Disease Information for Avitaminosis A

Clinical Manifestations
Signs & Symptoms
Coarsening skin
Dry brittle hair/Lank lifeless hair
Dry skin/scaling dry skin
Face skin lesions
Fissuring palms/soles
Follicular hyperkeratosis
Follicular plugging/broken hair/coarse skin
Hyperkeratosis/palms and soles
Papular Rash
Phrynoderma/toadskin sign
Anorexia Decreased appetite
Malnourished/poor nutrition status/signs
Poor weight gain/child
Painful coitus or dyspareunia
Growth/development delay
Absence of tears/on exam
Bitots spots/conjunctival foamy patches
Chronic Vision Loss, Persistent
Corneal dryness/irritation
Dry eyes/poor tearing
Dryness Conjunctiva
Eye symptoms/signs
Grainy/Gritty Eye Sensation
Inspissated secretions/mucus eye
Night blindness/Impaired night vision
Xerosis Conjunctiva/Cornea
Clinical Presentation & Variations
Presentation/ Papular Rash Face Upper Arms
Demographics & Risk Factors
Ethnic or Racial Factors
Asian Indian population
Asian population
Established Disease Population
Patient/Jejunocolic bypass
Patient/Malabsorption syndrome
Patient/Sprue/gluten enteropathy
Population Group
Population/Immigrant population
Laboratory Tests
Abnormal Lab Findings - Decreased
Carotene/Vitamin A level (Lab)
Plasma Retinol
Plasma Retinol Binding Protein
URINE Retinol binding protein
Abnormal Lab Findings - Increased
Hemoglobin (Lab)
Diagnostic Test Results
Electroretinogram abnormal
Associated Diseases & Rule outs
Associated Disease & Complications
Corneal Ectasia
Corneal perforation/penetration
Growth retardation/failure
Phthisis bulbi/Globe collapse
Toxic amblyopia syndrome
Vitamin A deficiency/Avitaminosis A
Disease Mechanism & Classification
Pathophysiology/Mucosal keratinization
Pathophysiology/Dark adaptation/vision defect
PROCESS/Deficiency (category)
PROCESS/Fat soluble vitamin deficiencies (ex)
Drug Therapy - Indication
RX/Vitamin A

Vitamin A (retinol) is fat soluble and is found mainly in fish liver oils, liver, egg yolks, butter, and cream. Green leafy and yellow vegetables contain -carotene and other provitamin carotenoids, which are converted to retinal in the mucosal cells of the small intestine; Retinal is reduced to retinol, then esterified; Most of the body"s vitamin A is stored in the liver as retinyl palmitate; It is released into the circulation as retinol bound to retinol binding protein and prealbumin (transthyretin); The 11-cis isomer of retinal (vitamin A aldehyde) combines with opsin to form rhodopsin, the prosthetic group of photoreceptor pigments in the retina; In somatic cells, retinol is converted to retinoic acid, which combines with receptors that bind to DNA and regulate gene expression to maintain epithelial tissues; Primary vitamin A deficiency is usually caused by prolonged dietary deprivation; It is endemic in areas, such as southern and eastern Asia, where rice, devoid of carotene, is the staple; Secondary vitamin A deficiency may be due to inadequate conversion of carotene to vitamin A or to interference with absorption, storage, or transport of vitamin A; Interference with absorption or storage is likely in celiac disease, sprue, cystic fibrosis, pancreatic disease, duodenal bypass, congenital partial obstruction of the jejunum, obstruction of the bile ducts, giardiasis, and cirrhosis; Vitamin A deficiency is common in protein-energy malnutrition (marasmus or kwashiorkor), principally because the diet is deficient but also because vitamin A storage and transport are defective; The severity of the effects of vitamin A deficiency is worse in young; Growth retardation is a common sign in children; this can cause impaired dark adaptation and night blindness; xerosis of the conjunctiva and cornea; xerophthalmia and keratomalacia; keratinization of lung, GI tract, and urinary tract epithelia; increased susceptibility to infections; and sometimes death; Follicular hyperkeratosis of the skin is common; rod dysfunction, can be detected by dark adaptometry, rod scotometry, or electroretinography (these tests require cooperative subjects); Dysfunction of the retina is followed by changes in the structure and function of epithelial cells; Xerosis of the bulbar conjunctiva consists of drying, thickening, wrinkling, and muddy pigmentation; the cornea becomes xerotic, infiltrated, and hazy at an early stage; Keratomalacia rapidly supervenes with liquefaction of part or all of the cornea, leading to rupture, with extrusion of the eye contents and subsequent shrinking of the globe (phthisis bulbi), or to anterior bulging (corneal ectasia and anterior staphyloma) and blindness; Bitot"s spots (superficial foamy patches composed of epithelial debris and secretions on the exposed bulbar conjunctiva) occur in advanced deficiency; Severe Vitamin A deficiency, in children, mortality can be 50% or more; Plasma retinol levels fall after liver stores are exhausted; Plasma levels of vitamin A and RBP also fall in acute infections; Secondary infection may complicate the corneal changes; Trial with therapeutic doses of vitamin A assists in the diagnosis----------[Merck Manual 17th]-----


External Links Related to Avitaminosis A
PubMed (National Library of Medicine)
NGC (National Guideline Clearinghouse)
Medscape (eMedicine)
Harrison's Online (accessmedicine)
NEJM (The New England Journal of Medicine)