Atrophic beriberi. A complication of jejunoileal bypass surgery for morbid obesity.
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Biomedical subjects
Publications and source records attributed to R E Hodges.
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Recent studies of experimental vitamin A deficiency in man led the authors to conclude that anemia may result from lack of vitamin A. A review of numerous nutrition surveys in underdeveloped countries enhanced the suspicion that deficiency of vitamin A does contribute to the prevalence of anemia. Preliminary studies of vitamin A-deficient rats confirmed previous observations that anemia may result from lack of this vitamin. The livers of these animals had very low concentrations of vitamin A but normal or increased concentrations of iron. The finding of anemia is in contrast with other reports that vitamin A deficiency may cause elevated values for hemoglobin and hematocrit. The authors suggest that loss of taste and smell as a result of deficiency may account for refusal of experimental animals to eat and drink enough to prevent inanitation and dehydration. The resulting hemoconcentration may mask the true hematological picture, which is one of anemia.
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In order to investigate the role of vitamin A nutriture in the prevalence of anemia in Central America, a retrospective evaluation of the data of the six Institute of Nutrition of Central Americal and Panama/Office for International Research nutrition surveys of Central America and Panama has been made. Three groups of children; 1 to 4, 5 to 8, and 9 to 12 years old, living between 0 and 2,5000 feet above sea level were studeid. Several biochemical and dietary parameters related to anemia were corrleated with plasma levels of retinol. Children between the ages of 5 and 12 years showed a significant positive correlation between hemoglobin and plasma retinol. Children aged 1 to 4 years did not show a similar correlation. In children of all age groups there were positive correlations between plasma retinol and serum iron. Percent saturation of transferrin was also found to be lower when plasma retinol levels were low. Children with an adequate intake of iron, as classified by both dietary information and socioeconomic level, showed a significant positive correlation between plasma retinol levels and iron in their serum. In contrast, no correlation was found when dietary iron was low. In the light of these findings, a possible relationship between vitamin A deficiency and anemia is suggested.
The sulfation of ascorbic acid by an ascorbic acid sulphotransferase was investigated using rat liver and colon homogenates. When Na2 35 SO4 or 3'-phosphoadenylyl [35S]sulfate (P-Ado-P-35S) and ascorbic acid were used as substrates, chromatographic behavior of the reaction products on thin-layer cellulose suggested that ascorbic acid 2-[35S]sulfate was formed. With Na2 35SO4 as the source of radioactive sulfate in the assay system, ATP was found to be an obligatory cofactor. Incorporation of [35S]sulfate frofrom Na2 35SO4 into ascorbic acid 2-[35S]sulfate was also decreased when ATP sulfurylase inhibitors were added to the system. P-Ado-O35S alone in the assay without ATP was an extemely effective sulfating agent. In addition, liver and colon homogenates from vitamin A deficient and sufficient rats were used in one of the studies. Vitamin A deficiency appeared to have little effect on ascorbic acid 2-sulfate formation.
Weekly determinations of serum copper (Cu) and zinc (Zn) were made in eight adult patients receiving total parenteral nutrition (TPN) for 3 to 13 weeks. Serum Cu decreased in all eight patients. Five of eight patients had hypocupremia lasting at least 2 consecutive weeks and three of the five had Cu levels of 30 mug/dl or lower. Low levels of serum ceruloplasmin provided supportive evidence of Cu deficiency in the three patients with the lowest Cu levels. Two patients who had Cu less than or equal to 20 mug/dl demonstrated declines in hemoglobin which were probably due to Cu deficiency. The mean rate of decline in serum Cu was 10.8 mug/dl/week. After resumption of oral feedings in five patients, the mean rate of increase in Cu was 14 mug/dl/week. The sharpest rise in Cu was seen during the 2nd week after oral feedings were resumed in four of the five patients. Three of eight patients had serum Zn levels less than 70 mug/dl for at least 2 consecutive weeks. Serum Zn decreased at a mean rate of 6.6 mug/dl/week. There was a further decline in serum Zn in three of five patients in whom measurements were made after resumption of oral intake. Concentrations of Zn in TPN solutions varied between 0.63 and 1.0 mg/liter. Cu was undetectable in TPN solutions.
