Water Soluble Vitamins

VITAMINS 

HISTORICAL BACKGROUND THIAMIN, ASCORBIC ACID, (VIT-A) (NIGHT BLINDNESS) [BERI – BERI] (SCURVY)

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DEFINITION: ESSENTIAL ORGANIC MICRONUTRIENTS MUST BE PROVIDED REGULARLY IN THE DIET FAT SOLUBLE, WATER SOLUBLE VITAMINS

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WATER SOLUBLE VITAMINS (FEATURES)

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NOT STORED EXCEPT VIT B12 NO TOXICITY BUT EXCESS EXCRETED IN URINE CO-ENZYMES IN METABOLIC PROCESSES OF CARBOHYDRATES, PROTEIN AND LIPID METABOLISM RESPIRATORY CHAIN

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WATER SOLUBLE VITAMINS 1. 2.

3.

4.

5.

THIAMINE (B-1) [BERI BERI] RIBOFLAVIN (B-2) [CHEILOSIS, GLOSSITIS, SEBHORRHOEA] NIACIN (B-3) [PELLEGRA PREVENTING FACTOR] PANTOTHENIC ACID (B-5) [Co-A SH] & [ACP] PYRIDOXINE (B-6) [PERIPHERAL NEURITIS)

6. BIOTIN (CO2 FIXATION) 7. COBALAMINES (B-12) [MEGALOBLASTIC AND PERNICIOUS ANAEMIA, METHYLMALONYL ACIDURIA HOMOCYSTEINMIA] 8. FOLIC ACID (MEGALOBLASTIC ANAEMIA) 9. ASCORBIC ACID (VIT C) [SCURVY]

THIAMINE( B – 1) 



ACTIVE THIAMINE IS THIAMINE DIPHOSPHATE ACTIVATION IN BRAIN & LIVER

1. BIOCHEMICAL ROLL OF THIAMINE (VIT – B1)

a. AN OXIDATIVE DECARBOXYLATION OF αKETO ACIDS PYRUVATE ACETYL COA o ENZYME PYRUVATE DEHYDROGENASE b.α -KETOGLUTARATE SUCCINYL COA o ENZYME α -KG DEHYDROGENASE c. α -KETOANALOGS OF BRANCHED CHAIN A ACIDS 

d. o   

TRANSKETOLASE REACTION (HMP)

ACTIVITY OF TRANSKETOLASE IS DECREASED IN VIT B1 DEFICIENCY RIBOSE-5P + XYLULOSE-5P SEDUHEPTULOSE + GLYCER ALDEYDE-3P XYLULOSE-5P + ERYTHROSE-4P FRUCTOSE-6P + GYCERALDEHYDE -3P GLYCERALDEHYDE – 3P + SEDUHEPTULOSE-7P FRUCTOSE – 6P + ERYTHROSE – 4P

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THIAMINE DEFICIENCY [BERI BERI]

HIGH CHO DIET, HEAVY ALCOHOL, I-V GLUCOSE AEROBIC METABOLISM OF GLUCOSE IS DISTURBED AND CELLS CAN NOT UTILIZE GLUCOSE (BRAIN) ACCUMULATION OF PYRUVIC AND LACTIC ACID CARDIAC FAILURE, PERIPHERAL NEUROPATHY & ENCEPHLOPATHY

TYPES OF BERI BERI (SEVERE WEAKNESS EVEN PARALYSIS)

1. WET AND DRY BERI BERI PREGNANCY, 2. INFANTILE BERI BERI LACTATIN 3. WERNICK’S ENCAPHELOPATHY INFANTS, AND 4. KORSAKOFF’S PSYCHOSIS DIALYSIS PRECIPITATE

