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Xerophthalmia and keratomalacia secondary to diet-induced vitamin A deficiency in Scottish adults
CASE SERIES
Xerophthalmia and keratomalacia secondary to diet-induced vitamin A deficiency in Scottish adults Ken Lee Lai, MBChB,* Jia Yu Ng, MBChB,* Sathish Srinivasan, FRCSEd, FRCOphth, FACS*,† ABSTRACT ● RÉSUMÉ Objective: To report the ocular features, underlying systemic conditions, and management of diet-induced vitamin A deficiency in Scottish adults. Design: Retrospective case series. Methods: Three middle-aged white adults presented with ocular signs of xerophthalmia and keratomalacia that led to the diagnosis of previously undiagnosed vitamin A deficiency. Case 1 presented with rapidly progressing bilateral keratomalacia with corneal perforation, whereas Cases 2 and 3 presented with conjunctival and corneal xerosis. Results: Corneal gluing was performed in Case 1. Cases 2 and 3 were treated topically with preservative-free tears, retinoic acid, and punctual plugs to optimize the ocular surface. This, combined with dietary supplementation, resulted in normalizing the ocular surface. Conclusions: Diet-induced vitamin A deficiency can occur in middle-aged white adults. Ocular surface changes may be the presenting sign of hypovitaminosis A in the Western world. A high degree of suspicion with prompt recognition and management of the underlying dietary deficiency can lead to complete reversal of the ocular surface changes. Objet : Compte-rendu des caractéristiques oculaires, des conditions systémiques sous-jacentes et la gestion de la déficience de vitamine A, induites par un régime alimentaire chez les adultes écossais. Méthodes : Rétrospective d'une série de cas. Résultats : Trois adultes caucasiens d'âge moyen présentaient des signes oculaires de xérophtalmie et de kératomalacie, qui induisent un diagnostic de déficience de vitamine A non diagnostiquée précédemment. Le premier cas présentait une progression rapide de kératomalacie bilatérale avec perforation de la cornée, alors que les deuxième et troisième cas avaient une xérosis conjonctivale et cornéenne. Dans le premier cas, on a fait un collage cornéen. Les deuxième et troisième cas ont été soignés topiquement avec des larmes sans préservatif, de l'acide rétinoïque et des bouchons lacrymaux pour optimiser la surface oculaire. Cela, combiné avec un supplément diététique, a eu comme résultat de normaliser la surface oculaire. Conclusions : La déficience de vitamine A induite par un régime alimentaire peut survenir chez les Caucasiens d'âge moyen. Un haut degré de suspicion avec une reconnaissance rapide et une prompte gestion de la déficience alimentaire sous-jacente peuvent mener à un renversement complet des changements au niveau de la surface oculaire.
Hypovitaminosis A caused by malnutrition is typically considered endemic only within regions of Southeast Asia and sub-Saharan Africa, where it is a leading cause of childhood blindness.1 This condition in the developed world is rare because of well-balanced nutritional measures; however, reduced vitamin A absorption, transport, and storage may still result from gastrointestinal surgery, malabsorptive disorders, and dietary inattention.2–7 We present 3 cases of xerophthalmia, keratomalacia, and hypovitaminosis A in Scottish adults secondary to alcohol-induced malnutrition.
