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Vitamin D3 And B12

Division of Drugs, Bombay Hospital Institute of Medical Sciences and Analysis, Mumbai, Maharashtra, India

Summary

Introduction

Dietary deficiencies are the commonest reason behind anemia within the tropical international locations.[1] Deficiencies of vitamin B12 and folate could cause extreme anemia and cytopenias as a result of ineffective hematopoiesis and may typically mirror hemolytic anemia. Additionally megaloblastic anemia, presenting solely as pyrexia, will be present in solely a small proportion of circumstances and is poorly characterised. This etiology can typically be missed and delay the prognosis if not actively regarded for in circumstances pyrexia of unknown origin (PUO).

Case Report

After 2 weeks, on follow-up, affected person was afebrile and repeat ranges of vitamin B12 ranges had been 2000 pg/l, LDH had decreased to-341 mU/ml, complete bilirubin to 0.5 mg/dl (with oblique bilirubin-0.1mg/dl) and homocsyteine had decreased to12 micromoles/l. The repeat CBC is as proven in [Table 1].

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Dialogue

A differential prognosis of fever, hemolytic anemia, and thrombocytopenia can vary from infections like malaria, dengue, cytomegalovirus, Ebstein barr virus, parvovirus, infective endocarditis, autoimmune dysfunction (systemic lupus erythromatosis), vasculitis, hemolytic uremic syndrome, thrombotic thrombocytopenic purpura (TTP), autoimmune hemolytic anemia/Evan’s syndrome, and so forth. The presence of very excessive LDH ranges and a low reticulocyte rely and a comparatively milder thrombocytopenia in our affected person additionally favors the trigger as pseudo-thrombotic microangiopathy (TMA) brought on by cobalamin deficiency over TTP.[5] Though testing for ADAMTS-13 ranges would have been best whether it is obtainable to rule out TTP. TTP and HUS had been dominated out as a result of absence of precipitating trigger (although not all the time essential), renal dysfunction and psychological adjustments.

Conclusion

All sufferers presenting with pyrexia and cytopenia with hemolytic image ought to be fastidiously evaluated for attainable vitamin B12 and folate deficiency so as to stop the pointless burden of investigations and coverings. Presence of hyperhomocysteinemia and hypovitaminosis D-induced hypophosphatemia in vitamin B12 deficiency are further danger issue for extreme hemolysis in megaloblastic anemias. Extra research evaluating the attainable roles of cytokine signaling and bone marrow stromal microenvironment would possibly assist in understanding the pathophysiological mechanism of pyrexia in megaloblastic anemia.

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Footnotes

References

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