WET BERI BERI

1. MECHANISM  ACCUMULATION OF PYRUVIC ACID AND LACTIC ACID, PERIPHERAL VASO DILATATION, Na+ RETENTION  HYPOPROTEINEMIA 2. CLINICAL FEATURES  HIGH CARDIAC OUTPUT FAILURE, OEDEMA  ECG CHANGES (INVERTED T WAVE , CONDUCTION DEFECTS), TACHYCARDIA, PRECARDIAL PAIN  SKIN FIRST WARM THEN LATER COLD 3. LAB TEST  PYRUVIC ACID AND LACTIC ACID INCREASED  LOW TRANSKETOLASE ACTIVITY IN RBCs  PLASMA AND URINARY THIAMIN LOW

DRY BERI BERI 

LONG STANDING DEFICIENCY OF VIT B1

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DEGENERATION AND DEMYELINATION OF SENSORY AND MOTOR NERVES MUSCLE WASTING, CALF MUSCLE BLOOD PYRUVIC ACID AND LACTATE ARE NORMAL PERIPHERAL NEUROPATHY (DUE TO COMBINED DEFICIENCYOF B GROUP e.g. B6, NIACIN & B12

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REFLEXES ARE LOW (KNEE JERK)

WERNICK’S ENCAPHALOPATHY 

OCCURS IN ALCOHALICS WITH DEFICIENCY OF VIT B1 IN DIET. PURELY INVOLVE CEREBRAL CORTEX

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CLINICAL FEATURES [IN ALCOHALICS, DIET DEF IN B1]

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CONFUSION, BILATERAL OPHTHALMOPLEGIA, ATAXIA, APATHY, DROWSINESS TRANSKETOLASE ACTIVITY IS LOW

KORSAKOFF’S PSYCHOSIS 

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UNTREATED WERNICK’S ENCAPHALOPATHY LEADS TO PERMANENT DAMAGE OF THE BRAIN PROFOUND IMPAIRMENT OF MEMORY, OTHERWISE CONSCOIUS INDIVIDUAL INCAPABLE OF LIVING INDEPENDENTLY REQUIRES INSTITUTIONAL CARE

RIBOFLAVIN (VIT B2)

RIBOFLAVIN (VIT B2) 1. SOURCE: YEAST, LIVER, KIDNEY, MILK. YELLOW FLORESCENT PIGMENT. DECOMPOSES IN LIGHT, HEAT STABLE IN LEAFY VEG. [MILK EXPOSED TO LIGHT] 2. BIOCHEMICAL ROLE ACTIVE FORM IS FLAVIN MONONEUCLEOTIDE (FMN) AND FLAVIN ADENINE DINEUCLEOTIDE (FAD). THESE ARE CALLED FLAVO PROTEINS [CONTAIN Mb & Fe] FLAVIN + ATP FMN FAD  SERVES AS CO-ENZYME OF OXIDO REDUCTASES ENZYMES

1. 2. 3. 4. 5. 6. 7. 8. 9.

α -AMINO OXIDASE (DEAMINATION) XANTHINEOXIDASE (PURINE CATABOLISM) ALDEHYDE DH (ALDEHYDE DEGRADATION) GLYCEROL-3-P DH [TPT OF REDUCING EQUIVALENT] SUCCINATE DH (TCA) ACYL-COA DH AND ELECTRON TRANSFER PROTEIN (FATTY ACID OXIDATION) OXIDATIVE DECARBOXYLATION (PYRUVATE AND α -KETOGLUTARATE) ELECTRON TRANSPORT CHAIN FAD AS COENZYME TO GLUTATHIONE REDUCTASE

DEFICIENCY 

CAUSES:

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SENSITIVE TO BOILING IN ALKALINE MEDIUM SENSITIVE TO UV LIGHT (VIT IS STORED IN BROWN BOTTLE) NEONATES WITH INCREASED SERUM BILIRUBIN TREATED BY PHOTOTHERAPY

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1. 

