Acquired Night Blindness Due to Bad Eating Patterns

CLINICAL CASE REPORT Acquired night blindness due to bad eating patterns

A Paraﬁta-Fernández1, MM Escalona-Fermín2, M Sampil1, N Moraña1, E Viso1 and PC Fernández-Vila1

We report a case of acquired night blindness in a developed country (Spain) without risk factors for nutritional deficiency disease or family history of hereditary retinal disease. A 76-year-old woman presented with acquired night blindness of 6-month progression. After a thorough inquiry about eating patterns she becomes suspicious of vitamin A low dietary intake, which is analytically confirmed and successfully treated. Despite being very uncommon in our environment and even more in patients without digestive problems, in a patient reporting acquired night blindness vitamin A deficiency should not be discarded until eating patterns have been investigated. It might be especially relevant in certain socioeconomic situations and eating disorders such as bulimia or anorexia nervosa.

European Journal of Clinical Nutrition (2015) 69, 752–754; doi:10.1038/ejcn.2015.35; published online 25 March 2015

INTRODUCTION (normal range 1.1–4.8 × 1.6 × 109/l). Initially, it supports a reasonably good Vitamin A deficiency can cause night blindness and xerophthalmia nutritional status. Best-corrected visual acuit was 20/20 in both eyes. Intraocular pressure (Bitot's spots, conjunctival and corneal xerosis), reaching corneal was 12 mm Hg OU. During slit lamp examination, slight cortical cataracts ulceration, keratomalacia and corneal scars in the most severe 1 that did not explain the visual disturbance were found, without altered cases. In developing countries, malnourishment is the main ocular surface. Both retinas and visual fields were within normal limits for cause, being a serious health issue for the population, affecting her age. survival and impaired growth and reproduction,2 whereas in Despite informing us that she followed a varied diet, when inquired developed countries most of them are secondary to malabsorp- about her regular habits, she literally confessed ‘Doctor, I eat everything... tion syndromes (intestinal resection because of tumor or everything I like’ (sic), which meant the absence of dairy products, fruits inflammatory bowel disease,3 bariatric surgery,4 hepatitis,5 cystic and plenty of vegetables during years voluntarily. Her main sources of food fi 4 fi fibrosis and alcoholism6). were certain meats and sh for 5 years. All this was con rmed by the family. Asked for a 24-h dietary recall, she referred having two scoops of A case of acquired night blindness in a developed country fl (Spain) is presented, without risk factors for deficiency disease or cocoa powder (not fat free) mixed in water (in 12 uid ounces) with some white bread (~75 g) for breakfast and dinner. A small ration of grilled record of hereditary retinal disease, as retinitis pigmentosa or rod chicken and half plate of baked beans, without dessert. This was reported dystrophy, which after a thorough inquire about feeding habits, as the usual intake, with slight variations. she becomes suspicious of vitamin A low dietary intake, which is Full-field electroretinography (ERG) was performed using Cadwell Sierra analytically confirmed and successfully treated. To the knowledge (Kennewick, WA, USA) wave 11.0 with a full-field flash Ganzfeld stimulator of the authors, this is the first case reported comprising such and surface electrodes were used for recording. Three stimulation protocols characteristics. were used, based on the recommendations of the International Society for the Clinical Electrophysiology of Vision:7,8 for rod evaluation (dim white flash stimulus of 0.01 cd/s/m2 in the dark adapted eye) and mixed rod–cone (dim white flash stimulus of 3 and 10 cd/s/m2 in the dark adapted eye). First ERG SUBJECTS AND METHODS shows bilateral absence of rod response, low amplitude (left: 30 μV; right: A 76-year-old woman referred by her primary care physician had a history 29.6 μV) and increased latency of waves ‘a’ (left: 24.8 ms; right: 26 ms) and ‘b’ 2 of progressive night blindness of ~ 6-month evolution. She reported (left: 45 ms; right: 45 ms) in both 3 and 10 cd/s/m stimulus in the mixed difficulty in dark environments that limited her regular life to the sunny responses (Figure 1). Schirmer test I OD 10 mm in 5 min, OS 8 mm in 5 min hours of the day. Nevertheless, she could watch television at nights, and tear breakup time 415 s. Laboratory test were normal, with the despite ignoring the rest of the room. There were no familial exception of vitamin A deficiency of 0.06 mg/l (reference: 0.30–1.00 mg/l), ophthalmological or general disease records. She presented arterial with negative markers of celiac and autoimmune disorders, and normal hypertension and aortic and mitral insufficiency, treated with acetilsalicilic values of blood proteins. acid, enalapril and hydrochlorothiazide. No digestive symptoms suggest- Given the habits of the patient and the findings in the work-up (low ing malabsorption were reported. vitamin A and ERG altered), she was supplemented with a multivitamin During regular follow-ups in the past year by her primary care physician complex (providing 800 μg of vitamin A/tablet) for 2 months, achieving for blood pressure control, no weight changes were observed, having great clinical improvement with significant changes in the patient's quality maintained a body mass index of 20.14 (normal range 18.5–24.9). Low- of life, normalizing vitamin A levels (0.60 mg/dl; reference: 0.30–1.00 mg/l) density lipoprotein cholesterol was 113 mg/dl (normal range 100–155 mg/ and ERG was performed with the same protocols and evidenced recovery dl), high-density lipoprotein cholesterol was 59 mg/dl (normal range 45- of the rod response, an improvement in the latency of the wave ‘a’ (left: 65 mg/dl), total cholesterol 183 mg/dl (normal range 140–240 mg/dl), 23 ms; right: 23 ms) and ‘b’ (left: 41 ms; right: 42 ms); and a normalization of albumin 4.2 mg/dl (normal range 3.5–5 mg/dl) and 1.6 × 109/l lymphocytes the amplitude (left: 65 μV; right: 67 μV) in mixed responses (Figure 2). The

