Severity Of Vitamin Research Articles

Prevalence of Vitamin D Deficiency in Chronic Liver Disease

Vitamin D deficiency has been associated with cholestatic liver disease such as primary biliary cirrhosis. Some studies have suggested that cirrhosis can predispose patients to development of osteoporosis because of altered calcium and vitamin D homeostasis. The aim of this study was to determine the prevalence of vitamin D deficiency in patients with chronic liver disease. One hundred and eighteen consecutive patients (43 with hepatitis C cirrhosis, 57 with hepatitis C but no cirrhosis, 18 with nonhepatitis C-related cirrhosis) attending the University of Tennessee Hepatology Clinic had their 25-hydroxyvitamin D level measured. Severity of vitamin D deficiency was graded as mild (20-32 ng/ml), moderate (7-19 ng/ml) or severe (<7 ng/ml), normal being >32 ng/ml. Of patients, 109/118 (92.4%) had some degree of vitamin D deficiency. In the hepatitis C cirrhosis group, 16.3% (7/43) had mild, 48.8% (21/43) had moderate, and 30.2% (13/43) had severe vitamin D deficiency. In the hepatitis C noncirrhotic group, 22.8% (19/57) had mild, 52.6% (30/57) had moderate, and 14% (8/57) had severe vitamin D deficiency. In the nonhepatitis C-related cirrhosis group, 38.9% (7/18) had mild, 27.8% (5/18) had moderate, and 27.8% (5/18) had severe vitamin D deficiency. Severe vitamin D deficiency (<7 ng/ml) was more common among patients with cirrhosis compared with noncirrhotics (29.5% versus 14.1%, P value=0.05). Female gender, African American race, and cirrhosis were independent predictors of severe vitamin D deficiency in chronic liver disease. Vitamin D deficiency is universal (92%) among patients with chronic liver disease, and at least one-third of them suffer from severe vitamin D deficiency. African American females are at highest risk of vitamin D deficiency.

Vitamin D Deficiency—A Clinical Spectrum: Is There a Symptomatic Nonosteomalacic State?

Vitamin D deficiency is not uncommon even in the sunny land of India. Lack of sun exposure and inadequate oral intake are both responsible for vitamin D deficiency. This article provides a retrospective, examining the effects of Vitamin D deficiency in 71 patients. The study's inclusion criterion was low vitamin D level combined with musculoskeletal symptoms but without the presence of osteomalacia. All patients in this study were suspected to have vitamin D deficiency. The data were retrieved from the case-charts of patients seen between 1996 and 2001 at the rheumatology services of Hinduja Hospital, Mumbai, India. This study found no correlation between Vitamin D levels and symptoms, or between the severity of Vitamin D deficiency and the number of symptoms displayed. Subclinical vitamin D deficiency or preosteomalacic state was the term coined for individuals with vitamin D deficiency producing nonspecific musculoskeletal symptoms in the absence of clinical osteomalacia.

Prevalence of Vitamin D Deficiency in Chronic Liver Disease

Purpose: Vitamin D deficiency has been reported in association with cholestatic liver diseases such as Primary biliary cirrhosis. Some studies have suggested that cirrhosis can predispose to osteoporosis due to alteration in calcium and vitamin D homeostasis. The aim of this study is to determine the prevalence of vitamin D deficiency in patients with chronic liver disease. Methods: 118 consecutive patients (43 Hepatitis C patients with cirrhosis; 57 Hepatitis C patients without cirrhosis; 18 Non Hepatitis C patients with cirhhosis) seen at the Methodist Hepatology clinic had their 25-OH vitamin D levels measured. Severity of Vitamin D deficiency was graded as mild (levels between 20–32 ng/ml), moderate (levels between 7–20 ng/ml) and severe (levels <7 ng/ml) respectively with normal being >32 ng/ml. Results: 109/118 (92.4%) patients had some degree of vitamin D deficiency. In the Hepatitis C cirrhosis group: 16.3% (7/43) had mild, 48.8% (21/43) had moderate and 30.2% (13/43) had severe vitamin D deficiency. In the Hepatitis C non cirrhotic group the numbers were: 22.8% (13/57), 52.6% (30/57) and 14% (8/57) respectively. In the non HCV cirrhosis group the numbers were: 38.9% (7/18), 27.8% (5/18) and 27.8% (5/18) respectively. Severe vitamin D deficiency (level < 7 ng/ml) is more common among cirrhotics. Conclusion: Vitamin D deficiency is universal (92%) in patients with chronic liver disease and at least one third suffer from severe deficiency. Measurement of vitamin D levels and replacement should be part of care to cirrhotic patients.

