of the mouth.
Symptoms of photophobia and eye discomfort may be present.
Generalized fatigue and weakness.

Past Medical History

History of malabsorptive disorders such as celiac disease or inflammatory bowel disease.
Chronic alcohol use disorder.
Previous episodes of nutritional deficiencies.
Pregnancy or recent lactation.

Family History

No significant hereditary pattern; riboflavin deficiency is typically acquired.

Physical Exam Findings

Presence of angular stomatitis characterized by fissures and erythema at the corners of the mouth.
Observation of cheilitis with dry, cracked, and inflamed lips.
Detection of magenta-colored glossitis, indicating inflammation and atrophy of the tongue papillae.
Possible seborrheic dermatitis with scaly, erythematous plaques on the face and scalp.

Diagnostic Workup

Diagnostic Criteria

Diagnosis of vitamin B2 deficiency is based on clinical signs such as cheilitis, glossitis, and seborrheic dermatitis combined with laboratory evidence including decreased activity of erythrocyte glutathione reductase and elevated urinary riboflavin metabolites. A thorough dietary history revealing inadequate riboflavin intake or conditions causing malabsorption supports the diagnosis. Additional findings may include anemia and ocular symptoms. Response to riboflavin supplementation further confirms the diagnosis.

Pathophysiology

Key Mechanisms

Vitamin B2 (riboflavin) deficiency impairs the function of flavoproteins involved in redox reactions essential for cellular metabolism.
Deficiency leads to decreased activity of flavin adenine dinucleotide (FAD) and flavin mononucleotide (FMN)-dependent enzymes, disrupting energy production.
Impaired metabolism affects the maintenance of mucous membranes, skin integrity, and antioxidant defenses.

Involvement	Details
Organs	Skin: Shows characteristic seborrheic dermatitis and scaling in deficiency.
Organs	Eyes: May develop photophobia and conjunctivitis related to riboflavin deficiency.
Tissues	Oral mucosa: Commonly exhibits inflammation and cracking in riboflavin deficiency.
Tissues	Corneal epithelium: Can develop vascularization and photophobia due to deficiency.
Cells	Epithelial cells: Highly affected by riboflavin deficiency leading to mucosal lesions.
Cells	Red blood cells: Require riboflavin for proper metabolism and energy production.
Chemical Mediators	Flavin adenine dinucleotide (FAD): A coenzyme derived from riboflavin essential for redox reactions.
Chemical Mediators	Flavin mononucleotide (FMN): Another riboflavin-derived coenzyme critical for mitochondrial electron transport.

Treatment

Pharmacological Treatments

Riboflavin supplementation
- Mechanism: Replenishes deficient vitamin B2 to restore normal enzymatic functions
- Side effects: rare allergic reactions, yellow-orange discoloration of urine

Non-pharmacological Treatments

Increase intake of riboflavin-rich foods such as milk, eggs, lean meats, and green vegetables.
Address underlying causes such as alcoholism or malabsorption to improve nutrient absorption.

Prevention

Pharmacological Prevention

Oral riboflavin supplementation at recommended daily allowances to prevent deficiency.
Multivitamin preparations containing riboflavin for at-risk populations.

Non-pharmacological Prevention

Maintaining a balanced diet rich in dairy products, eggs, green vegetables, and meats.
Addressing underlying causes such as alcoholism and malabsorption disorders.
Regular nutritional counseling for at-risk individuals.

Outcome & Complications

Complications

Development of peripheral neuropathy leading to sensory deficits.
Severe ocular involvement including corneal vascularization and photophobia.
Progression to combined vitamin B deficiencies causing anemia and neurological symptoms.

Short-term Sequelae	Long-term Sequelae
Persistent oral discomfort and difficulty eating due to stomatitis and glossitis. Mild skin irritation and dermatitis. Transient eye symptoms such as photophobia.	Chronic neuropathy with sensory loss and paresthesias. Potential irreversible ocular damage if untreated. Long-standing nutritional deficiencies leading to systemic complications.

Differential Diagnoses

Vitamin B2 (Riboflavin) Deficiency versus Iron Deficiency Anemia

Vitamin B2 (Riboflavin) Deficiency	Iron Deficiency Anemia
Presence of angular stomatitis and cheilitis.	Presence of microcytic hypochromic anemia on CBC.
Normal or slightly decreased hemoglobin with normocytic or macrocytic anemia.	Low serum ferritin and low iron levels.
Characteristic magenta-colored tongue and seborrheic dermatitis.	Symptoms include pica and koilonychia (spoon nails).

Vitamin B2 (Riboflavin) Deficiency versus Niacin (Vitamin B3) Deficiency

Vitamin B2 (Riboflavin) Deficiency	Niacin (Vitamin B3) Deficiency
Presence of magenta-colored tongue and angular stomatitis.	Classic triad of dermatitis, diarrhea, and dementia (pellagra).
No dementia or diarrhea symptoms.	Photosensitive broad, scaling rash on sun-exposed areas.
Seborrheic dermatitis localized to the face and scalp.	Associated with glossitis but not magenta tongue.

Vitamin B2 (Riboflavin) Deficiency versus Vitamin B6 (Pyridoxine) Deficiency

Vitamin B2 (Riboflavin) Deficiency	Vitamin B6 (Pyridoxine) Deficiency
Characteristic magenta-colored tongue and angular stomatitis.	Peripheral neuropathy and irritability.
Seborrheic dermatitis primarily affecting the face and scalp.	Seizures may be present in severe cases.
No peripheral neuropathy or seizures.	Cheilitis and glossitis without characteristic magenta tongue.