Low Serum B12 Research Articles

Localised Skin Hyperpigmentation as a Presenting Symptom of Vitamin B12 Deficiency Complicating Chronic Atrophic Gastritis.

Vitamin B12 deficiency is common in developing countries and should be suspected in patients with unexplained anaemia or neurological symptoms. Dermatological manifestations associated with this deficiency include skin hyper- or hypopigmentation, angular stomatitis and hair changes. We report a case of a 28-year-old man who presented to the Sultan Qaboos University Hospital in Muscat, Oman, in November 2013 with localised hyperpigmentation of the palmar and dorsal aspects of both hands of two months' duration. Other symptoms included numbness of the hands, anorexia, weight loss, dizziness, fatigability and a sore mouth and tongue. There was no evidence of hypocortisolaemia and a literature search revealed a possible B12 deficiency. The patient had low serum B12 levels and megaloblastic anaemia. An intrinsic factor antibody test was negative. A gastric biopsy revealed chronic gastritis. After B12 supplementation, the patient's symptoms resolved. Family physicians should familiarise themselves with atypical presentations of B12 deficiency. Many symptoms of this deficiency are reversible if detected and treated early.

Vitamin B12 deficiency in patients after enterocystoplasty

Serum B12 deficiency is a known sequlae of enterocystoplasty. The complications of B12 deficiency include megaloblastic anemia, neuropsychiatric disease, and demyelinating diseases such as peripheral neuropathy. Some studies have suggested that underlying disease states may be more important than enteric absorptive capacity in predicting acquired B12 deficiency. A 38% incidence of low or low-normal serum B12 in patients who have undergone enterocystoplasty has previously been reported, and oral B12 supplementation has been demonstrated to be an effective short-term therapy; however, the long-term results remain unclear. This study hypothesized that oral vitamin B12 supplementation in patients with B12 deficiency following enterocystoplasty is an effective long-term treatment. Additionally, it sought to determine if underlying disease state predicts B12 deficiency following enterocystoplasty. Children who underwent enterocystoplasty at the present institution prior to August 2007 were reviewed. Patients with non-ileal augment, insufficient follow-up or hematologic disorders were excluded. Patients with low or low-normal B12 levels were included. Treatment consisted of daily oral therapy of 250 mcg or monthly parenteral therapy of 1000 mcg IM. Separately, the institutional database of 898 patients who underwent enterocystoplasty was searched and patients with at least one post-operative B12 level were highlighted. The indication for enterocystoplasty was classified as neuropathic or non-neuropathic. Twenty-three patients met inclusion criteria. The mean follow-up was 49 months (range 5-85) following initial abnormal B12 level. On the last follow-up, 4/23 (17%) patients had normal serum B12 levels. No patients reported sequelae of long-term B12 deficiency. In the secondary investigation, 113 patients met inclusion criteria. A total of 101 had neuropathic indications for enterocystoplasty, and 12 had non-neuropathic indications. At any time during follow-up, 48/101 (47.5%) neuropathic patients had low or low-normal B12 levels, and 4/12 (33.3%) non-neuropathic patients had low or low-normal B12 levels during follow-up (P = 0.54) (Figure). The initial success of oral B12 deficiency treatment following enterocystoplasty does not persist over time. This contradicts previous results with short duration follow-up. Underlying disease as the indication for enterocystoplasty did not predict B12 deficiency risk. The study was limited by the small number of patients with B12 deficiency who were started on treatment, as well as by the small number of patients with non-neuropathic indications for enterocystoplasty. The aims of the study were met. Further investigation is required to assess predictors of B12 deficiency following enterocystoplasty.

PTH-249 Contraceptive pill and b12: low yield from investigating low serum b12 in women taking the ocp

