The clinical effects of vitamin A deficiency that are best recognised are those affecting the eye. However vitamin A deficiency affects all mucous membranes of the body and the impact on the eye is later than that on some other organs. The effects are seen most markedly in periods of greatest need; early growth, pregnancy and lactation.
Xerophthalmia and Keratomalacia: Xerophthalmia represents the ocular consequences of vitamin A deficiency and includes
Opsin, a protein binds covalently with 11- cis- retinal to form rhodopsin or visual purple. Light exposure even at low levels bleaches rhodopsin. This sends electrochemical impulses along the optic nerve to the brain that results in vision. The vitamin A aldehyde is returned to the rods to form rhodopsin once again and thus the visual cycle is completed. Due to a lack of vitamin A, this cycle is disabled resulting in poor vision in dim light followed by night blindness. This is commonly seen among preschool children and pregnant women.
Conjunctival xerosis with Bitot’s spots: Bitot’s spots are grey to yellowish white foamy patches of keratinized cells present usually on the temporal conjuctival surface. They respond to high potency vitamin A and disappear within two weeks. In some cases they may persist for many months despite overcoming vitamin A deficiency. Thus they may represent past rather than present deficiency.
Corneal xerosis, ulceration and necrosis: Corneal xerophthalmia represents an acute decompensation of the corneal epithelium and is a sight threatening emergency. It responds to vitamin A therapy if treated immediately. If untreated it leads to blindness. Small ulcers in the cornea also heal with a minimum damage if treated promptly. If it is not treated it will result in meltdown of the eye with irreversible blindness in the eye.
Last modified: Wednesday, 2 November 2011, 11:07 AM