scholarly journals Risk factors for folate deficiency differ from those for vitamin B12 deficiency in Cameroonian women and children (119.7)

2014 ◽  
Vol 28 (S1) ◽  
Author(s):  
Setareh Shahab‐Ferdows ◽  
Reina Engle‐Stone ◽  
Daniela Hampel ◽  
Alex Ndjebayi ◽  
Martin Nankap ◽  
...  
Author(s):  
Sanem Kayhan ◽  
Nazli Gulsoy Kirnap ◽  
Mercan Tastemur

Abstract. Vitamin B12 deficiency may have indirect cardiovascular effects in addition to hematological and neuropsychiatric symptoms. It was shown that the monocyte count-to-high density lipoprotein cholesterol (HDL-C) ratio (MHR) is a novel cardiovascular marker. In this study, the aim was to evaluate whether MHR was high in patients with vitamin B12 deficiency and its relationship with cardiometabolic risk factors. The study included 128 patients diagnosed with vitamin B12 deficiency and 93 healthy controls. Patients with vitamin B12 deficiency had significantly higher systolic blood pressure (SBP), diastolic blood pressure (DBP), MHR, C-reactive protein (CRP) and uric acid levels compared with the controls (median 139 vs 115 mmHg, p < 0.001; 80 vs 70 mmHg, p < 0.001; 14.2 vs 9.5, p < 0.001; 10.2 vs 4 mg/dl p < 0.001; 6.68 vs 4.8 mg/dl, p < 0.001 respectively). The prevalence of left ventricular hypertrophy was higher in vitamin B12 deficiency group (43.8%) than the control group (8.6%) (p < 0.001). In vitamin B12 deficiency group, a positive correlation was detected between MHR and SBP, CRP and uric acid (p < 0.001 r:0.34, p < 0.001 r:0.30, p < 0.001 r:0.5, respectively) and a significant negative correlation was detected between MHR and T-CHOL, LDL, HDL and B12 (p < 0.001 r: −0.39, p < 0.001 r: −0.34, p < 0.001 r: −0.57, p < 0.04 r: −0.17, respectively). MHR was high in vitamin B12 deficiency group, and correlated with the cardiometabolic risk factors in this group, which were SBP, CRP, uric acid and HDL. In conclusion, MRH, which can be easily calculated in clinical practice, can be a useful marker to assess cardiovascular risk in patients with vitamin B12 deficiency.


2021 ◽  
Vol 104 (2) ◽  
pp. 003685042110076
Author(s):  
Nazmi Mutlu Karakaş

Background: In this study, the aim was to evaluate the prevalence of vitamin D, vitamin B12, ferritin, and folate deficiencies in adolescence to clarify the need for early diagnosis and therapy. Methods: The medical records of adolescents between 10 and 18 years of age between 01 September 2018 and 28 February 2019 as healthy with non-specific complaints, or due to well-child care visits, were analyzed retrospectively. Results: A total of 1847/2507 (73.6%) adolescents were included in the study. The prevalence of vitamin D deficiency was 25.7% (n: 178/691). Vitamin B12 deficiency prevalence was 69.2% (n: 753/1088). The prevalence of anemia and ferritin deficiency was 4.8% and 13.26%. The prevalence of folate deficiency was 37.9% (n: 413/1088). VDD prevalence was statistically significantly higher in females than males (F/M:116/62). VB12D prevalence, the number and mean age of females with hemoglobin deficiency, and low ferritin levels was found to be statistically significantly higher in females than males. Conclusions: The prevalence of vitamin D, vitamin B12, folate deficiency and low ferritin levels was found to be high among adolescents. In particular, adolescents admitting with non-specific complaints and for control purposes in big cities must be considered to be at risk for the deficiency of these vitamins and low level of ferritin.


2021 ◽  
Vol 2021 ◽  
pp. 1-5
Author(s):  
John Rolshoven ◽  
Katelyn Fellows ◽  
Rolando Ania ◽  
Burton J. Tabaac

Background. The term cytotoxic lesions of the corpus callosum (CLOCCs) encompasses the entity reversible splenial lesion syndrome (RESLES). RESLES typically presents with altered levels of consciousness, seizures, and delirium and is distinguished radiographically by reversible focal lesions of the splenium of the corpus callosum. This disease pathology is associated with withdrawal of antiepileptic medications, infections, metabolic disturbance, or high-altitude cerebral edema. Methods. We presented an otherwise healthy 72-year-old female that was consulted for an episode of isolated vertigo lasting four hours. Initial workup included CT head without contrast, CT angiogram head and neck, and MRI brain with and without contrast. The patient experienced recurrent episodes of vertigo at one and four months after initial presentation. An extensive workup at one month included a wide spectrum of laboratory tests and repeat imaging. Results. Noncontrast CT of the head and CT angiogram of the head and neck were reassuring. MRI brain with and without contrast demonstrated hyperintensity in the splenium of the corpus callosum on FLAIR sequencing. A follow-up visit at one month revealed vitamin B12 deficiency and unchanged hyperintensity of the splenium of the corpus callosum. History and workup were negative for typical risk factors associated with RESLES. Conclusion. An otherwise healthy patient who presented with an isolated episode of vertigo was discovered to demonstrate radiographic features consistent with RESLES but lacked the common risk factors and typical presentation of RESLES. This case expands the possible clinical presentation of RESLES and highlights the possible relationship between vitamin B12 deficiency and radiographic features of RESLES.


