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Vitamin Deficiencies (vitamin + deficiency)
Selected AbstractsRelevance of post-methionine homocysteine and lipoprotein (a) in evaluating the cardiovascular risk in young CAD patientsEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 1 2005R. Marcucci Abstract Background, Aims of our study were to evaluate the prevalence of high lipoprotein (a) [Lp(a)] and homocysteine levels , both in the fasting state (FHcy) and post-methionine (PMHcy) , in young coronary artery disease (CAD) patients, and to investigate the role of genetic and environmental factors for hyperhomocysteinaemia. Materials and methods, We studied 140 patients with angiographically documented CAD (24 women , 55 years and 116 men , 50 years) and 140 healthy subjects as controls. Results, Both FHcy [13·2 (5·4,45·8) vs. 9·0 (5·1,24) µmol L,1); P < 0·0001] and PMHcy [(39·4 (9·0,66·4) vs. 25·2 (16·4,33·9); P < 0·0001] were significantly higher in patients than in controls. Lp(a) levels were significantly higher in patients than in controls (200 (3,1486) mg L,1 vs. 97 (10,412) mg L,1; P < 0·0001). At the multivariate analysis, adjusted for the classical cardiovascular risk factors and creatinine levels, the OR (95% CI) for CAD at young age significantly increased in the fourth quartile of the distribution of FHcy, PMHcy and Lp(a) levels [FHcy: 14·9 (4·1,58), P < 0·0001; PMHcy: 19·2 (4·0,86·3); P < 0·0001; Lp(a): 19·6 (4·7,78·6): < 0·0001]. Vitamin deficiencies were detected in 28/140 (20%) patients. The prevalence of the homozygous C677T (+/+) methylenetetrahydrofolatereductase genotype was higher, but not significantly different, in patients (22·8%) than in controls (18·6%). The allele frequency of the 844ins68 insertion variant in the cystathionine beta-synthase gene was 0·08 in the control group and 0·06 in the patient group. Conclusions, Results of the present study indicate the usefulness of including fasting and post-methionine Hcy, and Lp(a) determination in the diagnostic panels of young CAD patients, in order to obtain a better assessment of their cardiovascular risk profile. [source] Maternal vitamin B-6 and folate status and risk of oral cleft birth defects in the PhilippinesBIRTH DEFECTS RESEARCH, Issue 7 2004Ronald G. Munger Abstract BACKGROUND Vitamin deficiencies induce oral clefts in animal experiments, but the role of specific nutrients in human oral clefts is uncertain. METHODS Associations between maternal vitamin B-6 and folate status and risk of nonsyndromic cleft lip, with or without cleft palate (CL/P), were examined in case,control studies at two sites in the Philippines,Negros Occidental and Davao. Cases were mothers of affected children and control mothers were those who had no children with oral clefts. RESULTS The risk of having a CL/P-affected child increased with increasing tertile of vitamin B-6 deficiency in both Negros Occidental and Davao (odds ratios [ORs] and 95% confidence intervals [CIs] for sites combined = 1.0 [reference], OR, 2.94; 95% CI, 1.51,5.73; OR, 4.98; 95% CI, 2.56,9.67). Poor B-6 status had a stronger association with CL/P among mothers with lower versus higher plasma folate levels. Increasing tertiles of plasma folate were marginally associated with an increased risk of clefts in both sites combined (1.0 [reference]; OR, 1.58; 95% CI, 0.93,2.68; OR, 1.59; 95% CI, 0.94,2.70). Increasing tertiles of erythrocyte folate were associated with a decreased risk of CL/P in Negros Occidental (1.0 [reference]; OR, 0.34; 95% CI, 0.13,0.90; OR, 0.46; 95% CI, 0.20,1.09) and an increased risk in Davao (1.0 [reference]; OR, 1.23; 95% CI, 0.54,2.81; OR, 4.85; 95% CI, 2.24,10.50). The inconsistent associations between folate status and CL/P risk appeared to be a result of statistical interaction between folate, vitamin B-6, and case,control status that produced different results in study areas of higher versus lower prevalence of vitamin B-6 deficiency. CONCLUSIONS Poor maternal vitamin B-6 status was consistently associated with an increased risk of CL/P at two sites in the Philippines. Folate-CL/P associations were inconsistent and may be related to the vitamin B-6 status or other characteristics of the populations under study. Birth Defects Research (Part A), 2004. © 2004 Wiley-Liss, Inc. [source] The paradox of normal serum albumin in anorexia nervosa: A case reportINTERNATIONAL JOURNAL OF EATING DISORDERS, Issue 3 2005Mori J. Krantz MD Abstract Objective Anorexia nervosa (AN) is associated with marked decreases in caloric intake and a corresponding reduction in body weight due to abnormal self body image. Although counterintuitive, hypoalbuminemia and vitamin deficiencies are not expected consequences of this disorder. Etiologic considerations for hypoalbuminemia are discussed. Method The case report of a patient with AN and marked hypoalbuminemia is presented and a focused literature review is reported. Results Hypoalbuminemia was initially attributed to starvation. However, occult infection was ultimately responsible. Serum