Anemia terjadi ketika sel-sel darah merah berkurang jumlahnya. Sel darah merah merupakan komponen utama dalam darah dan melayani fungsi vital mengantar oksigen dari paru-paru ke seluruh jaringan dalam tubuh. Ketika anemia terjadi, tubuh kekurangan oksigen yang dibutuhkan untuk berfungsi dengan benar.

Ada banyak jenis anemia, yang semuanya memiliki perawatan mereka sendiri. Jenis yang paling umum termasuk:

anemia defisiensi besi Asam folat dan anemia defisiensi

anemia akibat kekurangan vitamin B12.

Anemia mungkin akibat dari penyakit kronis, obat, atau konsumsi alkohol yang berlebihan. Dalam beberapa kasus, mewarisi kondisi yang menghasilkan darah hasil cacat pada anemia.

Sebagian besar kasus anemia diperbaiki hanya dengan menambahkan asam folat besi atau lebih untuk diet. Jika Anda memiliki kekurangan vitamin B12, Anda mungkin memerlukan suntikan intramuskular. Beberapa kasus yang tidak mudah diperbaiki.

Seseorang yang sedikit anemia mungkin merasa lelah dan lemah dan tampak pucat. Mendapatkan tele dan mengalami sakit pada dada selama latihan adalah gejala lain dari anemia. Dalam kasus yang lebih serius, denyut jantung tidak teratur atau gejala neurologis seperti bingung, lekas marah, dan mati rasa atau kesemutan pada ekstremitas muncul.

Penyebab

Anemia defisiensi besi adalah jenis yang paling umum dari penyakit, dan paling sering disebabkan oleh kehilangan darah yang berlebihan. Ketika tubuh kehilangan darah, kehilangan besi-bagian penting dari sel darah merah. Zat besi dibutuhkan untuk membuat hemoglobin, protein dalam sel darah merah yang membawa oksigen. Bertahap, kehilangan darah yang berkepanjangan dari menstruasi berat adalah penyebab utama anemia defisiensi besi pada wanita. Perdarahan gastrointestinal dari wasir, ulkus lambung, atau kondisi inflamasi usus juga dapat membuat seseorang anemia. Darah akibat kanker usus besar dan usus kanker lainnya menyumbang sekitar 2% dari kasus kehilangan. Penggunaan jangka panjang dari aspirin atau obat anti-inflammatory drugs (NSAID) seperti ibuprofen dan naproxen dapat mengiritasi lapisan lambung dan perdarahan penyebab yang menghasilkan anemia. Wanita yang sedang hamil atau menyusui terkadang menjadi anemia ketika kebutuhan meningkat besi mereka tidak terpenuhi. Anak-anak tumbuh, yang juga membutuhkan zat besi lebih banyak, kadang-kadang menjadi anemia. Namun, kekurangan makanan jarang penyebab anemia defisiensi besi.

Kekurangan asam folat adalah jenis anemia yang terjadi ketika ada terlalu sedikit asam folat yang dikonsumsi dalam diet, atau jika tidak benar diserap di dalam tubuh. Tubuh membutuhkan asam folat untuk membuat sel darah merah. Terlalu sedikit ini (juga disebut folat) hasil vitamin dalam sel darah merah yang normal besar (makrositik), dan mati sebelum waktunya. Tubuh tidak menyimpan asam folat dalam jumlah besar, dan kadar asam folat karena itu perlu dipertahankan

melalui diet. Asam folat dan anemia defisiensi disebabkan oleh asupan yang tidak memadai atau ketidakmampuan untuk menyerap vitamin. Pada saat-saat tertentu, seperti selama kehamilan dan menyusui, tubuh membutuhkan lebih banyak asam folat dari biasanya. Kebanyakan wanita hamil disarankan untuk mengonsumsi suplemen (yang mencegah cacat lahir), dan pemerintah sekarang memerlukan bahwa banyak makanan (sereal, roti, pasta) diperkaya dengan vitamin. Orang dengan penyakit gastrointestinal dan kanker mungkin memiliki masalah menyerap asam folat, dan menjadi anemia. Demikian juga, orang yang memakai obat-obatan tertentu (antikonvulsan, antibiotika, keluarga berencana, pil, agen antikanker) kadang-kadang mengalami kesulitan menyerap atau metabolisme asam folat.