ANGULAR STOMATITIS

NOT SPECIFIC. RESULT DUE TO COMBINED DEFICIENCY OF NIACIN, PYRIDOXIN & IRON.\ CAN FOLLOW HERPES FIBRILIS AT THE ANGLES OF MOUTH

2. CHEILOSIS IS ZONE OF RED DENUDED EPITHELIUM AT THE LINE OF CLOSURE OF LIPS. COMBINED WITH NIACIN i.e. ALSO IN PELLAGRA 3. NASOLABIAL DYSSEBACEA (SCALINESS / GREASINESS)  CAN ALSO OCCUR IN PELLAGRA 4. VASCULARIZATOIN OF CORNEA 5. MAGENTAL COLOUR TONGUE AND ANAEMIA  DEFICIENCY IN EXPERIMENTAL ANIMALS INDUCE BIRTH DEFECTS DURING PREGNANCY  DIAGNOSIS  LOW ERYTHROCYTE GLUTATHIONE REDUCTASE ACTIVITY

NIACIN (VIT- B-3)

NIACIN (VIT- B-3) 

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SOURCE: WIDELY DISTRIBUTED PLANTS AND ANIMALS, COFFEE GOOD SOURCE, LIVER, MEAT, FISH TRYPTOPHAN (60 mg) CONVERTED TO VIT B6 (1mg) RESISTANT TO HEAT. DIFFERENT NAMES AS NIACIN, NICOTINAMIDE AND NICOTINIC ACID 60 GRAMS PROTEIN = 10 mg NIACIN

BIOCHEMICAL ROLE

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ACTIVE NIACIN IS NICOTINAMIDE ADENINE DINUCLEOTIDE (NAD) AND NICOTINAMIDE ADENINE DINUCLEOTIDE PHOSPHATE (NADP) NAD AND NADP ARE CO-ENZYMES OF ENZYMES OXIDOREDUCTASES [ADDITI OF H+ ION H+]

1. THEY ARE KEY COMPONENTS OF METABOLIC PATHWAYS FOR CARBOHYDRATES, LIPIDS AND AMINO ACID METABOLISM (TCA, HMP) 2. CO-ENZYME FOR DEHYDROGENASES ENZYMES  LACTATE DEHYROGENASE IN CYTOSOL  MALATE DEHYDROGENASE IN MITOCHONDRIA 3. NADP LINKED DH OR REDUCTASES IN CYTOSOL FOR REDUCTIVE SYNTHESIS OF CHO AND LIPIDS 4. PART OF RESPIRATORY CHAIN 5. PYRUVATE DEHYDROGENASE 6. α-KETOGLUTARATE DEHYDROGENASE 7. DECREASES CHOLESTEROL

NIACIN DEFICIENCY (PELLAGRA SYNDROME) 1. 

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WHEN STAPLE DIET IS MAIZE (NIACIN IS IN BOUND FROM i.e. NIACYTIN IN MAIZE) MAIZE IS ALSO DEFICIENT IN TRYPTOPHAN. HIGHLY LEUCIN DIET ALCOHOLICS WITH POOR DIET. VIT B6 LOW DIET HEARTNUP’S DISEASE, INH, CARCINOID SYNDROME

2. 

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CLINICAL FEATURES, DISEASE OF THREE Ds

DERMATITIS, DIARRHEA, DEMENTIA, WEIGHT LOSS, DEPRESSION

a. 

CAUSES:

SKIN (DERMATITIS)

ERYTHEMA AROUND THE NECK IN CHILD LEADING TO VESICULAION, EXUDATION AND ULCERS VULVA, PERINIAL AREA ALSO INVOLVED

b. ALIMENTARY TRACT [NON INFECTIVE INFLAMATION] ANNOREXIA, NAUSIA, DYSPHAGIA  GLOSSITIS, ANGULAR STOMATITIS LEADING TO INFLAMMATION OF GIT AND DIARRHEA 

c. NERVOUS SYSTEM (DELIRIUM AND DEMENTIA) URINARY METHYL NICOTINAMIDE OR RBC NAD IS THE BIOCHEMICAL TEST FOR DIAGNOSIS MANAGEMENT: 

d.

