Symptoms of Vitamin A Deficiency Due to Malabsorption
Beyond night blindness, vitamin A deficiency from malabsorption causes progressive ocular surface disease including xerophthalmia (dry eyes), Bitot spots, corneal keratinization, keratomalacia (corneal softening), and ultimately irreversible blindness if untreated. 1, 2
Ocular Manifestations
Early Signs
- Xerophthalmia (dry eyes) develops as an early manifestation, caused by loss of mucus-secreting goblet cells and reduced tear production 1, 3
- Night blindness remains the earliest symptom, resulting from insufficient rhodopsin synthesis in the retina 2, 4
- Bitot spots appear as gray/white foamy lesions on the conjunctiva, representing keratinized epithelium 2
- Superficial punctate keratopathy develops on the corneal surface 3
Progressive Disease
- Conjunctival keratinization occurs as deficiency worsens, with abnormal differentiation of nonsquamous epithelium 3
- Corneal keratinization and ulceration represent more severe stages 1, 3
- Keratomalacia (corneal softening and melting) can develop even without bacterial infection or inflammatory infiltration 1, 3
- Permanent blindness results from corneal maceration and secondary infection if left untreated 1
Non-Ocular Manifestations
Dermatologic Changes
- Generalized xerosis (dry skin) can occur without night blindness in some cases 5
- Dry hair has been reported 1
Systemic Effects
- Impaired immune function increases susceptibility to secondary infections that worsen eye damage 2
- Growth disturbances may occur, particularly in younger patients 6
High-Risk Populations for Malabsorption-Related Deficiency
Gastrointestinal Conditions
- Short bowel syndrome carries significant risk due to reduced fat absorption 1
- Cystic fibrosis patients are at elevated risk 1, 7
- Celiac disease increases deficiency risk 1
- Chronic diarrhea of any etiology 1
Surgical Interventions
- Bariatric surgery patients, particularly after malabsorptive procedures like BPD/DS and RYGB, show the highest risk 1, 5, 7
- Small bowel resection significantly impairs vitamin A absorption 7
Hepatic Disease
- Chronic liver disease shows high prevalence of deficiency, with severity correlating to disease progression 1
- Liver transplant candidates demonstrate deficiency in 69.8% of cases 1
- Chronic alcohol consumption depletes hepatic vitamin A stores, though serum levels may remain falsely normal 1
Other Conditions
- Chronic kidney disease requires regular monitoring as levels fluctuate unpredictably 1
- Patients on octreotide treatment are at increased risk 7
Clinical Pitfalls
A critical caveat: serum retinol levels may remain in the normal range despite depleted liver stores, particularly in chronic alcohol consumption, creating a false sense of adequacy. 1 Additionally, during inflammation, retinol-binding protein release is reduced, potentially masking deficiency 2. Interpretation of serum levels should therefore be treated with caution as they do not directly reflect total body vitamin A stores 1.
Surface abnormalities respond rapidly to systemic vitamin A supplementation, with corneal changes disappearing long before goblet cells reappear, indicating that clinical improvement precedes complete tissue restoration 3.