Blood ◽  
1982 ◽  
Vol 59 (3) ◽  
pp. 634-640
Author(s):  
MR Taheri ◽  
RG Wickremasinghe ◽  
BF Jackson ◽  
AV Hoffbrand

The role of vitamin B12 in the folate dependent biosynthesis of thymidine nucleotides is controversial. In an attempt to clarify this, three methods have been used to assess the relative efficacy of vitamin B12 (hydroxocobalamin) and various folate analogues in titrated concentrations at correcting ‘de novo’ thymidylate synthesis by megaloblastic human marrow cells: (1) The deoxyuridine (dU) suppression test which analyses the reduction in (3H)-thymidine labeling of DNA by unlabeled dU. Marrow cells were also labeled with (6–3H)-dU with assessment of (2) its incorporation into DNA and (3) the accumulation of (6–3H)-deoxyuridine monophosphate (3H-dUMP). The three methods gave similar results. In both, N6-formyl tetrahydrofolate (formyl-FH4) was the most effective agent at correcting thymidylate synthesis in megaloblastic anemia due to vitamin B12 or folate deficiency. Vitamin B12 corrected the lesion in vitamin B12 deficiency but not in folate deficiency. Tetrahydrofolate (FH4) and folic acid were effective in deficiency of vitamin B12 or folate, although in both deficiencies they were less effective than formyl-FH4. Methyl-FH4 was effective in folate deficiency but not in vitamin B12 deficiency. These results confirm the failure of methyl-FH4 utilisation in vitamin B12 deficiency. They suggest that if vitamin B12 is needed in the formylation of FH4, this is a minor role in provision of the correct coenzyme for thymidylate synthesis compared with its major role of provision of FH4 from methyl- FH4.


2017 ◽  
Vol 35 (5) ◽  
pp. 463-471
Author(s):  
Shuzi Zheng ◽  
Chaoqun Wu ◽  
Wei Yang ◽  
Xuanping Xia ◽  
Xiuqing Lin ◽  
...  

Objectives: The study aimed to investigate the association of Crohn's disease (CD) with transcobalamin II (TCN2) polymorphisms and serum homocysteine, folate, and vitamin B12 levels. Methods:TCN2 (rs1801198, rs9606756) were genotyped by iMLDR in 389 CD patients and 746 controls. Furthermore, 102 CD patients and 153 controls were randomly selected for examination of serum homocysteine, folate, and vitamin B12 levels by enzymatic cycling assay and chemiluminescence immunoassay, respectively. Results: Mutant allele (G) and genotype (AG + GG) of (rs9606756) were higher in CD patients than in controls (both p < 0.05). So were they in ileocolonic CD patients and stricturing CD patients compared to controls (all p < 0.05). Mutant allele (G) and genotype (CG + GG) of (rs1801198) were more prevalent in stricturing CD patients than in controls (both p < 0.05). Compared to controls, average homocysteine level was enhanced in CD patients (p = 0.003), whereas average folate and vitamin B12 levels were reduced in CD patients (both p < 0.001). The prevalence of hyperhomocysteinemia, folate deficiency, and vitamin B12 deficiency was higher in CD patients than in controls (all p < 0.01). Both folate deficiency and vitamin B12 deficiency were independently related to risk of CD (both p < 0.01). Conclusion:TCN2 (rs1801198, rs9606756) polymorphisms as well as folate deficiency and vitamin B12 deficiency are correlated with CD.


Stroke ◽  
2015 ◽  
Vol 46 (suppl_1) ◽  
Author(s):  
Zarah Yusuf ◽  
Jayanthi Alamelu ◽  
Ming Lim ◽  
Nomazulu Dlamini

