Three infants with megaloblastic anemia caused by maternal vitamin B 12 deficiency

2020 ◽  
Vol 62 (7) ◽  
pp. 864-865
Author(s):  
Jun Okamura ◽  
Yoshishige Miyake ◽  
Michi Kamei ◽  
Yasuhiko Ito ◽  
Tadashi Matsubayashi
Keyword(s):  
Megaloblastic Anemia ◽  
Vitamin B ◽  
Maternal Vitamin ◽  
Vitamin B 12

Maternal vitamin B-12 and folate status during pregnancy and excessive infant crying

2011 ◽  
Vol 87 (4) ◽  
pp. 309-314 ◽  
Author(s):  
Geertje Goedhart ◽  
Marcel F. van der Wal ◽  
Manon van Eijsden ◽  
Gouke J. Bonsel
Keyword(s):  
Vitamin B ◽  
Maternal Vitamin ◽  
Infant Crying ◽  
Folate Status ◽  
Vitamin B 12

scholarly journals Homocystinuria masquerading as vitamin B12 deficiency

2012 ◽  
Vol 4 (2) ◽  
pp. 326-328
Author(s):  
M Wadhwani ◽  
S Beri ◽  
A Saili ◽  
S Garg
Keyword(s):  
Vitamin B12 ◽  
Megaloblastic Anemia ◽  
Vitamin B12 Deficiency ◽  
Interesting Case ◽  
Vitamin B ◽  
Ophthalmological Examination ◽  
Ophthalmic Manifestations ◽  
History Of ◽  
B12 Deficiency ◽  
Vitamin B 12

Background: Homocystinuria is a rare metabolic disorder charcterised by excess homocysteine in the urine. Vitamin B12 deficiency has diverse cutaneous, nervous and ophthalmic manifestations. Objective: To report a case of homocystinuria masquerading as vitamin B 12 deficiency. Case: We hereby are presenting an interesting case of a 4 year old boy who was being treated for Vitamin B 12 deficiency on the basis of history of delayed milestone, abdominal pain and hyperpigmentation of skin which was diagnosed as homocystinuria. Conclusion: It is important to carry out ophthalmological examination in every case of megaloblastic anemia if associated with blurring of vision and mental retardation.DOI: http://dx.doi.org/10.3126/nepjoph.v4i2.6554 Nepal J Ophthalmol 2012; 4 (8): 326-328

scholarly journals Low Maternal Vitamin B-12 Status Is Associated with Offspring Insulin Resistance Regardless of Antenatal Micronutrient Supplementation in Rural Nepal

2011 ◽  
Vol 141 (10) ◽  
pp. 1912-1917 ◽  
Author(s):  
Christine P. Stewart ◽  
Parul Christian ◽  
Kerry J. Schulze ◽  
Margia Arguello ◽  
Steven C. LeClerq ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Vitamin B ◽  
Micronutrient Supplementation ◽  
Maternal Vitamin ◽  
Vitamin B 12 ◽  
Rural Nepal

scholarly journals KNUCKLE HYPERPIGMENTATION AS A PRELIMINARY MARKER OF VITAMIN B 12 DEFICIENCY: A CASE SERIES

2021 ◽  
pp. 36-38
Author(s):  
Manali Patil ◽  
S. N. Agrawal ◽  
V. V. Saoji
Keyword(s):  
Vitamin B12 ◽  
Megaloblastic Anemia ◽  
Case Series ◽  
Vitamin B12 Deficiency ◽  
Neurological Deficits ◽  
Vitamin B ◽  
Important Clue ◽  
B12 Deficiency ◽  
Systemic Manifestations ◽  
Vitamin B 12

Vitamin B12 deficiency is common in vegetarian population in India and can present with variable Hematological (megaloblastic anemia), Neuropsychiatric, Mucocutaneous (glossitis, angular stomatitis), Skin (pallor, hyperpigmentation) and Hair changes (dry, brittle, thin, lustreless, prematurely grey). Knuckle hyperpigmentation has been described in vitamin B12 deficiency but usually these patients are dermatologically asymptomatic but they have systemic manifestations like megaloblastic anemia, pancytopenia or neurological deficits. The foreground of this study is highlighting the importance of knuckle hyperpigmentation as an early cutaneous sign of vitamin B12 deficiency which points an important clue towards the aetiology of Megaloblastic anemia.

