Mean Serum B12 Research Articles

Ramifications of Pancytopenia in Children in a Tertiary Care Center in North Indian

BACKGROUND: Pancytopenia generally suggests the likelihood of bone marrow failure syndromes or leukemias. However, other easily treatable entities can also cause pancytopenia. To know the underlying cause of pancytopenia is essential for definite management and prognosis. AIM: The aim of this study is to study the prevalence, clinico-hematological profile, and etiology of pancytopenia in hospitalized children of 1 month to 18 years of age. METHODS: Descriptive study conducted in a tertiary care center included children of age 1 month to 18 years hospitalized with pancytopenia. Sociodemographic data, presenting complaints, and detailed history were noted. Detailed clinical examination and relevant investigations were done. RESULTS: The prevalence of pancytopenia was 2%. Majority of the patients were >10 years of age. Female: Male ratio was 1.15:1. The most common presentation was progressive pallor, followed by fever, icterus, and bleeding manifestations. The most common clinical examination finding was pallor, followed by splenomegaly, hepatomegaly, icterus, and lymphadenopathy. Macrocytic blood picture was most common, followed by microcytic, atypical cells, and normocytic picture. Mean serum ferritin (ng/ml) was 374.77 ± 1662.64. Mean serum B12 (pg/ml) was 117.72 ± 64.71. In bone marrow aspirate examination, megaloblastic erythropoiesis was most common, followed by normoblastic erythropoiesis, dual deficiency, malignant cells of lymphoid series, hypocellular marrow, and malignant cells of myeloid series. Megaloblastic anemia was the most common etiology, followed by dimorphic anemia amid acute leukemia. CONCLUSION: The study showed that megaloblastic anemia and infections (tuberculosis, dengue fever, and enteric fever) both of which are eminently treatable, cause nearly 65% of pancytopenia cases in pediatric patients.

Nitrous oxide-induced myeloneuropathy.

Nitrous oxide misuse is a recognized issue worldwide. Prolonged misuse inactivates vitamin B12, causing a myeloneuropathy. Twenty patients presenting between 2016 and 2020 to tertiary hospitals in Sydney with myeloneuropathy due to nitrous oxide misuse were reviewed. The average age was 24years, and mean canister consumption was 148 per day for 9months. At presentation, paresthesias and gait unsteadiness were common, and seven patients were bedbound. Mean serum B12 was normal (258pmol/L, normal range [NR]=140-750) as was active B12 (87pmol/L, normal>35). In contrast, mean serum homocysteine was high (51μmol/L, NR=5-15). Spinal magnetic resonance imaging (MRI) showed characteristic dorsal column T2 hyperintensities in all 20 patients. Nerve conduction studies showed a predominantly axonal sensorimotor neuropathy (n=5). Patients were treated with intramuscular vitamin B12, with variable functional recovery. Three of the seven patients who were bedbound at presentation were able to walk again with an aid at discharge. Of eight patients with follow-up data, most had persistent paresthesias and/or sensory ataxia. Mobility scores at admission and discharge were not significantly correlated with the serum total and active B12 levels or cumulative nitrous oxide use. There were no significant trends between serum active B12 level and cumulative nitrous oxide use (Spearman rho = -0.331, p=0.195). Nitrous oxide misuse can cause a severe but potentially reversible subacute myeloneuropathy. Serum and active B12 can be normal, while elevated homocysteine and dorsal column high T2 signal on MRI strongly suggest the diagnosis. Neurological deficits can improve with abstinence and B12 supplementation, even in the most severely affected patients.

Abstract 50: Elevated Serum Cobalamin associated Increased Mortality in Advanced Heart Failure

Introduction: Elevated serum cobalamin (B12) has been associated with liver dysfunction in decompensated heart failure. We hypothesize that elevated B12 is associated with worse outcomes in advanced heart failure. Methods: We examined 115 consecutive patients with advanced heart failure undergoing evaluation for advanced therapies. Patients receiving B12 injections were excluded. Our lab considers B12 >900pg/mL as elevated. Linear regression was performed to determine significant predictors. Survival was assessed by Kaplan Meier curves. Results: Mean and median serum B12: 843± 362pg/mL, 795 pg/mL (IQR 551-1046). Patients with elevated values were more likely to be have diabetes, dyslipidemia, COPD, CAD, and CKD. Less likely to be on spironolactone or be transplanted. Patients had higher total bilirubin and RDW; lower MVO2 and cardiac index. Hepatic, cholestatic, inflammatory and renal biomarkers were not found to be predictive of elevated B12, but MVO 2 (OR: 0.93, [95%CI 0.87,0.99]) was. At 2-yr, transplanted patients with increased B12 had higher mortality (logrank p=0.006). Conclusions: Serum B12 is elevated in patients with advanced heart failure. Decreased MVO2 and markers of chronic inflammation are predictive of higher B12 levels. Elevated B12 is a significant predictor of mortality. Mechanistic studies of B12 in heart failure could provide key insights into the complexity of heart failure pathophysiology. Figure 1: Survival Analysis of Elevated versus normal Serum B12 levels

Behavioural and Psychological Symptoms of Alzheimer Type Dementia Are Not Correlated with Plasma Homocysteine Concentration

Background/Aims: Vitamin B12 and folate deficiencies have been associated with cognitive impairment and various psychiatric symptoms but not specifically with behavioural and psychological symptoms of dementia (BPSD). A limitation of previous studies in dementia was lack of concurrent homocysteine measurement especially as it may provide a better indicator of tissue activities of these vitamins. This study was designed to clarify whether a relationship exists between plasma homocysteine concentration and BPSD. Methods: Plasma homocysteine, serum vitamin B12 and folate were measured in23Alzheimer’s disease (AD) patients with BPSD and 27 AD patients without BPSD as determined through the use of the Neuropsychiatric Inventory (NPI). Blood levels of measured substances were also correlated with individual NPI scores and with cumulative NPI scores for different cluster of symptoms. Results: There was no significant difference (p = 0.956) in the mean plasma homocysteine levels between AD patients with BPSD (17.48 µmol/l) and AD patients without BPSD (17.34 µmol/l). Similarly, there was no significant difference between the two groups in the mean serum B12 (382.61 and 391.60 pg/ml, respectively) and folate (7.95 and 10.02 ng/ml, respectively). Mean levels for both vitamins were well within the laboratory reference range. Neither individual nor cluster NPI scores correlated significantly with plasma homocysteine. Conclusion: This study shows for the first time that BPSD are not associated with hyperhomocysteinaemia in Alzheimer dementia. Although previous studies have identified homocysteine as an independent risk factor in AD, the results reported here do not lend weight to an aetiological role for homocysteine specifically in BPSD.