CASE REPORTS Case 1
A 50-year-old white male presented to the emergency department with chronic abdominal pain, weight loss, and From the *Department of Ophthalmology, University Hospital Ayr, Ayr; and †Faculty of Medicine, University of Glasgow, Glasgow, Scotland, United Kingdom
red, sticky eyes of 2 days’ duration. Medical history identified chronic alcohol consumption and poor dietary intake. He was cachectic and had hepatomegaly. Best corrected visual acuity (BCVA) was 6/48 right eye (RE) and 6/60 left eye (LE). Bilateral inferior corneal epithelial defects were noted. He had iron-deficiency anemia with hemoglobin of 8.6 g/dL (range 13.3–16.7) and deranged liver function. Initially, he was treated with topical ofloxacin; however, bilateral corneal thinning rapidly supervened, resulting in corneal perforation in LE and descemetocele formation with impending perforation in the right eye (RE; Fig. 1). The LE perforation was sealed with cyanoacrylate glue and bandage contact lens. Oral ascorbic acid 1 g daily and doxycycline 200 mg daily was commenced. Punctual plugs were inserted in both eyes, and intense topical therapy with preservative-free (PF) carmellose sodium 1% and PF chloramphenicol 0.5% were commenced. No organisms were identified from Can J Ophthalmol 2014;49:109–112 0008-4182/14/$-see front matter & 2014 Canadian Ophthalmological Society. Published by Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.jcjo.2013.09.003
Originally received Apr. 28, 2013. Final revision Aug. 14, 2013. Accepted Sep. 13, 2013 Correspondence to Sathish Srinivasan, FRCSEd, FRCOphth, FACS, Department of Ophthalmology, 3rd Floor, University Hospital Ayr, Dalmellington Road, Ayr, KA6 6DX, United Kingdom; sathish.srinivasan@ gmail.com CAN J OPHTHALMOL — VOL. 49, NO. 1, FEBRUARY 2014
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Vitamin A deficiency in Scottish adults—Lai et al.
Fig. 1 — A, Slit-lamp photograph of the left eye (Case 1) showing descemetocele formation involving the inferior cornea. B, Slitlamp photograph of the right eye (Case 1) showing a corneal perforation sealed with cyanoacrylate glue. C, Slit-lamp photograph of the left eye (Case 1) after treatment showing inferior corneal scar. D, Slit-lamp photograph of the right eye (Case 1) after treatment showing dense stromal scar with vascularization.
corneal scrapes. Although no classic signs of coniunctival or corneal xerosis were evident, hypovitaminosis A was suspected and serum testing confirmed reduced vitamin A at 0.1 mmol/L (range 1.0–3.0) and retinol binding protein at 8 mg/L (range 20–40) levels. A dietary plan was
initiated and he was commenced on a course of highdose oral vitamin A (4000 IU vitamin A/D complex). At 2-month review, BCVA was 6/9 OD and 6/24 OS, with bilateral inferior corneal scars noted with no thinning (Fig. 1).
Fig. 2 — A, Slit-lamp photograph of the temporal bulbar conjunctiva of the right eye (Case 2) showing inflamed, dry ocular surface with keratinization. B, Slit-lamp photograph of the inferotemporal aspect of the bulbar conjunctiva in the left eye (Case 2) showing keratinized surface. Post-treatment pictures showing normalized ocular surface in the right (C) and left eye (D).
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Vitamin A deficiency in Scottish adults—Lai et al. Case 2
A 48-year-old female presented with a 1-year history of decreased vision and redness. Medical history included pancreaticojejunostomy and bowel resection secondary to alcohol-induced pancreatitis. BCVA was 6/7.5 RE and 6/6 LE. Slit-lamp biomicroscopy showed bilateral diffuse punctate staining of conjunctiva and cornea. The temporal bulbar conjunctiva in both eyes displayed areas of keratinized surface with hyperemia (Fig. 2). Schirmer test and tear film breakup time were reduced bilaterally. She admitted to having a sparse and poorly varied diet. Serum assay revealed low levels of serum vitamin A at less than 0.3 μmol/L (range 1.0–3.0) and serum vitamin E at 5 μmol/L (range 15–45). A balanced diet was advocated, and high-dose oral vitamin A and multivitamin supplements were commenced. Her ocular surface was optimized with punctual plugs, PF artificial tears, and topical retinoic acid. At 3-month review, the areas of conjunctival xerosis normalized (Fig. 2). Case 3
A 44-year-old male with history of depression, alcoholrelated seizures, and psychosis was assessed for bilateral redness and poor visual function at night. He had history of excessive alcohol consumption and dietary neglect. BCVA was 6/9 bilaterally. Slit-lamp biomicroscopy demonstrated marked superficial punctate keratitis, rapid tear film breakup time, and keratinization of the conjunctivae. Xerophthalmia was suspected and treatment with topical retinoic acid, oral multivitamin supplements, and a course of daily oral vitamin A daily was initiated, with good resolution of his symptoms weeks afterward. Subsequent serum vitamin assay testing confirmed low levels of vitamin A less than 0.3 μmol/L (range 1.0–3.0) and retinol binding protein of 12 mg/L (range 20–40).