CLINICAL AND EPIDEMIOLOGICAL PROFILE OF CHILDREN WITH MEGALOBLASTIC ANEMIA AT A TERTIARY CARE HOSPITAL IN WESTERN INDIA: A CROSS SECTIONAL STUDY

2021 ◽  
pp. 35-38
Author(s):  
Anjali Sharma ◽  
Anand Deshpande ◽  
Chhavi Sauparna ◽  
Zeeshan Ahmed
Keyword(s):  
Bone Marrow ◽  
Folic Acid ◽  
Vitamin B12 ◽  
Megaloblastic Anemia ◽  
Tertiary Care ◽  
Neurological Manifestation ◽  
Vitamin B ◽  
Western India ◽  
Care Hospital ◽  
Vitamin B 12

Background: In India most cases of Megaloblastic anemia are caused by nutritional deciency of vitamin B12 and Folic acid. Initial workup include Complete Blood Count(CBC), Peripheral blood smear(PBS) ,Vitamin B12 asssay, folic acid assay and Bone marrow if required. Therefore, this study is planned to study the clinical and laboratory prole of children with Megaloblastic anemia and to study the clinical outcome of children with Megaloblastic anemia Methods: The study was a prospective observational study conducted among 60 children with megaloblastic anemia, aged 1- 12 years. Demographic data, clinical symptoms and signs, laboratory ndings, serum B12 and Folic acid ,Bone marrow report and stool routine microscopy report were collected. Chi square test was applied. Results: Among the 60 children 40% were female sand 60% were males. The age of the study population ranged from a minimum of 1 month to a maximum of 12 years with a mean(SD) of 8.08 (± 5.45).Majority of children (41.6%) were in age group of 6 months- 1 year. Most common symptoms fever and most common sign is pallor. More than fty percent cases presented with severe anemia. Many cases reported late, leading to delay in diagnosis leads to poor outcome. Developmental delay (neurological manifestation) is strongly associated with vitamin B 12 deciency as compared to folic acid deciency. (p value <0.05) Conclusions: There is a slight female preponderance seen in megaloblastic anemia, probably due to reduced attention to girl children in the study group. neurological manifestation is strongly associated with vitamin B 12 deciency as compared to folic acid deciency.

scholarly journals Megaloblastic Anemia Probably Caused by Defective Utilization of Folinic Acid

Blood ◽  
1960 ◽  
Vol 16 (5) ◽  
pp. 1546-1554 ◽  
Author(s):  
FARID I. HAURANI ◽  
GEORGE WANG ◽  
L. M. TOCANTINS
Keyword(s):  
Folic Acid ◽  
Vitamin C ◽  
Clinical Response ◽  
Folinic Acid ◽  
Similar Condition ◽  
Megaloblastic Anemia ◽  
Vitamin B ◽  
Negro Girl ◽  
Vitamin B 12 ◽  
Hereditary Nature

Abstract A 12 year old negro girl was studied who presented a picture of megaloblastic anemia refractory to physiologic doses of vitamin B-12 and to folic acid. However, remission could be induced and maintained by pharmacologic doses of vitamin B-12 (1000 µg. per week), by folinic acid or by a combination of vitamin C (or homocysteine) and folic acid. Folinic acid determinations and the clinical response to various metabolites indicated the existence of a metabolic defect in the utilization of folinic acid. The hereditary nature of this defect was suggested by the fact that two siblings might have had a similar condition.

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