1.HIGH PROTEIN DIET 2. VIT B COMPLEX 3.

ALCOHOL SHOULD BE AVOIDED

PYRIDOXINE (VIT B6)

PYRIDOXINE (VIT B6)   

SOURCE: WIDELY DISTRIBUTED IN PLANTS, LIVER, EGG, FRUIT [BANANA] WHOLE GRAIN CEREALS FORMS: PYRIDOXINE, PYRIDOXAL, PYRIDOXAMINE, ALL HAVE EQUAL VIT ACTIVITY

BIOCHEMICAL ROLE  

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PYRIDOXAL PHOSPHATE IS THE COENZYME OF SEVERAL ENZYMES OF AMINO ACID METABOLISM ACTIVATED TO PYRIDOXAL PHOSPHATE IN BODY PYRIDOXAL PYRIDOXAL PYRIDOXAL PO4 (PLP) + ATP KINASE

1. CO-ENZYME OF AMINO ACID METABOLISM i. TRANSAMINATION (SGOT, SGPT) ii. DECARBOXYLATION OF DOPA TO DOPAMINE ALDOLASE iii. THREONINE GLYCINE + ACETALDEHYDE iv. TRYPTOPHANE DEGRADATION 2. CO-ENZYME FOR GLYGENOLYSIS  INTEGRAL PART OF PHOSPHORELASE: 70-80% VIT B6 IS WITH MUSCLE PHOSPHORELASE 3. CO-ENZYME FOR SYNTHESIS OF DELTA AMINO LEVULINIC ACID (PORPHYRIN SYNTHESIS)

DEFICIENCY

SOLITARY DEFICIENCY IS RARE  SOLITARY DEFICIENCY CAN OCCUR IN LACTATION, ALCOHOLICS AND ISONIAZID THERAPY OF TUBERCULOSIS LACTATION  MOTHER ARE DEPLETED OF VIT B6 DUE TO ORAL CONTRACEPTIVES ALCOHALICS  ETHANOL CONVERTED TO ACETALDEHYDE WHICH HYDROLYZE PYRIDOXAL PHOSPHATE TO PYRIDOXINE ISONIAZID (INH) [CHEMICAL ANTAGONIST]  PYRIDOXINE PYRIDOXAL HYDRAZINE TOXICITY  NEUROLOGICAL INVOLVEMENT IF >.2 gm / Day 

BIOTIN

BIOTIN

COLOURLESS, HEAT STABLE, MONOCARBOXYLIC ACID SOURCE  

INTESTINAL BACTERIAS NATURAL FOODS, LIVER, KIDNEY, YEAST, ROYAL JELLY, EGG YOLK

BIOCHEMICAL ROLE

ACTIVE FORM AS BIOTNYL CARBOXYLASE  CO-ENZYME OF CARBOXYLASE ENZYMES FOR FIXATION OF CO2 IN THE FORM OF ACTIVATED COOH GROUP 1. PYRUVATE CARBOXYLASE (PYRUVATE TO GLUCOSE, REPLENISH OXALOACITATE FOR TCA) 2. ACETYL CoA CARBOXYLASE (FATTY ACIDS SYNTHESIS) ACETYL CoA TO MALONYL - CoA 3. PROPIONYL COA CARBOXYLASE (PROPIONATE TO SUCCINATE) 4. B-METHYLE CROTONYL COA CARBOXYLASE (CATABOLIZE LEUCINE AND ISOPRENOID UNITS) 5. FIXATION OF CO2 AS CARBAMYOL PO4 

DEFICIENCY (RARE) CAUSE: (RAW EGGS (BIOTIN ANTAGONIST    

AVIDIN) LONG TERM PARENTRAL NUTRITION SCALY DERMATITIS ALOPECIA PARAESTHESIA SEBORRHIC TYPE OF DERMATITIS

CLINICAL FEATURES OF BIOTIN  

DERMATITIS, ALOPECIA, PARAESTHESIA, DEPRESSION, HALLUCINATIONS, MUSCLE PAIN IMMUNODEFICIENCY DISEASE RELATED TO ACCUMULATION OF LACTATE, βMETHYLCROTONATE, βHYDROXYISOVALERATE, βHYDROXYPROAONATE