albumin concentration normalized with antibiotic therapy despite minimal restoration of body weight. Discussion Hypoalbuminemia should not be considered a characteristic feature of AN even in the setting of progressive weight loss. The presence of other potentially life-threatening conditions should be sought, as reduced serum albumin concentration is a marker of inflammation in AN. © 2005 by Wiley Periodicals, Inc. [source] Resolution of alcoholic neuropathy following liver transplantationLIVER TRANSPLANTATION, Issue 12 2004Edward Gane Between 10 and 20% of adult liver transplants are performed for end-stage alcoholic liver disease. Severe extrahepatic end-organ damage from alcoholism (cardiomyopathy, pancreatitis, central nervous system injury, and neuropathy) is widely regarded as an absolute contraindication to liver transplantation, despite a lack of data on the effect of transplantation on these complications. We describe such a patient who presented with decompensated alcoholic liver disease and moderately severe peripheral neuropathy. Both his liver failure and neuropathy progressed despite 9 months abstinence and intensive nutritional support. By 12 months post-transplant, however, this patient had regained almost normal muscle strength, with associated recovery in sensory and motor conduction velocities. Direct alcohol toxicity, nutritional and vitamin deficiencies, and liver failure were all likely etiologic factors in this patient's neuropathy. In conclusion, this case suggests that peripheral neuropathy in a patient with alcoholic cirrhosis may resolve following liver transplantation and should not constitute a contraindication to transplantation, even when it is disabling. (Liver Transpl 2004;10:1545,1548.) [source] G1793A polymorphisms in the methyl- enetetrahydrofolate gene: Effect of folic acid on homocysteine levelsMOLECULAR NUTRITION & FOOD RESEARCH (FORMERLY NAHRUNG/FOOD), Issue 8 2006Sandra Soares Melo Abstract Mutations or polymorphisms in the gene of the enzyme methylenetetrahydrofolate (MTHFR) are associated with hyperhomocysteinemia and possibly with an elevated risk for vascular diseases. A study was conducted on 83 individuals with type 2 diabetes in order to determine the allelic and genotypic frequencies of the G1793A mutation and to assess the effect of folic acid supplementation on plasma homocysteine concentrations. The patients were attended by the Diabetes and Hypertension Program , Balneario Camboriu/SC and received daily supplements containing 1 mg of folic acid for 3 months. DNA was previously extracted from leukocytes and the G1793A mutation was detected by PCR-RFLP. Blood samples were collected during the basal period and after supplementation for the determination of homocysteine by HPLC, and of folic acid and vitamin B12 by RIA. The allele frequency for the G1793A mutation was 3.01% and no homozygous individuals with mutant alleles were detected. Hyperhomocysteinemia was diagnosed in 27.71% of the patients, folic acid deficiency in 15.66%, and vitamin B12 deficiency in 7.23%. Plasma homocysteine concentrations were inversely correlated with folic acid (r = ,0.27, p = 0.01) and vitamin B12 (r = ,0.21; p = 0.05) concentrations. The individuals with a heterozygous genotype for the G1793A mutation showed borderlines or deficient values in folic acid and vitamin B12 concentrations compared to individuals with a normal genotype. Hyperhomocysteinemia and the vitamin deficiencies presented by type 2 diabetic individuals, included with a heterozygous genotype for the G1793A mutation in the MTHFR gene, reached normal values by daily folic acid supplementation. [source] The neurology and neuropathology of coeliac diseaseNEUROPATHOLOGY & APPLIED NEUROBIOLOGY, Issue 6 2000A. J. Wills A number of neurological syndromes have been described in association with coeliac disease. These include disorders of the central nervous system encompassing epilepsy, myoclonus, ataxia, internuclear opthalmoplegia, multifocal leukoencephalopathy and dementia. Most of these associated conditions show a poor response to gluten restriction. Peripheral neuropathies, of axonal and demyelinating types, have also been reported and may respond to elimination of gluten from the diet. The mechanism underlying these processes remains obscure but may be immunological or related to trace vitamin deficiencies. Controversially, it has also been claimed that occult coeliac disease accounts for a substantial proportion of patients with neurological dysfunction of unknown cause. Some authorities recommend that cryptogenic ataxias and neuropathies should be routinely screened for the presence of gluten-sensitivity but this remains contentious and has not been universally accepted. This review will attempt to review the clinical and pathological findings in this condition and speculate on pathogenesis and directions for future research. [source] Iron and vitamin deficiencies, endocrine and immune status in patients with primary Sjögren's syndromeORAL DISEASES, Issue 3 