Akibat Defisiensi Vitamin AXerophtalmia Merenggut Penglihatan Balita Hellen Keller InternationalKondisi mata yang terserang xe

Akibat Defisiensi Vitamin AXerophtalmia Merenggut Penglihatan Balita

JAKARTA Betapa malang nasib Desak Made Ratna. Perempuan cilik berusia 5,5 tahun itu seumur hidup harus menggunakan bola mata palsu di mata kanannya. Mata kirinya tak kalah mengenaskan, harus terus menjalani perawatan hingga sembuh total dari xerophtalmia. Kalau terlambat sedikit saja diobati, maka putri seorang penjual janur di Mataram, Nusa Tenggara Barat (NTB) itu bisa menderita buta total di kedua indra penglihatannya.Ratna adalah contoh seorang anak korban kekurangan vitamin A dan gizi buruk akibat kemiskinan. Sejak usia dua tahun orangtuanya bercerai. Ibunya yang hanya berpenghasilan Rp4.000 per hari tak mampu memberi gizi cukup bagi Ratna. Lengkap sudah derita anak yang kini bersekolah di Sekolah Luar Biasa (SLB) tersebut.Sekolah pun hanya bisa dilakukan sebulan sekali. Ini karena jarak antara rumah Ratna dengan SLB sangat jauh, bisa menghabiskan biaya Rp20.000. Tapi itu lebih baik, setidaknya dia sudah bisa berbuat sesuatu daripada buta sama sekali, jelas Dr.Siti Farida Santyowibowo, SpM, ahli mata dari Balai Kesehatan Mata Masyarakat NTB dalam sebuah seminar mengenai penanggulangan defisiensi di Jakarta, Kamis (12/6).Ratna hanya satu dari begitu banyak anak di pelosok Indonesia yang terancam kebutaan akibat kekurangan konsumsi vitamin A. Walau selintas terkesan remeh, ternyata vitamin A bisa berakibat fatal kalau kurang dikonsumsi. Kasus xeropthalmia, sebuah kelainan pada mata akibat kekurangan vitamin A tak bisa dipandang enteng. Dulu ada asumsi bahwa penyakit ini sudah tidak ada lagi di Indonesia. Tapi fakta berbicara bahwa xerophtalmia masih bisa dikatakan sebagai momok mengerikan bagi anak usia bawah lima tahun (balita).Pada 19781980 Departemen Kesehatan (Depkes) bersama dengan Hellen Keller International (HKI) dan RS Mata Cocendo, Bandung mengadakan survei ihwal gangguan mata akibat kekurangan vitamin A. Didapat hasil bahwa prevalensi xerophtalmia status X1B sebanyak 1,2 persen, dan status X2 atau X3 sebanyak 9,8 persen per sepuluh ribu. Dari sini tergambar bahwa problem ini tergolong masalah kesehatan masyarakat.Survei yang dilakukan kembali pada 1992 di 15 provinsi Indonesia mengungkapkan penurunan yang cukup lumayan. Prevalensi xerophtalmia status X1B tinggal 0,33 persen. Dan tipe X2 dan X3 menjadi 0,5 per 10.000. Namun bukan berarti Indonesia terbebas dari penyakit mengerikan ini.

MalnutrisiMenurut Siti, xerophtalmia merupakan suatu tahap lanjutan akibat kekurangan vitamin A setelah seorang anak mengalami tahap seperti diare, kista, anemia, gangguan pertumbuhan. Ini diawali dengan kondisi kekurangan gizi yang dibiarkan saja. Xerophtalmia sendiri bisa berakibat kebutaan kalau tak mendapat pengobatan, tutur Siti.Seorang anak yang mendapat asupan vitamin A cukup, kalau terganggu kesehatannya hanya akan mengalami penyakit yang tidak terlalu berbahaya. Demam, cacar dan sebagainya bisa sembuh dalam waktu singkat. Sedangkan anak yang mendapat asupan vitamin A berstatus marjinal cenderung mengidap suatu penyakit lebih lama dan berat. Dan pada anak yang memiliki status asupan vitamin A buruk, bisa terancam kebutaan dan bahkan kematian. Biasanya faktor kemiskinan dan malnutrisi menjadi penyebab gangguan mata ini. Daerah gersang seperti NTB cenderung dihinggapi problem kurang gizi pada anak-anak. Maka tak heran di daerah beriklim panas ini kasus xerophtalmia masih tergolong tinggi. Dari 4.000 jiwa terdapat 4 persen kasus xerophtalmia.Kalau seorang anak balita bertubuh kurus dan menderita malnutrisi mengalami gejala rabun senja maka harus segera diwaspadai. Rabun senja, yakni tak bisa melihat dengan jelas pada waktu senja dan malam menjadi gejala klinis xerophtalmia. Terlebih kalau disertai dengan diare, demam atau infeksi saluran pernapasan. Pada tahap ini berarti seorang anak sudah mencapai klasifikasi xerophtalmia XN, demikian menurut klasifikasi Badan Kesehatan Dunia WHO. Jika dibiarkan maka bisa beranjak ke kondisi yang lebih parah, yakni status X1A di mana terjadi kekeringan konjungtiva pada mata dan munculnya kerut di sekitar mata.Stadium berikutnya adalah munculnya serosis dan bercak bito di mata, yakni bercak putih menyerupai keju.Kondisi ini terjadi pada tahap X1B. Makin lama kalau tidak dirawat kondisi ini berkembang ke status X2 di mana kornea dan selaput mengering dan tampak suram. Pada tahap ini pasien masih bisa diobati dengan memberi asupan vitamin A dan gizi lain. Mata bisa kembali normal seperti semula kalau cepat ditangani, tutur Siti.Tapi kalau tak dirawat maka akan kian parah menjadi status X3A, yakni sepertiga kornea mata tertutup atau lebih populer dengan istilah keratomalcia. Dan status yang lebih buruk lagi adalah X3B, di mana lebih dari sepertiga kornea tertutup. Dan yang paling parah adalah status XS, seluruh mata sudah tertutup hingga tak bisa melihat.Menurut Siti, selama bertugas di NTB ia mendapati bahwa jumlah penderita xerophtalmia cenderung menurun seiring dengan penyuluhan gizi terhadap masyarakat. Mereka juga melakukan pelatihan bagi dokter dan perawat agar bisa segera mendeteksi sejak dini gejala penyakit berakibat kebutaan tersebut.

Fungsi Vitamin ALalu mengapa vitamin A begitu penting bagi mata? Vitamin A makanan dalam bentuk retinol ester dan sebelum diserap dalam pencernaan diubah menjadi retinol. Dari mukosa sel retinol tersebut diesterfikasi kembali, kemudian diangkut oleh khilomikron, dibawa ke hati untuk disimpan, papar Profesor Muhilal dari Puslitbang Gizi Institut Pertanian Bogor (IPB) dalam kesempatan serupa. Bentuk aktif vitamin A sebagian berupa asam retinoat yang akan berperan dalam ekspresi gen. Di retina mata retinol ini diubah menjadi 11 cis retinal-dehida yang mampu berkonyugasi dengan opsin membentuk rhodopsin yang berperan dalam proses penglihatan. Maka jelas sudah mengapa mata amat membutuhkan kehadiran vitamin A. Selama ini masyarakat beranggapan bahwa vitamin A cukup banyak terkandung dalam sayuran dan buah. Itu memang betul. Namun jumlahnya masih kurang mencukupi terkecuali buah dan sayur dikonsumsi dalam porsi banyak. Pada riset yang dilakukan HKI tahun 1980-an, ditemukan bahwa kandungan vitamin A yang terdapat pada sayur dan buah tidak sebanyak yang terdapat pada produk hewani seperti hati, telur, daging dan susu. Tidak disebutkan berapa banyak asupan vitamin A yang diperlukan tubuh setiap hari. Yang jelas, balita yang menjadi sasaran utama xerophalmia harus mendapat konsumsi gizi baik. Depkes berkerjasama dengan HKI memulai pemberian kapsul vitamin A gratis sebanyak dua kali dalam setahun, tiap Februari dan Agustus. Kapsul ini disebarkan ke 240.000 Posyandu dan 7.000 Puskesmas seluruh Indonesia. Targetnya adalah anak usia antara enam bulan hingga 59 bulan. Selain itu disebarkan pula buklet Deteksi Dini Xerophtalmia yang dirancang untuk memberi informasi yang diperlukan petugas kesehatan. Lebih dari 58.000 buklet telah dicetak dan akan disebarkan ke seluruh Puskesmas di Indonesia dan rumah sakit. Dengan program ini diharap masyarakat bisa segera menyadari pentingnya vitamin A. (mer)