Introduction Vitamin B12 deficiency causes megaloblastic anaemia, cytopenias and neurological deficits and deficiency is usually a result of defective absorption, either through lack of intrinsic factor, gastric pathology or ileal pathology although dietary deficiency may occur. Serum B12 assays have low specificity and up to 50% of results below 200 ng/l appear erroneous. Patients could be committed to unnecessary B12 replacement therapy and symptoms may be wrongly ascribed to B12 deficiency as the real cause is overlooked. 70–90% of serum B12 is bound to holohaptocorrin, the remainder being bound to holotranscobalamin. These carrier proteins are affected by pregnancy and the oral contraceptive pill (OCP), resulting in a low B12 level in the absence of anaemia or macrocytosis. Our aim was to evaluate B12 testing in women of childbearing age by assessing firstly, concomitant use of the OCP and secondly where, the result was felt to indicate true deficiency, whether appropriate assessment was conducted. Method Over a 12-month period, all women of childbearing age who were shown to have a low serum B12 level were eligible to be included. Repeat tests were excluded. We then reviewed Hb, MCV and ferritin and folate. Results of investigation were noted when performed including intrinsic factor, anti-GPC and TTG antibodies; endoscopy and small bowel imaging. Results 180 case records were identified, complete data was available from 166. The two key groups are those with isolated low B12 and those with macrocytic anaemia. Of those with macrocytic anaemia, 4/10 had coexisting folate deficiency. Further assessment was inconsistent- 4/10 no further assessment, 2/10 further blood tests but no imaging and 4/10 had various tests. One patient was subsequently diagnosed with Crohn’s disease. Those patients with an isolated low B12 result, 68 were taking the OCP. For the remainder there was no documentation to confirm or deny use. Of the 68 patients, 30/68 had undergone some form of further investigation. In 2/30 women taking the OCP with low B12 without anaemia, one had coeliac disease and one had anti-GC antibodies (but no IF antibodies). Conclusion In those patients who are identified as having a low B12 level in the absence of anaemia or macrocytosis; use of the OCP should be considered. Investigation of low B12, when there is no anaemia and normocytosis, is unrewarding. Repeating the serum B12 level after stopping the OCP should confirm the cause and prevent unnecessary investigation. Where anaemia or macrocytosis is present a structured approach to further investigation should made to seek and identify significant pathology. This includes antibody testing, thyroid function and gastric + ileal assessment. Disclosure of interest None Declared.

Effect of vitamin B12 supplementation on B12 status and neurophysiological function in older Chileans analyzed by the combined indicator of B12 status

Since 2005 the National Feeding Program for the Elderly (PACAM) in Chile has provided a B12 fortified milk drink (1.7 µg B12/d) which is insufficient to ensure B12 adequacy in many individuals. The objective was to evaluate effects of adding 1 mg B12/d to PACAM vs 1 mg B12/d as a pill with PACAM on B12 status and neurophysiological function in Chilean elderly. The cluster RCT had 3 arms: fortified PACAM (1 mg B12, n=101), pill with PACAM (1 mg B12, n=97) and placebo with PACAM (control, 1.7 ug B12, n=89). B12 status was defined as cB12, which combines serum B12, holoTC, MMA and tHcy. cB12 and peripheral sensory and motor nerve conduction were assessed at baseline and after 4 (efficacy), 9 and 18 mo (effectiveness). A linear mixed-effect model was performed. Based on cB12, 7.6% of elderly were B12 deficient and 27.3% had low status at screening. Subjects with very low serum B12 were excluded and treated. cB12 correlated more strongly (-~0.40, p<0.0001) with the average distal latency of the sural nerve at baseline than did any individual B12 marker. cB12 did not differ among groups at baseline. After 4 mo, B12 provided by PACAM or a pill equally (p<0.0001) improved B12 status. The effect was maintained at 9 and 18 mo. Sensory nerve conduction latencies of the sural nerves were reduced (p<0.0001) after 4 mo in both supplement groups. Giving elderly B12 fortified milk was as effective and efficacious as B12 in pills for improving B12 status and peripheral nerve conduction, and cB12 was the best marker of status and function. Funding: Chilean FONDECYT #1070592 and USDA, ARS WHNRC Figure 1. Impact of supplemental B12 on B12 status