DISCUSSION
treatment programs are imperative in the cessation of alcohol misuse.11 The recommended maximum oral dosage of oral vitamin A for treatment of xeropthalmia is 30,000 IU in 4-month dosages.12 An alternative delivery of systemic vitamin A is via intramuscular injections.13 Comprehensive nutritional supplementation is also key and should include oral multivitamins containing Bcomplex compounds, thiamine, folate, and zinc.10 In vitamin A deficiency, the conjunctiva undergoes squamous metaplasia and hyperkeratosis. Eventually the corneal surface becomes dry with superficial punctuate keratitis. Ocular dryness is managed with intense lubrication agents addressing the lack of mucin and aqueous secretion. Deploying punctal plugs can increase tear film availability, and topical retinoic acid preparations may help to optimize the ocular surface. Topical PF antibiotics are initiated in the setting of epithelial erosions/defects to prevent any secondary infection. Xerophthalmic keratomalacia may develop, leading to descemetocele formation and ultimately corneal perforation. Macsai et al.14 reported a case of bilateral corneal ulcers leading to bilateral perforation requiring bilateral corneal transplantation in an alcoholic patient with vitamin A deficiency. It is unclear in this case whether the corneal perforation was secondary to infectious keratitis or keratomalacia. Case 1 in this series presented with corneal perforation in 1 eye (managed with corneal glueing) and descemetocele with impending perforation in the fellow eye secondary to keratomalacia. All subjects in this cohort were diagnosed with underlying vitamin A deficiency based on the ocular signs. With alcohol consumption doubling in the United Kingdom compared with 50 years ago,15 dietary deficiency and secondary vitamin deficiencies may be more prevalent and ophthalmologists should have a high index of suspicion.
Disclosure: The authors have no proprietary or commercial interest in any materials discussed in this article.
A true vitamin A deficiency state results only after the vitamin stores in the liver are depleted completely. Although the main cause of vitamin A deficiency worldwide is malnutrition, in developed countries, the cause is mostly due to malabsorption. This malabsorption of vitamin A can be caused by structural or functional abnormality of the gastrointestinal system. Previous cases of vitamin A deficiency in the developed world have been reported after cystic fibrosis,2 primary biliary cirrhosis,3 jejunoileal bypass surgery,4 hemicolectomy,5 and bariatric surgery.6 Selective dietary restrictions leading to hypovitaminosis A can also be influenced by behavioural challenges in food faddism, psychoses, as well as neurodevelopmental8–10 and psychiatric disorders.7 Treatment must be directed to address the systemic entities of malnutrition, alcoholism, and the ophthalmic complications from xerosis. Alcohol rehabilitation and
REFERENCES 1. Thylefors B, Négrel AD, Pararajasegaram R, Dadzie KY. Global data on blindness. Bull World Health Organ. 1995;73:115-21. 2. Rayner RJ, Tyrell JC, Hiller EJ, et al. Night blindness and conjunctival xerosis caused by vitamin A deficiency in patients with cystic fibrosis. Arch Dis Child. 1989;64:1151-6. 3. Walt PR, Kemp CM, Lyness L, et al. Vitamin A treatment for night blindness in primary biliary cirrhosis. Br Med J Clin Res Ed. 1984;288:1030-1. 4. Tripathi RC, Tripathi BJ, Raja SC, Partamian LS. Iatrogenic ocular complications in patients after jejunoileal bypass surgery. Int Surg. 1993;78:68-72. 5. Sloan DB, Wood WJ, Isernhagen RD, Schmeisser ET. Short-term night blindness associated with colon resection and hypovitaminosis A. Arch Ophthalmol. 1994;112:162-3. 6. Fok JS, Li JY, Yong TY. Visual deterioration caused by vitamin A deficiency in patients after bariatric surgery. Eat Weight Disord. 2012;17:e144-6.
