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At least 19 recordsLinked to original sources
PubMed1993

[Vitamin deficiency and marginal vitamin deficiency].

Fat-soluble vitamin deficiency and marginal deficiency of this type of vitamin will be discussed. The trias of vitamin A deficiency is composed of nyctalopia, xerophthalmia and hyperkeratosis follicularis. Vitamin D deficiency causes rachitis and osteomalacia. In Japan, vitamin D deficiency is more often caused by impaired vitamin D activation due to renal failure, than by a lack of sunbathing or insufficient ingestion of vitamin D from diet. At present, it is quite rare that the physician encounters patients with deficiency of vitamin E or other vitamins. According to surveys of occult vitamin deficiency, the prevalence of marginal fat-soluble vitamin deficiency was lower than that of marginal water-soluble vitamin deficiency. Marginal vitamin deficiency seems to be absent or very rare among healthy individuals. In patients, however, marginal vitamin deficiency is sometimes observed. Since marginal vitamin deficiency can modify the underlying disease or trigger complications, the physician should take adequate measures to prevent the onset of marginal vitamin deficiency in managing patients with various diseases.

Humans↗
PubMed1999

Diagnosis and detection of vitamin deficiencies.

Vitamin deficiencies can be detected in several ways, none of which is entirely unambiguous. Evidence of several types is, therefore, required. For instance, it is rare for clinical signs to result from a single cause, except in controlled experiments. Natural diets are rarely deficient in only a single nutrient, and individual requirements vary considerably. Biochemical and functional status indices can help bridge the gap between inadequate diet and resulting pathology. Some indices are very specific for individual vitamins; others, although only semi-specific, are useful if closely linked to tissue malfunction and hence to pathology. Ideally, biochemical indices should separate severe deficiency, mild subclinical deficiency, normal status and overload toxicity. Vitamin concentrations in plasma, serum, red cells, urine, and other accessible tissues have been used, and metabolic products of vitamin-dependent metabolic pathways have been exploited. However, many of the assays are difficult to perform and interpret, and are limited to few laboratories, world-wide. There is a need for simpler and more 'portable' tests, for routine laboratories and for the medical profession.

Avitaminosis↗
PubMed1985

[Subclinical alcoholic optic neuritis without vitamin deficiency].

Vitamin B1, Folic acid Vitamin B12, whole blood Lead level, and plasma Zinc level were determined in 82 patients admitted to an alcoholism rehabilitation program. Each patient was examined for an optic neuritis. Thirty-two of the patients had sub-clinical abnormalities suggestive of optic neuritis like dyschromatopsias and/or field visual defects. No differences were found in the blood levels of Vitamin B1, Folic acid, and Vitamin B12 between the 32% affected and the 68% unaffected subjects. Moreover vitamins blood levels were found to be within the limits of normal values in both groups. A negative correlation between whole blood Lead levels and plasma Zinc levels was found. When an optic neuritis occurs the lead level tends to be higher and the Zinc lower. Abnormalities of the more usual alcoholism tests: gamma glutamyl Transpeptidase (gamma GT), mean red cell volume (V.G.M.) and glutamic Oxaloacetic transferase (T.G.O.), were more pronounced in alcoholics with optic neuritis.

Adult↗
PubMed1979

Relevance of a borderline vitamin deficiency in relation to the question of vitamin requirement.

A definition is given for the terms of latent and borderline vitamin deficiency, and the vitamin requirement and optimal vitamin supply, respectively, are discussed in relation to these two terms. The upper limit of the latent vitamin deficiency status can be used to define the optimal intake of vitamins, whereas the lower limit indicates the minimum requirement. The impact on health of a latent vitamin deficiency lies in the risk of falling into a manifest vitamin deficiency during sudden stress, whereas, in borderline vitamin deficiency status, some health functions are affected so that a problem of public health may arise and countermeasures should be taken.

Adolescent↗
PubMed1981

Fat soluble vitamin deficiency in biliary atresia.

Between January 1973 and January 1980, 29 patients with biliary atresia treated by Kasai hepatic portoenterostomy were evaluated for deficiencies of vitamin A, D, and E. The mean vitamin A level in 11 patients with successful operations was 25.5 +/- 3.8 (SE) micrograms/100 ml whereas the level was 16.0 +/- 8.8 (SE) micrograms/100 ml in three patients with failed operations (normal: greater than 30 micrograms/100 ml). Vitamin E levels in 6 children (5 with sustained bile drainage) were 2.9 +/- 1.7 (SD) micrograms/ml (normal: greater than 4 micrograms/ml). Vitamin D deficiency was evaluated in 22 patients by serial radiographs of knees and wrists. Four children (18%) had pure osteomalacia and 13 children (59%) had combined osteoporosis and osteomalacia. The four oldest survivors (age 5-5.5 yr) resolved their bone disease without specific treatment. Serologic deficiencies of vitamins A and E and radiographic evidence of vitamin D deficiency exist in patients with biliary atresia despite operative establishment of bile flow. These deficiencies are present in both the younger and the older children. In the case of vitamin D, resolution may occur without specific treatment.

Bile↗
PubMedDate not supplied

Direct in vitro effect of 1,25-dihydroxyvitamin D3 on islets insulin secretion in vitamin deficient rats: influence of vitamin D3 pretreatment.

Vitamin D3 deficiency decreased glucose-induced insulin release from isolated rat islets. In vivo, vitamin D3 treatment restored the B-cell response within 3 days; this delay suggests an effect of vitamin D3 metabolites. The effect of 1,25-dihydroxyvitamin D3 was studied in vitro on isolated islets from vitamin D3 deficient rats. When it was added to the incubation medium, it increased in a dose-dependent manner islet insulin secretion. However this effect only occurred when the vitamin D3-deficient rats received at least a single injection of vitamin D3 24 hours earlier; these results sustain the hypothesis of a direct but delayed in vitro stimulation of B cell function by 1,25-dihydroxyvitamin D3.

Animals↗
PubMed1980

Drugs producing vitamin deficiencies.

Many drugs produce vitamin deficiencies. They belong to the most important and common therapeutical classes: analgesics, antianemics, antibacterial and antiblastic agents, antibiotics, antidiabetics, antimalarials, antiphlogistics, antipyretics, diuretics, laxatives and purgatives, tranquilizers and anticonvulsives, radiomimetics, hormones and vitamins themselves. The vitamin deprivation processes may be produced by a variety of mechanisms and may involve all vitamins. Recent experiments indicate that there is a competition for binding sites on proteins between vitamin C and salicylate and between dicoumarol and vitamin K. Usually a drug exerts a "devitaminizing" action with respect to only one vitamin. However there are examples of multiple vitamin deficiencies induced by a single drug, like salicylate which deprives the organism of vitamins C, K and pantothenate. These deficiencies may develop either all at the same time or successively. A direct and concomitant vitamin depriving action occurs when an antibiotic blocks the production of vitamins by the enteric flora. A different mode of action occurs in the drug induced folic acid deficiency, which in turn induces a deficiency of vitamin B12. It has been reported that a vitamin deficiency may result from intake of high pharmacological doses of other vitamins. These data need confirmation in patients treated with high doses of nicotinic acid. The drug induced vitamin deficiencies are studied with the same methodology employed for avitaminoses in general; hence they can be diagnosed using the same criteria.

Analgesics↗