Vitamin B12 Status in a Cohort of Canadian Pregnant Women and Newborn Infants

Low maternal concentrations of vitamin B12 (B12) adversely affect fetal development. In Canada, low serum B12 concentrations (&lt;148 pmol/L) are prevalent among women of reproductive age. We measured concentrations of serum B12 and its functional biomarkers, plasma total homocysteine (tHcy) and methylmalonic acid (MMA), in 368 pregnant women at 12‐16 wk gestation, at delivery and in cord blood. We also determined the effect of major fetal genetic variants of B12 metabolism on cord plasma concentrations of B12, tHcy and MMA. The prevalence of low serum B12 concentrations at recruitment and delivery was 17% and 37%, respectively. Elevated plasma MMA concentrations (&gt;270 nmol/L) were only observed in 2% and 5% of women at recruitment and delivery, respectively, and no women had plasma tHcy concentrations &gt;13 μmol/L. During pregnancy, mean serum B12 concentrations decreased by 23%, while plasma tHcy and MMA increased by 20% and 24%, respectively (p&lt;0.0001). Mean cord blood concentrations of B12, tHcy and MMA were 1.9, 0.8 and 2.3 times maternal concentrations at delivery (p&lt;0.0001). Cord plasma MMA concentrations were significantly altered by the MTR rs1805087, MUT rs1141321 and MMAA rs2270655 genotypes (p&lt;0.04), while cord serum B12 and plasma tHcy concentrations were altered by the TCN1 rs34324219 genotype (p=0.04). Our data suggest that although “suboptimal” serum B12 levels are prevalent in Canadian pregnant women, they are unlikely functionally significant as evidenced by MMA and tHcy status. Fetal genetic variants appear to influence cord blood concentrations of B12, MMA and tHcy. Funded by CIHR MOP#106446

Vitamin B12 in obese adolescents with clinical features of insulin resistance.

Emerging evidence indicates an association between obesity, metformin use and reduced vitamin B12 status, which can have serious hematologic, neurologic and psychiatric consequences. This study aimed to examine B12 status in obese adolescents with pre-diabetes and/or clinical features of insulin resistance. Serum B12 was measured using chemiluminescence immunoassay in 103 (43 male, 60 female) obese (mean body mass index (BMI) z-score ± SD (2.36 ± 0.29)), adolescents aged 10 to 17 years, median (range) insulin sensitivity index of 1.27 (0.27 to 3.38) and 13.6% had pre-diabetes. Low B12 (<148 pmol/L) was identified in eight (7.8%) and borderline status (148 to 221 pmol/L) in an additional 25 (24.3%) adolescents. Adolescents with borderline B12 concentrations had higher BMI z-scores compared to those with normal concentrations (2.50 ± 0.22 vs. 2.32 ± 0.30, p = 0.008) or those with low B12 concentration (2.50 ± 0.22 vs. 2.27 ± 0.226, p = 0.041). In conclusion, nearly a third of obese adolescents with clinical insulin resistance had a low or borderline serum B12 status. Therefore, further investigations are warranted to explore the cause and the impact of low B12 status in obese pediatric populations.

Low serum vitamin B12 levels among psychiatric patients admitted in Butabika mental hospital in Uganda

BackgroundPsychiatric manifestations have been noted in patients with low serum vitamin B12 levels even in the absence of other neurologic and/or haematologic abnormalities. There is no literature on low serum B12 prevalence among Ugandans with psychiatric illnesses. The aim of this study was to establish the prevalence, risk factors, and clinical manifestations of low serum vitamin B12 among psychiatric patients admitted in a Mental Health Hospital in Uganda.MethodUsing a cross sectional descriptive study design, 280 in-patients selected by systematic sampling were studied using a standardized protocol. Low serum vitamin B12 was defined as a level < 240 pg /mL.ResultsWe found a prevalence of low serum B12 in 28.6% of the participants. Absent vibration sense which was significantly associated (58.3% Vs. 26.7%: OR = 3.84 (95% C.I. 1.18, 12.49); p-value = 0.025) with low vitamin B12 was observed among 12 participants. Macro-ovalocytes present among 23 participants on peripheral film were significantly associated with low serum levels (73.9% Vs. 26.2%: OR = 7.99 (95% C.I. 3.01, 21.19) p-value < 0.0001). Factors significantly associated with low serum B12 levels included psychiatric diagnosis of schizophrenia (AOR 1.74 (95% C.I. 1.00, 3.02); p-value = 0.049), duration of psychiatric illness > or = 3 years (AOR 2.27 (95% C.I. 1.29, 3.98); p-value = 0.004), and hospitalization < 3 weeks (AOR 4.01 (95% C.I. 1.02, 15.79); p-value = 0.047). Female participants were associated with protection from low serum levels (AOR 0.4 (95% C.I. 0.22, 0.73); p-value = 0.003).ConclusionLow serum B12 is common among hospitalized psychiatric patients with the majority having no haematological findings. Associated risk factors included having a psychiatric diagnosis of schizophrenia, a shorter duration of hospitalization and longer duration of psychiatric illness. Female participants were less likely to have low serum vitamin B12 levels. Routine screening for serum vitamin B12 levels should be adopted by all hospitals for admitted psychiatric patients.