Effects of dietary vitamins C and E on alternative complement activity, hematology, tissue composition, vitamin concentrations and response to heat stress in juvenile golden shiner ( Notemigonus crysoleucas)

The objective of this study was to characterize the response of golden shiner fed one of eight purified diets with either 0 or 38 mg α-tocopherol (α-T) kg −1 and one of four levels of ascorbic acid (AA) (23, 43, 98, or 222 mg kg −1 diet) in a 2×4 factorial design. Growth, survival, signs of vitamin E deficiency, and immune and stress responses were monitored in groups of 30 golden shiners (mean average initial weight=0.79 g) fed the diets to apparent satiation twice daily in triplicate aquaria for 14–19 weeks. The average individual weight gain was not affected by dietary α-T concentrations at 14 weeks, but the survival of fish fed the α-T-unsupplemented diets was lower than that of fish fed the α-T-supplemented diets. After 10 weeks, fish fed the α-T-unsupplemented diets began to show vitamin-E-deficiency signs such as increased prevalence of fish with darkened skin. After 17 weeks the deficient fish had lower α-T concentrations in viscera, lower whole-body crude protein, total lipid, dry matter, hematocrit, hemoglobin, lymphocyte (%), alternative complement activity (ACH50), and survival after exposure to stressful water temperatures (36–37 °C) than those fed the α-T-supplemented diets. A sparing effect of vitamin E on vitamin C was evident. Elevated dietary vitamin C reduced the incidence and severity of vitamin E deficiency signs in a dose-dependent manner. The interactive effect of vitamins C and E on ACH50 activity and percentage of thrombocytes was also significant. Regardless of vitamin E levels, different vitamin C levels did not influence the α-T concentration in viscera and other interactions between vitamins C and E were not evident.

Serum osteocalcin is increased in patients with osteomalacia: correlations with biochemical and histomorphometric findings.

The synthesis of osteocalcin or bone gla protein by osteoblasts is markedly stimulated by 1,25-(OH)2D, a key hormone in the regulation of bone mineralization. The circulating levels of osteocalcin have been shown to reflect both the osteoid matrix production and the formation rate of mineralized bone in several metabolic bone diseases (osteoporosis, thyrotoxicosis, primary hyperparathyroidism) in which both mechanisms are tightly coupled because of the absence of mineralization defect. In this study, we measured in 12 patients (7 women, 5 men, 56 +/- 15 yr old) with untreated osteomalacia serum osteocalcin and vitamin D metabolites (25OHD and 1,25-(OH)2D). The results were correlated with biochemical and histomorphometric assessment of bone remodeling. Osteomalacia was due to vitamin D deficiency (5 cases), to vitamin D malabsorption (6 cases), and to hypophosphataemia in 1 case. When compared to control values, serum osteocalcin was increased in patients with osteomalacia (7.4 +/- 4 vs. 3.7 +/- 1.3 ng/mL; P less than 0.001) and was positively correlated with serum alkaline phosphatase (r = 0.65; P = 0.03) and negatively with 25 OHD (r = -0.61; P = 0.04). Serum osteocalcin was not correlated with 1,25-(OH)2D [r = -0.45; not significant (NS)] even after exclusion of the patient with hypophosphataemia. Serum osteocalcin was positively correlated with the osteoid volume and osteoid perimeter (r = 0.71 and 0.69 respectively; P less than 0.01) but not with any of the tetracycline-based parameter of bone mineralization at the tissue level (r ranging from -0.41 to +0.42, NS). Serum 25 OHD, but not 1,25-(OH)2D, was positively correlated with the mineralization rate (r = 0.59; P less than 0.05 and r = 0.54; NS). We conclude that in patients with osteomalacia, a condition which is characterized by an increased osteoid accumulation due to a decreased mineralization rate, the increased level of serum osteocalcin reflects the increased osteoid synthesis but not the mineralization defect. In this disease, serum osteocalcin is inversely correlated to the severity of vitamin D deficiency reflected by serum 25 OHD, but not to the serum levels of 1,25-(OH)2D.

Megadose Effects of Vitamin C on Vitamin B-12 Status in the Rat

Effects of ascorbic acid ingestion on the severity of vitamin B-12 deficiency were investigated by feeding weanling rats experimental diets containing 0-100 micrograms of vitamin B-12 activity per kg of diet, with or without 6.0 mg of ascorbic acid per ml supplied in drinking water for 15 wk. This daily consumption of up to 150 mg of ascorbic acid did not impair growth, but did result in significantly higher concentrations of ascorbic acid in plasma, liver, adrenal glands and feces. When rats were fed diets deficient or marginally deficient in vitamin B-12, liver concentrations of vitamin B-12 were markedly lower than in liver of rats fed adequate vitamin B-12. Ascorbic acid ingestion raised values significantly in the vitamin B-12-deficient diet group. Urinary methylmalonic acid was significantly elevated in the deficient rats. However, it was significantly reduced to more normal values by ascorbic acid in rats with both low and marginal vitamin B-12 status, as defined by dietary and liver concentrations of vitamin B-12 activity. Although coprophagy was not prevented, rats showed no increased consumption of feces with the higher ascorbic acid content. Thus, the results of this research indicate that vitamin C ingestion partially protects rats from vitamin B-12 deficiency.