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In seven adult patients receiving fat-free total parenteral nutrition (TPN) for 4 to 8 weeks, weekly determinations of plasma fatty acids and total plasma tocopherols were made. Four patients were deficient in essential fatty acids, as defined by triene: tetraene ratio greater than 0.4, at the end of the second week of TPN. Six patients were deficient by the end of the third week and all seven were deficient by the end of the fifth week of TPN treatment. One patient who was deficient in both essential fatty acids and zinc developed a scaling, eczemoid dermatitis that disappeared within 3 weeks after cessation of TPN and resumption of oral feedings containing both fat and zinc. After resumption of oral feedings by three patients, the triene: tetraene ratio returned to normal within 2 weeks. The mean of total plasma tocopherols fell over a period of 7 weeks and in three individuals, reached levels generally associated with deficiency. There were not any obvious clinical manifestations of vitamin E deficiency.
Weanling rats were fed diets with and without the addition of retinyl palmitate at 6,500 units/kg. The supplemented groups were fed either ad libitum or food was restricted daily to that amount consumed by the group of rats receiving the unsupplemented diet. After a 10 week experimental period, signs of vitamin A deficiency were observed (growth plateau, xerophthalmia) and liver values as retinol were only 1% of control values. Relative to the two control groups, vitamin A deficiency resulted in approximately 30% lower liver, 50% lower blood and 40% lower urinary ascorbic acid. Vitamin A deficiency did not appear to result in significant and direct impairment of GAG sulfate metabolism. Although the total amount of GAG in rat skin was increased, the composition of GAG fractions did not appear to be altered by vitamin A deficiency. Studies regarding the incorporation and disappearance of 35S-sulfate in vivo into GAG fractions obtained from skin indicated no serious impairment in GAG turnover with vitamin A deficiency. Twenty-four hour urine samples were also collected for estimation of 35SO4 excreted in GAG and non-GAG fractions. Likewise, little change was observed with respect to radioactivity associated with sulfate fractions excreted in urine. Although many previous studies have directly linked vitamin A with sulfation of GAG, the results reported here suggest that if there is an alteration in GAG sulfate metabolism, it is probably an indirect consequence of vitamin A status.
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Twenty-five young couples consumed either a saturated or polyunsaturated fat diet for a 20-week period. The polyunsaturated beef, lamb and dairy products, high in linoleic acid, were produced by feeding ruminant animals "protected lipid" feeds which prevent hydrogenation of fats in the rumen. The experimental design provided for four dietary groups: A) saturated diet for 20 weeks; B) polyunsaturated diet for 20 weeks; C) saturated diet for 10 weeks then polyunsaturated diet for 10 weeks; and D) polyunsaturated for 10 weeks then saturated diet for 10 weeks. Polyunsaturated-to-saturated ratios (linoleic: total saturated fatty acids) for the diets were: prestudy, 0.43-0.56; saturated 0.11-0.14; polyunsaturated, 0.56-0.62. Factors other than diet that appeared to affect cholesterol responses were carefully considered. During the initial 3 weeks (regimentation period) plasma cholesterol concentration decreased in all groups irrespective of diet. This was followed by two experimental periods in which the effects of the prescribed diets were readily apparent (response periods I and II). The final 4 weeks of the study were characterized by diminishing compliance with the dietary discipline (abatement period). Subjects in each group (A,B,C,D) were subdivided into high and low on a basis of each group's initial median cholesterol level. Those in the high subgroups were very responsive to dietary changes whereas those in the low subgroups were not. Combined responses of high subjects were: polyunsaturated diet, -10.7 mg/dl (P less than 0.025), saturated diet, d8 mg/dl (P less than 0.05). Combined difference between saturated and polyunsaturated diets was 18.5 mg/dl or approximately a 10% cholesterol difference between the experimental polyunsaturated and saturated diets.
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