1Ophthalmology Department, Complejo Hospitalario de Pontevedra, Pontevedra, Spain and 2Neurophysiology Department, Complejo Hospitalario de Pontevedra, Pontevedra, Spain. Correspondence: Dr A P Fernández, Ophthalmology Department, Complejo Hospitalario de Pontevedra, Loureiro Crespo, 2, 36002 Pontevedra, Spain. E-mail: alberto.paraﬁ[email protected] Received 22 December 2014; revised 27 January 2015; accepted 29 January 2015; published online 25 March 2015 Night blindness A Paraﬁta-Fernández et al 753

Figure 1. Scotopic flash (a) 0.01 cd/m2 (b) 10 cd/m2 and (c) 30 cd/m2. Diminished amplitude is observed for every stimuli. patient was highly encouraged to change her lifestyle for the benefit of her it more susceptible to infections.2 It is often accompanied by other health. deficiencies, which worsens the prognosis of these patients. In developed countries, vitamin A deficiency comes secondary to 5 3 fi DISCUSSION digestive pathology (hepatitis C), Chron's disease or cystic brosis among others, due to malabsorption syndromes of different causes. fi It is called night blindness to the dif culty of viewing under Bariatric surgery, as intestinal resections in inflammatory bowel scotopic (low light) circumstances. Clinical disorders affecting disease do, can produce a short bowel syndrome and secondary mesopic vision, during transition from photopic to scotopic, can malabsorption. Meanwhile, in alcoholism6 occurs a competition for cause night blindness due to poor adaptation of the photo- the absorption which interferes with vitamin A metabolism, or receptors to this new situation.9 We will avoid in this discussion 10 secondary to cirrhosis when present. the terms nyctalopia and hemeralopia by its frequent confusion, Acquired night blindness presented by the patient in the as many times are used as synonyms, despite not being so, present case is not a consequence of deficiency associated to depending on the root considered. systemic disease, but poor dietary habits. On her own, she When facing a patient with night blindness it is necessary, first excluded from her regular diet foods that provide essential of all, to define if it is hereditary or acquired. Among hereditary conditions, retinitis pigmentosa, fundus albipunctatus or retinitis nutrients, such as dairy, fruits and vegetables, so she lacks an appropriate carotene intake.1 Her serum protein concentration punctata albescens should be considered among others, but – seems unlikely in this case as she is 76 year-old and the absence of (6.60 g/dl) was in the lower limit of reference values (6.50 8.50 g/ familial records of such retinal disease. Among acquired, besides dl), suggesting the authors that a probable eating disorder that fi toxic retinopathies (drugs like quinin or vigabatrin) and the tumor will include some other de ciencies might be present despite associated (melanoma), the most frequent is vitamin A deficiency. having normal biometric markers as shown in the case report. As As it is well known, thanks to all the research performed by only vitamin A was checked, some other trace element could be George Wald (awarded the 1967 Nobel Prize in Medicine), decreased, but the multivitamin complex prescribed would have, rhodopsin cannot be regenerated in the absence of vitamin A, at least partially, compensated this supposed deficiency. being rods more sensitives to its lack than cones.11 To our knowledge, there is only one case report in which Vitamin A deficiency is a common cause of blindness in vitamin A deficiency appears in a patient with anorexia nervosa in developing countries and it also causes a rise in child mortality.1,2 a developed country,12 but this case also presents a history of Vitamin A is involved in the formation and regeneration of kidney transplantation, so as the rest of the cases reported in epithelia and immunocompetence, making the individual lacking Europe and US, she suffers a mayor systemic disease.

