Vitamin B9 ,folate ,folic acid deficiency , megaloblastic anemia , Neural tube disorders .

1. Gunjita Negi
AIIMS Rishikesh

2. Folate
 Folic acid , folate or vitamin B9 consists of 3
components -
Pteridine ring
PABA(p-amino benzoic acid)
Glutamic acid residue (1-7)
Hence it is known as Pteroyl-glutamic acid.
 Tetrahydrofolate (THF) is the reduced ,active form of
folic acid.

3. Biochemical Functions
 THF , the coenzyme ,receives one carbon fragments from
donors such as serine ,glycine and histidine and transfers
them to intermediates in the synthesis of amino acids,
purines, TMP .

4. RDA
 Men – 0.1mg/day
 Women-0.1mg/day
 Pregnancy-0.4mg/day
 Lactation-0.15mg/day

5. Deficiency
 Dietary
• Inadequate intake – seen in alcoholics
• Overcooking of food –loss of folic acid activity
 Impaired absorption- small intestine disease
 Drug interference – eg methotrexate
 Increased demand – pregnancy
 Hemolytic anemia
 Other-loss , as seen in patients undergoing dialysis

6. Clinical manifestation
 Megaloblastic anemia
accumulation of large, immature RBC
precursors(megaloblasts)- due to diminished purine
and TMP synthesis
hyperchromic macrocytic anemia

7. Biochemical Findings
 Low plasma folic acid levels (<3ng/ml)
 Low red cell folic acid levels (<150ng/ml)
 Normal plasma Vitamin B12 levels
 Increased plasma LDH levels

8. Neural Tube Defects
 Folic acid deficiency results in impaired and aberrant
neural tube defects.
 Anencephaly and spina bifida –most common NTDs
 This is because critical folate dependant development
occurs in first weeks of fetal life.
 Folic acid supplementation during the first trimester
greatly reduces NTDs.

9. Spina bifida and anencephaly

10. Homocysteinemia
 Homocysteine is a risk factor for CHD
 Folic acid is required for the conversion of
homocysteine to methionine
 Deficiency will result in increased
 levels of homocystiene