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Fig. 19. Seasonality of xerophthalmia in Tianjin, China. (Reprinted from ref. 897.)

jan feb mar april may june July aug sept oct nov dec

Fig. 19. Seasonality of xerophthalmia in Tianjin, China. (Reprinted from ref. 897.)

(369). In Tunisia, cases of xerophthalmia were also reportedly more common at the end of the hot summer and were associated with chronic diarrhea (872). The seasonal incidence of more than 15,000 cases of xerophthalmia among children was examined in four ophthalmic hospitals in India, Indonesia, and Vietnam (898). In Bangalore, India, there were more cases of xerophthalmia seen from April to June, and this coincided with a relative scarcity of green vegetables and milk and with a higher prevalence of summer diarrhea. In Surabaya and Bandung, Indonesia, the incidence of xerophthalmia was highest from about March to September. In Hanoi, Vietnam, there were two periods in which xerophthalmia was highest, from April to June and from October to December (898). In a longitudinal study of 312 children, aged 0-4 yr, in rural West Bengal, the incidence of night blindness and/or Bitot spots had a small peak in November-December and in a larger peak in May-June (899). The prevalence of Bitot spots was highest in the pre-monsoon season in West Bengal (899). In longitudinal field studies in Indonesia, the number of children with corneal involvement in xerophthalmia was highest in March through August (285). Among children admitted to Cicendo Eye Hospital in Bandung, Indonesia, the peak month of admissions was in March, which corresponds to the dry season (623). The periodicity of xerophthalmia in some populations needs to be taken in account when conducting epidemiological surveys of vitamin A deficiency. Xerophthalmia was also reported to increase after crop failure in Russia (900).

5.3.12. Malabsorption

Cystic fibrosis. Cystic fibrosis is an autosomal recessive disease that affects primarily Caucasian populations and is characterized by exocrine pancreatic insufficiency, altered pulmonary mucosal immunity, and other abnormalities affecting the liver, sweat glands, and genitourinary tract (901). Exocrine pancreatic insufficiency causes malabsorption of fat and fat-soluble vitamins such as vitamin A, and problems such as steatorrhea and poor weight gain. Cystic fibrosis is caused by a mutation in the FES1 gene that encodes the cystic fibrosis transmembrane conductance regulator. Individuals with cystic fibrosis are at a high risk of developing vitamin A deficiency because of malabsorption of vitamin A (902). One study of 36 infants less than 2 mo of age in Colorado showed that vitamin A deficiency was present among 21% of those diagnosed with cystic fibrosis by newborn screening (903). There have been many case reports of xerophthalmia associated with cystic fibrosis (904-913). Low plasma vitamin A concentrations and impaired dark adaptation appear to occur frequently in cystic fibrosis, even among clinically stable, eutrophic, and retinol-supplemented adolescents (914). Night blindness and conjunctival xerosis may still occur despite vitamin A-supplementation among adolescents with cystic fibrosis, especially if they have liver disease (909).

Pulmonary exacerbations of cystic fibrosis are associated with an increase in inflammation and a decrease in plasma retinol concentrations (915). Xerophthalmic fundus has been reported in an 18-yr-old girl with cystic fibrosis who developed night blindness (908). Regular monitoring of serum retinol concentrations in individuals with cystic fibrosis has been recommended because vitamin A deficiency may still occur despite vitamin A supplementation (902). Low serum retinol concentrations were reported to have no correlation with pancreatic sufficiency in cystic fibrosis (916). Regular monitoring of serum retinol concentrations and adherence to vitamin A supplementation may help patients with cystic fibrosis avoid problems with night blindness (917,918). A study of vitamin A concentrations in the liver among fifteen patients with cystic fibrosis from 8 to 34 yr of age show that hepatic retinol concentrations decrease with age (919). These findings are suggestive that long-term vitamin A supplementation is unlikely to increase the risk of hypervitaminosis A in patients with cystic fibrosis (919). A transient increase in intracranial pressure, as manifested by a bulging anterior fontanelle, was reported in two 9-mo-old infants with cystic fibrosis and xerophthalmia after receiving high-dose vitamin A (913).

Celiac sprue. Celiac sprue, also known as celiac disease and gluten-sensitive enteropathy, is a condition of the proximal small intestine that is characterized by malabsorption (920,921). The condition is associated with injury to the small intestine after the ingestion of wheat gluten or related rye and barley proteins and improves on treatment with a gluten-free diet. The condition has a genetic predisposition and may occur in one of every 120-300 persons in both Europe and the United States (921). It mostly occurs in Caucasians but has been reported occasionally in other ethnic groups. Abnormal T-cell mediated immune responses against ingested gluten may occur in those that are genetically predisposed together the disease (921). Common clinical manifestations include diarrhea, failure to thrive, and abdominal distention in children, and diarrhea and iron deficiency anemia in adults. Children and adults with celiac disease may have abnormal absorption of oral vitamin A (922). During active sprue, vitamin A absorption is severely impaired, but during remission of disease, the absorption of vitamin A may be satisfactory (923). Plasma retinol concentrations are reduced in patients with sprue compared with normal individuals (924). Keratomalacia was reported in a 64-yr-old man with a history of celiac sprue after he developed persistent diarrhea in spite of adherence to a gluten-free diet (925).

