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We report two patients of Afro-Caribbean origin with an ataxic neuropathy combined with visual loss and deafness. In previous reports of a similar syndrome most patients have been malnourished and have had mucocutaneous lesions, features which were absent in our patients.
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We measured serum, blood, or red cell concentrations of various vitamins in 24 patients with Crohn's disease who had been free from any nutritional treatment, and compared them with those in 24 healthy controls. Twelve of the patients were affected in the small bowel only, two in the large bowel only, and the remaining 10 in both the small and large bowel. The fat-soluble vitamins A and E were significantly decreased in patients with Crohn's disease compared to controls. Among the water-soluble vitamins, vitamins B1, B2 and B6 and folic acid were more depleted in patients with Crohn's disease than in the controls, whereas vitamins B12 and C, nicotinic acid, and biotin were not different between the two groups, and pantothenic acid was increased in patients with Crohn's disease. In addition, vitamin B2 and nicotinic acid showed a negative correlation with the Crohn's disease activity index. These findings suggest that there is a variety of vitamin deficiencies in Crohn's disease prior to treatment and also that concentrations of some vitamins, such as vitamin B2 and nicotinic acid, may reflect the severity of the disease.
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Biotin deficiency in Aspergillus nidulans has been found to increase the uptake of ammonium ions, associated with a marked increase in the activity of NADP-linked glutamate dehydrogenase, which is found to be the major route of ammonia assimilation in this culture. The results obtained are discussed with respect to the growth of Aspergillus nidulans during biotin deficiency.
Liver fibrosis was induced in rats by simulating human alcoholic eating and drinking patterns. Alcohol addiction was established by gradually increasing the ethanol concentration in the drinking water; salts were added at the terminal stage. The hepatocytes of rats receiving alcohol concentrations exceeding 50% (v/v) (similar to vodka) exhibited alcoholic hyaline (Mallory bodies). Alcoholic liver fibrosis was induced by alternating between regular and autoclaved (vitamin-depleted) diets, simulating the irregular eating habits of human alcoholics. In the livers of rats receiving 70% (v/v) ethanol (comparable to absinthe) with 25% saline and fed the alternating diets, pericellular fibrosis was induced. No significant difference in calorie intake between control and alcohol rats was detected except when rats underwent drinking bouts (heavy drinking phase). This indicates that neither a high-fat diet nor a choline-depleted diet is necessary to induce the alcoholic fibrosis seen in human alcoholics.
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The comparison between complaints, functional defects and vitamin deficiencies is reported for several professional groups characterized by different work conditions. Results suggest that complaints are an useful indicator of visual load and that retinal sensitivity to the light is especially tried. Longitudinal studies are required to verify whether some functional alterations on the aging process of the eye can be aggravated by a visual overload. Visual complaints, functional defects and vitamin deficiencies as indicators of visual load.
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OBJECTIVE: To perform a comprehensive laboratory assessment of nutritional status in two elderly patients selected for the presence of atrophic glossitis, a classic physical sign of malnutrition. DESIGN: Case report. SETTING: Inpatient internal medicine ward at the William S. Middleton Memorial Veterans Medical Center, Madison, Wisconsin. MEASUREMENTS AND MAIN RESULTS: Blood specimens were analyzed by the Nutrition Evaluation Laboratory at the USDA Human Nutrition Research Center on Aging at Tufts University. Both subjects had biochemical evidence of protein-calorie malnutrition and were deficient or marginally deficient in several vitamins and trace minerals. CONCLUSIONS: Much work needs to be done to determine the sensitivity and positive predictive value of the classic physical signs of malnutrition as predictors of low biochemical levels and adverse clinical outcomes. The presence of atrophic glossitis should prompt the clinician to consider a basic nutritional assessment.