PANTOTHENIC ACID

STRUCTURE: (PANTOIC ACID + B-ALANINE) SOURCE: WIDELY DISTRIBUTED [PANTOS MEANS EVERY WHERE] BIOCHEMICAL ROLE: (-SH IS REACTIVE THIOL GP)  ACTIVE IN THE FORM OF CO-ENZYME-A (CoASH)  ACYLE CARRIER PROTEIN (ACP) 1. REQUIRED IN THE FOLLOWING AS CoA  TCA, FATTY ACID OXIDATION, ACETYLATION OF DRUGS, CHOLESTEROL SYNTHESIS 2. REQUIRED AS ACP IN FATTY ACID SYNTHESIS DEFICIENCY  NOT SPECIFIC  BURNING FEET SYNDROME CAN BE ASSIGNED TO ITS DEFICIENCY [DUE TO DECREASED ACETYLATION REACTION]  RESTLESSNESS, FATIGUE, GIT DISTURBANCES

ASCORBIC ACID (VIT C) (RESEMBLE GLUCOSE)

SOURCE:  

FRESH FRUITS (GAUVA, LEMON, ORANGE), GREEN LEAFY VEGETABLES, MILK IS DEFICIENT ANIMALS WITH GULONOLACTONE OXIDASE CAN SYNTHESIZE

BIOCHEMICAL ROLE 

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ACTIVE VIT C IS ASCORBIC ACID WHICH IS DONOR OF REDUCING EQUIVALENTS IN CERTAIN REACTIONS ASCORBIC ACIDS DEHYDRO ASCROBIC ACID CAN REDUCE, MOLECULAR OXYGEN, NITRATES, CYTOCHROMES a&c

FOLLOWING ARE THE ROLES 1. 2.  

3. 

4. 5. 6. 7. 8.

HYDROXYLATION OF PROLINE TO HYDROXY PROLINE (POSTTRANSLATIONAL MODIFICAITON OF COLLAGEN) + HYDROXYLATION OF LYSINE TYROSINE METABOLISM CU++ P-OH PHENYLE ALANINE HOMOGENSTITATE HOMOGENSTITATE MALEYL ACETOACETATE Fe++ SYNTHESIS OF EPINEPHRINE DOPAMINE-β-HYDROXYLASE STEP TO FORM NOR EPINEPHRINE BILE ACIDS FORMATION-7 α - HYDROXYLASE STEROIDOGENESIS IN ADRENAL CORTEX ABSORPTION OF IRON ASCORBIC ACID ACTS AS ANTIOXIDANT AND INHIBIT NITROSAMINE FORMATION IN GUT PREVENT LIPID PEROXIDATION INDIRECTLY TO REDUCE VIT-E REQUIREMENT

PREVENTION DIET SHOULD CONTAIN CITRUS FRUITS AND FRESH VEGETABLES  BREAST FEEDING, MOTHER’S DIET WITH JUICES  INFANT SHOULD BE GIVEN JUICES  DIFFERENT FRUITS HAVE FOLLOWING CONCENT RATIONS OF VIT C.  LEMON 50 mg/g  ORANGE 49 mg/g  GUAVA 300 mg/dl BLOOD LEVEL OF VIT C IS 1 mg/dl  LESS THAN 0.4 mg/dl DEFICIENCY OCCUR  LESS THAN 0.2 mg/dl SCURVY APPEARS  NORMAL STORES OF VIT-C ARE SUFFICIET FOR 3-4 MONTHS BEFORE SCURVY APPEARS 

DEFICIENCY (SCURVY)

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ABNORMAL FORMATION OF CONNECTIVE TISSUE DUE TO ABNORMAL COLLAGEN RESULT INTO: DELAYED WOUND HEELING SUBCUTANEOUS & CAPILLARY HEMORRHAGES SUBNORMAL PLATELET ADHESIVENESS