Copyright Sinar Harapan 2003

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dr. Rachmi Untoro, MPH: Mata Jendela Kehidupan

Jumat, 25 April, 2003 oleh: Gsianturidr. Rachmi Untoro, MPH: Mata Jendela KehidupanGizi.net - Perspektif Baru 14.2.2003dr. Rachmi Untoro, MPH: Mata Jendela Kehidupan

Mata adalah jendela kehidupan, itu satu hal yang rasanya perlu kita camkan dalam hati. Karena itu memelihara kesehatan mata adalah prioritas utama bagi kita semua, tapi tahukah anda bahwa menjaga kesehatan mata sebaiknya diawali sejak dini, sejak anak masih berusia balita atau bahkan sejak berada dalam kandungan. Sayangnya tidak banyak yang paham tentang hal ini, sehingga berbagai kasus penyakit mata yang muncul sudah berada pada kondisi yang buruk hingga sulit untuk diobati, terutama penyakit mata yang disebabkan oleh kekurangan vitamin A. Banyak juga yang tidak tahu bahwa penyakit mata yang disebabkan oleh kekurangan vitamin A itu relatif sulit untuk disembuhkan dan bisa menyebabkan terjadinya resiko kebutaan. Perspektif Baru kali ini akan berbincang-bincang tentang vitamin A dan kesehatan Mata dengan Ibu dr. Rachmi Untoro MPH. Direktur Gizi Masyarakat Departemen Kesehatan RI. Dengan Ibu Rachmi kita akan berbincang-bincang tentang bagaimana pentingnya vitamin A dalam meningkatkan kualitas kesehatan mata dan mencegah kerusakan mata. Perspektif Baru dipandu oleh Ruddy Gobel.

Dr. Rahmi, saya ingin memulai dengan pertanyaan yang sangat mendasar yang mungkin sebagian mungkin sudah tahu tapi saya yakin banyak juga yang belum tahu tentang apa sebetulnya vitamin A dan darimana sumber-sumber vitamin A itu bisa didapatkan?

Kita sebetulnya sudah belajar sejak SD tentang Ilmu Hayat, vitamin A adalah suatu zat gizi yang sangat penting bagi manusia, karena zat gizi ini tidak dibuat oleh tubuh jadi harus dipenuhi dari luar yaitu makanan. Vitamin A dapat kita konsumsi dari bahan makanan yang berwarna hijau, seperti sayur-sayuran warna hijau atau berwarna jingga sebagai contoh adalah bayam, daun singkong, pepaya yang warnanya jingga yang matang, hati kuning telur dan juga Air Susu Ibu (ASI), itu bahan makanan yang kaya dengan vitamin A. Jika kita tidak bisa mengkonsumsi dari makanan. kita bisa mendapatkannya dari bahan makanan yang sudah diperkaya dengan vitamin A. Berbagai makanan sekarang di dalam labelnya disebutkan sudah diperkaya dengan vitamin A atau untuk balita saat ini tersedia kapsul vitamin A dengan dosis tinggi.

Jadi dari apa yang dikatakan oleh Ibu dokter tadi, sebenarnya tidak semua kebutuhan vitamin A itu diperoleh dari makanan yang mahal harganya, artinya gizi yang cukup bisa didapatkan dari sumber-sumber yang banyak tersedia disekitar kita. Kekurangan vitamin A seperti yang kita semua sudah pahami menyebabkan kerusakan mata, tapi Ibu bisa jelaskan bagaimana itu bisa terjadi? Kemudian kerusakan mata seperti apa yang disebabkan oleh kekurangan vitamin A?

Sebelum kita bicara tentang kerusakan mata akibat kekurangan vitamin A, kita melihat dulu mata yang sehat. Mata yang sehat itu ditandai dengan selaput bening mata yang menutupi bagian hitam dari mata yang dikenal dengan kornea itu benar-benar jernih transparan, tembus sinar dan bagian putih mata itu terlihat putih warnanya. Bagian hitam itu benar-benar hitam, kelopak warna yang sehat itu dapat membuka dan menutup dengan baik dan bulu matanya teratur mengarah keluar pertumbuhannya. Sedangkan mata yang kekurangan vitamin A , selaput matanya pada daerah hitam dan daerah putih itu menjadi kering dan bila tidak segera diobati, selaput mata yang kering ini akan mengakibatkan kebutaan. Kita tadi sudah mendengar bahwa mata adalah jendela hati, itu artinya indera mata sangat penting dari 5 indra kita untuk kita dapat menangkap stimulus2 atau rangsangan2 dari luar dan itu berkaitan juga dengan kecerdasan.

Salah satu penyakit mata yang disebabkan karena kekurangan vitamin A adalah Xeroftalmia atau keringnya selaput bening mata. Bisa Ibu jelaskan gejalanya seperti apa dan kemudian bagaimana mendeteksinya secara dini sehingga masih bisa untuk diobati?

Mata yang sehat itu bening, mula-mula saya akan ceritakan kasusnya pada balita, bila kita melihat balita kita pada waktu menjelang magrib atau sudah agak menjelang malam terantuk-antuk jalannya, itu dikenal dengan buta senja. Kemudian bagian putih mata itu mengalami kekeringan, kusam dan tidak bersinar. Kalau pada bagian putih mata itu ada satu bercak seperti busa sabun, itu tandanya sudah makin parah. Bila selaput bening yang ada pada bagian hitam atau yang ada pada kornea sudah mulai kering dan kusam, itu berarti sudah terjadi kekeringan pada selaput korneanya dan lebih lanjut lagi sebagian hitam mata itu akan melunak seperti bubur dan pada akhirnya bagian kornea itu seluruh bagian hitam melunak dan bola matanya mengecil atau mengempis. Itulah ciri-ciri orang yang terkena Xeroftalmia atau keringnya selaput bening mata.

Bagaimana cara memberikan pengobatan terhadap kasus penyakit mata ini?

Seperti yang tadi saya katakan, kita harus mendapatkan makanan dari luar karena zat gizi ini harus didapatkan melalui makanan. Pada anak balita, kita sudah mempunyai program untuk mencegah kering mata ini dengan memberikan kapsul vitamin A dengan dosis yang tinggi. Kapsul vitamin A ini dibagikan setiap bulan Februari dan Agustus setiap tahun, bisa didapatkan di Puskesmas dan Posyandu terdekat didaerah masing-masing. Jadi sebetulnya dengan pemberian kapsul yang relatif mudah ini akan menentukan bagaimana masa depan dari seorang anak. Bila Ibu terlambat memberikannya maka pencegahannya juga akan membawa akibat pada kebutaan nanti.

Kita akan berbicara lebih general tentang kondisi Indonesia karena ada yang mengatakan bahwa Indonesia mengalami apa yang disebut dengan defisiensi vitamin A, apa maksud pernyataan tersebut sebetulnya?

Tadi saya sampaikan bahwa kekurangan vitamin A akan menyebabkan kebutaan. Saya ingin mengingatkan bahwa satu lagi fungsi dari vitamin A ini adalah meningkatkan daya tahan tubuh atau meningkatkan kekebalan anak. Anak yang kekurangan vitamin A akan mudah terserang infeksi, yang untuk anak sehat penyakit itu tidak menyebabkan kematian atau tidak menyebabkan kecacatan yang parah, sebagai contoh penyakit yang sering diderita anak-anak seperti campak, diare, itu akan menjadi lebih parah bila anak tersebut kurang vitamin A. Sebetulnya masalah kekurangan vitamin A di Indonesia secara klinis dan dari segi kesehatan masyarakat bukan lagi masalah kesehatan masyarakat karena angkanya kurang dari 0,3% (menurut WHO), tetapi jika diperiksa secara laboratorium masih terdapat 50% balita yang menderita vitamin A sub klinis. Kalau diperiksa di laboratorium oleh ahli, batasannya adalah anak itu mempunyai serum retinol (calon vitamin A) kurang dari 20 mikrogram /desiliter, karena itu secara klinis sudah cukup rendah angkanya tapi secara sub klinis cukup memprihatinkan. karena 50% dari balita kita yang berjumlah 20 juta balita atau sekitar 10 juta balita indonesia berpotensi untuk kekurangan vitamin A. Karena itulah kita membuat program yang menyeluruh untuk para balita kita.

Berkaitan dengan defisiensi vitamin A, kelompok mana saja atau kelompok masyarakat mana saja atau kelompok balita mana saja yang memiliki resiko tinggi untuk mengalami resiko kekurangan vitamin A?