CAN J OPHTHALMOL — VOL. 49, NO. 1, FEBRUARY 2014
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Vitamin A deficiency in Scottish adults—Lai et al. 7. Cooney TM, Johnson CS, Elner VM. Keratomalacia caused by psychiatric-induced dietary restrictions. Cornea. 2007;26:995-7. 8. Collins CE, Koay P. Xerophthalmia because of dietary-induced vitamin a deficiency in a young Scottish man. Cornea. 2010;29:828-9. 9. Steinemann TL, Christiansen SP. Vitamin A deficiency and xerophthalmia in an autistic child. Arch Ophthalmol. 1998;116:392-3. 10. Pyott AAE, Kirkness CM. Nutritional disorders. In: Krachmer JH, Mannis MJ, Holland EF, eds. Cornea. Vol. 2. St Louis, Mo.: Mosby-Year Book; 1997:955-66.
112
11. Sommer A, West KP. The duration of the effect of vitamin A supplementation. Am J Public Health. 1997;87:467-9. 12. Roncone DP. Xerophthalmia secondary to alcohol-induced malnutrition. Optometry. 2006;77:124-33. 13. Levitsky J, Mailliard ME. Diagnosis and therapy of alcoholic liver disease. Semin Liver Dis. 2004;3:233-47. 14. Macsai MS, Agarwal S, Gamponia E. Bilateral corneal ulcers in primary vitamin A deficiency. Cornea. 1998;17:227-9. 15. Leon DA, McCambridge J. Liver cirrhosis mortality rates in Britain, 1950 to 2002. Lancet. 2006;367:52-6.
CAN J OPHTHALMOL — VOL. 49, NO. 1, FEBRUARY 2014
Xerophthalmia and keratomalacia secondary to diet-induced vitamin A deficiency in Scottish adults Ken Lee Lai, MBChB,* Jia Yu Ng, MBChB,* Sathish Srinivasan, FRCSEd, FRCOphth, FACS*,† ABSTRACT ● RÉSUMÉ Objective: To report the ocular features, underlying systemic conditions, and management of diet-induced vitamin A deficiency in Scottish adults. Design: Retrospective case series. Methods: Three middle-aged white adults presented with ocular signs of xerophthalmia and keratomalacia that led to the diagnosis of previously undiagnosed vitamin A deficiency. Case 1 presented with rapidly progressing bilateral keratomalacia with corneal perforation, whereas Cases 2 and 3 presented with conjunctival and corneal xerosis. Results: Corneal gluing was performed in Case 1. Cases 2 and 3 were treated topically with preservative-free tears, retinoic acid, and punctual plugs to optimize the ocular surface. This, combined with dietary supplementation, resulted in normalizing the ocular surface. Conclusions: Diet-induced vitamin A deficiency can occur in middle-aged white adults. Ocular surface changes may be the presenting sign of hypovitaminosis A in the Western world. A high degree of suspicion with prompt recognition and management of the underlying dietary deficiency can lead to complete reversal of the ocular surface changes. Objet : Compte-rendu des caractéristiques oculaires, des conditions systémiques sous-jacentes et la gestion de la déficience de vitamine A, induites par un régime alimentaire chez les adultes écossais. Méthodes : Rétrospective d'une série de cas. Résultats : Trois adultes caucasiens d'âge moyen présentaient des signes oculaires de xérophtalmie et de kératomalacie, qui induisent un diagnostic de déficience de vitamine A non diagnostiquée précédemment. Le premier cas présentait une progression rapide de kératomalacie bilatérale avec perforation de la cornée, alors que les deuxième et troisième cas avaient une xérosis conjonctivale et cornéenne. Dans le premier cas, on a fait un collage cornéen. Les deuxième et troisième cas ont été soignés topiquement avec des larmes sans préservatif, de l'acide rétinoïque et des bouchons lacrymaux pour optimiser la surface oculaire. Cela, combiné avec un supplément diététique, a eu comme résultat de normaliser la surface oculaire. Conclusions : La déficience de vitamine A induite par un régime alimentaire peut survenir chez les Caucasiens d'âge moyen. Un haut degré de suspicion avec une reconnaissance rapide et une prompte gestion de la déficience alimentaire sous-jacente peuvent mener à un renversement complet des changements au niveau de la surface oculaire.