The migration and maturation of Langerhans cells (LCs) in rat tracheal squamous metaplasia due to vitamin A deficiency were investigated immunohistochemically and electron microscopically. In the early stage of metaplasia, i.e. basal cell hyperplasia, no LCs with Birbeck granules (BGs) could be found, but there were desmosome-free cells which had the morphological characteristic of immature LCs. They were clearly different from inflammatory cells such as macrophages and lymphocytes, and were, therefore, considered to be precursors of LCs. In the stage of stratification, small numbers of Ia- and protein kinase C type II (PKCII)-positive cells were recognized. Ultrastructurally they were immature LCs with ovoid nuclei, many free ribosomes and few dendrites. The cytoplasm was dark and a few BGs and atypical granules (AGs) could be seen in the Golgi area. In the early stage of cornification, LCs with partially intended nuclei, prominent nucleoli and well-developed Golgi complexes were found. There were many BGs and AGs and structures transitional between them in the Golgi areas. In epithelium showing mature squamous metaplasia, many Ia- and PKCII-positive dendritic cells could be seen. Most of these were typical mature LCs with lobulated nuclei, clear cytoplasm and prominent dendritic processes. The number of BGs and AGs were fewer than in the LCs found in the early stage of cornification, and these granules were distributed throughout the cytoplasm. In the final stage, where the basal cells had differentiated into a flatter epithelium, few LCs could be seen.(ABSTRACT TRUNCATED AT 250 WORDS)
Vitamins, either as coenzymes or hormone-like substances play an important role in the expression of genetic information and in the regulation of cellular metabolism, differentiation, and maturation. Recent epidemiologic evidence suggests that certain forms of cancer are more prevalent among populations with a limited intake of certain nutrients. Other evidence indicates that localized deficiency of a nutrient can occur in hormone-sensitive cells without overt systemic manifestations of deficiency disease. Folic acid, because of its key role in nucleic acid biosynthesis, and vitamin A, because of its role in epithelial maintenance are of particular interest. The recognition of folate-dependent fragile sites on chromosomes suggests that folate and related compounds may play a role in preventing tumor-specific chromosome translocations and the insertion of viral oncogenes. Improved understanding of the role of nutrients in cellular maturation could provide clues for primary cancer prevention and better methods of treatment.
Vitamins contain reactive functional groups necessary to their established roles as coenzymes and reducing agents. Their reactive potential may produce injury if vitamin concentration, distribution, or metabolism is altered. However, identification of vitamin toxicity has been difficult. The only well-established human vitamin neurotoxic effects are those due to hypervitaminosis A (pseudotumor cerebri) and pyridoxine (sensory neuropathy). In each case, the neurological effects of vitamin deficiency and vitamin excess are similar. Closely related to the neurological symptoms of hypervitaminosis A are symptoms including headache, pseudotumor cerebri, and embryotoxic effects reported in patients given vitamin A analogs or retinoids. Most tissues contain retinoic acid (RA) and vitamin D receptors, members of a steroid receptor superfamily known to regulate development and gene expression. Vitamin D3 effects on central nervous system (CNS) gene expression are predictable, in addition to the indirect effects owing to its influence on calcium and phosphorus homeostasis. Folates and thiamine cause seizures and excitation when administered in high dosage directly into the brain or cerebrospinal fluid (CSF) of experimental animals but have rarely been reported to cause human neurotoxicity, although fatal reactions to i.v. thiamine are well known. Ascorbic acid influences CNS function after peripheral administration and influences brain cell differentiation and 2-deoxyglucose accumulation by cultured glial cells. Biotin influences gene expression in animals that are not vitamin-deficient and alters astrocyte glucose utilization. The multiple enzymes and binding proteins involved in regeneration of retinal vitamin A illustrate the complexity of vitamin processing in the body. Vitamin A toxicity is also a good general model of vitamin neurotoxicity, because it shows the importance of the ratio of vitamin and vitamin-binding proteins in producing vitamin toxicity and of CNS permeability barriers. Because vitamin A and analogs enter the CNS better than most vitamins, and because retinoids have many effects on enzyme activity and gene expression, Vitamin A neurotoxicity is more likely than that of most, perhaps all other vitamins. Megadose vitamin therapy may cause injury that is confused with disease symptoms. High vitamin intake is more hazardous to peripheral organs than to the nervous system, because CNS vitamin entry is restricted. Vitamin administration into the brain or CSF, recommended in certain disease states, is hazardous and best avoided. The lack of controlled trials prevents us from defining the lowest human neurotoxic dose of any vitamin. Large differences in individual susceptibility to vitamin neurotoxicity probably exist, and ordinary vitamin doses may harm occasional patients with genetic disorders.(ABSTRACT TRUNCATED AT 400 WORDS)
BACKGROUND: Deficiencies of vitamins and trace elements are frequent in inflammatory bowel disease. Aim of this study was to evaluate retrospectively the prevalence of these deficiencies and of liver complications in a large population. PATIENTS AND METHODS: The records from 392 out-patients, 279 with Crohn's disease (160 female, 119 male) and 113 with ulcerative colitis (56 female, 57 male) were analyzed. RESULTS: Deficiencies were found in 85% of patients with Crohn's disease vs 68% with ulcerative colitis during the course of the disease, predominantly a deficiency of iron and of calcium. Less frequently deficiencies of zinc, protein, cyanocobalamin, and folic acid were found. Elevated liver enzymes were seen in 38% of patients with Crohn's disease vs 27% with ulcerative colitis. In order of frequency: gamma-glutamyl-transferase, ALAT, AP, ASAT, and bilirubin. Gallstones were present in 12% of patients with Crohn's disease and 4% with ulcerative colitis. 6% of patients with Crohn's disease and 4% with ulcerative colitis had kidney stones. CONCLUSIONS: In view of the high frequency of deficiencies in patients with inflammatory bowel disease it seems to be important to check frequently for extraintestinal complications.