Resolution Of Vitamin Research Articles

Comparison of Home-Blenderized Formula and Commercial Enteral Formulas for Gastrostomy Tube-Fed Children: A Retrospective, Prospective Cohort Study.

Background Blenderized gastrostomy tube feedings (BGTFs) consist of pureed table foods and liquids that are administered as enteral tube feedings. Compared to commercial enteral formulas (CEFs), BGTF has been shown to have fewer side effects. Despite these results, apprehensions have been raised about microbial contamination, nutritional deficiencies or surplus, risk of gastrostomy tube (GT) blockages, and lack of consistency in clinical outcomes. The goal of this retrospective, prospective, 18-month-long study is to report the clinical and nutritional outcomes of GT-dependent pediatric patients who attended a multidisciplinary feeding clinic. Methodology After Institutional Review Board (IRB) approval and consent were obtained, 25 children who were receiving tube feeding via G were enrolled in a retrospective, prospective, observational, cohort study from August 2019 to February 2021. A multidisciplinary team was formed, and multivariate logistic regression was performed comparing subjects on BGTF versus CEF, per os diet versus nil per os, CEF versus homemadeblenderized tube feeding (HBTF) versus blenderized tube feeding (BTF), and how they compared at the beginning and end of the study. Results The mean age of the patients was 4.4 years (SD ±2.2). Gastroesophageal reflux disease (GERD) and short bowel syndrome (SBS) were the most common comorbid gastrointestinal (GI) conditions. Of the 25 patients enrolled in the study, seven were initially on BGTF, while 14 ended the study on BGTF. There were no statistically significant differences in malnutrition status, feeding intolerance, emergency room visits, hospitalizations, and GT blockages between all different comparison groups when comparing between the CEF versus HBTF versus commercial blenderized tube feeding (CBTF) groups. Of the patients who were in the BGTF group, there was a resolution of vitamin A deficiency, vitamin D deficiency, and anemia (n = 1). In total, two patients had resolved vitamindeficiencies, namely, vitamins A and D. Conclusions When comparing BGTF and CEF, there was no statistically significant difference in outcomes. This study suggests that BGTF is at least equivalent to CEF in clinical outcomes, meaning BGTF should be considered standard nutrition for GT-dependent patients.

Long-term anti-epileptic drug therapy and metabolic bone disase in children

Epilepsy is a common chronic brain dysfunction in children. Studies have showed that antiepi- leptic drugs （AED） affect the hydroxylation of vitamin D in liver and kidney and inhibit the calcification of bone, mainly by up-regulating cytochrome oxidase P450 and promoting the resolution of vitamin D, and then increasing serum parathyroid hormone compensatory. Long-term use can cause children metabolic bone disease occurrence, clinical manifestations include bone pain, short stature, rickets, teeth agenesis, fracture, etc. AED firstly affect the hormones related to bone metabolism in vivo,so that the present researches focus on biochemical tests and meas- urement of sclerotin and bone density. In the children＇s long-term use of antiepileptic drug treatment at the same time,the application of Vitamin D,calcium and exercise can prevent the occurrence of metabolic bone disease. Key words: Antiepileptic drug; Metabolic bone disease in children

Resolution of vitamin A cis/trans isomers resolves proficiency test assessments

Proficiency tests run by FAPAS for vitamin A analysis in cod liver oil were observed to give rise to multi-modal distributions of data. For this reason, setting the assigned value for the tests was difficult or even impossible, without too high uncertainty values. The methods used by participants could broadly be categorised into normal phase or reversed-phase high performance liquid chromatography. In a recent test, participants were asked if their method could separate the cis and trans isomers of vitamin A. Results from participants who could separate the isomers gave rise to a unimodal distribution of data. This was synonymous with participants using the normal phase chromatography method. Conversely, results from participants who were unable to separate the isomers, or who were using reversed-phase chromatography, gave rise to multi-modal distributions of data. The recommendation for future tests is to set the assigned value on the basis of the ability to separate the isomers.

