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Results for “ASCORBIC ACID DEFICIENCY”

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PubMed1999

Trace element and vitamin concentrations and losses in critically ill patients treated with continuous venovenous hemofiltration.

OBJECTIVES: To measure the blood concentrations of a number of trace elements and vitamins in critically ill patients and examine their elimination by continuous venovenous hemofiltration (CVVH). SETTING: Intensive care unit of a tertiary institution. DESIGN: Prospective, controlled, clinical study. PATIENTS: Eight critically ill patients requiring renal replacement therapy, nine patients requiring intensive care treatment but not requiring renal replacement therapy, and nine healthy controls. INTERVENTIONS: Measurement of trace element and vitamin concentrations in blood and ultrafiltrate. MEASUREMENTS AND MAIN RESULTS: Compared with normal volunteers, critically ill patients requiring CVVH had significantly lower median blood concentrations of vitamin C, vitamin E, selenium, and zinc. During the first 24 hrs of CVVH, there were no changes in the trace element and vitamin concentrations in blood, nor were there differences between pre- and postfilter samples. Micronutrient losses in the ultrafiltrate were small or undetectable except for Vitamin C, chromium, and copper. Compared with normal volunteers, critically ill patients not requiring CVVH also had significantly lower median blood concentrations of vitamin C, vitamin E, selenium, and zinc. There were no differences between the two critically ill groups. CONCLUSIONS: The clinical significance of the reductions in blood concentrations of selenium, zinc, vitamin C, and vitamin E in critically ill patients and the ultrafiltrate losses of Vitamin C, copper, and chromium remains unclear.

Ascorbic Acid Deficiency↗
PubMed1986

Vitamin C status in 137 outpatients with Crohn's disease. Effect of diet counseling.

Vitamin C intake, and serum and leukocyte ascorbate levels were assessed serially over 6 months in 137 outpatients with Crohn's disease. Vitamin C intake was low in 18% of males and 37% of females. Serum ascorbate levels were suboptimal in 11% of males and 18% of females. Leukocyte ascorbate levels were low in 26% of males and 49% of females. Serum ascorbate levels were more frequently below the reference range in patients who smoked, but neither the serum nor the leukocyte ascorbate levels were affected by Crohn's disease activity, the use of an oral contraceptive agent, or by taking prednisone or sulfasalazine. Monthly diet counseling sessions significantly increased vitamin C intake, led to more patients consuming a normal ascorbate intake, and to a normalization of serum ascorbate values. We did not establish the importance of these ascorbate abnormalities on the clinical course of Crohn's disease. We conclude that low serum or leukocyte ascorbate levels are relatively common in patients with active or inactive Crohn's disease; these abnormalities are due in part to the reduced intake of dietary ascorbate; and the ascorbate status in patients with Crohn's disease may be normalized by improving the dietary intake of vitamin C.

Adult↗
PubMed1997

Vitamin B6, vitamin C, and carpal tunnel syndrome. A cross-sectional study of 441 adults.

As part of an ongoing study of carpal tunnel syndrome (CTS) in industry, we measured plasma concentrations of pyridoxal 5'-phosphate (PLP, a measure of vitamin B6 status) and total ascorbate (ASC, a measure of vitamin C status) in 441 adult volunteers from six industries and a university exercise study. In the entire study group and in non-vitamin users (n = 218), there were no significant differences in mean plasma PLP or ASC concentrations between controls (neither symptoms nor slowing), subjects with symptoms only, subjects with median nerve slowing only, or subjects with CTS (symptoms + slowing). In male non-vitamin users (n = 137), there were significant inverse univariate associations between plasma PLP concentration and the prevalence of pain, the frequency of tingling and nocturnal awakening, and the Phalen test result. In this same subgroup, the ASC/PLP ratio was directly associated with the prevalence of pain and nocturnal awakening, and with the frequency of pain, tingling, and nocturnal awakening. In multivariate analyses, plasma ASC concentration predicted more median nerve slowing and confirmed CTS, and vitamin or vitamin interaction variables were independent predictors of 20 CTS-related outcomes. These multivariate relationships often occurred only after adjustment for age, gender, body mass index, serum alkaline phosphatase activity, or tobacco use. We conclude that there are significant relationships between plasma vitamin levels and both components of CTS (specific symptoms and median nerve slowing). The interaction between plasma PLP and ASC appears to be particularly important with respect to symptoms.

Adult↗
PubMed1980

Prolyl and lysyl hydroxylase activities of human skin fibroblasts: effect of donor age and ascorbate.

Prolyl and lysyl hydroxylase activities in cultures of human skin fibroblasts from fetal to 94-yr-old donors were measured. In contrast to earlier studies with whole skin, neither prolyl nor lysyl hydroxylase activity was found related to donor age. Prolyl hydroxylase activity increased 3- to 6-fold when cell extracts were incubated with ascorbate and other hydroxylation cofactors before assay. A similar increase in prolyl hydroxylase activity occurred when cells were incubated with ascorbate. Lysyl hydroxylase activity remained unaltered under these conditions.

Adolescent↗
PubMed1983

Serum ascorbic acid in patients undergoing chronic hemodialysis.

Serum presupplementation ascorbic acid levels were subnormal in 8 out of 10 patients undergoing chronic hemodialysis with capillary film and capillary flow dialyzers, the mean duration of treatment being 11 months. Supplementation with 100 mg ascorbic acid daily for two weeks raised the ascorbic acid values to normal in 9 out of 10 patients. After supplementation with 500 mg daily, all patients had ascorbic acid levels exceeding the normal upper limit, and 3 of them had gastrointestinal side-effects. The mean blood pH value, measured in 24 patients on chronic hemodialysis, showed a significant, though slight, decrease during supplementation with 500 mg daily as compared with the mean presupplementation value, but no statistically significant changes were observed in blood bicarbonate, base excess or PCO2 values.

Acid-Base Equilibrium↗
PubMed1968

Chronic scurvy.

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Adult↗
PubMed1983

Tissue ferritin in scorbutic guinea-pigs.

Tissue ferritin metabolism was compared in control and ascorbic acid (AA) deficient guinea-pigs. Concentrations of ferritin protein in the liver (0.98 +/- 0.61 mg/g wet weight) and spleen (0.48 +/- 0.23 mg/g) of control animals did not change after tissue depletion of AA. Iron dextran (75 mg/kg weight, i.m.) caused a 4-5-fold increase in tissue ferritin concentrations in controls whereas no increase in tissue ferritin occurred in scorbutic animals. The rise in tissue total iron concentration was similar in the two groups. Liver ferritin synthesis was similar in control and scorbutic animals. After stimulation with iron (8 mg/kg iron dextran i.v.), ferritin synthesis rose in both groups of animals. However, the pattern of response differed. At 24 h after iron dextran, ferritin synthesis in controls was still significantly elevated (P less than 0.001) and liver ferritin protein continued to rise, whereas in scorbutic animals, ferritin synthesis had declined to pre-iron injection levels, and no rise in ferritin protein values occurred. It is concluded that the ferritin synthetic apparatus in AA deficient tissues remained intact and capable of responding to added iron. The absence of a sustained elevation in tissue ferritin protein after an iron load appeared to be due to inadequate stimulation of ferritin synthesis by intracellular iron. It is suggested that AA has a physiological role in the reduction of intracellular iron and that it is the reduced form of iron which stimulates ferritin synthesis. Abnormalities of iron metabolism occur in AA depleted tissues when the quantity of Fe3+ entering cells exceeds the residual reducing capacity of those cells.

Animals↗