Introduction: Risk factors in childhood stroke are multiple and causality hard to determine. Current guidelines recommend prothrombotic workup, yet yield is variable, often without therapeutic consequence. Raised homocysteine is associated with vitamin B12 deficiency (B12), which is not routinely measured. Hypothesis: We hypothesised that B12 deficiency is a treatable risk factor for stroke in children not reliably identified by analysis of homocysteine only. Method: We retrospectively reviewed paediatric stroke patients admitted to a tertiary care hospital from 2010-2014. All patients with plasma homocysteine measured as part of their prothrombotic workup were selected. All clinical data closest to stroke diagnosis were reviewed. B12 deficiency was defined as low total and/or holo (functional) vitamin B12 with/without raised methylmalonic acid (MMA). Parental prothrombotic workup and B12 status was analysed where available. Results: Of 134 patients, 61 had homocysteine levels, 20 were tested for vitamin B12 (age range 0-14.8 years), 14/20 for MMA. B12 deficiency was found in 7/20 with median age of acute stroke presentation of 1 day (25th percentile= 0; 75th percentile= 51days). Median age of stroke presentation in B12 replete group was 3.5 years (25th percentile=2.0;75th percentile=7.0years). There was a statistical difference in age of stroke presentation between the B12 deficient and replete groups (Kruskal-Wallis, p=0.001). Raised homocysteine (10/20) was not sensitive in detecting B12 deficiency (sensitivity 42.8%, 95% CI 15.82-74.95). Two of seven had additional risk factors (1/7 iron deficiency, 1/7 MTHFR 667 homozygous). Seizures were the most common stroke presentation regardless of B12 status. Vitamin B12 (im) was given in 4/7 children and 3/9 parents (2 mothers, 1 father). Five of seven were breast fed. All treated parents were vegetarian. Conclusion: Our study suggests vitamin B12 deficiency is associated with early childhood stroke. Homocysteine alone is not a sensitive screen for this. Investigation with functional biomarkers such as holo B12 and MMA would allow for improved detection of a treatable risk factor in childhood stroke. Further studies may support this recommendation being added to guidelines.


2008 ◽  
Vol 14 (2) ◽  
pp. 217-223 ◽  
Author(s):  
Peggy D. Headstrom ◽  
Stephen J. Rulyak ◽  
Scott D. Lee

2020 ◽  
Vol 154 (Supplement_1) ◽  
pp. S87-S87
Author(s):  
S N Mattox ◽  
D Kozman ◽  
G Singh

Abstract Introduction/Objective To identify clinical/laboratory factors associated with folate deficiency in tertiary care patients. Methods We reviewed the medical records of 1019 patients with serum folate &lt;7.0 ng/mL, 301 patients with serum folate of 15 ng/mL, and 300 patients with serum folate &gt; 23 ng/mL. Results Serum prealbumin levels were subnormal in 54.8% of patients with serum folate &lt;7.0 ng/mL. Vitamin B12, hemoglobin, and serum albumin levels were significantly lower in the &lt;7.0 ng/mL folate group. In 62.4% of patients with serum folate &lt;7.0 ng/mL, 1 or more markers of malnutrition were present. The low-folate group had a significantly higher prevalence of gastrointestinal (GI) disorders, sepsis, and abnormal serum creatinine level. There were no significant differences in the 2 groups regarding diabetes; behavioral/neurological disorders, including drug and alcohol abuse; bariatric surgery; or a diagnosis of malnutrition. The average body mass index (BMI) for the &lt;7.0 ng/mL and 15 ng/mL folate groups was significantly different (28.89 and 28.31, respectively), although the difference does not appear to be clinically meaningful. Conclusion The prevalence of folate deficiency depends on what is considered a normal serum folate level. Approximately 10% of tertiary care patients have levels &lt;7.0 ng/mL and exhibit other markers of malnutrition. It is recommended that patients with GI disorders, chronic kidney disease, and sepsis be routinely tested for serum folate levels, before administration of vitamin supplements. Patients with serum folate levels &lt;7.0 ng/mL should be evaluated for malnutrition, despite BMI &gt; 25. Folate supplementation should be administered only after excluding coexisting vitamin B12 deficiency.


2018 ◽  
Vol 72 (4) ◽  
pp. 265-271 ◽  
Author(s):  
Ili Margalit ◽  
Eytan Cohen ◽  
Elad Goldberg ◽  
Ilan Krause

Background: Vitamin B12 deficiency is associated with hematological, neurological, and cardiovascular consequences. Epidemiologic data on these related illnesses indicate gender differences. Methods: A cross-sectional study was designed to examine gender differences in vitamin B12 deficiency among a healthy population. Data from healthy individuals aged 18–65, who were provided with a routine medical evaluation during 2000–2014, were retrieved from the medical charts. Individuals with background illnesses and those who had used medications or nutritional supplements were excluded. Vitamin B12 deficiency was defined by 2 cutoff values (206 and 140 pmol/L). The multivariate analysis was adjusted for age, body mass index, estimated glomerular filtration rate, hyperhomocysteinemia, folate deficiency, albumin, and transferrin saturation. Sensitivity analyses were implemented by excluding individuals with anemia, hyperhomocysteinemia, or folate deficiency and by age stratification. Results: In all, 7,963 individuals met the inclusion criteria. Serum vitamin B12 mean levels were 312.36 and 284.31 pmol/L for women and men respectively (p < 0.001). Deficiency prevalence was greater for men (25.5%) in comparison with women (18.9%; p < 0.001). Men were strongly associated with severe deficiency (adjusted OR 2.26; 95% CI 1.43–3.56). Conclusions: Among the healthy population, men are susceptible to vitamin B12 deficiency. This can be explained by neither diet habits nor estrogen effects. Genetic variations are therefore hypothesized to play a role.


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