Hypovitaminosis A caused by malnutrition is typically considered endemic only within regions of Southeast Asia and sub-Saharan Africa, where it is a leading cause of childhood blindness.1 This condition in the developed world is rare because of well-balanced nutritional measures; however, reduced vitamin A absorption, transport, and storage may still result from gastrointestinal surgery, malabsorptive disorders, and dietary inattention.2–7 We present 3 cases of xerophthalmia, keratomalacia, and hypovitaminosis A in Scottish adults secondary to alcohol-induced malnutrition.
CASE REPORTS Case 1
A 50-year-old white male presented to the emergency department with chronic abdominal pain, weight loss, and From the *Department of Ophthalmology, University Hospital Ayr, Ayr; and †Faculty of Medicine, University of Glasgow, Glasgow, Scotland, United Kingdom
red, sticky eyes of 2 days’ duration. Medical history identified chronic alcohol consumption and poor dietary intake. He was cachectic and had hepatomegaly. Best corrected visual acuity (BCVA) was 6/48 right eye (RE) and 6/60 left eye (LE). Bilateral inferior corneal epithelial defects were noted. He had iron-deficiency anemia with hemoglobin of 8.6 g/dL (range 13.3–16.7) and deranged liver function. Initially, he was treated with topical ofloxacin; however, bilateral corneal thinning rapidly supervened, resulting in corneal perforation in LE and descemetocele formation with impending perforation in the right eye (RE; Fig. 1). The LE perforation was sealed with cyanoacrylate glue and bandage contact lens. Oral ascorbic acid 1 g daily and doxycycline 200 mg daily was commenced. Punctual plugs were inserted in both eyes, and intense topical therapy with preservative-free (PF) carmellose sodium 1% and PF chloramphenicol 0.5% were commenced. No organisms were identified from Can J Ophthalmol 2014;49:109–112 0008-4182/14/$-see front matter & 2014 Canadian Ophthalmological Society. Published by Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.jcjo.2013.09.003
Originally received Apr. 28, 2013. Final revision Aug. 14, 2013. Accepted Sep. 13, 2013 Correspondence to Sathish Srinivasan, FRCSEd, FRCOphth, FACS, Department of Ophthalmology, 3rd Floor, University Hospital Ayr, Dalmellington Road, Ayr, KA6 6DX, United Kingdom; sathish.srinivasan@ gmail.com CAN J OPHTHALMOL — VOL. 49, NO. 1, FEBRUARY 2014
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Vitamin A deficiency in Scottish adults—Lai et al.
Fig. 1 — A, Slit-lamp photograph of the left eye (Case 1) showing descemetocele formation involving the inferior cornea. B, Slitlamp photograph of the right eye (Case 1) showing a corneal perforation sealed with cyanoacrylate glue. C, Slit-lamp photograph of the left eye (Case 1) after treatment showing inferior corneal scar. D, Slit-lamp photograph of the right eye (Case 1) after treatment showing dense stromal scar with vascularization.
corneal scrapes. Although no classic signs of coniunctival or corneal xerosis were evident, hypovitaminosis A was suspected and serum testing confirmed reduced vitamin A at 0.1 mmol/L (range 1.0–3.0) and retinol binding protein at 8 mg/L (range 20–40) levels. A dietary plan was
initiated and he was commenced on a course of highdose oral vitamin A (4000 IU vitamin A/D complex). At 2-month review, BCVA was 6/9 OD and 6/24 OS, with bilateral inferior corneal scars noted with no thinning (Fig. 1).