Kelompok-kelompok yang beresiko kekurangan vitamin A, pertama adalah bayi berat lahir rendah yaitu bayi yang waktu lahir beratnya kurang dari 2500 gram. Bayi berat lahir rendah ini pada umumnya berasal dari Ibu yang kekurangan gizi. Jadi Ibu yang kurang gizi akan melahirkan anak yang kurang gizi juga dan anak ini juga berpotensi menderita gangguan gizi lain disamping kekurangan vitamin A. Yang kedua adalah anak yang tidak mendapatkan ASI pada usia dininya. Jadi ASI adalah makanan yang terbaik bagi bayi dan 99% sebetulnya Ibu bisa menyusui, hanya masalah psikologis saja yang bisa mempengaruhi tidak keluarnya ASI. Jadi tidak beralasan apabila ada Ibu yang mengatakan tidak bisa memberi ASI karena air susunya tidak keluar padahal semakin sering dihisap akan semakin banyak pula produksinya. Air Susu Ibu adalah sumber vitamin A yang paling baik untuk bayi dan anak sampai 2 tahun. Anak yang tidak mendapatkan ASI sesudah berumur 6 bulan maka membutuhkan makanan pendamping ASI yang bermutu artinya cukup sumber energinya, cukup proteinnya, cukup lemaknya, cukup vitamin dan mineralnya sesuai dengan yang ditetapkan oleh pakar. Anak yang kurang gizi bisa kita lihat dari grafik pertumbuhannya yang ditujunka oleh garis merah dan hijau pada Kartu Menuju Sehat yang terdapat di Posyandu . Jika anak sudah di ditimbang beratnya di Posyandu dan beratnya berada di bawah garis merah maka anak tersebut berpotensi beresiko untuk menderita kekurangan vitamin A dan anak yang sering menderita infeksi, campak, diare, TBC, infeksi saluran pernapasan akut dan cacingan akan lebih beresiko kekurangan vitamin A. Secara ekonomis, anak-anak yang berasal dari lingkungan yang miskin dan keluarga miskin, seperti anak yang tinggal di daerah pengungsian, anak yang tinggal di daerah yang kekurangan sumber vitamin A, kekurangan sayur-sayuran hijau, buah-buahan berwarna jingga, merupakan anak-anak yang lebih berpotensi mengalami kekurangan vitamin A. Anak-anak yang tidak mendapat imunisasi, tidak mendapat kapsul vitamin A dan Ibu yang kurang menyediakan sumber vitamin A pada makanan keluarganya juga sangat beresiko mengalami kekurangan vitamin A.

Tadi kita sudah berbicara tentang sebagian besar penyakit mata itu disebabkan karena kekurangan vitamin A, tapi kita juga ingin tahu adakah penyebab lain selain kekurangan vitamin A, yang dapat menyebabkan terjadinya penyakit mata seperti mungkin katarak dan penyakitpenyakit lain, ini perbedaannya dimana? Kemudian tingkat resiko atau tingkat keberhasilan dalam penyembuhan itu lebih berat yang mana, apakah kekurangan vitamin A atau karena faktor faktor lain?

Kalau xeroftalmia terjadi akibat dari kekurangan vitamian A, karena salah gizi atau di dalam konsumsi makanan kita tidak mengandung cukup vitamin A. Kalau katarak itu penyakit degeneratif, siapapun itu akan beresiko mengalami karena terjadi sesuai dengan proses ketuaan, tetapi orang yang menderita kurang gizi cenderung lebih cepat menderita katarak. Kalau katarak mudah pengobatannya dengan operasi yang sederhana saja, diganti lensanya sudah bisa segera melihat.. Tetapi kalau akibat xeroftalmia tidak mungkin diperbaiki dengan operasi karena sudah terjadi kerusakan pada alat mata. Kalau katarak kerusakan terjadi karena adanya kekeruhan pada lensa dan lensanya bisa diganti.

Ada satu hal penting yang bisa kita pahami dari perbincangan diatas bahwa kalau penyakit mata yang disebabkan karena kekurangan vitamin A itu lebih beresiko untuk tidak bisa sembuh dan menyebabkan kebutaan dibandingkan dengan penyakit penyakit mata yang disebabkan oleh faktor-faktor yang lain. Tadi terungkap bahwa Indonesia meskipun secara klinis jumlah penderita kekurangan vitamin A tidak terlalu besar, tapi secara sub klinis masih banyak balita kita yang mengalami defisiensi vitamin A. Saya ingin bertanya kepada Ibu tentang seberapa seriuskah Defisiensi vitamin A yang terjadi di Indonesia dibandingkan dengan negara-negara lain sehingga kita perlu membuat sebuah program khusus untuk melakukan atau menanggulangi persoalan ini?

Angka kebutaan yang terjadi karena akibat kekurangan vitamin A cukup tinggi. Informasi yang penting untuk disampaikan bahwa salah satu fungsi dari vitamin A adalah meningkatkan kekebalan tubuh. Jadi kalau anak sudah menderita kekurangan gizi dan terkena infeksi akan lebih parah dibandingkan anak yang kena infeksi dalam keadaan gizi yang baik. Tadi kita sudah melihat bahwa yang sub klinis itu 10 juta dan itu bukan angka yang kecil, angka yang cukup besar. Disamping itu kita juga sudah melihat bahwa sebagian besar anak-anak kita hidup berada dibawah garis kemiskinan mengingat lebih dari 20% masyarakat Indonesia adalah masyarakat miskin. Ditambah lagi sekarang banyak terjadi pengungsian, sehingga menambah jumlah yang beresiko menderita defisiensi vitamin A ini.

Ibu sempat mengatakan tentang pembagian vitamin A secara gratis, bisa Ibu jelaskan lagi dimana masyarakat bisa mendapatkan kapsul vitamin A ini, kemudian kapan waktu pelaksanaannya?

Kapsul vitamin A sebagai satu upaya untuk mencegah kekurangan vitamin A ini dibagikan untuk bayi berusia antara 6-11 bulan, balita berusia 1259 bulan atau kurang lebih 5 tahun dan Ibu nifas, karena Ibu nifas itu menyusui dan melalui darah Ibu akan dikeluarkan ASI yang mengandung vitamin A. Untuk bayi berumur 6 sampai 11 bulan diberikan kapsul vitamin A berwarna biru, dosisnya 100.000 Internasional unit. Untuk balita berusia diatas satu sampai lima tahun diberikan kapsul berwarna merah dengan dosis 200.000 Internasional unit dan Ibu nifas juga diberikan 200.000 internasional unit. Jadi ada tiga target populasi kita yaitu bayi, balita dan Ibu nifas. Kapsul ini tersedia di semua Puskesmas dan diberikan antara lain pada hari-hari Posyandu. Jadi bagi Ibu-Ibu yang tidak bisa ke Puskesmas untuk daerah-daerah terpencil tapi kegiatan Posyandu-nya berjalan, bisa mendapatkan pelayanan ini di Posyandu.

Ini mungkin jadi isu bagi masyarakat dari kelompok ekonomi lemah, apakah pembagian ini gratis atau adakah biaya yang harus dikeluarkan ketika Ibu-Ibu harus membawa anaknya?

Kapsul vitamin A ini diberikan gratis untuk semua balita, karena itu disediakan di seluruh Puskesmas dan Posyandu. Kita kurang lebih mempunyai 7000 Puskesmas dan 240.000 Posyandu. Semua kita sediakan kapsul vitamin A secara gratis dan tidak dipungut bayaran apapun untuk pemberian ini.

Kita kembali ke soal kekurangan gizi tadi dan satu hal yang menarik perhatian saya adalah sejak didalam kandungan bayi pun sebetulnya sudah harus kita persiapkan agar supaya dia tidak mengalami kekurangan atau Defisiensi Vitamin A. Hal berarti ini adalah treatment yang diberikan kepada Ibu-Ibu yang sedang hamil dan yang sedang menyusui. Ibu barangkali bisa memberikan semacam tips atau nasehat bagi Ibu yang sedang hamil atau yang sedang menyusui?