2001IMC Lundström OBJECTIVES: To study the prevalence of iron and vitamin deficiencies, endocrine disorders and immunological parameters in patients with primary Sjögren's syndrome (1°SS). DESIGN AND SUBJECTS: At the time of the establishment of the diagnosis of 1°SS in 43 consecutive patients, a clinical examination including haematological analyses was performed. The patients' medical records were also reviewed. SETTING: Patients referred for diagnosis to The University Hospital, Linköping, a secondary or tertiary referral hospital serving the middle part of southern Sweden. RESULTS: In total, current or previously treated iron and vitamin deficiencies were registered for 63% of the 1°SS patients (iron 51%, vitamin B12 25%, folate 9%). Current low ferritin was noted in 24%, low iron saturation in 37%, decreased vitamin B12 in 13% and folate in 9%. Thyroid disease was found in a total of 33% and 30% had had autoimmune thyroiditis. Three patients (7%) had verified diabetes mellitus. Erythrocyte sedimentation rate (ESR) was raised in 65% of the patients and 84% had a polyclonal increase of Ig. Rheumatoid factor (RF) was detected in 85%, antinuclear antibody (ANA) in 74%, anti-SS-A in 88% and anti-SS-B in 73% of the patients. CONCLUSION: Iron and vitamin deficiencies and thyroid diseases are common in patients with 1°SS. Since these disorders often are treatable and may affect the patients' distress as well as their immune and exocrine function, an active, recurrent search for deficiencies, endocrine diseases and other frequently recorded disorders is recommended. [source] Nutritional deficiencies in iron overloaded patients with hemoglobinopathies,AMERICAN JOURNAL OF HEMATOLOGY, Issue 6 2009Susan Claster One of the hallmarks of both sickle cell disease (SCD) and thalassemia major (TM) is accelerated oxidative damage. Decreased antioxidant levels and increased oxidant stress biomarkers are found in both diseases. Although isolated vitamin deficiencies have been reported in TM and nontransfused SCD patients, a comprehensive evaluation of vitamin and trace mineral levels has never been performed in chronically transfused SCD or TM patients. As vitamins and trace minerals may be consumed as a result of chronic oxidative stress; we hypothesized that levels of these compounds would correlate with surrogates of iron overload, hemolysis, and inflammation in chronically transfused patients. Using a convenience sample of our group of chronically transfused patients we studied 43 patients with SCD (17 male, 26 female) and 24 patients with TM (13 male and 11 female). The age range for our patients varied from 1.5 to 31.4 years. Levels of vitamins A, thiamin, B6, B12, C, D, E as well as selenium, zinc, copper, and ceruloplasmin were measured. We found that 40,75% of the patients were deficient in A, C, D and selenium and 28,38% of the patients had low levels of B vitamins and folate. There was little association with iron overload, hemolysis, or inflammation. Although the precise mechanism of these deficiencies is unclear, they may contribute to the morbidity of chronically transfused hemoglobinopathy patients. Am. J. Hematol., 2009. © 2009 Wiley-Liss, Inc. [source] Water-soluble vitamins in fish ontogenyAQUACULTURE RESEARCH, Issue 5 2010Rune Waagbø Abstract Studies on vitamin requirement at early stages are difficult and vary in quality, both due to the scientific approach and vitamin analysis. Focus has been on water-soluble vitamins that cause dramatic losses of the offspring in practical farming situations or in wild life, like vitamin C and thiamine deficiencies respectively. Practical solutions including vitamin administration through brood stock and larvae diets have confirmed and corrected the vitamin deficiencies. For the other water-soluble vitamins, the situation is not so obvious. Descriptive studies of folate and vitamin B6 during fish ontogeny have shown a net loss of vitamin during endogenous feeding and a steady transfer of vitamin from the yolk sac into the body compartment, and finally, dramatic increases in body vitamin levels after the start of feeding. The kinetics of mass transfer with ontogeny appears, however, to differ between vitamins. Start of feeding of fish larvae with live or formulated feeds includes several challenges with respect to water-soluble vitamins, including aspects of live feed enrichment and stability, micro-diet leaching, variable feed intakes, immature gastrointestinal tract, variable bioavailability of vitamins and larvae vitamin storage capacity. Consequently, the exact minimum requirements are difficult to estimate and vitamin recommendations need to consider such conditions. [source] Clinical trial: B vitamins improve health in patients with coeliac disease living on a gluten-free dietALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 8 2009C. HALLERT Summary Background, Patients with coeliac disease living on a gluten-free diet show vitamin deficiency and reduced subjective health status. Aim, To study the biochemical and clinical