Vitamin Deficiency Disorders Abdelaziz Elamin MD, PhD, FRCPCH Professor of Child Health College of Medicine Sultan Qaboos University Muscat, Oman.

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Presentation transcript:

Vitamin Deficiency Disorders Abdelaziz Elamin MD, PhD, FRCPCH Professor of Child Health College of Medicine Sultan Qaboos University Muscat, Oman

BACKGROUND  Vitamins are organic substances that are essential for several enzymatic functions in human metabolism  Thiamine was discovered in 1912 & was thought to be a vital amine compound & thus the term vitamin was invented

VITAMINS  Vitamins are classified according to solubility into fat soluble & water soluble.  13 vitamins are known, 4 fat soluble (KEDA) & 9 water soluble (C, Folate & the B group).

VITAMIN A  Vitamin A is a generic term for many related compounds.  Retinol (alcohol), Retinal (aldehyde) are often called preformed vitamin A. Retinal can be converted by the body to retinoic acid which is known to affect gene transcription.  Body can convert  -carotene to retinol, thus called provitamin A.

FUNCTIONS Vision:Vision: integrity of eye & formation of rodopsin necessary for dark adaptation. Regulation of gene expressionRegulation of gene expression: vital to cell differentiation & physiologic processes Growth & developmentGrowth & development ImmunityImmunity: important for activation of T lymphocyte, maturation of WBC & integrity of physiological barrier.

Nutrient Interactions Zinc deficiency interfere with vitamin A metabolism in several ways: It decreases the synthesis of retinol binding protein, which transports retinol to tissues. It decreases the activity of the enzyme retinyl palmitate, which is necessary for release of retinol from the liver. Zn is needed for the enzyme that convert retinol into retinal.

Nutrient Interactions/2 Iron & vitamin A.Iron & vitamin A. Vitamin A deficiency may exacerbate IDF Vitamin A supplementation improves iron status among children & pregnant women. Combining vitamin A with iron controls IDA more quickly & effectively than using iron alone.

VITAMIN A UNITS  1  g of retinol = 6  g of  -carotene.  3  g of retinol = 10 international units of vitamin A.  100 mg carrots contain 10 mg of  - carotene.

Life stage  g/day Infants Children Adolescent 900M- 700F Adult Pregnant women Lactating women Recommended Allowance

Animal Foods Plant Foods Cod liver oil Sweet potato Liver & kidney Carrots EggCantaloupe ButterSpinach Milk & cheese Apricot Fish & meet Papaya RICH DIETARY SOURCES

Vitamin A deficiency Deficiency of vitamin A leads to:  Night blindness & xerophthalmia  Growth retardation  Acquired immune deficiency  Keritinization of epithelia in RT, GIT & UT with increased risk of RTI, malabsorption & UTI.

THERAPEUTIC USES  Vitamin A deficiency  Boosting immunity of infants  Skin disorders  Acute promyelotic leukemia  Cancer prevention (lung & breast)

TOXICITY Vitamin A in excess leads to:Vitamin A in excess leads to: Dermatitis with xanthosis cutis Hepatosplenomegaly Bone pain & increased risk of fracture Pseudotumor Cerebri

VITAMIN D  Vitamin D comprises a group of sterols; the most important of which are cholecalciferol (vitamin D3) & ergosterol (vitamin D2).  Humans & animal utilize only vitamin D3 & they can produce it inside their bodies from cholesterol.  Cholesterol is converted to 7-dehydro- cholesterol (7DC), which is a precursor of vitamin D3.

VITAMIN D  Exposure to the ultraviolet rays in the sunlight convert 7DC to cholecalciferol.  Vitamin D3 is metabolically inactive until it is hydroxylated in the kidney & the liver to the active form 1,25 Dihydroxycholecalciferol.  1,25 DHC acts as a hormone rather than a vitamin endocrine & paracrine properties.

FUNCTIONS Calcium metabolismCalcium metabolism: vitamin D enhances ca absorption in the gut & renal tubules. Cell differentiationCell differentiation: particularly of collagen & skin epithelium ImmunityImmunity: important for Cell Mediated Immunity & coordination of the immune response.

Vitamin D deficiency Deficiency of vitamin D leads to:Deficiency of vitamin D leads to:  Rickets in small children.  Osteomalacia  Osteoporosis

GROUPS AT RISK Infants Elderly Dark skinned Covered women Kidney failure patients Patients with chronic liver disease Fat malabsorption disorders Genetic types of rickets Patients on anticonvulsant drugs

Sources of Vitamin D  Sunlight is the most important source  Fish liver oil  Fish & sea food (herring & salmon)  Eggs  Plants do not contain vitamin D3

THERAPEUTIC USES  Rickets & Osteomalacia  Osteoporosis  Psoriasis  Cancer prevention (prostate & colorectal)  Autoimmune diseases

TOXICITY Hypervitaminosis DHypervitaminosis D causes hypercalcemia, which manifest as: Nausea & vomiting Excessive thirst & polyuria Severe itching Joint & muscle pains Disorientation & coma.

RICKETS