Saya ingin mengingatkan, Ibu yang sedang hamil sebetulnya mempersiapkan calon sumberdaya manusia yang baru, karena itu Ibu harus memberi makan untuk dua orang. Ibu hamil harus makan lebih banyak dibandingkan kalau Ibu tidak hamil. Ibu juga harus menimbang berat badannya, karena dengan menimbang berat badan maka kita bisa mengetahui secara tidak langsung bagaimana tumbuh kembang anak. Ibu yang sehat. Sampai akhir kehamilannya kenaikan berat badan ibu hamil harus sekitar 10 sampai 15 kilo, tergantung pada kondisi Ibunya. Kalau dibawah itu berarti Ibu harus waspada . Yang penting sekali bahwa awal dari kehidupan dalam kandungan itu menentukan kualitas masa depan anak yang dilahirkannya, karena di dalam kandungan sampai usia balita terjadi suatu pesat tumbuh yang sangat cepat dan kita mengenalnya sebagai masa emas yang berkaitan dengan panca indera kita seperti otak, mata. Untuk otak porsi pesat tumbuhnya sebesar 80% terjadi pada waktu kehamilan sampai umur kurang lebih tiga tahun, sedangkan 20%-nya terjadi sesudah masuk usia sekolah. Jadi bayangkan saja kalau Ibu menderita gizi kurang pada waktu hamil dan balita itu kekurangan gizi, maka otaknya tentu tidak berkembang dengan optimal. Jadi secara kasar dia akan kehilangan sekitar 80% kemampuan otak dan kalau diibaratkan sekarang kita analogikan seperti komputer, anak yang Ibunya cukup gizi selama hamil dan waktu balita akan mempunyai kapasitas yang mungkin dianalogikan sudah pentium 4, sedangkan anak yang kurang gizi itu hanya pentium 1 atau kalau di iklan televisi disebutkan tulalit atau jaringan telepon yang tidak nyambung dikarenakan sel-sel otak tidak berkembang baik pada waktu dalam kandungan sampai pada usia balita.

Sumber:http://articles.perspektif.net/view.asp?id=361

www.gizi.net/cgi-bin/berita/fullnews.cgi?newsid1051160589,86320, -

Defisiensi vitamin Sementara betakaroten adalah pigmen tumbuh-tumbuhan yang merupakan precusor dari vitamin A yang biasanya terdapat pada sayuran hijau atau kuning dan buah-buahan. Selama proses absorbsi (penyerapan), betakaroten akan dimetabolisme menjadi vitamin A pada dinding usus.

Vitamin A tersebut, kata Ermi, berperan dalam pembentukan fotoreseptor seperti pada siklus rhodopsin. ''Bila tejadi defisiensi vitamin A maka regenerasi rhodopsin akan terhalang atau berlangsung lambat sehingga kemampuan adaptasi gelap agak berkurang dan timbul lah keadaan yang disebut dengan buta senja atau niktalopia,'' tambahnya.

Ermi menjelaskan, pada Bio Vision juga terkandung vitamin B2 (riboflavin). Di dalam tubuh riboflavin diubah menjadi koenzim riboflavin fosfat atau flavin mononukleotida (FMN) dan flavin adenosin di nukleotida (FAD) yang berperan dalam berbagai proses metabolisme.

Gejala pada mata yang ditimbulkan akibat defisiensi vitamin ini adalah konjunctivitis, fotopobia, lakrimasi, gatal dan panas. ''Pada pemeriksaan, defisiensi vitamin tersebut bisa menimbulkan vaskularisasi kornea dan katarak,'' ujarnya.

( ) www.republika.co.id/suplemen/cetak_detail. asp?mid=2&id=197142&kat_id=105&kat_id1=150 - 35k

Vitamin A Deficiency Vitamin A (retinol) is fat soluble and is found mainly in fish liver oils, liver, egg yolks, butter, and cream. Green leafy and yellow vegetables contain -carotene and other provitamin carotenoids, which are converted to retinal in the mucosal cells of the small intestine. Retinal is reduced to retinol, then esterified. Most of the body's vitamin A is stored in the liver as retinyl palmitate. It is released into the circulation as retinol bound to retinol binding protein and prealbumin (transthyretin). The 11-cis isomer of retinal (vitamin A aldehyde) combines with opsin to form rhodopsin, the prosthetic group of photoreceptor pigments in the retina. In somatic cells, retinol is converted to retinoic acid, which combines with receptors that bind to DNA and regulate gene expression to maintain epithelial tissues and guide differentiation of a variety of other tissues.

Biologic equivalents, for diets with different proportions of retinol and -carotene, are as follows: 1 USP U equals 1 IU; 1 IU equals 0.3 g of retinol; 1 g of -carotene equals 0.167 g of retinol. Other provitamin carotenoids are half as active as -carotene.

Synthetic vitamin analogs (retinoids) are used increasingly in dermatology. The possible protective role of -carotene, retinol, and retinoids against some epithelial cancers is under investigation.

Etiology Primary vitamin A deficiency is usually caused by prolonged dietary deprivation. It is endemic in areas, such as southern and eastern Asia, where rice, devoid of carotene, is the staple.

Secondary vitamin A deficiency may be due to inadequate conversion of carotene to vitamin A or to interference with absorption, storage, or transport of vitamin A. Interference with absorption or storage is likely in celiac disease, sprue, cystic fibrosis, pancreatic disease, duodenal bypass, congenital partial obstruction of the jejunum, obstruction of the bile ducts, giardiasis, and cirrhosis. Vitamin A deficiency is common in protein-energy malnutrition (marasmus or kwashiorkor), principally because the diet is deficient but also because vitamin A storage and transport are defective.

Symptoms and Signs The severity of the effects of vitamin A deficiency is inversely related to age. Growth retardation is a common sign in children. Inadequate intake or utilization of vitamin A can cause impaired dark adaptation and night blindness; xerosis of the conjunctiva and cornea; xerophthalmia and keratomalacia; keratinization of lung, GI tract, and urinary tract epithelia; increased susceptibility to infections; and sometimes death. Follicular hyperkeratosis of the skin is common.

Pathognomonic changes are confined to the eye (see Keratomalacia in Ch. 96). The earliest change, rod dysfunction, can be detected by dark adaptometry, rod scotometry, or electroretinography (these tests require cooperative subjects). Dysfunction of the retina is followed by changes in the structure and function of epithelial cells. Xerosis of the bulbar conjunctiva consists of drying, thickening, wrinkling, and muddy pigmentation; the cornea becomes xerotic, infiltrated, and hazy at an early stage. Keratomalacia rapidly supervenes with liquefaction of part or all of the cornea, leading to rupture, with extrusion of the eye contents and subsequent shrinking of the globe (phthisis bulbi), or to anterior bulging (corneal ectasia and anterior staphyloma) and blindness. Bitot's spots (superficial foamy patches composed of epithelial debris and secretions on the exposed bulbar conjunctiva) occur in advanced deficiency; they are most likely due to vitamin A deficiency when they occur in young children who have other indications of vitamin A deficiency. In severe vitamin A deficiency in children, mortality can be 50% or more.

Laboratory Findings and Diagnosis Evidence of vitamin A depletion is unobtainable in the preclinical stage, except for a history of inadequate intake. Plasma retinol levels fall after liver stores are exhausted. The normal range is 20 to 80 g/dL (0.7 to 2.8 mol/L); 10 to 19 g/dL (0.35 to 0.66 mol/L) is low, and < 10 g/dL (< 0.35 mol/L) is deficient. Mean plasma retinol binding protein (RBP) is 47 g/mL for adult males and 42 g/mL for adult females. Up to the age of 10 yr, the range is 20 to 30 g/mL. Plasma levels of vitamin A and RBP fall in deficiency states and in acute infections. Other causes of night blindness (eg, retinitis pigmentosa) must be excluded. Secondary infection may complicate the corneal changes. Trial with therapeutic doses of vitamin A assists in the diagnosis.

Prophylaxis Xerophthalmia is the major cause of blindness among young children in most developing countries, where prophylactic doses of 66,000 g (200,000 IU) of vitamin A palmitate in oil orally once every 3 to 6 mo are advised for all children aged 1 to 4 yr; the dose is halved for those < 1 yr. The diet should include dark green leafy vegetables and yellow fruits, such as mango and papaw. Bread, sugar, and monosodium glutamate are fortified with vitamin A. For secondary deficiency, vitamin A supplements should be given routinely. Infants suspected of being allergic to milk should be given adequate vitamin A in the substitute formula.

Treatment The cause should be corrected, and vitamin A should be given in therapeutic doses at once. Oral vitamin A palmitate in oil 20,000 g (60,000 IU) daily for 2 days and once before discharge from the hospital after 7 to 10 days is usually effective. In the presence of vomiting or malabsorption, water-miscible vitamin A must be given IM (oil preparations are not used IM). Thereafter, 3,200 to 8,000 g (10,000 to 25,000 IU)/day is given orally in three divided doses as cod liver oil, red palm oil, or another concentrate. Prolonged daily administration of large doses, especially to infants, must be avoided because toxicity may result.

During pregnancy and lactation, prophylactic or therapeutic doses should not exceed two times the RDA to avoid possible damage to the fetus.