MTHFR C677T genotype and cardiovascular risk in a general population without mandatory folic acid fortification

Meta-analyses have suggested an effect of MTHFR C677T genotype (rs1801133), a proxy for blood total homocysteine, on cardiovascular disease (CVD) in populations with low population dietary folate. The aim was to examine the association and effect modification by serum folate and vitamin B12 levels between MTHFR and CVD-related outcomes in a general population with no mandatory folic acid fortification policy. The study population included 13,748 adults retrieved from pooling of four population-based studies conducted in Denmark. MTHFR genotype, serum folate (measured in approximately 9,356 individuals), and serum vitamin B12 (9,215 individuals), hypertension, and dyslipidemia were measured at baseline, and participants were followed for a mean of 10.5-11.7 years in central registries for diagnoses of stroke (623 incidents), ischaemic heart disease (IHD) (835 incidents), and all-cause mortality (1,272 incidents). The MTHFR genotype (TT vs. CC/CT) was not associated with hypertension [OR (95% CI) 1.09 (0.95-1.25)], dyslipidemia [OR (95% CI) 0.97 (0.84-1.11)], stroke [HR (95% CI) 0.92 (0.69-1.23)], and all-cause mortality [HR (95% CI) 0.94 (0.77-1.14)], either overall, or in participants with low serum folate or B12 status (P values for interactions 0.15-0.94). Individuals with the MTHFR TT genotype had a higher risk of IHD (HR (95% CI) 1.38 (1.11-1.71)), but this association was not modified by folate status (P value for interaction 0.45). Our results do not support a causal relationship between homocysteine and CVD. However, we cannot exclude a direct causal effect of MTHFR C677T genotype on IHD.

SERUM B12 DEFICIENCY;

Objective: To determine the frequency of various neurological and psychiatric symptoms associated with B12 deficiency.Study design: Observational and descriptive study. Place and duration of study: The study was conducted on patients presenting to theneurology clinics and inpatients who were admitted through the emergency department at Aga khan University Hospital Karachi, from 1stJuly 2011 to March 2012. Subjects and methods: 150 patients of either gender and age more than 18 years. Detailed history was takenfrom all the patients with special regard to anemia. Inclusion criteria were that patients above 18 years of age of either sex with low serumB12 levels. Patients having any type of neurological tumors, major ischemic stroke, major intracranial haemorrhage, patients onneuroleptic medications and any evidence of toxin induced neuropathy were excluded. All patients underwent for specific investigationcomplete blood count, serum B12 levels (derived by Radio Assay method (RIA). Further investigations Nerve Conduction Studies /Electromyography and CT Scan / Magnetic resonance Imaging of the Brain / spinal cord were carried out as and when required,depending on the clinical scenario. Results: There were 69 (46%) males and 81(54%) females. Female to male ratio was 1:0.8. The ageranged between 18 to 90 years with the mean age of 45.7+ 5.6. Out of 150 patients 107 patients (71.3 %) had severe vitamin B 12deficiency while 43 (28.7%) had mild to moderate deficiency. Neurological manifestations which were observed included; Memory wasimpaired in 13 (8.7%) of the patients. Dysarthia, along with other cerebellar signs (Nystagmus and dysdiadochokinesia) was present in9 patients (6%). 4 patients (2.7%) sought medical attention regarding their abnormal gait and their neurological examination revealedextensor planter responses and hyperreflexia. Cranial nerve examination revealed Anosmia in 2 (1.3%) and upper motor neuron facialweakness in 1 (0.66%) patients. Motor weakness was found in 2 patients (1. 3%), and spasticity in 2 (1.3%) patients. 5 patients (3.3%)had sensory complains and were found to have impaired pain and touch perception. Proximal muscle weakness in one patient whileanother patient had asymmetric muscle weakness and rest of the patients had normal muscle power. None of the patient had autonomicdysfunction. In six neuropsychiatric problems were commonly seen in vitamin B 12 deficient people. In these patients depression wasobserved in 16%, agitation 12.7 %, memory impairment 8.7%, cerebellar signs and dysarthria 6%, sensory symptoms 3.3% and gaitabnormality and hyperreflexia and extensor planters 2.7 %. Conclusions: Various Neuropsychiatric problems are associated with vitaminB 12 deficiency and the most common Neuropsychiatric illness found in these patients were depression, agitation, and memoryimpairment.