effects of B vitamin supplementation in adults with longstanding coeliac disease. Methods, In a double blind placebo controlled multicentre trial, 65 coeliac patients (61% women) aged 45,64 years on a strict gluten-free diet for several years were randomized to a daily dose of 0.8 mg folic acid,0.5 mg cyanocobalamin and 3 mg pyridoxine or placebo for 6 months. The outcome measures were psychological general well-being (PGWB) and the plasma total homocysteine (tHcy) level, marker of B vitamin status. Results, Fifty-seven patients (88%) completed the trial. The tHcy level was baseline median 11.7 ,mol/L (7.4,23.0), significantly higher than in matched population controls [10.2 ,mol/L (6.7,22.6) (P < 0.01)]. Following vitamin supplementation, tHcy dropped a median of 34% (P < 0.001), accompanied by significant improvement in well-being (P < 0.01), notably Anxiety (P < 0.05) and Depressed Mood (P < 0.05) for patients with poor well-being. Conclusions, Adults with longstanding coeliac disease taking extra B vitamins for 6 months showed normalized tHcy and significant improvement in general well-being, suggesting that B vitamins should be considered in people advised to follow a gluten-free diet. [source] Electrocardiographic Changes Due to Pyridoxine DeficiencyPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 5 2003EDUARDO MALMIERCA A young woman presented with marked alterations in the ECG without cardiological symptoms or evidence of structural heart disease after further evaluation. There was evidence of vitamin deficiency and the ECG normalized after 10 days of treatment with vitamins. Similar alterations have been described in several experimental studies with rats, but this is the first case reported in humans. (PACE 2003; 26:1289,1291) [source] Thiamine-responsive megaloblastic anaemia: a cause of syndromic diabetes in childhoodPEDIATRIC DIABETES, Issue 4 2007Birthe S Olsen Abstract:, Thiamine-responsive megaloblastic anaemia (TRMA) is a rare autosomal recessive condition, characterized by megaloblastic anaemia, non-autoimmune diabetes mellitus, and sensorineural hearing loss. We describe three infants with TRMA from two consanguineous Pakistani families, who were not known to be related but originated from the same area in Pakistan. All children were homozygous, and the parents were heterozygous for a c.196G>T mutation in the SLC19A2 gene on chromosome 1q23.3, which encodes a high-affinity thiamine transporter. The result is an abnormal thiamine transportation and vitamin deficiency in the cells. Thiamine in high doses (100,200 mg/d) reversed the anaemia in all our patients. Two patients discontinued insulin treatment successfully after a short period, while the third patient had to continue with insulin. The hearing loss persisted in all three children. The diagnosis of TRMA should be suspected in patients with syndromic diabetes including hearing loss and anaemia, even if the latter is only very mild and, particularly, in the case of consanguinity. [source] Endothelial markers and homocysteine in patients with classic Fabry diseaseACTA PAEDIATRICA, Issue 2002K Demuth Aim: Fabry disease is an X-linked inborn error of glycosphingolipid metabolism due to the deficient activity of ,-galactosidase A, a lysosomal enzyme. It is a multisystem disorder characterized by progressive renal insufficiency, with added morbidity from cardio- and cerebrovascular involvement. The recent availability of genetically engineered enzyme offers an effective targeted treatment approach, but also emphasizes the need for surrogate markers to delineate organ damage and monitor the efficacy of enzyme replacement therapy (ERT). Methods: Multiple endothelial factors and plasma homocysteine concentrations were investigated in 12 consecutive hemizygous males with classic Fabry disease and 15 controls as part of an exhaustive baseline evaluation prior to ERT. Results: Compared with the controls, plasma concentrations of homocysteine were significantly (p > 0.01) higher in patients with Fabry disease in the absence of chronic renal failure or vitamin deficiency. Plasma concentrations of vascular cell adhesion molecule-1 were also significantly (p > 0.05) higher in the patients, and there was a trend for decreased endothelin-1 levels. No difference was found in serum intercellular adhesion molecule-1, plasma P-selectin, serum E-selectin and plasma thrombomodulin between the patients and controls. Conclusions: The results do not reveal measurable evidence for endothelial and leukocyte activation that could reliably serve as surrogate markers for routine monitoring of the efficacy of ERT in patients with Fabry disease. While the exact origin and clinical significance of hyperhomocysteinaemia in Fabry disease remains to be studied in a larger cohort of patients carefully monitored for their concurrent medications, especially carbamazepine, we suggest that patients may benefit from folic acid or multivitamin therapy to treat this additional vascular risk factor, when present. [source] | |||||||||||||