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The Merck Manual of Diagnosis and Therapy

Section 8. Ophthalmologic Disorders

Chapter 96. Corneal Disorders Topics

Superficial Punctate Keratitis Corneal Ulcer Herpes Simplex Keratitis Herpes Zoster Ophthalmicus Keratoconjunctivitis Sicca Phlyctenular Keratoconjunctivitis Interstitial Keratitis Peripheral Ulcerative Keratitis Keratomalacia Keratoconus Bullous Keratopathy Corneal Transplantation

Keratomalacia(Xerotic Keratitis; Xerophthalmia)A condition associated with vitamin A deficiency and protein-calorie malnutrition, characterized by a hazy, dry cornea that becomes denuded.Corneal ulceration with secondary infection is common. The lacrimal glands and conjunctiva are also affected. Lack of tears causes extreme dryness of the eyes, and foamy Bitot's spots appear on the bulbar conjunctiva. Night blindness may be associated. Further details, including specific therapy, can be found under Vitamin A Deficiency in Ch. 3.

www.merck.com/pubs/mmanual/section1/chapter3/3b.htm - 41k - Cached - Save - BlockPENCEGAHAN DAN PENGOBATAN PENYAKIT DEFISIENSIVITAMIN A DENGAN VITAMIN A DOSIS BESAR PERORAL.Angka kebutaan (rate of blindness) untuk Indonesia cukup tinggi. Di Jawa Timurangka ini dilaporkan sebesar 250/100.000 penduduk, dan pada anak-anak sebagianbesar disebabkan oleh keratomalacia.Mengingat pentingnya peranan vitamin A dalam kebutaan ini, telah dilakukan suatupenyelidikan mengenai pencegahan dan pengobatan defisiensi vitamin A di Cibatok,Bogor. Orang-orang percobaan ialah anak-anak prasekolah (berumur 1 -- 6 tahun)yang terdiri dari penderita-penderita defisiensi vitamin A dan anak-anak normalsebagai kontrol. Vitamin A dalam dosis 300.000 IU bersama-sama vitamin E50 IUdiberikan satu kali secara oral dalam bentuk emulsi.6 bulan kemudian hasil percobaan dinilai. Ternyata 90% penderita penyakitdefisiensi vitamin A yang mendapat pengobatan menjadi sembuh, sedangkan 88,9%penderita yang mendapat plasebo masih tetap menderita defisiensi vitamin A.Pemberian vitamin A dengan cara tersebut juga dapat mencegah timbulnya defisiensivitamin A dengan hasil yang memuaskan (I00%).Disimpulkan bahwa pemberian kombinasi vitamin A dan vitamin E dalam dosisbesar, secara oral, dapat mencegah dan mengobati penyakit defisiensi vitamin A padaanak-anak prasekolah dalam waktu 6 bulan.www.kalbefarma.com/files/cdk/ files/14Abstrak005.pdf/14Abstrak005.html - 38k - Hasil Tambahan Jenis VitaminVitamin A

Dibutuhkan untuk pertumbuhan dan pembangunan jaringan yang normal (normal development of tissues); memelihara kesehatan kulit dari dalam dan melindungi kulit luar terhadap infeksi. Juga melindungi dari berbagai bentuk kanker. Vitamin A juga perlu untuk penglihatan;

Gejala Defisiensi (Kekurangan) : Sariawan, rabun malam, jerawat, sering terkena pilek dan infeksi, kulit kering dan pecah-pecah, ketombe, kista, diare;

Sumber : Melon, mangga, tomat, aprikot (apricot), pepaya, dan jeruk kepruk (tangerines); www.kvmi-online.org/v2/viewnutrition.php?id=5 - 17k

Vitamin A Overview

The following is from "Programs Against Micronutrient Malnutrition: Ending Hidden Hunger" by Maberly, G.F. et al., Annu.Rev. Public Health. 1994. 15:277-301.

The most widely known vitamin A deficiency problems are related to the eye, collectively referred to as xerophthalmia, Greek for "dry eyes"; night blindness, caused by a reversible lack of retinol in the retina; conjunctival xerosis; Bitot's spot, an accumulation of cell debris on the conjunctival surface; corneal xerosis; corneal ulceration; and keratomalacia, which results in irreversible blindness. Vitamin A deficiency is the most preventable cause of blindness worldwide (87). These conditions are typically accompanied by serum retinol levels below 0.35 mol/l, well below the normal lower limit of 0.70 mol/l. Corneal xerophthalmia constitutes a medical emergency, because it progresses to irreversible blindness and is associated with increased mortality related to overwhelming infection and malnutrition (87).

The impact of vitamin A deficiency, however, is more extensive than the ocular effects. Xerophthalmia and low vitamin A levels are associated with increased mortality and severity of morbidity from respiratory and gastrointestinal disease (30, 56, 77, 78, 79). Thus, the extent of vitamin A deficiency is often not noticed in affected communities, either by the people themselves or by researchers carrying out cross-sectional studies, because of the high mortality (82, 85). Vitamin A deficiency impairs the body's defenses against infections (88, 64, 70) by breakdown of resistant barriers at epithelial and mucosal surfaces and impairment of both humoral and cellular immunity. The effect of vitamin A may be more likely to be related to inadequate response to infection rather thai impaired resistance to becoming infected, based on meta-analysis in whic:h vitamin A supplementation trials were shown not to affect incidence and duration of disease, but to reduce both severity and mortality rates associated with diarrheal and respiratory infections and with measles (9, 76). One meta-analyses of six randomized controlled trials reported a reduction in mortality of 30% (32) while another of eight trials found a reduction in mortality of 23% in children from 6 months to 5 years (9).

www.sph.emory.edu/PAMM/vitamina.htm - 19k - DEFISIENCY VIT A

KESEHATAN MASYARAKAT"Separo warga kena masalah gizi". Masalah gizi tidak hanya dialami masyarakat miskin, tapi juga masyarakat ekonomi menengah keatas. Riset birektorat Gizi Masyarakat Depkes menemukan sekitar 100 juta atau nyaris separo penduduk Indonesia memiliki masalah dengan angka kecukupan gizi. Direktur Gizi Masyarakat Depkes, Rahmi Untoro mengatakan masalah gizi yang kerap ditemukan pada masyarakat miskin adalah anemia, defisiensi iodium, serta defisiensi vitamin A. Data hasil survei sosial ekonomi nasional 2000 menyebutkan, sekitar 3-4 juta balita menderita kekurangan gizi. Sebanyak 1,5 juta di antaranya terkategori bergizi buruk sehingga mudah terkena diare, infeksi, dan mengalami gangguan pertumbuhan. (Indo Pos 26/6/05)

www.depkes.go.id/index.php?option=news& task=viewarticle&sid=1011&Itemid=2 - 21k

Vitamin A deficiency

DefinitionVitamin A deficiency exists when the chronic failure to eat sufficient amounts of vitamin A or beta-carotene results in levels of blood-serum vitamin A that are below a defined range. Beta-carotene is a form of pre-vitamin A, which is readily converted to vitamin A in the body. Night blindness is the first symptom of vitamin A deficiency. Prolonged and severe vitamin A deficiency can produce total and irreversible blindness.

DescriptionVitamin A (called retinol in mammals) is a fat-soluble vitamin. The recommended dietary allowance (RDA) for vitamin A is 1.0 mg/day for the adult man and 0.8 mg/day for the adult woman. Since beta-carotene is converted to vitamin A in the body, the body's requirement for vitamin A can be supplied entirely by beta-carotene. Six mg of beta-carotene are considered to be the equivalent of 1 mg of vitamin A. The best sources of vitamin A are eggs, milk, butter, liver, and fish, such as herring, sardines, and tuna. Beef is a poor source of vitamin A. Plants do not contain vitamin A, but they do contain beta-carotene and other carotenoids. The best sources of beta-carotene are dark-green, orange, and yellow vegetables; spinach, carrots, oranges, and sweet potatoes are excellent examples. Cereals are poor sources of beta-carotene.

Vitamin A is used for two functions in the body. Used in the eye, it is a component of the eye's light-sensitive parts, containing rods and cones, that allow for night-vision or for seeing in dim-light circumstances. Vitamin A (retinol) occurs in the rods. Another form of Vitamin A, retinoic acid, is used in the body for regulating the development of various tissues, such as the cells of the skin, and the lining of the lungs and intestines. Vitamin A is important during embryological development, since, without vitamin A, the fertilized egg cannot develop into a fetus.