ADULT SCURVY

CLASSICAL SYNDROME OF VIT C DEFICIENCY 1. SWOLLEN AND SPONGY GUMS (SCURVY BUDS) 2. PERIFOLLICULAR AND PETICHIAL HEMORRHAGES, ECHYMOSIS 3. DELAYED WOUND HEELING 

LAB DIAGNOSIS 

PLASMA LEVEL OF ASCORBIC ACID LOW

INFANTILE SCURVY   

LASSITIDE, SUBPERIOSTEAL HEMORRHAGES, ANOREXIA, GINGIVITIS PAINFUL LIMBS ENLARGEMENT OF COSTROCHONDRAL JUNCTIONS

COBALAMINES (VIT B12)

COBALAMINES (VIT B12 ) EXTRINSIC FACTOR  ANTI-PERNICIOUS ANAEMIC FACTOR CHEMICAL STRUCTURE [CORRIN RING + COBALT ] SOURCE: ANIMAL ORIGIN (LIVER), MICROORGANISMS RDA = 3 MICROGRAM/DAY ABSORPTION, TRANSPORT AND STORAGE  INTRINSIC FACTOR (IF) MANDATORY FOR ABSORPTION, STORED IN LIVER [UNIQUE SITUATION] 

ABSORPTION AND TRANSPORT OF VITAMIN B12 

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ENTEROHEPATIC CIRCULATION OF VIT B12 THIS SYSTEM IS DISTURBED IN FOLLOWING CONDITIONS [INTESTINAL LOOP SYNDROME – SPRUE AND CROHN’S DISEASE] ALL THESE LEAD TO MALABSORPTION AND REQUIREMNET OF EXOGENOUS VIT B12 IS INCREASED

BIOCHEMICAL ROLE THE ACTIVE VIT B12 ACTS AS COENZYMES IN THE FOL FORMS: 1. METHYL COBALAMINE (CYTOSOLE) 3% IN PLASMA 2. DEOXYADENOSYL COBALAMINE (MITOCHONDRIA) 70% 3. HYDROXYCOBALAMINE (PLASMA) 

ACTS AS A CO-ENZYME IN FOLLOWING REACTIONS MUTASE 1. METHYL MALONYL COA SUCCINYL COA (DEOXYADENOSYL FORM) 2. HOMOCYSTEINE METHIONIEN 

METHIONINE SYNTHASE

+ + N5 -METHYL H4 FA H4 FOLATE METHYL COBALAMIN

PURINES, PYRIMIDINE & DNA SYNTHESIS NUCLEIC ACID SYNTHESIS DECREASED VIT B12 [FOLATE TRAP] [FOLATE SINK]

DEFICIENCY

(PERNICIOUS ANEMIA)

CAUSES:  

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DIETARY (VEGANS) INTRINSIC FACTOR DEFICIENCY GASTRIC ATROPHY CONGENITAL DEFICIENCY TOTAL GASTRECTOMY DISEASE OF TERMINAL ILLEUM PARASITIC INFESTATION (TAPE WORM) DRUGS

LABORATORY DIAGNOSIS: 

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LEVEL IN RBCs, SHAPE OF RBCs (MEGALOBLASTIS) SERUM VIT B12 SCHILLING TEST ANTIBODY TO INTRINSIC FACTOR METHYL MALONYL ACIDURIA HOMOCYSTINURIA

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RBC-COUNT IS DRASTICALLY DECREASED IN PERNICIOUS ANAEMIA SCHILLING TEST ORAL VIT B12 RADIOACTIVE PARENTRAL NON RADIOACTIVE % EXCRETION OF RADIOACTIVE VIT B12

