Adequate Vitamin Supplementation Research Articles

Deficiency of vitamins E and A in cystic fibrosis is independent of pancreatic function and current enzyme and vitamin supplementation.

The aim of this study was to evaluate to what extent serum vitamins A and E cystic fibrosis are affected by the underlying disease, pancreatic sufficiency or insufficiency, meconium ileus, nutritional status, age and treatment (enzyme and vitamin supplementation). Serum vitamin A and E levels were determined by high performance liquid chromatography in 210 cystic fibrosis patients, subdivided according to clinical condition into four subgroups (unsupplemented pancreatic insufficiency, supplemented meconium ileus, pancreatic sufficiency, supplemented pancreatic insufficiency) and compared with 42 control subjects. Vitamin A and E levels were generally lower in cystic fibrosis patients than in controls (P < 0.002 and P < 0.001 respectively). Subjects with pancreatic insufficiency regularly receiving enzyme and vitamin supplementation had significantly lower vitamin A (P < 0.05) and vitamin E (P < 0.01) levels than controls. In subjects with pancreatic sufficiency only vitamin A was significantly lower than in controls (P < 0.01). Vitamin levels were not age-dependent in cystic fibrosis, and no significant correlation with standardized body weight (Z-score) was observed. Cystic fibrosis patients show a clear tendency to vitamin A and E deficiency, irrespective of pancreatic function, body weight and standardized supplementation with pancreatic extract and liposoluble vitamins. Since the clinical significance of this deficiency is still not clear, longitudinal studies of cystic fibrosis patients with and without adequate vitamin supplementation are required.

Thiamine Deficiency: Probable Wernicke's Encephalopathy Successfully Treated in a Child With Acute Lymphocytic Leukemia

The classical clinical picture of the syndrome described by Wernicke1 consists of disturbances of consciousness, ophthalmoplegia, and ataxia. It has been ascribed to thiamine deficiency, although other dietary deficiencies may contribute to its development. The fullblown triad is frequently not present, a confused state often being the only manifestation. This may progress to stupor or coma. The condition has been described in adults with alcoholism, in chronic gastrointestinal disease, in prisoners of war maintained on very precarious diets and in obese patients kept on restricted diets without adequate vitamin supplementation.2 Guerrero3 in 1949 reported two infants with Wernicke's syndrome due to vitamin B deficiency.

Infant Nutrition.

This is a good updating of current practices in infant feeding. The author attributes the improvement in infant nutrition, which dates from the 1920s, to improved sanitation, alteration of curd tension of milk, and adequate vitamin supplementation. Marriott's contribution, however, we feel was more than that which could be accounted for either by the smaller curd of evaporated milk or reduction of buffer by lactic acid. In analyzing the content of nutritional disturbances admitted to an infants' ward in the 1920s, one of the largest groups was that hospitalized for "regulation of feeding." Common to practically all of the histories of this group was the story of dilute, low-calorie feedings, repeatedly made more dilute when regurgitation or discomfort was complained of. The standard correction was merely the concentration of the feeding to at least 20 calories per ounce. In 1927, the reviewer and Dr. K. D. Blackfan reported a study