Correction of vitamin E deficiency in children with chronic cholestasis. II. Effect on gastrointestinal and hepatic function.

Although secondary vitamin E deficiency causes a reversible neurologic disorder in children with chronic cholestasis, the effect of this deficiency state on other organ systems is unknown. We studied the effects of vitamin E therapy on selected gastrointestinal and hepatic functions in five children with chronic cholestasis and well-documented biochemical and neurologic evidence of vitamin E deficiency. After 2 to 3 years of oral or parenteral vitamin E therapy, there was no improvement in fecal fat losses, severity of vitamin E malabsorption (as measured by an oral vitamin E tolerance test) or total serum fatty acid concentrations. Serial analyses of liver function blood tests demonstrated a marked decline in fasting serum cholylglycine concentrations during 18 to 31 months of vitamin E therapy, while other liver function tests showed no consistent changes. We conclude that vitamin E deficiency does not appear to alter intestinal absorption of fat or vitamin E; however, vitamin E deficiency may further impair already compromised hepatic function during pathologic conditions such as cholestasis.

Comparison of vitamin E and 25-hydroxyvitamin D absorption during childhood cholestasis

To characterize differences in intestinal absorption of fat-soluble vitamins during cholestasis, intestinal absorption of vitamin E was compared with that of 25-hydroxyvitamin D in eight infants and young children with prolonged neonatal cholestasis. Oral tolerance tests were performed using 100 IU/kg/dose dl-alpha-tocopherol and 10 micrograms/kg/dose 25-hydroxyvitamin D. Mean vitamin E absorption was only 1.0% to 1.9% of that of control children, whereas 25-hydroxyvitamin D absorption was 22.5% to 25.1% of that of controls. Although intestinal absorption of both vitamins is impaired during cholestasis, the severity of vitamin E malabsorption far exceeds that of 25-hydroxyvitamin D.

Vitamin E deficiency and neurologic disease in childrenwith cholestasis: A prospective study

CHILDREN WITH CHRONIC CHOLESTASIS may develop a characteristic progressive and disabling neurologic disease related to vitamin E deficiency, ~4 but neither the earliest signs nor the time required for its development is known. Therefore we thought it important to ascertain the incidence and severity of vitamin E deficiency in children with cholestasis. In this prospective clinical study we determined serum vitamin E concentration and performed systematic and sequential neurologic examinations in 48 children with previously identified cholestasis and in 23 others with either noncholestatic malabsorption or progressive ataxia.

Breast feeding

A survey of available data shows that the reaction of infants to human and cow's milk differs in many respects. The differences are reflected in shape of the growth curve, in the amounts of nitrogen, calcium, and phosphorus which are retained, in the plasma vitamin C levels, in the response of the blood sugar to lactose ingestion, in the incidence and severity of vitamin D deficiency disease and eczema, in the incidence of tetany during the newborn period, and in the frequency of respiratory infections. It is not our intention to present these data as evidence of the superiority of human over cow's milk in feeding babies, although the lowered incidence of respiratory infections and severe eczema in the breast-fed infant is a very real, practical consideration. Reasoning from the meager available information, it would appear that breast feeding is superior to artificial feeding from the psychologic viewpoint. In the last analysis, the choice of one or the other method of feeding stems from a general attitude. The physician who is impressed by the remarkable adaptibility of the human organism will, whether giving advice in the care of a well child or in ministering to the sick, interfere minimally with natural processes. We have erred too often in the past. This is not meant to minimize in any way the enormous value of artificial feeding for those infants who, for one reason or another, are unable to be fed at the breast. We do feel, however, that artificial feeding should be reserved for the instances where an honest attempt at breast feeding has failed. A survey of available data shows that the reaction of infants to human and cow's milk differs in many respects. The differences are reflected in shape of the growth curve, in the amounts of nitrogen, calcium, and phosphorus which are retained, in the plasma vitamin C levels, in the response of the blood sugar to lactose ingestion, in the incidence and severity of vitamin D deficiency disease and eczema, in the incidence of tetany during the newborn period, and in the frequency of respiratory infections. It is not our intention to present these data as evidence of the superiority of human over cow's milk in feeding babies, although the lowered incidence of respiratory infections and severe eczema in the breast-fed infant is a very real, practical consideration. Reasoning from the meager available information, it would appear that breast feeding is superior to artificial feeding from the psychologic viewpoint. In the last analysis, the choice of one or the other method of feeding stems from a general attitude. The physician who is impressed by the remarkable adaptibility of the human organism will, whether giving advice in the care of a well child or in ministering to the sick, interfere minimally with natural processes. We have erred too often in the past. This is not meant to minimize in any way the enormous value of artificial feeding for those infants who, for one reason or another, are unable to be fed at the breast. We do feel, however, that artificial feeding should be reserved for the instances where an honest attempt at breast feeding has failed.