CLINICAL FEATURES 

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PERNICIOUS ANAEMIA (DEFICIENCY OF INTRINSIC FACTOR) MEGALOBLASTIC ANAEMIA THERE IS DELAYED DIVISION OF DNA AND THE TIME BETWEEN DIVISION INCREASES WHICH GIVE TIME TO CELL FOR GROWING INTO MEGALOBLAST GIT PROBLEMS INTERMITTENT SORNESS OF TONGUE PERIODIC DIARRHEA

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o o o

NEUROLOGICAL PROBLEMS PARAESTHESIA OF FINGER AND TOES DEMENTIA MAY OCCUR UNSTEADINESS OF GAIT SPINAL CORD AND PERIPHERAL NERVES ARE CLEARLY INVOLVED

FOLATE OR FOLACIN (FOLIC ACID) FOLIUM (LEAF)

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FOLATE OR FOLACIN (FOLIC ACID) (LEAF) CHEMICALFOLIUM STRUCTURE

PTERIDINE + PABA + GLUTAMATE ACID SOURCE PLANT ORIGIN, LEAFY VEGETABLES (POLYGLUTAMATE CONGUGATES) SYNTHESIZED IN GIT ABSORPTION AND TRANSPORT IN BLOOD IN GIT EXISTS AS POLYGLUTAMATES MONOGLUTAMATE IN BLOOD 2/3 OF FOLATE IS BOUND WITH PROTEIN IN LIVER MAJOR FOLATE IS STORED AS PENTAGLUT-AMATE CONGUGATE

BIOCHEMICAL ROLE      

ACTIVE FOLATE IS TETRAHYDROFOLIC ACID (H4 FOLATE) 1. H4 FOLATE IS CARRIER OF ACTIVATED ONE CARBON UNIT IN DIFFERENT OXIDATION STATES METHYL -CH3 ALL ARE METHYLENE -CH2METABOLICALLY METHENYL -CH= INTERCONVERTABLE

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FORMYL C O H FORMIMINO HN=CH-

SERINE IS A THE MAJOR SOURCE OF ONE CARBON UNIT (METHYLENE – CH2 –) 2. FOR SYNTHESIS OF PURINES i.e. THYMIDYLATE FOR DNA SYNTHSIS  N5 , N10 METHYLENE-H4 FOLATE PROVIDES METHYL GROUP IN THE FORMATION OF THYMIDYLATE FROM URIDYLATE, A NECESSARY PRECURSOR OF DNA SYNTHESIS & ERYTHROPOISIS 

TRIMETHOPRIM

FOLIC ACID

DIHYDRO FOLIC ACID

METHOTREXATE FOLATE REDUCTASE

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TETRA HYDRO FOLATE (H4 FOALTE) TRIMETHOPRIM (ANTIBACTERIAL) AND METHOTRAXATE (ANTICANCER) ACT AS FOLATE ANTAGONISTS

DEFICIENCY CAUSES   

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INADEQUATE DIET UPPER GIT DISEASE (COELIAC AND SPRUE) INCREASED BODY DEMAND THAN INTAKE  PREGNANCY (COMMON)  ACTIVE CELL PROLIFERATION  HEMOLYTIC ANAEMIAS  LEUKEMIAS  EXTENSIVE PSORIASIS DRUGS, METHOTREXATE DECREASED DEHYDRO FOLATE REDUCTASE ALCOHOL, PHENYTOIN AND PRIMIDONE

CLINICAL FEATURES   

MEGALOBLASTIC ANAEMIA IN TROPICAL COUNTRIES DUE TO MALNUTRITION, PREGNANCY: ANAEMIA IS DIFFERENTIATED FROM VIT B12 DEFICIENCY BY FOLLOWING GLOSSITIS IS LESS APPARENT,NEUROLOGICAL SYMPTOMS ARE NOT THERE SPERMATOGENESIS AND OOGENESIS FAILURE

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LAB DIAGNOSIS

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FIGLU TEST SERUM & ERYTHROCYTE CONCENTRATION OF FOLIC ACID THERAPEUTIC DOSE RESPONSE 300-500 mg / DAY

 