1. Vitamin A Deficiency Nutrition Department Medical Faculty of Sumatera Utara November 2009 DKS09

2. 2 Background “Nutrition Related Disease” Nutrition problem in Indonesia Nutrition Status Survey  1998-2002, 10 million Indonesian children  risk of Vit A deff >> (sub klinis)  xeropthalmia  blindness

3. 3 What caused deficiency? Primary (‘NUTRITION’): –Protein energy malnutrition (defect on absorption) –Minimum daily vit A or β-carotene intakes (long period) –No ‘exclusive breast feeding’ for babies –Imbalanced diet (less fat, protein, Zn, or other nutrients)  help absorption and utilization

4. 4 Secondary (diseases related to absorption and metabolism ) –Celiac disease –Sprue –Cystic fibrosis –Pancreatic disease –Congenital partial obstruction of duodenum –Giardiasis –Cirrhosis –Chronic hepatitis –Chronic diarrhea

5. 5 Other signs of defficiency Frequent infections like measles, diarrhea, and malaria Stunted growth Anemia Malnutrition Thickened toad like skin, goose flesh

6. 6 Skin Manifestation

7. 7 XS X3B X3A X2 X1B X1A XN: night blindness is the earliest symptom of vit A deff. Which is often reported by the mother as reduced visual acuity of the child in the evening and the night time X1A: conjungtival xerosis or drying of the conjungtiva X1B: bito’s spot on the conjungtiva X2: corneal xerosis or dryness of the cornea with a granular looking swurface X3A: keratomalacia involving less than a third of the cornea X3B: Keratomalacia > 1/3 XF: funduscopy changes in visible in opthalmoscopy XS:Corneal scarring, compromising severly on visual acuity Clinical signs of vit A deff

8. 8 Vitamin A deff and toxicity

9. 9 Toxicity Excessive dietary intakes of vitamin A produce symptoms of acute and chronic toxicity including teratogenecity in developing fetuses Normally results from the indiscriminate use of pharmaceutical supplements, not from the consumption of usual diets Sign: –Serum vit A of 75-2000 RAE/100mL –Bone pain & fragility –Hydrochepalus and vomiting –Dry, fissured skin –Brittle nail –Alopecia –Gingivitis, cheilosis, anorexia, irritability, fatique –Hepatomegaly and abnormal liver function –Ascites and portal hypertention

10. 10 How to diagnosed Funduscopic examination Laboratorium: Serum retinol Retinol binding protein level < 10  g/dL Clinical sign < 20  g/dL Sub clinic

11. Vitamin A

12. 12 Vitamin A Vitamin A-active compounds are represented by retinoids (designated as vitamin A) and their carotenoid precursors (provitamin A carotenoids) Structure: –Retinoids: retinol, retinaldehyde, and retinoic acids –Provitamin A carotenoid (α-carotene, β-carotene, and β-cryptoxanthin)

13. 13 Functions  Retinal is a structural component of the visual pigments of the rod and cone cells  photoreception  RA  acts as hormon to affect gene expression  Glycoprotein  important for normal cell surface function such as cell aggregation and cell recognition  Normal reproduction (retinol), bone development, immune function

14. 14 Absorption and convertion vitamin A and β-carotene β-Carotene bile 2-50% mixed micelle Retinyl ester Retinol INTESTINAL LUMEN ENTEROCYTE β -carotene Central cleavage Retinaldehyde Retinol Retinoic acid Portal blood flow (albumin) Fatty acids Retinyl esters Chylomicron Lymph Sumber: Erdman dkk, 1993

15. 15 Stability (vitamin A) In foods, the indigenous retinyl ester are dissolved in the lipid matrix, protected from the oxidizing action of oxygen by vitamin E and antioxidants Destructions of vitamin A compounds related to accelerated lipid oxidation, such as exposure to air, heat, traces of certain metals (Co and Fe), and storage time

16. 16 Stability (carotenoids) Carotenoids in foods influenced by food processing and domestic cooking, such as nonenzymatic or enzymatic oxidation Cutting of fruits and vegetables into small pieces or maceration (non-enzymatic) increase exposure to carotenoids  mix up carotenoid and lipoxygenase Lipoxygenase in plant tissues catalyzes lipid peroxidation  hydroperoxides attack carotenoids (enzymatic)

17. 17 Moderate heat, such as blanching and cooking denature carotenoid binding proteins  releasing the carotenoid Optimal retention of carotene is obtained by steaming vegetables of cooking with minimal water until the vegetables are cooked