Vitamin B12 Deficiency Masquerading as Clozapine-Resistant Psychotic Symptoms in Schizophrenia

Vitamin B₁₂ Deficiency Masquerading as Clozapine-Resistant Psychotic Symptoms in Schizophrenia

Response Letter to Lawrence Solomon

To the Editor: We appreciate Dr. Solomon's interest in our recent study of vitamin B12 and peripheral nerve function. We agree that B12 deficiency is only one risk factor for poor peripheral nerve function, and many older adults with “normal” B12 levels may have subclinical B12 deficiency, as shown according to methylmalonic acid (MMA) levels, and have poor peripheral nerve function. Because diabetes mellitus accounts for only approximately 40% of prevalent cases of peripheral neuropathy and half of incident cases,1 additional risk factors need to be identified in individuals without diabetes mellitus. Clinicians are often unable to determine a reasonable cause of neuropathy in older adults. We recognize that older adults with “normal” serum B12 levels (>260 pmol/L) can still have high MMA levels. A recent review showed that homocysteine and MMA levels may be high for serum B12 levels up to 400 pmol/L.2 Therefore, the cut point of 260 pmol/L may be inadequate for determining associations with poor peripheral nerve function. More importantly, the clinical deficient cutpoint of 148 pmol/L may need to be reexamined because many older adults with “clinically normal” B12 levels may have nerve deficits caused by low B12 availability. Thus, clinicians may believe that, because their patients' serum B12 level is “clinically normal,” poor B12 is not causing the symptoms of peripheral neuropathy and B12 replacement is not needed. Unfortunately, MMA or homocysteine levels are not available for those with B12 levels greater than 260 pmol/L to determine those with “functional B12 deficiency.” In our study, in those with low serum B12 (<260 pmol/L), no significant difference existed in MMA levels between older adults with (358.9 ± 252.1 nmol/L) and without diabetes mellitus (323.5 ± 213 nmol/L) (P = .20). The analysis that Dr. Solomon has performed is important to determine that “functional B12 deficiency” is probably present in a substantial proportion of older adults, particularly in older adults with diabetes mellitus. The use of metformin, which impairs absorption of B12 found naturally in food (animal products), accentuates this relationship in older adults with diabetes mellitus.3,4 The role of “functional B12 deficiency” and the threshold of vitamin B12 levels affecting peripheral nerve function in older adults is a critical future direction of our work.

Neural tube defects on the Texas‐Mexico border: What we've learned in the 20 years since the Brownsville cluster

We reviewed the published findings from the Texas Neural Tube Defect Project, a 6-year case-control study (1995-2000) of neural tube defects (NTDs) on the Texas-Mexico border. In this review, we highlight what was learned about environmental, genetic, and nutritional factors (i.e., those related to the folate and other metabolic pathways) and the novel putative risk factors that emerged from this study of Mexican American women living on the Texas-Mexico border. Our investigations of the micronutrients and metabolic pathways involved confirmed the findings of other researchers that increased folate intake has a protective effect and that low serum B(12) , high serum homocysteine levels, and obesity independently contribute to risk. Studies of this population also have implicated hyperinsulinemia and low ferritin, metabolic risk factors, which require additional study to elucidate their physiologic mechanism. Environmental contaminants such as heavy metals, pesticides, and polychlorinated biphenyls (PCBs), which were of community concern, did little to explain NTD risk. Studies in this folic acid deficit-population also revealed several novel risk factors, namely, diarrhea, stress, fumonisins, and the combination of nitrosatable drug exposure with high nitrate/nitrite intake. In conclusion, the 23 studies among the Mexican American women living along the Texas-Mexico border have demonstrated the multifactorial nature of NTDs and that a population deficient in folic acid will be vulnerable to a variety of insults whether brought on by individual behaviors (e.g., obesity) or through the surrounding environment (e.g., fumonisins). Birth Defects Research (Part A), 2012. © 2012 Wiley Periodicals, Inc.