Other conditions. Night blindness associated with vitamin A deficiency has been reported with intestinal bypass surgery for morbid obesity (926-930). In addition to night blindness, conjunctival xerosis (926) and Bitot spots (927) have also been reported after intestinal bypass surgery. Xerophthalmia and keratomalacia have been described in an infant with obstructive biliary cirrhosis (931). Night blindness has been associated with alcoholic liver disease (932-934). Severe protein energy malnutrition is associated with impaired intestinal absorption of vitamin A (935).

5.3.13. Pregnancy

Night blindness has long been recognized among pregnant women, with hundreds of cases reported in the literature (936-961). The requirement for vitamin A increases during pregnancy, and many women may not have adequate intake of vitamin A and subsequently develop night blindness. In general, night blindness is more common in pregnant women from poor families and in association with complications of pregnancy such as hyperemesis, anorexia, diarrhea, and other concomitant infections. In a study conducted in 1889-1892 in Nishne Tagilsk in the Urals, O. Walter noted that night blindness among pregnant women seemed to peak in February through April, and a large proportion indicated that they had repeatedly been night blind during pregnancy (941). At a time when vitamin A deficiency was prevalent in Europe, Theodor Birnbacher and Emanuel Klaften noted that night blindness was more common among pregnant women than nonpregnant women of childbearing age (944), and Birnbacher attributed the night blindness to lack of vitamin A (946). Carsten Edmund (b. 1897) and Svend Clemmesen (b. 1901) in Copenhagen concluded that night blindness in pregnant women was due to vitamin A deficiency because the night blindness was promptly cured after treatment with parenteral vitamin A (947). After margarine was fortified with vitamin A in 1936-1937 in Denmark, they noted a decrease in the number of cases of pregnant women with night blindness (947). Parul Christian has recently brought attention to night blindness during pregnancy as an indicator of vitamin A deficiency (962).

5.3.14. Nonpregnant Women of Childbearing Age

Night blindness has also been reported among nonpregnant women of childbearing age in India (963), Bangladesh (964), Nepal (965), and Cambodia (603). In the 1930s, Adalbert Fuchs reported that night blindness and keratomalacia occurred among lactat-ing women in Mysore, India (966). A strong risk factor for night blindness among women of childbearing age is night blindness during the most recent pregnancy (603). However, it does not appear that vitamin A deficiency during the last pregnancy alone is the main determinant of night blindness, as one might expect that the point prevalence of night blindness would be highest immediately following pregnancy. Instead, the risk of night blindness appears to be consistently high and steady for many months following delivery (Fig. 20), which suggests that there are women who have greater risk overall of night blindness because of poor intake of vitamin A-rich foods (603). Among nonpregnant women in Cambodia, in a final multivariate analysis, risk factors for night blindness included materials of the wall of the house (OR 1.4, 95% CI 0.9-2.0), land ownership >0.5 hectares (OR 1.4, 95% CI 1.0-1.9), night blindness in the last pregnancy (OR 44.5, 95% CI 29.2-67.8), parity >3 (OR 1.5, 95% CI 1.0-2.1), diarrhea within the last 2 wk (OR 1.9, 95% CI 1.3-2.8), maternal body mass index (OR 1.8, 95% CI 1.2-2.7), and lack of consumption of vitamin A-rich animal foods in the last 24 h (1-60 REs, OR 1.1, 95% CI 0.7-1.6, >60 retinol equivalents, OR 0.7, 95% CI 0.4-1.0) (603).

0 to <3 3 to <6 6 to <9 9 to <12 12 to <24 24 to <36 36 to <48 48 to <60

Months Since Delivery of Last Pregnancy

0 to <3 3 to <6 6 to <9 9 to <12 12 to <24 24 to <36 36 to <48 48 to <60

Months Since Delivery of Last Pregnancy

N 1194 1515 1310 1247 3318 2164 1611 979 Fig. 20. Point prevalence of night blindness after delivery among women in Cambodia. (Reprinted from ref. 603.)

5.1.15. Institutionalization

Xerophthalmia has been reported in mental hospitals, prisons, and orphanages where the diet may be inadequate in vitamin A (967-970). In Calcutta, corneal ulceration occurred among prisoners recovering from cholera and was thought to be the result of malnutrition (971). Bitot spots and corneal leucomas were described among inmates of a mental hospital in Mathari, Kenya (969). In Kampala and Luzira Prisons in Uganda in the 1920s, corneal ulceration was observed among inmates who were fed a diet poor in vitamin A (970). No cases of xerophthalmia and corneal ulceration were reported from Mengo Prison, where the inmates were fed four pounds of sweet potato (a rich plant source of vitamin A) each day (970). Xerophthalmia was noted to be common in local prisons in Malawi in the 1980s (Moses Chirambo, personal communication). Medical staff and aid workers who deal with prisoners in developing countries should be aware that the presence of night blindness, Bitot spots, or corneal xerosis among inmates indicate a poor quality diet that is low or devoid of vitamin A-rich foods.

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