Causes and symptomsVitamin A deficiency occurs with the chronic consumption of diets that are deficient in both vitamin A and beta-carotene. When vitamin A deficiency exists in the developed world, it tends to happen in alcoholics or in people with diseases that affect the intestine's ability to absorb fat. Examples of such diseases are celiac disease (chronic nutritional disorder), cystic fibrosis, and cholestasis (bile-flow failure or interference). Vitamin A deficiency occurred in infants during the early 1900s in Denmark. The deficiency resulted when milk fat was made into butter for export, leaving the by-product (skimmed milk) for infant feeding. Vitamin A deficiency has taken place in infants in impoverished populations in India, where the only foods fed to the infants were low in beta-carotene. Vitamin A deficiency is also common in areas like Southeast Asia, where polished rice, which lacks the vitamin, is a major part of the diet.

The earliest symptom of vitamin A deficiency is night blindness. Prolonged deficiency results in drying of the conjunctiva (the mucous membrane that lines the inner surface of the eyelids and extends over the forepart of the eyeball). With continued vitamin A deficiency, the drying extends to the cornea (xerophthalamia). The cornea eventually shrivels up and becomes ulcerated (keratinomalacia). Superficial, foamy gray triangular spots may appear in the white of the eye (Bitot's spots). Finally, inflammation and infection occur in the interior of the eye, resulting in total and irreversible blindness.

DiagnosisVitamin A status is measured by tests for retinol. Blood-serum retinol concentrations of 30-60 mg/dl are considered in the normal range. Levels that fall below this range indicate vitamin A deficiency. Night blindness is measured by a technique called electroretinography. Xerophthalamia, keratinomalacia, and Bitot's spots are diagnosed visually by trained medical personnel.

TreatmentVitamin A deficiency can be prevented or treated by taking vitamin supplements or by getting injections of the vitamin. The specific doses given are oral retinyl palmitate (110 mg), retinyl acetate (66 mg), or injected retinyl palmitate (55 mg) administered on each of two successive days, and once a few weeks later if symptoms are not relieved.

PrognosisThe prognosis for correcting night blindness is excellent. Xerophthalamia can be corrected with vitamin A therapy. Ulcerations, tissue death, and total blindness, caused by severe vitamin A deficiency, cannot be treated with vitamin A.

PreventionVitamin A deficiency can be prevented by including foods rich in vitamin A or beta-carotene as a regular component of the diet; liver, meat, eggs, milk, and dairy products are examples. Foods rich in beta-carotene include red peppers, carrots, pumpkins, as well as those just mentioned. Margarine is rich in beta-carotene, because this chemical is used as a coloring agent in margarine production. In Africa, Indonesia, and the Philippines, vitamin A deficiency is prevented by public health programs that supply children with injections of the vitamin.

Key TermsBitot's spots

Bitot's spots are superficial, foamy gray, triangular spots on the white of the eyeball.

Carotenoids

Carotenoids are yellow to deep-red pigments.

Conjunctiva

The conjunctiva is a clear layer of cells that covers the eye and directly contacts the atmosphere. The conjunctiva is about five-cells thick.

Cornea

The cornea is a clear layer of cells that covers the eye, just under the conjunctiva. The cornea is about 50-cells thick.

Fat-soluble vitamin

Fat-soluble vitamins can be dissolved in oil or in melted fat. Water-soluble vitamins can be dissolved in water or juice.

Keratinomalacia

Keratinomalacia is ulceration of the cornea.

Recommended Dietary Allowance (RDA)

The Recommended Dietary Allowances are quantities of nutrients in the diet that are required to maintain good health in people. RDAs are established by the Food and Nutrition Board of the National Academy of Sciences, and may be revised every few years. A separate RDA value exists for each nutrient. The RDA values refer to the amount of nutrient expected to maintain good health in people. The actual amounts of each nutrient required to maintain good health in specific individuals differ from person to person.

Xerophthalmia

Xerophthalmia is a dry, thickened, lusterless condition of the eyeball resulting from vitamin A deficiency

www.healthatoz.com/healthatoz/Atoz/ency/vitamin_a_deficiency.jsp - 26k -

Vitamin A Deficiency

April 21, 1999 MicSem Monthly Discussion Topic #21

What's the Problem?

Vitamin A Deficiency is doing serious damage to our children. Although some of its other symptoms can be more critical, its best known symptom is night blindness, when young people simply can't see anything in the evening because their eyes are no longer capable of making the proper adjustments. Some children show clouding of the eyes and eye spots. In more extreme cases, the deficiency destroys the eyeball, eating away at it until it is gone. But these are the most obvious symptoms of Vitamin A deficiency. It does even more serious damage covertly-by weakening the immune system and so making the child susceptible to other diseases such as flu or even infections. Those who suffer the most from this deficiency are the children who do not survive long enough to experience the effects of the ghastly degeneration of the eyes, for they have already died of a condition that has been brought on, or at least worsened by, Vitamin A deficiency.

Vitamin A deficiency is a form of malnutrition. Like all kinds of malnutrition it weakens the body generally so that it makes the person susceptible to any number of diseases. In a small child these can often prove fatal. It's anyone's guess just what this might mean in terms of mortality, but medical researchers have suggested that Vitamin A deficiency could be responsible for 30 percent of all child deaths on Pohnpei.

How Bad Is It?

The answer to this varies from place to place, but there are two states in FSM-Chuuk and Pohnpei-that show especially high rates of this deficiency. The data is difficult to compare because it is sometimes based on different sorts of tests, but it points to a serious problem. In Chuuk about 18 percent of the children tested showed physical degeneration of their eyes (what is called xerophthalmia) as a result of Vitamin A deficiency. Pohnpei had no tests done for clinical Vitamin A deficiency, but if we were to extrapolate from other studies we might conclude that about 10 percent of Pohnpeian children show the same level of deficiency. Kiribati, which is also high, shows a rate of 15 percent, while the Marshalls rate is only 4 percent. The rate in the Solomons is 1.7 percent, while in the rest of the Pacific it is negligible. Interestingly enough, Palau shows a very low rate of Vitamin A deficiency. The World Health Organization (WHO) considers a prevalence rate over 1.5 percent to be a "major public health problem." Pohnpei is probably six times higher than this, and Chuuk is twelve times this rate.

Within Chuuk, the prevalence of Vitamin A deficiency is highest in the lagoon and on the capital, Weno Island. It is much lower in the remote outer islands to the west and northwest of Chuuk. This may indicate that a traditional lifestyle and diet guards against the deficiency, but other factors may also be involved. It also suggests that Vitamin A deficiency follows the pattern of many other forms of malnutrition in that it shows up the most in those geographical areas and social groups that are neither traditional nor fully modernized, but in the groups that are on the fringe of the modern sector. Characteristically, these groups live in the peri-urban areas, near but not in the center of town. Such groups lack the vitamin-rich traditional foods but often do not have the money to purchase adequate substitutes or do not understand the importance of including substitutes.

What Does It Do?

Vitamin A, also known as retinol, is found in certain kinds of foods: for example, fish oils, liver, butter and egg yolk. Beta-carotene, a precursor of Vitamin A and something that can be converted into Vitamin A by the cells in our intestines, is found in green leafy and yellow vegetables such as pele, mango, papaya, carrots, and a type of sweeet, reddish banana known as the karat. Excess Vitamin A can be stored in our liver and called upon when our intake decreases. Vitamin A is vital for the functioning of the immune system. It is also an important ingredient in the proteins that form the structure of the eye. While overdoses of Vitamin A can occur, they are difficult to achieve and are rare. On the other hand, lack of retinol leads to a host of health problems that can lead to an early death.

What Causes the Problem?

Although the problem is often thought to be dietary, our panel of experts pointed out that there is no single cause for Vitamin A deficiency. Deficiency might be due to inadequate intake of Vitamin A in the diet, but it could also be due to inadequate absorption (through malfunctions in our bodily system) or excess wastage (drained off through infections or diarrhea). This deficiency can, therefore, be linked to other conditions, such as the cleanliness of the water supply, since impure water will cause diarrhea, leading to the rapid expulsion of Vitamin A from the system. This deficiency also seems to depend on whether the body is getting its other requirements, such as iron and iodine, for there is a complex interrelationship between such elements in the human body. Yet, the condition is more directly related to the intake of foods that produce Vitamin A than anything else.

Then and Now

Are we worse off today than in former times? Because we do not have baseline studies that give us any hint of what the level of Vitamin A deficiency was in the past, we cannot conclusively answer that question. Someone suggested that the fact that Pohnpeians have no word for night blindness implies that this condition was not recognized as important in the past because the disorder was not commonly found in those days. On the other hand, it may have been that, while the problem was just as common then, those suffering from the deficiency simply didn't live long enough to develop the eye symptoms that mark long-term sufferers.