Use of Serum Vitamin B12 Level as a Marker to Differentiate Idiopathic Noncirrhotic Intrahepatic Portal Hypertension from Cryptogenic Cirrhosis

Idiopathic non-cirrhotic intrahepatic portal hypertension (NCIPH) is often mis-diagnosed as cryptogenic cirrhosis. Serum vitamin B12 levels can be raised in cirrhosis, probably because of excess release or reduced clearance. Because NCIPH is characterised by long periods of preserved liver function, we examined whether serum B12 level could be used as a marker to differentiate NCIPH from cryptogenic cirrhosis. We analysed serum B12 levels in 45 NCIPH and 43 cryptogenic cirrhosis patients from January 2009 to September 2011. Serum B12 levels were significantly lower in NCIPH patients than in cryptogenic cirrhosis patients (p < 0.001) and were useful in differentiating the two disorders (area under ROC: 0.84; 95% C.I: 0.76-0.93). Low serum B12 level (≤250 pg/ml) was noted in 25/72 (35%) healthy controls, 14/42 (33%) NCIPH patients, and 1/38 (3 %) cryptogenic cirrhosis patients. In patients with intrahepatic portal hypertension of unknown cause, serum B12 level ≤ 250 pg/ml was useful for diagnosing NCIPH (positive predictive value: 93 %, positive likelihood ratio 12.7), and serum B12 level >1,000 pg/ml was useful in ruling out NCIPH (negative predictive value: 86 %, negative likelihood ratio: 6.67). Low serum B12 levels (≤250 pg/ml) correlated with diagnosis of NCIPH after adjusting for possible confounders (O.R: 13.6; 95% C.I:1.5-126.2). Among patients in Child's class A, serum B12 level was ≤250 pg/ml in 14/35 NCIPH patients compared with 1/21 cryptogenic cirrhosis patients (O.R: 13.3; 95% C.I: 1.6-111). Serum vitamin B12 level seems to be a useful non-invasive marker for differentiation of NCIPH from cryptogenic cirrhosis.

Relationship between vitamin B12 and sensory and motor peripheral nerve function in older adults.

To examine whether deficient B12 status or low serum B12 levels are associated with worse sensory and motor peripheral nerve function in older adults. Cross-sectional. Health, Aging and Body Composition Study. Two thousand two hundred and eighty-seven adults aged 72 to 83 (mean 76.5 ± 2.9; 51.4% female; 38.3% black). Low serum B12 was defined as serum B12 less than 260 pmol/L, and deficient B12 status was defined as B12 less than 260 pmol/L, methylmalonic acid (MMA) greater than 271 nmol/L, and MMA greater than 2-methylcitrate. Peripheral nerve function was assessed according to peroneal nerve conduction amplitude and velocity (NCV) (motor), 1.4 g/10 g monofilament detection, average vibration threshold detection, and peripheral neuropathy symptoms (numbness, aching or burning pain, or both) (sensory). B12-deficient status was found in 7.0% of participants, and an additional 10.1% had low serum B12 levels. B12 deficient status was associated with greater insensitivity to light (1.4 g) touch (odds ratio = 1.50, 95% confidence interval = 1.06-2.13) and worse NCV (42.3 vs 43.5 m/s) (β = -1.16, P = .01) after multivariable adjustment for demographics, lifestyle factors, and health conditions. Associations were consistent for the alternative definition using low serum B12 only. No significant associations were found for deficient B12 status or the alternative low serum B12 definition and vibration detection, nerve conduction amplitude, or peripheral neuropathy symptoms. Poor B12 (deficient B12 status and low serum B12) is associated with worse sensory and motor peripheral nerve function. Nerve function impairments may lead to physical function declines and disability in older adults, suggesting that prevention and treatment of low B12 levels may be important to evaluate.