18. 18 Bioavailability When meals containing natural amounts of vitamin A and provitamin A carotenoids consumed, efficiency vitamin A: 70-90% compared with 20-50% for the provitamins Present of fat in milk protects vitamin A from degradation Pulped better than pieces for carotene bioaccessibility (carrots), and addition of cooking oil is more effective

19. 19 Host related factors affecting bioavailability: –Malnourished –Presence of intestinal parasites –Atrophic gastritis –Elderly people with little or no acid in stomach –Drug: Omeprazole  pH>4.5  reduced β- carotene serum

20. Medical Nutrition Therapy and Prevention

21. 21 Therapy GejalaHari 1Hari 2Hari 15 (mgg II) XN (buta senja), XIA (xerosis conjungtiva) tanpa pernah sakit campak 3 bulan terakhir Beri kapsul vitamin A dengan dosis sesuai umur -- Ada salah satu gejala X1B (bercak bitot- nanah/radang-kornea keruh-ulkus kornea- pernah sakit campak Beri kapsul vitamin A dengan dosis sesuai umur UmurDosis <6 bulan3 x 50.000 SI (1/2 kapsul biru) 6 bulan – 1 tahun100.000 SI (1 kapsul biru) 1-5 tahun200.000 SI (1 kapsulmerah) (Sumber: Deteksi dan Tatalaksana Kasus Xeroftalmia,Depkes RI, 2003)

22. 22 Prevention Prevention: –< 6 months: 50.000 IU oral –6-12 months: 100.000 IU oral –>1-5 year: 200.000 IU oral February and August

23. 23 Requirement Not exceed 2 times the RDA (AKG ’04)

24. 24 Medical Nutrition Therapy Goals: –Provided an adequate food to reach normal nutrition status –Provided high vitamin A food sources

25. 25 Energy: –Adequate energy to prevent protein break- down (energy supply and recovery) –Malnutrition (poor nutrition status): Stabilization phase: 80-100 cal/kg BW Trantition phase: 150 cal/kg BW Rehabilitation phase: 200 cal/kg BW

26. 26 Protein –High protein –To form Retinol Binding Protein and Rhodopsin –Malnutrition (poor), step by step: 1-1.5 g/kg BW/ day 2-3 g/kg BW/day 3-4 g/kg BW/day

27. 27 Fat –20-25% –For optimal vit A absorption: 3-4 g per meal –MCT –PUFA>>SFA –Palm oil (red), coconut oil

28. 28 High vit A food sources How to cooked (fry or light fry) Food form: destructive gastrointestinal epitel condition  easy to digest

29. 29 Vitamin A Sources Vitamin A sources (retinol per 100 g edible portion) Cow’s milk30 Semi-skimmed19 Skimmed1 Cheese958 Egg190 Chicken11 Liver19,700 Sardines6 Butter958 Sumber: Food Standard Agency(2002)

30. 30 Sumber β-karoten β-carotene sources (μg/100g) Carrot (cooked): 9800Daun selada: 1200 Sweet potatoes (cooked): 8800Bawang prei: 1000 Carrot : 7900Tomato juice: 900 Spinach (cooked): 5500Celery : 710 Tomato ketchup: 5000Green beans: 630 Pumpkin : 3100Tomatoes: 520, sawi : 530 Blewah:3000Watermelon : 230 Daun singkong:3000Pickles : 180 Bit: 2560Papaya: 99 Red pepper: 2200Corn : 51 Broccoli : 1300Avocado : 34 Mango: 1300Apple: 26 and orange: 39 Sumber: Mangels dkk, 1993

31. 31 Contoh makanan lunak kaya vitamin A Pagi: –Bubur ayam + tomat cincang Selingan: –Kue sus isi wortel Siang: –Bubur/tim nasi –Semur daging giling –Oseng tempe –Sayur lodeh (kcg pjg dan melinjo) –Pepaya Sore: –Kolak biji salak (ubi merah/oranye) Malam: –Lontong –Telur bumbu opor –Tumis buncis –Pisang ambon Malam: –susu

32. 32 Contoh makanan biasa kaya vitamin A Pagi: –Nasi goreng –Telur ceplok Selingan: –Cake wortel Siang: –Nasi –Goreng ayam mentega –Tumis kacang merah –Cah wortel dan caisim –Jeruk Sore: –Pastel isi sayuran Malam: –Nasi –Gulai ikan –Tahu telur –Tumis kangkung Malam: –susu

33. 33 Thank you