Severe vitamin D deficiency, myopathy, and rhabdomyolysis

In the report by Rasheed et al.,[1] a 33-year-old female developed proximal myopathy and rhabdomyolysis associated with very low serum 25 (OH) vitamin D (4 ng/mL, laboratory lower normal limit 31 ng/mL). Rasheed et al.,[1] noted that serum 25 (OH) vitamin D levels >20 ng/mL can cause increased body sway, while >10 can lead to inability to rise from a chair, or ascend stairs, coupled with muscle pain. We have recently assessed exercise-induced severe rhabdomyolysis in a thin, athletic, dark-skinned (Meztizo), highly conditioned, nondiabetic young man, occurring in the setting of a 5 K race. He was subsequently found to have severe 25 (OH) vitamin D deficiency (6 ng/mL). Rhabdomyolysis, myoglobinemia, and even mild renal failure can occur as sequelae of marathon races, military recruit training, strength training, and endurance athletics.[2] Often this muscle damage resolves without incident or treatment and may be detected only upon laboratory testing.[2] We speculate that subjects with preexisting low serum 25 (OH) vitamin D are selected out for exertional rhabdomyolysis during strenuous activities. In subjects not receiving statins, low serum 25 (OH) D levels have been associated with myositi[3] and reduced muscle function.[4] Vitamin D may improve muscle strength through a highly specific nuclear receptor in muscle tissue.[5] Serum 25 (OH) D is related to physical performance.[6] Since myositis-myalgia is the major cause of statin intolerance,[7] and the tripartite association of serum 25 (OH) vitamin D deficiency, statins, and myositis-myalgia has physiologic plausibility,[3,4,6,8,9] resolution of vitamin D deficiency interacting with statins to produce myositis-myalgia would have significant clinical importance, allowing reinstitution of statins to optimize low-density lipoprotein (LDL) cholesterol and prevent cardiovascular disease (CVD). Recently, we prospectively studied 150 hypercholesterolemic patients, unable to tolerate ≥1 statin because of myositis-myalgia, selected by low (>32 ng/mL) serum 25 (OH) vitamin D.[10] On no statins, 50,000 units of vitamin D was given twice a week for 3 weeks and then continued once a week. After 3 weeks on vitamin D, statins were restarted. On vitamin D supplementation plus reinstituted statins for a median of 8.1 months, 131 of 150 patients (87%) were free of myositis-myalgia and tolerated reinstituted statins well. Serum 25 (OH) vitamin D increased from median 21 to 40 ng/mL (P > 0.001), and normalized (≥32 ng/mL) in 117 (78%) of 150 previously vitamin D deficient, statin-intolerant patients. Median LDL cholesterol decreased from 146 to 95 mg/dL, P > 0.001. We concluded[10] that symptomatic myositis-myalgia in hypercholesterolemic statin-treated patients with concurrent serum 25 (OH) vitamin D deficiency may reflect a reversible interaction between vitamin D deficiency and statins on skeletal muscle causing myalgia. We believe vitamin D deficiency places subjects at higher risk for rhabdomyolysis, which develops during severe exertion. We suggest that when exercise-induced rhabdomyolysis develops, after full recovery and back at normal nutrition, serum 25OH vitamin D be measured. We suggest that when very low vitamin D is documented, it be normalized before major prolonged exertion. We hypothesize that normalization of vitamin D before heavy exertion could perhaps prevent severe muscle damage events and sequelae, which may occur in previously asymptomatic athletes.

Symptomatic myositis-myalgia in hypercholesterolemic statin-treated patients with concurrent vitamin D deficiency leading to statin intolerance may reflect a reversible interaction between vitamin D deficiency and statins on skeletal muscle

Myositis-myalgia is the most common cause of statin intolerance, leading to cessation of statin use, with consequent failure to lower LDL cholesterol to target levels for primary and secondary prevention of cardiovascular disease (CVD). We hypothesize that symptomatic myositis-myalgia in hypercholesterolemic statin-treated patients with concurrent 25 (OH) vitamin D deficiency and statin intolerance may reflect a reversible interaction between vitamin D deficiency and statins on skeletal muscle. In hypercholesterolemic, vitamin D deficient patients, intolerant to statins because of myositis-myalgia, three non-blinded clinical case series have uniformly demonstrated that after supplementation with oral vitamin D2 which normalizes serum 25 (OH) vitamin D levels, statins can be successfully re-instituted in >90% of patients, without recurrent myositis-myalgia, with reduction of LDL cholesterol to target levels. Empirically, in 68 hypercholesterolemic patients, unable to tolerate ⩾ 1 statin because of myositis-myalgia, selected by low (<32 ng/ml) serum 25 (OH) vitamin D, we have prospectively assessed whether resolution of vitamin D deficiency would result in statin tolerance, free of myositis-myalgia. On no statins, 50,000 units of vitamin D2 was given twice/week for 3 weeks, and was then continued once/week. After 3 weeks on vitamin D supplementation, statins were restarted, and patients were re-assessed after 3 months on statins while continuing vitamin D supplementation. At 3 months follow-up, on vitamin D supplementation and re-instituted statins, 62 of 68 (91%) previously statin-intolerant patients now tolerated statins well and were asymptomatic without myositis-myalgia. In these 68 patients, on vitamin D supplementation and statins, mean ± SD vitamin D rose from 22 ± 7 to 43 ± 13 ng/ml ( p < 0.0001), and LDL cholesterol fell from 162 ± 55 to 101 ± 35 mg/dl ( p < 0.0001). Despite published and new empirical evidence, the medical establishment has refused to accept the hypothesis, requiring placebo-controlled, double-blind studies, none having been reported to date. A placebo-controlled, double-blind study is needed to document that normalization of serum 25 (OH) vitamin D levels in vitamin D deficient, statin intolerant patients would facilitate re-introduction of statins with concurrent freedom from myositis-myalgia. The ability to reverse myositis-myalgia in vitamin D deficient, statin intolerant, hypercholesterolemic patients by vitamin D supplementation would be extraordinarily valuable, facilitating reinstitution of statins to lower LDL cholesterol to reduce risk of CVD events. We hypothesize that symptomatic myositis-myalgia in hypercholesterolemic statin-treated patients with concurrent vitamin D deficiency producing statin intolerance may reflect a reversible interaction between vitamin D deficiency and statins on skeletal muscle.