Vitamin B12 deficiency in a case followed as schizophrenia

Medical disorders may be mistaken for a primary psychiatric disturbance because of prominent and commonly associated psychiatric or behavioral manifestations. The lack of recognition of the underlying medical condition precludes optimal treatment even though the psychiatric treatment might be appropriate for the symptoms, often manifesting as inadequate response or psychotropic treatment resistance. Deficiency of vitamin B12 has a well-established association with a wide variety of neurologic and psychiatric presentations includes slowed mentation, delirium, affective disorder, personality change, and acute or chronic psychosis. We present here a 41 year-old female patient who was previously hospitalized and then followed as schizophrenia without remission. During our current hospitalization, laboratory investigations confirmed very low serum B12 level and consequent megaloblastic anemia. She recovered dramatically with short term antipsychotic medication and intramuscular vitamin B12 supplementation. She remained asymptomatic and functionally independent at four months follow up. This case underscores the importance of considering vitamin B12 deficiency in the differential diagnosis of patients with schizophrenia.

Evaluation of serum vitamin B12 levels in type 1 diabetics attending a tertiary care hospital: A preliminary cross - sectional study

Aims and Objectives:To estimate serum vitamin B12 levels in type 1 diabetes and to evaluate the influence of duration of diabetes, diabetic control, and age on B 12 levels.Importance of Study:Vitamin B12 deficiency is known to be associated with autoimmune disorders. However, currently there is very limited and controversial data regarding the prevalence of B12 deficiency in type 1 diabetes in South Indian population. If our study demonstrates the presence of low serum B12 levels in type1 diabetes in our population, a recommendation for regular screening and supplementation of vitamin B12 could be considered in these patients.Materials and Methods:This was a cross- sectional study. Ninety type 1 diabetic patients (44 males and 46 females) were randomly selected based on inclusion/ exclusion criteria from the diabetes registry at Bangalore Diabetes Centre. Serum vitamin B12 level and parameters for diabetic controls were estimated using fully automated methods. All statistical analysis was carried out using SPSS version 16.Results:The study showed that 45.5% of the diabetics had low B12 using the manufacturer's cut – off of 180 pg/mL and 54% had low B12 using the published cut – off of 148 pmol/l (200pg/mL). There was no significant difference in B12 levels between males and females (mean difference = - 14.3: P > 0.05). The study did not demonstrate any significant correlation between vitamin B12 levels and age, duration of diabetes, and diabetes control (the r values being – 0.18, - 0.11, and - 0.08 respectively and the P-value > 0.05).Conclusion:Results of our study shows the presence of low serum B12 levels in type 1 diabetics. These findings merits further research on a larger population to investigate into the cause of deficiency and the benefit of B12 supplementation in these patients.

Nutritional Supplements and its Effect on Quality of Life and Sleep

Problem statement: Inadequate sleep has been recognized as a risk factor for poor health status. Mental stress, body pains, melatonin deficiency, late night awakening disturbing the body clock are triggers for poor quality of sleep and fatigue. Fatigue due to insomnia is a major cause for poor quality of life. Evidences suggest certain nutrients to exert profound influence on quality of sleep which in turn could affect quality of life. In the present study we examine to study the effects of food and nutrients on sleep and quality of life. Approach: 800 subjects were screened for sleep quality and presence of insomnia out of which, 34 subjects of both sexes aged 21-45 years included for the “Nutrition Intervention Study”. Nutrients and food components were assessed by three days Diet Diary Method and Sleep quality was assessed by Sleep Behavior and Insomnia Screening Questionnaire (ISQ) as well as the Pittsburgh sleep quality index. Blood and urine parameters were examined by standard methods. A prepost assessment method was adopted. Subjects were assessed for blood parameters like-serum cortisol, vitamin B12, ferritin, iron and magnesium; urine profile included was pH and Sp.Gr. Intervention period was 15 days and subjects were divided in to three groups depending upon criteria of diagnosis, i.e., Gr.1, subjects (n = 12) with low serum B12 levels, who were given B12 injections. Gr. 2(n = 12) and Gr. 3: (n = 10) subjects respectively were provided with beet root and poppy seeds drinks to be consumed every night (4 h before bed time). Results: Beet root consumption increased the ferritin level. B12 level increased significantly with beet root powder intervention. B12 supplementation effectively increased (from 152.87±23.9-1375.6±804.4 pg mL-1) serum levels of this vitamin and the difference was extremely significant statistically (p<0.01). It was highly encouraging to note a significant reduction in cortisol levels with B12 supplementation within a period of 15 days. Mean value of ferritin increased after poppy seed intervention; this improvement can be attributed to the iron content of poppy seed. A decrease in serum cortisol level was also noted, the mean levels before and after intervention being 16.6±3.4-11.7±2.5 mcg dL-1 affect a mean reduction of 4.9 mcg dL-1, although a striking difference was observed, it was statistically not significant. The maximum improvement in insomnia was found with poppy seed drink (63.6%) followed by beet root drink and B12 supplementation which varied from 54.6 and 33.4% respectively. Improvement of anxiety as a factor affecting insomnia was noted in 20% of subjects in B12 and 66.6% in beetroot drink supplementation groups. It was encouraging to witness a 100% improvement in the group with poppy seed intervention. Significant improvement was noted in the Circadian rhythm disorder in all intervention groups Parasomnia and Restless Leg Syndrome (RLS) recovery was seen in all the intervention groups while highest proportion RLS improvement was noted in B12 group. (Please give data) Significant improvement was seen in sleep quality among all the intervention groups administered either vitamin B12, or beet root or poppy seeds. Marked reduction in co-morbid symptoms like fatigue, memory function and improvement in scores for quality of life was observed. Conclusion: Nutritional supplements appear to be effective in improving sleep quality which might influence quality of life.