Anemia pernisiosa adalah kondisi kurang umum tapi serius yang terjadi ketika tubuh tidak dapat menyerap vitamin B12. Anemia pernisiosa adalah gangguan di mana sistem kekebalan tubuh menyerang sel-sel di lambung yang menghasilkan faktor intrinsik (IF)-zat yang dibutuhkan untuk mengangkut vitamin B12. Tanpa IF, kekurangan B12 mengembangkan dan sel darah merah tumbuh terlalu besar dan mati terlalu dini. Anemia pernisiosa kadang-kadang timbul setelah operasi usus atau dari masalah usus dari metabolisme merusak vitamin ini. Pada orang tua, kerusakan lapisan lambung (gastritis atrofik) dan kegagalan berikutnya untuk menghasilkan JIKA merupakan penyebab umum. Diet jarang terlibat dalam kekurangan vitamin B12, meskipun dapat menjadi penyebab di vegetarian yang ketat, atau vegan, yang tidak makan daging atau produk susu yang kaya akan vitamin.

Penyakit kronis seperti kanker, rheumatoid arthritis, HIV / AIDS, atau kecanduan alkohol, dan obat-obatan tertentu juga dapat menyebabkan anemia. Penyakit ginjal kronis adalah juga merupakan penyebab penting anemia kronis. Orang dengan kanker yang mempengaruhi sumsum tulang, yang mana sebagian besar sel darah merah yang diproduksi, sering menjadi anemia; begitu juga orang dengan penyakit yang memicu proses inflamasi, seperti rheumatoid arthritis, lupus, penyakit Grave, penyakit Crohn, dan ulseratif kolitis. Sitokin, yang adalah protein yang dilepaskan selama peradangan, tampaknya akan bertanggung jawab. Sitokin adalah penting untuk penyembuhan, tetapi bila berlebihan dapat mengganggu besi dan hormon bertanggung jawab untuk merangsang produksi sel darah merah (erythropoietin).

Pecandu alkohol kadang-kadang mengalami anemia karena kekurangan gizi. Alkohol menghambat penyerapan vitamin, dan pecandu alkohol cenderung makan buruk.

Obat-obatan juga dapat menyebabkan anemia. Penggunaan jangka panjang NSAID dapat menyebabkan pendarahan yang mengakibatkan anemia. Obat yang menekan sistem kekebalan tubuh dan melawan kanker dapat menyebabkan anemia aplastik-anemia yang terjadi ketika sumsum tulang tidak membuat cukup sel darah merah. Selain itu, antibiotik tertentu, obat tekanan darah, dan obat-obatan digunakan untuk mengobati arrythmias jantung jarang dapat menyebabkan anemia hemolitik anemia-yang terjadi ketika sel darah merah yang hancur sebelum waktunya.

Anemia yang jarang namun serius seperti anemia sel sabit dan talasemia diwariskan. Sesuai namanya, anemia sel sabit ditandai dengan sabit berbentuk sel darah merah. Sel-sel ini kaku, dan tidak dapat melewati pembuluh darah yang sangat baik. Akibatnya, mereka mati setelah sekitar 20 hari (masa hidup rata-rata untuk sel darah normal merah adalah 120 hari). Anemia yang

dihasilkan, yang mempengaruhi sekitar 0,6% dari populasi, serius, dan dapat mematikan. Thalassemia adalah kelainan darah bawaan yang berasal dari cacat dalam tingkat di mana hemoglobin diproduksi. Dua jenis utama adalah talasemia mayor (anemia Cooley) dan talasemia minor (lebih umum dari dua). Thalassemia bisa sangat serius, tapi kondisi ini jarang terjadi, tetapi lebih sering ditemukan pada orang keturunan Mediterania.

Efek hematologi

Anemia kadang-kadang terlihat pada pasien yang menerima NSAIDs, termasuk kapsul piroksikam. Ini mungkin karena retensi cairan, okultisme atau kotor kehilangan GI darah, atau efek tidak lengkap dijelaskan pada eritropoiesis. Pasien pada pengobatan jangka panjang dengan NSAID, termasuk kapsul piroksikam, harus memiliki hemoglobin atau hematokrit diperiksa jika mereka menunjukkan tanda-tanda atau gejala anemia.