Figure 2. Scotopic ﬂash (a) 0.01 cd/m2 (b) 10 cd/m2 and (c) 30 cd/m2. Amplitude, latency and morphology are recovered after treatment.

The case report presented here is different from the rest in the REFERENCES absence of systemic or psychological medical records. It is not the 1 Sommer A. Mortality associated with mild, untreated xerophthalmia. Trans Am typical case of eating disorder but a case of bad eating habits. The Ophthalmol Soc 1983; 81: 825–8253. key for diagnosis and for proper treatment has been a thorough 2 Underwood BA. Vitamin A deficiency disorders: international efforts to control anamnesis after the guide symptom of night blindness, as ocular a preventable ‘Pox’. JNutr2004; 134: 231 S–236 S. 3 Da Rocha Lima B, Pichi F, Lowder CY. Night blindness and Chron’s disease. surface was better than expected, with no xerophthalmia 34 – fi Int Ophthalmol 2014; : 1141 1144. accompanying the de ciency, which is uncommon, followed by 4 Fok JS, Li JY, Yong TY. Visual deterioration caused by vitamin A deficiency in the performance of laboratory tests and ERG. patients after bariatric surgery. Eat Weight Disord 2012; 17: e144–e146. 5 Elison JR, Friedman AH, Brodie SE. Acquired subretinal flecks secondary to hypovitaminosis A in a patient with hepatitis C. Doc Ophthalmol 2004; 109: CONCLUSIONS 279–281. Despite being very uncommon in our environment and even 6 Roncone DP. Xerophtalmia secondary to alcohol-induced malnutrition. Optometry 77 – more in patients without digestive problems, vitamin A deficiency 2006; :124 133. 7 Marmor MF, Fulton AB, Holder GE, Miyake Y, Brigell M, Bach M et al. ISCEV should not be discarded in a patient reporting acquired night standard for full-field clinical electroretinography (2008 update). Doc Ophthalmol blindness until eating patterns have been investigated, even if no 2009; 118:69–77. other ocular symptoms suggesting xerophthalmia are present. It 8 Papathanasiou ES, Papacostas SS. Flash electroretinography: normative values might be especially relevant in certain socioeconomic situations with surface skin electrodes and no pupil dilation using a standard stimulation and eating disorders as bulimia or anorexia nervosa that could protocol. Doc Ophthalmol 2008; 116:61–73. also affect older people despite being less frequent. Also, it is 9 Petzold A, Plant GT. Clinical disorders affecting mesopic vision. Ophthalmol Physiol 26 – necessary to ask about digestive symptoms, since they may have Opt 2006; :326 341. 10 Murube J, Murube E, Mompeán B. Why should the terms ‘nyctalopia’ and not been a reason for assistance but still be a clue for diagnosis. ‘hemeralopia’ be avoided? Arch Soc Esp Oftalmol 2002; 77:227–228. 11 Wald G. The chemistry of rod vision. Science 1951; 113:287–291. 12 Lengyel D, Török B. Acquired temporary night blindness in vitamin A and zinc CONFLICT OF INTEREST deficiency in anorexia nervosa nine years after kidney transplantation. Klin Monbl The authors declare no conflict of interests. Augenheilkd 2006; 223:453–455.