Journal francais d'ophtalmologie · 2007
[The eye and anorexia nervosa. A case report].
Клинический случайАннотация на английскомСтатьяНазвание и аннотация: Перевод в очереди
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Berthout A, Sellam M, Denimal F, Lalau J-D, Milazzo S
Аннотация
INTRODUCTION: Vitamin A deficiency occurs in the poor in developing countries and is one of the main causes of blindness by perforative corneal complications. It is a rare pathology in industrialized countries and it is associated with an absorption syndrome. The authors report the first case of hypovitaminosis A in a patient suffering from chronic and severe anorexia nervosa.
CASE REPORT: The patient suffered from epiphora, photophobia, and hesperanopia. The ophthalmologic findings were keratoconjunctival xerosis with bilateral corneal ulcerations. The visual field showed a concentric bilateral restriction of isopters with tubular central vision, a similar aspect to retinitis pigmentosa. The ERG was modified with a b2 reduction and normal photopic and impaired scotopic responses. The fluorescein angiography was normal. The serum concentration of retinol confirmed the diagnosis of hypovitaminosis A. Corneoconjunctival improvement was obtained with vitamin supplementation, but no campimetric improvement was observed.
DISCUSSION: The corneoconjunctival signs result from direct destruction of goblet cells, whereas the campimetric deficit is explained by a dysfunction of rod cells. Rhodopsin, necessary to the survival of the cell, cannot be renewed if retinol is not present, which causes a permanent bright light stimulation that is lethal for the photoreceptor.
CONCLUSION: Vitamin A deficiency is rarely caused by psychiatric disease. Even if the main clinical finding is xerophthalmia with a high risk of keratomalacia, the visual prognosis can also be engaged by dysfunction of photoreceptors.
CASE REPORT: The patient suffered from epiphora, photophobia, and hesperanopia. The ophthalmologic findings were keratoconjunctival xerosis with bilateral corneal ulcerations. The visual field showed a concentric bilateral restriction of isopters with tubular central vision, a similar aspect to retinitis pigmentosa. The ERG was modified with a b2 reduction and normal photopic and impaired scotopic responses. The fluorescein angiography was normal. The serum concentration of retinol confirmed the diagnosis of hypovitaminosis A. Corneoconjunctival improvement was obtained with vitamin supplementation, but no campimetric improvement was observed.
DISCUSSION: The corneoconjunctival signs result from direct destruction of goblet cells, whereas the campimetric deficit is explained by a dysfunction of rod cells. Rhodopsin, necessary to the survival of the cell, cannot be renewed if retinol is not present, which causes a permanent bright light stimulation that is lethal for the photoreceptor.
CONCLUSION: Vitamin A deficiency is rarely caused by psychiatric disease. Even if the main clinical finding is xerophthalmia with a high risk of keratomalacia, the visual prognosis can also be engaged by dysfunction of photoreceptors.