If, as seems to be suggested by these medical studies, changes in the diet in recent years have contributed to the problem, we might ask what specific changes we might blame. Several were pointed out. Breastfeeding has given way to bottle feeding in some areas, so the baby is getting less Vitamin A, not to mention the problems that can be associated with the use of contaminated water that is often used to mix formula or the improper preparation of the formula. Many more people today are eating unenriched white rice, poor in Vitamin A, rather than breadfruit. There may be less fresh fish eaten today and more canned fish being consumed. Even mangoes, which are eaten in great quantities by kids lucky enough to find some, are being eaten green today (that is, without the Vitamin A) rather than being eaten when they are ripe (and full of Vitamin A).

The problem may be not only the food items consumed but the way in which they are prepared today. Some participants pointed out that, although it was accurate to say that Micronesians in general did not have a real predilection for green leafy vegetables, they absorbed some of the vitamins from these greens in other ways. Food was prepared in pots, which were covered with plant leaves and boiled, allowing some of the juices of the plant to seep down into the water. Today no one uses these plants much anymore since their taste is not appreciated and gathering them is regarded as too much trouble in any case. Modern life styles, especially whe women work full-time, also lead to changes in food choices and preparation, practices that may lead to decreases in Vitamin A intake.

Strategies

Health Services in the FSM has been giving supplemental doses of Vitamin A to as many children as it can reach twice a year. Someone suggested that possibly more could be reached if the treatment were mixed with the candy (or other treats) that is distributed to the island children by Santa Claus around Christmas time. However it is done, distribution of Vitamin A supplements was presented as a strategy that is not only justifiable but also imperative, even if it is a short-term solution. In the long term, however, we must educate the population on the ways in which an adequate level of Vitamin A can be restored to their diet.

There are two basic strategies that can be used to accomplish this. We can have the people look back to their diet in the old days with an eye to restoring as much of the traditional diet and the ways of preparing it as are feasible. Alternatively, we can propose new solutions in lieu of any hope of restoring the old customs. In other words, instead of trying to persuade people to eat lots of breadfruit and certain tree crops, we may urge them to get used to eating new items that are demonstrably rich in Vitamin A. This could mean pushing the karat banana, pele, and other sources of the vitamin that might not have been used so often in the past. Perhaps the best strategy is one that combines bits of both. Or there may be some as yet unthought of innovative strategy. Whatever strategies are used, they must be culturally satisfying.

http://www.micsem.org/pubs/conferences/frames/vitadeffr.htm?http&&&www.micsem.org/pubs/conferences/vitadef.htmVitamin A (Retinol)

Vitamin A and its metabolites play diverse roles in physiology, ranging from incorporation into vision pigments to controlling transcription of a host of important genes. Health depends on maintaining vitamin A levels within a normal range, as either too little or too much of this vitamin lead to serious disease.

Structure

Vitamin A or retinol has a structure depicted to the right. Retinol is the immediate precursor to two important active metabolites: retinal, which plays a critical role in vision, and retinoic acid, which serves as an intracellular messenger that affects transcription of a number of genes. Vitamin A does not occur in plants, but many plates contain carotenoids such as beta-carotene that can be converted to vitamin A within the intestine and other tissues.

Physiologic Effects of Vitamin A

Vitamin A and its metabolites retinal and retinoic acid appear to serve a number of critical roles in physiology, as evidenced by the myriad of disorders that accompany deficiency or excess states. In many cases, precise mechanisms are poorly understood. Some of the well-characterized effects of vitamin A include:

Vision: Retinal is a necessary structural component of rhodopsin or visual purple , the light sensitive pigment within rod and cone cells of the retina. If inadequate quantities of vitamin A are present, vision is impaired.

Resistance to infectious disease: In almost every infectious disease studied, vitamin A deficiency has been shown to increase the frequency and severity of disease. Several large trials with malnourished children have demonstrated dramatic reductions in mortality from diseases such as measles by the simple and inexpensive procedure of providing vitamin A supplementation. This "anti-infective" effect is undoubtedly complex, but is due, in part, to the necessity for vitamin A in normal immune responses. Additionally, many infections are associated with inflammatory reactions that lead to reduced synthesis of retinol-binding protein and thus, reduced circulating levels of retinol.

Epithelial cell "integrity": Many epithelial cells appear to require vitamin A for proper differentiation and maintenance. Lack of vitamin A leads to dysfunction of many epithelia - the skin becomes keratinized and scaly, and mucus secretion is suppressed. It seems likely that many of these effects are due to impaired transcriptional regulation due to deficits in retinoic acid signalling.

Bone remodeling: Normal functioning of osteoblasts and osteoclasts is dependent upon vitamin A.

Reproduction: Normal levels of vitamin A are required for sperm production, reflecting a requirement for vitamin A by spermatogenic epithelial (Sertoli) cells. Similarly, normal reproductive cycles in females require adequate availability of vitamin A.

Sources of Vitamin A

Vitamin A is present in many animal tissues, and is readily absorbed from such dietary sources in the terminal small intestine. Liver is clearly the richest dietary source of vitamin A.

Plants do not contain vitamin A, but many dark-green or dark-yellow plants (including the famous carrot) contain carotenoids such as beta-carotene that serve as provitamins because they are converted within the intestinal mucosa to retinol during absorption.

Vitamin A is stored in the liver as retinyl esters and, when needed, exported into blood, where it is carried by retinol binding protein for delivery to other tissues.

Vitamin A Deficiency and Excess States

Both too much and too little vitamin A are well known causes of disease in man and animals.

Vitamin A deficiency usually results from malnutrition, but can also be due to abnormalities in intestinal absorption of retinol or carotenoids. Deficiency is prevalent in humans, especially children, in certain underdeveloped countries. In herbivores such as cattle, vitamin A deficiency is usually due to lack of green feed, such as in animals coming off of dry summer pastures or those fed poor quality hay. Because the liver stores rather large amounts of retinol, deficiency states typically take several months to develop. Some of the more serious manifestations of vitamin A deficiency include:

Blindness due to inability to synthesize adequate quantities of rhodopsin. Moderate deficiency leads to deficits in vision under conditions of low light ("night blindness"), while severe deficiency can result in severe dryness and opacity of the cornea (xeropthalmia).

Increased risk of mortality from infectious disease has been best studied in malnourished children, but also is seen in animals. In such cases, supplementation with vitamin A has been shown to substantially reduce mortality from diseases such as measles and gastrointestinal infections.

Abnormal function of many epithelial cells, manifest by such diverse conditions as dry, scaly skin, inadequate secretion from mucosal surfaces, infertility, decreased synthesis of thyroid hormones and elevated cerebrospinal fluid pressure due to inadequate absorption in meninges.

Abnormal bone growth in vitamin A-deficient animals can result in malformations and, when the skull is affected, disorders of the central nervous system and optic nerve.

Vitamin A excess states, while not as common as deficiency, also lead to disease. Vitamin A and most retinoids are highly toxic when taken in large amounts, and the most common cause of this disorder in both man and animals is excessive supplementation. In contrast, excessive intake of carotinoids are not reported to cause disease - you cannot use the excuse of potential vitamin A toxicity to avoid eating carrots or green vegetables!

Teratogenic effects: Both hypovitaminosis A and hypervitaminosis A are known to cause congenital defects in animals and likely to have deleterious effects in humans. Pregnant women are advised not to take excessive vitamin A supplements, and some medical authorities also recommend that they consume liver only in moderation, which is usually not a hard sell to make.

Back to the index of Vitamins

References and Reviews Bates CJ: Vitamin A. Lancet 345:31, 1995.

Last updated on July 4, 1999

Author: R. Bowen

Send comments via form or email to rbowen@lamar.colostate.edu

arbl.cvmbs.colostate.edu/hbooks/pathphys/misc_topics/vitamina.html - 8k

VIT A

A. Background

Description

Vitamin A is a general term that refers to fat-soluble compounds that are similar in structure and biologic activity to retinol. Vitamin A also refers to dietary precursors of vitamin A (6,11). The precursors of vitamin A (retinol) are the carotenoids (most commonly beta-carotene). The term retinoid refers to any compound that is structurally similar to retinal (aldehyde), retinol (alcohol), or any other substance that exhibits vitamin A activity (1). Retinoic acid, which is a metabolite of retinal (6), is such a substance that is often studied. Synthetic compounds within the vitamin A family have similar structures as the natural form, but may have few or no functions that the natural vitamin posses (11). Most compounds within the vitamin A family are soluble in fat and essential to numerous processes within the body. There have been several water-soluble retinoids, extracted from plasma, bile, and other tissue (11). For the purposes of this literature review any discussion of vitamin A will focus on those retinoids with fat-soluble properties. The main discussion will involve retinol. Retinol is chemically a "pale yellow crystalline solid" (6). The solid and its metabolites exist in nature as various isomers. The biologic metabolites of retinol are unique in that they contain five conjugated double bonds within their six-carbon ring (B-ionone) and isoform specific side chains (11). The double bonds contribute special properties; for example, the double bonding in retinol plays a unique role in multiple vision processes, which will be discussed in a subsequent section of this review. As mentioned earlier most retinoids are soluble in organic solvents and fat. However, oxidation and polymerization are all detrimental to retinoids; therefore, the compounds must be protected from light, oxygen and high temperature.

