Nutritional Megaloblastic Anemia in Young Turkish Children is Associated With Vitamin B-12 Deficiency and Psychomotor Retardation

2006 ◽  
Vol 28 (9) ◽  
pp. 559-562 ◽  
Author(s):  
Selahattin Katar ◽  
Mehmet Nuri ??zbek ◽  
Ahmet Yaram?? ◽  
Sultan Ecer
2012 ◽  
Vol 4 (2) ◽  
pp. 326-328
Author(s):  
M Wadhwani ◽  
S Beri ◽  
A Saili ◽  
S Garg

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


2020 ◽  
Vol 62 (7) ◽  
pp. 864-865
Author(s):  
Jun Okamura ◽  
Yoshishige Miyake ◽  
Michi Kamei ◽  
Yasuhiko Ito ◽  
Tadashi Matsubayashi

2021 ◽  
pp. 36-38
Author(s):  
Manali Patil ◽  
S. N. Agrawal ◽  
V. V. Saoji

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.


2021 ◽  
pp. 35-38
Author(s):  
Anjali Sharma ◽  
Anand Deshpande ◽  
Chhavi Sauparna ◽  
Zeeshan Ahmed

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.


Blood ◽  
1960 ◽  
Vol 16 (5) ◽  
pp. 1546-1554 ◽  
Author(s):  
FARID I. HAURANI ◽  
GEORGE WANG ◽  
L. M. TOCANTINS

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.


2011 ◽  
Vol 81 (5) ◽  
pp. 328-334 ◽  
Author(s):  
Oya Halicioglu ◽  
Sezin Asik Akman ◽  
Sumer Sutcuoglu ◽  
Berna Atabay ◽  
Meral Turker ◽  
...  

Aim: 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. Subjects and Methods: 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. Results: 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. Conclusion: 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.


2006 ◽  
Vol 210 (S 5) ◽  
Author(s):  
N Haiden ◽  
K Klebermass ◽  
F Cardona ◽  
J Schwindt ◽  
A Berger ◽  
...  

2006 ◽  
Vol 210 (S 5) ◽  
Author(s):  
N Haiden ◽  
K Klebermass ◽  
F Cardona ◽  
J Schwindt ◽  
A Berger ◽  
...  

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