Vitamin D deficiency, myositis–myalgia, and reversible statin intolerance

Objective:In 150 hypercholesterolemic patients, unable to tolerate ≥1 statin because of myositis-myalgia, selected by low (<32 ng/ml) serum 25 (OH) vitamin D, we prospectively assessed whether vitamin D supplementation with resolution of vitamin D deficiency would result in statin tolerance, free of myositis–myalgia.Research design and methods:We studied 74 men, 76 women, median age 60, 131 white, 17 black and 2 other. On no statins, 50,000 units of vitamin D was given twice a week for 3 weeks, and then continued once a week. After 3 weeks on vitamin D, statins were restarted. Patients were re-assessed on statins and vitamin D every 3 to 4 months, with serial measures of serum 25 (OH) vitamin D, creatine phosphokinase (CPK), LDL cholesterol (LDLC) and assessment of myositis–myalgia.Main outcome measures:Percentage of patients myalgia-free on vitamin D plus reinstituted statins, serum 25 (OH) vitamin D, CPK, and LDLC on reinstituted statins and concurrent vitamin D supplementation.Results:On vitamin D supplementation plus re-instituted statins for a median of 8.1 months, 131 of the 150 patients (87%) were free of myositis–myalgia and tolerated the statins well. Serum 25 (OH) vitamin D increased from median 21 to 40 ng/ml (p < 0.001), and normalized (≥32 ng/ml) in 117 (78%) of 150 previously vitamin D deficient, statin-intolerant patients. Median LDLC decreased from 146 mg/dl to 95 mg/dl, p < 0.001.Conclusion:Symptomatic myositis–myalgia in hypercholesterolemic statin-treated patients with concurrent serum 25 (OH) vitamin D deficiency may reflect a reversible interaction between vitamin D deficiency and statins on skeletal muscle causing myalgia.

Resolution of vitamin D insufficiency in osteopenic patients results in rapid recovery of bone mineral density.

Vitamin D insufficiency is characterized biochemically by the presence of secondary hyperparathyroidism, which can contribute to bone loss in osteopenic patients. Over a 2-yr period of evaluation of 118 consecutive, free living patients with osteopenia or osteoporosis, we identified 18 subjects with depressed serum 25-hydroxyvitamin D (250HD; < or = 14 ng/mL). Twelve of these subjects harbored a low 25OHD level and consented to undergo replacement with 50,000 IU vitamin D2 twice weekly for 5 weeks. Five hundred thousand units of oral vitamin D2 resulted in significant increases in 25OHD (+24.3+/-16.9 ng/mL; P < 0.001) and the fasting urinary calcium/creatinine excretion ratio (+0.06+/-0.004; P = 0.01) and significant decreases in the serum concentration of PTH (-32.9+/-36.9 pg/mL; P < 0.001) and osteocalcin (-4.9+/-2.4 ng/mL; P < 0.001). Vitamin D repletion was associated with a significant 4-5% annualized increase in bone mineral density at both the lumbar spine (P < 0.001) and the femoral neck (P = 0.03), indicating that resolution of vitamin D insufficiency in a population of patients with low bone mass results in a rapid rebound increase in bone mineral density.

Resolution of Vitamin D Insufficiency in Osteopenic Patients Results in Rapid Recovery of Bone Mineral Density

Resolution of Vitamin D Insufficiency in Osteopenic Patients Results in Rapid Recovery of Bone Mineral Density

Gains in bone mineral density with resolution of vitamin D intoxication.

Vitamin D intoxication is associated with the mobilization of skeletal calcium. To ascertain how the resolution of vitamin D intoxication affects bone density. Case series. Referral service for metabolic bone disease in a tertiary care teaching hospital. Four patients with osteoporosis who were each using several nonprescription dietary supplements and were found to have fasting hypercalciuria. Discontinuation of use of dietary supplements. Serial measurement of serum levels of 25-hydroxyvitamin D, ratio of fasting urinary calcium to creatinine, and bone mineral density for 3 years. Discontinuation of use of dietary supplements resulted in the normalization of serum levels of 25-hydroxyvitamin D, the normalization of the ratio of urinary calcium to creatinine, and a mean annual increase in bone mineral density (+/- SD) of 1.9% +/- 0.5%. Occult vitamin D intoxication was detected in patients who were using dietary supplements that contained an unadvertised high level of vitamin D. Resolution of vitamin D intoxication was associated with a rebound in bone mineral density.

Quantitative analysis of phylloquinone (vitamin k 1) in soy bean oils by high-performance liquid chromatography

A high-performance liquid chromatographic method for determining phylloquinone (vitamin K 1) in soy bean oils is described. Resolution of vitamin K 1 from interfering peaks of the matrix was obtained after enzymatic digestion, extraction and liquid—solid chromatography on alumina. An isocratic reversed-phase chromatography with UV detection was used in the final stage. The quantitation was carried out by the standard addition method, and the recovery of the whole procedure was 88.2%.