Fig. 2 — A, Slit-lamp photograph of the temporal bulbar conjunctiva of the right eye (Case 2) showing inflamed, dry ocular surface with keratinization. B, Slit-lamp photograph of the inferotemporal aspect of the bulbar conjunctiva in the left eye (Case 2) showing keratinized surface. Post-treatment pictures showing normalized ocular surface in the right (C) and left eye (D).
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Vitamin A deficiency in Scottish adults—Lai et al. Case 2
A 48-year-old female presented with a 1-year history of decreased vision and redness. Medical history included pancreaticojejunostomy and bowel resection secondary to alcohol-induced pancreatitis. BCVA was 6/7.5 RE and 6/6 LE. Slit-lamp biomicroscopy showed bilateral diffuse punctate staining of conjunctiva and cornea. The temporal bulbar conjunctiva in both eyes displayed areas of keratinized surface with hyperemia (Fig. 2). Schirmer test and tear film breakup time were reduced bilaterally. She admitted to having a sparse and poorly varied diet. Serum assay revealed low levels of serum vitamin A at less than 0.3 μmol/L (range 1.0–3.0) and serum vitamin E at 5 μmol/L (range 15–45). A balanced diet was advocated, and high-dose oral vitamin A and multivitamin supplements were commenced. Her ocular surface was optimized with punctual plugs, PF artificial tears, and topical retinoic acid. At 3-month review, the areas of conjunctival xerosis normalized (Fig. 2). Case 3
A 44-year-old male with history of depression, alcoholrelated seizures, and psychosis was assessed for bilateral redness and poor visual function at night. He had history of excessive alcohol consumption and dietary neglect. BCVA was 6/9 bilaterally. Slit-lamp biomicroscopy demonstrated marked superficial punctate keratitis, rapid tear film breakup time, and keratinization of the conjunctivae. Xerophthalmia was suspected and treatment with topical retinoic acid, oral multivitamin supplements, and a course of daily oral vitamin A daily was initiated, with good resolution of his symptoms weeks afterward. Subsequent serum vitamin assay testing confirmed low levels of vitamin A less than 0.3 μmol/L (range 1.0–3.0) and retinol binding protein of 12 mg/L (range 20–40).
DISCUSSION
treatment programs are imperative in the cessation of alcohol misuse.11 The recommended maximum oral dosage of oral vitamin A for treatment of xeropthalmia is 30,000 IU in 4-month dosages.12 An alternative delivery of systemic vitamin A is via intramuscular injections.13 Comprehensive nutritional supplementation is also key and should include oral multivitamins containing Bcomplex compounds, thiamine, folate, and zinc.10 In vitamin A deficiency, the conjunctiva undergoes squamous metaplasia and hyperkeratosis. Eventually the corneal surface becomes dry with superficial punctuate keratitis. Ocular dryness is managed with intense lubrication agents addressing the lack of mucin and aqueous secretion. Deploying punctal plugs can increase tear film availability, and topical retinoic acid preparations may help to optimize the ocular surface. Topical PF antibiotics are initiated in the setting of epithelial erosions/defects to prevent any secondary infection. Xerophthalmic keratomalacia may develop, leading to descemetocele formation and ultimately corneal perforation. Macsai et al.14 reported a case of bilateral corneal ulcers leading to bilateral perforation requiring bilateral corneal transplantation in an alcoholic patient with vitamin A deficiency. It is unclear in this case whether the corneal perforation was secondary to infectious keratitis or keratomalacia. Case 1 in this series presented with corneal perforation in 1 eye (managed with corneal glueing) and descemetocele with impending perforation in the fellow eye secondary to keratomalacia. All subjects in this cohort were diagnosed with underlying vitamin A deficiency based on the ocular signs. With alcohol consumption doubling in the United Kingdom compared with 50 years ago,15 dietary deficiency and secondary vitamin deficiencies may be more prevalent and ophthalmologists should have a high index of suspicion.