Nutritional B12 Deficiency in Infants of Vitamin B12-Deficient Mothers

Nutritional vitamin B₁₂ deficiency in infants may occur because the maternal diet contains inadequate animal products. Clinical presentations of the infants who had nutritional vitamin B₁₂ deficiency were analyzed in this study. Patients with nutritional vitamin B₁₂ deficiency were enrolled in the study between 2003 and 2010. The diagnosis was based on a nutritional history of mothers and infants, clinical findings, hematological evaluation, and low level of serum vitamin B₁₂. Thirty children aged 1 - 21 months constituted the study group. Poverty was the main cause of inadequate consumption of animal products of the mothers. All infants had predominantly breastfed. The most common symptoms were developmental delay, paleness, apathy, lethargy, anorexia, and failure to thrive. Hematological findings were megaloblastic anemia (83.3 %), thrombocytopenia (30 %), and severe anemia (13.3 %). All of the mothers had low serum B₁₂ levels; eight of them had megaloblastic anemia. The unusual clinical manifestations of vitamin B₁₂ deficiency may also be seen apart from neurological and hematological findings. Nutritional vitamin B₁₂ deficiency due to maternal deficiency might be a serious health problem in infants. Therefore, screening and supplementation of pregnant and lactating women to prevent infantile vitamin B₁₂ deficiency should be considered.

Vitamin B12Deficiency and Depression in the Elderly

Vitamin B₁₂Deficiency and Depression in the Elderly

Association between vitamin B12-containing supplement consumption and prevalence of biochemically defined B12 deficiency in adults in NHANES III (Third National Health and Nutrition Examination Survey)

To explore the association between vitamin B(12) (B(12))-containing supplement use, low B(12) concentrations and biochemically defined B(12) deficiency in US adults. A cross-sectional study with adjustment for survey design. Prevalence ratios for two age groups (18-50 and >50 years) were estimated using unconditional logistic models. Outcome measures included prevalence of low serum B(12) concentration (<148 pmol/l) and biochemical B(12) deficiency (serum B(12)< 148 pmol/l with concomitant homocysteine > 10 mumol/l). A population survey of health and nutritional measures. Subjects were non-institutionalized adults, aged 18 years and older, who participated in Phase 2 of NHANES III (Third National Health and Nutrition Examination Survey). Low B(12) concentrations were less prevalent among persons consuming B(12)-containing supplements (P = 0.001) with an adjusted prevalence ratio of 0.6 (95 % CI 0.3, 1.0). Biochemical B(12) deficiency showed a similar trend (P = 0.0002), with an adjusted prevalence ratio of 0.3 (95 % CI 0.1, 0.8). Prevalence ratios were similar in adults >50 years of age, although the prevalence of low B(12) and biochemical deficiency was proportionally higher. Consumption of B(12)-containing supplements was associated with at least 50 % lower prevalence of both low serum B(12) and biochemical B12 deficiency in a nationally representative sample of US adults, suggesting increased consumption of B(12) from supplements or from fortified foods may reduce the prevalence of B(12) deficiency. Additionally, the current Recommended Daily Allowance for B(12) of 2.4 microg may be insufficient for those aged >50 years.