Night-blindness

The oxa2ohdinedione trimethadione [127-48-0] C H NO (50), at one time the dmg of choice for the treatment of absence sei2ures, has been replaced by ethosuximide (41) and valproate (49). (50) has a distinct profile from that of phenytoin but causes photophobia and night blindness in approximately 30% of the patients taking it and has the CNS and sedative properties seen for other anticonvulsants together with moderate neutropenia, hepatitis, and skin rashes (13). Trimethadione does not appear to produce its effects via modulation of GABA-mediated responses. 

In this period, the empirical healing of certain diseases by foods was estabUshed. Examples (3) were the treatment of night blindness (vitamin A deficiency) with hver ia many cultures over centuries, of beriberi (vitamin deficiency) by use of unpoHshed rice by the Japanese navy, of scurvy (vitamin C deficiency) by citms fmits ia the British navy or piae needle extracts by North American natives, and pellagra (niacia deficiency) by a dietary shift away from corn-based foods ia many countries. Other, nondietary empirical treatments iavolved, eg, exposure of children ia northern latitudes to sunlight to cute tickets (vitamin D deficiency) (4). 

In humans, vitamin A deficiency manifests itself in the following ways night blindness, xerophthalmia, Bitot s spots, and corneal involvement and ulceration. Changes in the skin have also been observed. Although vitamin A deficiency is seen in adults, the condition is particularly harmful in the very young. Often, this results from malnutrition (56). 

Nacht-blau, n. night blue, -blindhelt, /. night blindness, nyctalopia. 

Disorder characterized by atrophy ofthe choroid (the thin membrane covering most of the posterior of the eye between the retina and sclera) and degeneration of the retinal pigment epithelium resulting in night blindness. The disease is caused by mutations in Rab escort protein Repl (component A of Rab geranylgeranyl transferase). 

Mutation of the human Cavl.l gene is associated with hypokalemic periodic paralysis. Deletion of the Cav1.3 gene leads to viable pups that are deaf and have cardiac arrhythmia at rest. Mutation of the human Cavl. 4 gene is associated with X-linked congenital stationary night blindness. 

DISTUR0ED SENSORY PERCEPTION VISUAL. The patient taking chloroquine may experience a number of visual disturbances, such as disturbed color vision, blurred vision, night blindness, diminished visual fields, or optic atrophy. The nurse questions die patient about visual disturbances. 

A Retinol, p-carotene Visual pigments in the retina regulation of gene expression and cell differentiation p-carotene is an antioxidant Night blindness, xerophthalmia keratinization of skin... 

Health benefits — Research reports indicate that natural (3-carotene possesses numerous benefits for the human body and consistently supports the use of (3-carotene as part of the human diet. The human body converts (3-carotene to vitamin A via body tissues as opposed to the liver, hence avoiding a build-up of toxins in the liver. Vitamin A is essential for the human body in that it assists the immune system and helps battle eye diseases such as cataracts and night blindness, various skin ailments such as acne, signs of aging, and various forms of cancer. 

Patients with vitamin A deficiency may report visual disturbances, night blindness, and dry skin. 

Oka, S. (1955). Experience with adaptinol (Bayer) in night blindness (Japanese). Ophthalmol. Japonica Folia 6(4) 156-160. 

Sole, P., D. Rigal et al. (1984). Effects of cyaninoside chloride and heleniene on mesopic and scotopic vision in myopia and night blindness (French). J. Fr. Ophthalmol. 7(1) 35-39. 

There is additional evidence of wide variation in needs in the fact that high vitamin A intakes (much higher than the supposed normal) have been found beneficial in the treatment, in certain individuals, of skin lesions, night blindness, etc., when lower doses failed. Part of the difficulty in some cases may have involved faulty absorption. Even so, a difference in need is involved, and if one individual needs to consume ten times as much as another because of difficulty in absorption, the augmented need is just as real as if the difficulty involved some other step in utilization. 

Deficienqr of vitamin A results in night blindness (rod cells are responsible for vision in low light), metaplasia of the corneal epithelium, dry eyes, bronchitis, pneumonia, and follicular hyperkeratosis. 

G protein-coupled receptor kinase 1, rhodopsin kinase RHOK/ GRKl) 13q34 Exon 5 deletion Oguchi disease, reces-sively inherited stationary night blindness Impairment of GRKl-mediated desensitization of rhodopsin (189-191)... 

Dryja, T. P. (2000) Molecular genetics of Oguchi disease, fundus albipunctatus, and other forms of stationary night blindness LVII Edward Jackson Memorial Lecture. Am. J. Ophthalmol. 130, 547-563. 

Night Blindness, Retinitis Pigmentosa, and Rhodopsin Phosphorylation... 

In the absence of sufficient vitamin A, one consequence is a vision defect termed night blindness or, more technically, xerophthalmia. The rod cells in the retina are largely responsible for vision in low light. If they have too little retinal, they cannot do their job and night blindness, the inability to see in low light, results. If the condition persists, it is characterized by extreme dryness of the conjunctiva and can result in permanent blindness. 

Xerophthaimia night blindness, occasioned by a deficiency of vitamin A. 

A deficiency of vitamin A results in night blindness. A chronic deficiency results in a thickening of membranes in the cornea which, if untreated, can lead to blindness through perforation of the cornea and loss of the lens. It is estimated that half a million children develop blindness due to vitamin A deficiency every year. Refeeding malnourished children can produce a deficiency of vitamin A (see below). 

A deficiency of vitamin A leads to vision defects, including a visual impairment at low light levels, termed night blindness. For the processes of vision, retinol needs to be converted first by oxidation into the aldehyde retinal, and then by enzymic isomerization to cw-retinal. c -Retinal is then bound to the protein opsin in the retina via an imine linkage (see Section 7.7.1) to give the red visual pigment rhodopsin. 

Vitamin A deficiency can result from insufficient dietary intake, from malabsorption and it has been recognized that also malfunction of RAR-receptors can lead to symptoms of vitamin A deficiency. These symptoms include skin lesions, night blindness, corneal ulcerations and conjunctivitis and poor bone remodeling. Vitamin A deficiency associated with malnutrition is wide spread in large parts of the world and may be fatal in infants and young children suffering from kwashiorkor or marasmus. 

The duration of treatment for skin diseases is often longer than it is for malaria, and therefore, dose-related toxicities are important. The most serious toxicities are ophthalmological. Reversible alterations include ciliary body dysfunction and corneal changes with edema and deposits. Irreversible retinopathy also occurs however, it is less common with quinacrine than with the other two drugs. Toxicity may be asymptomatic, but the earliest symptoms are night blindness, scotoma, or tunnel vision. 

Since alcohol dehydrogenase is required for the conversion of retinol to retinal, excessive and prolonged ethanol ingestion can impair the physiological function of vitamin A. The decreased conversion of retinol to retinal results from competitive use of the enzyme by ethanol. Night blindness may result, since the visual cycle is a retinol-dependent physiological process. 

L B. Supplement with vitamin A. Vitamin A deficiency symptoms include night blindness that can lead to corneal ulceration. This deficiency can occur in patients with impaired liver storage or fat malabsorption. Dairy products, such as milk, are a good source of vitamin A. (3-Carotene, a vitamin A precursor, is found in pigmented vegetables, such as carrots. When a deficiency is diagnosed, it is appropriate to treat the patient with a supplement rather than to rely on increased consumption of vitamin A-rich foods. A patient with pancreatic disease and malabsorption syndrome will need parenteral supplementation. 

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