Dietary Function

Vitamin A is essential for numerous intrinsic processes. The most well-known and understood process is that of vision. The 11-cis retinal form of vitamin A is essential for the neural transmission of light into vision (11). Epithelial cells are highly dependent on retinoic acid and are commonly used to treat a variety of skin diseases. A developing fetus is also highly dependent on retinoic acid, as it is essential to the growth of the eyes, lungs, ears and heart (6). The retinoids are not only the most active form of vitamin A, but also a current area of interest to many scientists. The role of vitamin A as an antioxidant is debatable. Vitamin A has been shown to possibly have some antioxidant characteristics. However, the carotenoids such as beta-carotene have in recent years received more attention from the scientific community because of the harmful role they may play as pro-oxidants (14). A great deal more research is needed that addresses the role of vitamin A as an antioxidant to determine the exact role the vitamin and precursors play.

Sources

Retinol, the active form of vitamin A, is rarely found in foods. Instead, precursors to retinol, fatty acid retinyl esters, are found in the human diet. The esters are commonly found in foods of animal origin, such as egg yolks, liver, fish oil, whole milk and butter (6). Plants can synthesize the carotenoids, but cannot convert them to retinoids; this process occurs in the human body (11). The carotenoids are red, yellow, and orange in color and substantial in number (over 400 types). It is estimated that only 10% of the pigments have "vitamin A activity", with beta-carotene having the greatest activity, followed by the alpha and gamma forms (6). Fruits and vegetables that appear bright orange or yellow in color are usually high in carotenoids. All green vegetables also contain substantial amounts of carotenoids, but the orange or yellow color is masked by chlorophyll (6). The wide variety of vitamin A precursors allows for adequate amounts of the vitamin in all diet types.

B. Metabolism

Absorption and Bioavailability

Seventy to ninety percent of vitamin A from the diet is absorbed in the intestine. The efficiency of absorption for vitamin A continues to be high (60-80%) as intake continues to increase. Greater than 90% of the retinol store within the body enters as retinyl esters that are subsequently found within the lipid portion of the chylomicron (11). Absorption of vitamin A is very rapid, with maximum absorption occurring two to six hours after digestion (11). Within the intestinal lumen the vitamin is incorporated into a micelle and absorbed across the brush border into the enterocytes. Within the enterocyte, precursors of vitamin A (carotenoids) are converted to active forms of the vitamin. The newly formed products and additional precursors are then packaged into chylomicrons and readied for transport throughout the body (6).

Transport

After leaving the enterocytes chylomicrons, which carry retinyl esters, carotenoids, and unesterfired retinol along with triglycerides, are circulated first through the lymphatic system and then through the general circulation. Upon arriving at extra-hepatic cells chylomicrons release triglycerides, however vitamin A remains within the chylomicron. The vitamin A is then incorporated into a chylomicron remnant (6). The chylomicron remnant then travels back to the liver where it is taken up and further metabolized or stored. When needed retinol is mobilized from the liver and requires the use of a carrier for transport through the blood. Retinol-binding protein (RBP) is the specific carrier used to transport all-trans retinol in the plasma. The all-trans isoform accounts for more than 90% of all plasma vitamin A (11). This specific carrier is manufactured and secreted by the parenchymal cells of the liver (6,11). Each mole of retinol released binds equivocally with RBP to form holo-RBP. This compound then binds with a molecule of transthyretin (TTR), formerly known as prealbumin. This newly formed retinol-RBP-TTR complex is not filtered by the glomerulus, but instead freely circulates throughout the plasma. Tissues are then able to take the retinol up as needed via cellular retinoid-binding protein (11). Retinoic acid is believed to be manufactured by the cells as needed. Therefore, transport of retinoic acid is likely not substantial. Instead, the cell possesses intra-cellular proteins that regulate the amount of retinoic acid produced. The proteins also help to determine the intracellular usage of retinoic acid (6).

Storage

Approximately 50 to 85% of the total body retinol are stored in the liver when vitamin A status is adequate (11). Retinol returning to the liver is re-esterfied before storage. Because of this, over 90% of the retinol is stored in the form of retinyl esters. The retinol is stored in hepatic stellate (star-shaped) cells along with droplets of lipid (6,11). Thus constitutes the fat-soluble property of vitamin A. The size of stellate cells increase linearly with increasing retinol levels. Once hepatic stellate cells are saturated with all the retinol they can hold, hypervitaminosis can result. (11). The precursor to vitamin A, beta-carotene, can be stored in adipose cells of fat depots throughout the body (2). To date the only side effect of excess beta-carotene supplementation appears to be yellowing of the skin. Serum levels of beta-carotene are an indicator of recent intake and not body stores (6).

Excretion

The kidneys are the main paths of RBP and retinol excretion from the body. This is achieved manly via renal catabolism and glomerular filtration (11). Those persons suffering from renal disease often experience elevated serum levels of RBP and retinol and therefore must be more aware of vitamin A toxicity.

Physiological Role

As previously mentioned vitamin A is essential to vision. Within the photoreceptor cells of the retina are the rods, which detect small amounts of light and are specialized for motion detection and vision in dim light, and the cones that are specialized for color vision in bright light (11). Both rods and cones posses specialized outer segment disks that contain high amounts of rhodopsin and iodopsin respectively. These compounds are often referred to as the "visual pigment" (11). Photoreceptor cells detect light and undergo a series of reactions, which send signals to the brain, where they are deciphered as a particular visual image. A second very important function of vitamin A involves retinoic acid. Acting as a hormone, retinoic acid first binds to retinoic acid receptors. The receptors then interact with specific nucleotide sequences of DNA. The interaction directly affects gene expression and transcription, which in turn control cellular development and body processes (6). For example, epithelial cells depend on retinoic acid for structural and functional maintenance. This role of vitamin A is important for growth mechanisms in a manner that is not completely understood (6). Retinoic acid is especially important in heart, eye, lung and ear development (11). The development of gap junctions between cells is also affected by retinoic acid (6). Besides the previously mentioned functions, vitamin A plays a role in numerous other processes. Vitamin A is thought to play a key role in glycoprotein synthesis. Once formed, glycoproteins are important in multiple cellular processes including: communication, recognition, adhesion, and aggregation. Reproductive processes, bone development, along with maintenance, and immune system function (6,11) are dependent upon different isoforms of vitamin A. Retinoids are most commonly used in the treatment of skin diseases. The role the retinoids play in epithelial cell formation is very important in the treatment of skin cancer, acne, and acne-related diseases (11). Vitamin A also has antioxidant properties. However, beta-carotene has been noted as having pro-oxidant properties. Despite these discrepancies vitamin A is known to help repair damaged tissue and therefore may be beneficial in counter-acting free radical damage (11).

C. Daily Reference Intakes (DRI)

Current DRI

The Recommended Dietary Allowance (RDA) established in 1980 for vitamin A was set at 800-ug retinol equivalent (RE) for adult women and 1000 ug (1mg) retinol equivalent (RE) for adult men (6). It should be noted that 1 RE of vitamin A is equal to 3.33 IU of the vitamin. The levels (RDA) were not changed in 1989 when the RDAs were revised (6,11). One RE is equivalent to 1 ug of all-trans retinol, or 6 ug of all-trans beta-carotene (6). The RDA was based on the amount of vitamin needed to reverse night-blindness in vitamin A deficient subjects. The RDA has also been based on the amount needed to raise the plasma vitamin A levels to normal in depleted subjects. Starting in 2000 Dietary Reference Intakes (DRI) were developed to replace the RDA. A DRI for vitamin was not established. The DRI incorporates a safety ceiling into the recommendation, however due to a lack of evidence a safe upper limit could not established. The absence of a safe upper limit plus the numerous carotenoids has led the National Academy of Sciences to not establish a DRI at this time. The RDA is the current dietary guideline being used in place of the DRI. For men the RDA is 1000 mg of retinol equivalents (RE) and for women the RDA currently stands at 800 mg RE (10).

Deficiency

Deficiency of vitamin A is very rare in the United States, unless confounding malabsorption conditions such as steatorrhea, or diseases of the liver, pancreas, or gallbladder are present. In contrast vitamin A deficiency is prominent in young children (