Disclosure: The authors have no proprietary or commercial interest in any materials discussed in this article.
A true vitamin A deficiency state results only after the vitamin stores in the liver are depleted completely. Although the main cause of vitamin A deficiency worldwide is malnutrition, in developed countries, the cause is mostly due to malabsorption. This malabsorption of vitamin A can be caused by structural or functional abnormality of the gastrointestinal system. Previous cases of vitamin A deficiency in the developed world have been reported after cystic fibrosis,2 primary biliary cirrhosis,3 jejunoileal bypass surgery,4 hemicolectomy,5 and bariatric surgery.6 Selective dietary restrictions leading to hypovitaminosis A can also be influenced by behavioural challenges in food faddism, psychoses, as well as neurodevelopmental8–10 and psychiatric disorders.7 Treatment must be directed to address the systemic entities of malnutrition, alcoholism, and the ophthalmic complications from xerosis. Alcohol rehabilitation and
REFERENCES 1. Thylefors B, Négrel AD, Pararajasegaram R, Dadzie KY. Global data on blindness. Bull World Health Organ. 1995;73:115-21. 2. Rayner RJ, Tyrell JC, Hiller EJ, et al. Night blindness and conjunctival xerosis caused by vitamin A deficiency in patients with cystic fibrosis. Arch Dis Child. 1989;64:1151-6. 3. Walt PR, Kemp CM, Lyness L, et al. Vitamin A treatment for night blindness in primary biliary cirrhosis. Br Med J Clin Res Ed. 1984;288:1030-1. 4. Tripathi RC, Tripathi BJ, Raja SC, Partamian LS. Iatrogenic ocular complications in patients after jejunoileal bypass surgery. Int Surg. 1993;78:68-72. 5. Sloan DB, Wood WJ, Isernhagen RD, Schmeisser ET. Short-term night blindness associated with colon resection and hypovitaminosis A. Arch Ophthalmol. 1994;112:162-3. 6. Fok JS, Li JY, Yong TY. Visual deterioration caused by vitamin A deficiency in patients after bariatric surgery. Eat Weight Disord. 2012;17:e144-6.
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Vitamin A deficiency in Scottish adults—Lai et al. 7. Cooney TM, Johnson CS, Elner VM. Keratomalacia caused by psychiatric-induced dietary restrictions. Cornea. 2007;26:995-7. 8. Collins CE, Koay P. Xerophthalmia because of dietary-induced vitamin a deficiency in a young Scottish man. Cornea. 2010;29:828-9. 9. Steinemann TL, Christiansen SP. Vitamin A deficiency and xerophthalmia in an autistic child. Arch Ophthalmol. 1998;116:392-3. 10. Pyott AAE, Kirkness CM. Nutritional disorders. In: Krachmer JH, Mannis MJ, Holland EF, eds. Cornea. Vol. 2. St Louis, Mo.: Mosby-Year Book; 1997:955-66.
112
11. Sommer A, West KP. The duration of the effect of vitamin A supplementation. Am J Public Health. 1997;87:467-9. 12. Roncone DP. Xerophthalmia secondary to alcohol-induced malnutrition. Optometry. 2006;77:124-33. 13. Levitsky J, Mailliard ME. Diagnosis and therapy of alcoholic liver disease. Semin Liver Dis. 2004;3:233-47. 14. Macsai MS, Agarwal S, Gamponia E. Bilateral corneal ulcers in primary vitamin A deficiency. Cornea. 1998;17:227-9. 15. Leon DA, McCambridge J. Liver cirrhosis mortality rates in Britain, 1950 to 2002. Lancet. 2006;367:52-6.
CAN J OPHTHALMOL — VOL. 49, NO. 1, FEBRUARY 2014