Megaloblastic Anemia and Other Causes of Macrocytosis

Department of Internal Medicine, Marshfield Clinic, 1000 North Oak Avenue, Marshfield, WI 54449, USA.
Clinical Medicine &amp Research 10/2006; 4(3):236-41. DOI: 10.3121/cmr.4.3.236
Source: PubMed
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    • "Vitamin B12 deficiency is classically associated with overt haematological findings like macrocytic red blood cells (mean cell volume [MCV]> 100 fl) with/without anaemia, ovalocytes, hyper segmented white blood cells (i.e. >5% of neutrophils with ≥5 lobes) and pancytopenia [9]. Due to defective cell repair processes, atrophic glossitis, stomatitis and malabsorption due to villi atrophy and mucositis are also common. "
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    ABSTRACT: Vitamin B12 is an essential micronutrient required for optimal hemopoetic, neuro-cognitive and cardiovascular function. Biochemical and clinical vitamin B12 deficiency has been demonstrated to be highly prevalent among patients with type 1 and type 2 diabetes mellitus. It presents with diverse clinical manifestations ranging from impaired memory, dementia, delirium, peripheral neuropathy, sub acute combined degeneration of the spinal cord, megaloblastic anemia and pancytopenia. This review article offers a current perspective on the physiological roles of vitamin B12, proposed pathophysiological mechanisms of vitamin B12 deficiency, screening for vitamin B12 deficiency and vitamin B12 supplementation among patients with diabetes mellitus.
    Journal of Diabetes and Metabolic Disorders 05/2013; 12(1):17. DOI:10.1186/2251-6581-12-17
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    • "Number of red blood cells was slightly decreased (Fig. 2A), the mean corpuscular volume (Fig. 2B) and mean corpuscular hemoglobin (Fig. 2C) were significantly increased. This observation might indicate impaired cell division during erythropoiesis [34]. "
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    ABSTRACT: Nuclear myosin I (NM1) is a nuclear isoform of the well-known "cytoplasmic" Myosin 1c protein (Myo1c). Located on the 11(th) chromosome in mice, NM1 results from an alternative start of transcription of the Myo1c gene adding an extra 16 amino acids at the N-terminus. Previous studies revealed its roles in RNA Polymerase I and RNA Polymerase II transcription, chromatin remodeling, and chromosomal movements. Its nuclear localization signal is localized in the middle of the molecule and therefore directs both Myosin 1c isoforms to the nucleus. In order to trace specific functions of the NM1 isoform, we generated mice lacking the NM1 start codon without affecting the cytoplasmic Myo1c protein. Mutant mice were analyzed in a comprehensive phenotypic screen in cooperation with the German Mouse Clinic. Strikingly, no obvious phenotype related to previously described functions has been observed. However, we found minor changes in bone mineral density and the number and size of red blood cells in knock-out mice, which are most probably not related to previously described functions of NM1 in the nucleus. In Myo1c/NM1 depleted U2OS cells, the level of Pol I transcription was restored by overexpression of shRNA-resistant mouse Myo1c. Moreover, we found Myo1c interacting with Pol II. The ratio between Myo1c and NM1 proteins were similar in the nucleus and deletion of NM1 did not cause any compensatory overexpression of Myo1c protein. We observed that Myo1c can replace NM1 in its nuclear functions. Amount of both proteins is nearly equal and NM1 knock-out does not cause any compensatory overexpression of Myo1c. We therefore suggest that both isoforms can substitute each other in nuclear processes.
    PLoS ONE 04/2013; 8(4):e61406. DOI:10.1371/journal.pone.0061406 · 3.23 Impact Factor
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    • "Macrocytosis is considered a structural and functional abnormality of the erythrocyte membrane. The spectrum of etiologies associated with macrocytosis accompanied by anemia includes malnutrition, such as vitamin B12 and folate deficiency, use of chemotherapeutic and anticonvulsant agents, alcoholism with chronic liver damage, chronic obstructive pulmonary disease (COPD) and bone marrow disorders [18] [19]. In the present study, although univariate analysis showed significant differences between patients with and without macrocytosis in age, BMI and prescription of statins (Table 1), multivariate analysis using multiple logistic regression analysis showed that only advanced age (75 years old) and low prescription rate of statins were significant and independent predictors of macrocytosis. "
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    ABSTRACT: Macrocytosis, as a qualitative abnormality of erythrocytes, has not drawn attention as a prognostic indicator after PCI, while anemia, as a quantitative abnormality of erythrocytes, has been recognized as a predictor of adverse outcomes. The aim of this study was to perform prognostic risk stratification of patients after PCI based on the presence or absence of macrocytosis. The clinical records of 941 consecutive patients who underwent PCI at a single institution were retrospectively reviewed. The prognostic implication of macrocytosis was evaluated by univariate and multivariate Cox's proportional hazard regression analysis. There were 130 (13.8%) patients with macrocytosis. A significantly higher all-cause and cardiac mortality, as well as incidence of composite adverse events were observed in the Macrocytic group. Kaplan-Meier analysis also showed a significantly poorer overall survival in patients with macrocytosis. Even after exclusion of anemic patients, this tendency was still observed. Furthermore, macrocytosis was significantly and independently associated with adverse outcomes after PCI (aHR of cardiac death: 3.45, 95%CI: 1.22-9.80, P=0.019). Interestingly, fewer patients with macrocytosis were prescribed statins compared with those without it (33.8% vs. 47.1%, P=0.005). The results of the study indicate that measuring mean corpuscular volume (MCV) as a qualitative index of erythrocytes might be helpful for a prognostic risk stratification of patients subjected to PCI.
    Atherosclerosis 03/2012; 221(1):148-53. DOI:10.1016/j.atherosclerosis.2011.11.044 · 3.99 Impact Factor
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