NSAID menghambat agregasi platelet dan telah ditunjukkan untuk memperpanjang waktu perdarahan pada beberapa pasien. Tidak seperti aspirin, efeknya pada fungsi trombosit adalah kuantitatif kurang, dari durasi yang lebih singkat, dan reversibel. Pasien yang menerima kapsul piroksikam yang dapat terpengaruh oleh perubahan dalam fungsi platelet, seperti yang dengan gangguan koagulasi atau pasien yang menerima antikoagulan, harus dimonitor dengan baik.

PENYULUHAN ANEMIA DEFISIENSI BESI (ADB) PADA REMAJA PUTRI

DI SEKOLAH MENENGAH ATAS NEGERI 1 BANGLI

Dharmadi, M., Seri Ani, L., Sutarsa, IN., Ayu Kartika, dan Aryani, P.

Bagian Ilmu Kedokteran Komunitas dan Pencegahan

Fakultas Kedokteran Universitas Udayana

ABSTRACT

           The incidence of Iron Deficiency Anemia (IDA) among pregnant women in Indonesia is 63,5%, and in Bali is found 46,2%. The prevalence of IDA in Bangli Regency is 45,6%. It is suspected that latent iron deficiency is being existed during pre pregnancy stage. It is required, however that campaign of IDA and the prevention is need to be conducted in order to reduce the incidence of IDA either in pre pregnancy or pregnancy stages. This activity aims to capture the level of knowledge of female students in SMAN 1 Bangli before and after the campaign. The result showed that the level of knowledge of female students related to IDA is increasing from mean 3,47 to 6,14.

Keywords: iron deficiency anemia, female students, knowledge

ABSTRAK

            Angka kejadian anemia defisiensi besi (ADB) pada wanita hamil di Indonesia adalah sekitar 63,5% dan di Bali sebesar 46,2%. Angka kejadian di Kabupaten Bangli juga ditemukan masih tinggi yaitu sebesar 45,8%. Diduga hal ini terjadi karena telah terjadi defisiensi besi laten sejak masa prahamil. Penyuluhan ADB menjadi penting untuk menaggulangi masalah ADB pada wanita prahamil dan pada saat mereka mengalami kehamilan. Penyuluhan ini bertujuan untuk melihat pengetahuan remaja putri terkait anemia dan peningkatan pengetahuan yang terjadi setelah diberikan penyuluhan. Meteri penyuluhan meliputi penjelasan tentang ADB, paparan penyebab, dampak, dan strategi pencegahan secara mandiri. Penyuluhan ini berhasil meningkatkan pengetahuan remaja putri terkait ADB dengan peningkatan mean dari 3,47 menjadi 6,14 di SMAN 1 Bangli.

Kata kunci: ADB, remaja putri, pengetahuan

PENDAHULUAN

       Penurunan pasokan zat besi (fe) dalam mencukupi kebutuhan tubuh dapat berakibat pada

terjadinya Anemia Defisiensi Besi (ADB). Defisiensi Fe kronis akan berdampak pula pada

penurunan fungsi fisiologis penderitanya. Hal ini juga terjadi pada kasus ADB, dimana para

penderitanya karena mengalami defisiensi besi, maka fungsi sistem organnya juga mengalami

penurunan. Berbagai penelitian melaporkan bahwa kejadian ADB pada wanita hamil dapat

menimbulkan dampak baik bagi bayi ataupun ibu, mulai dari dalam kandungan, proses

persalinan, setelah bayi dilahirkan, usia sekolah, hingga memasuki fase hidup dewasa. Dampak

yang sering dijumpai adalah peningkatan partus prematurus yang berkaitan dengan masalah

ADB. Konsekuensinya adalah timbulnya berbagai permasalahan baru bagi si bayi seperti berat

badan lahir yang rendah (BBLR), penurunan status imunitas, peningkatan risiko gangguan

fisiologis dan tumbuh kembang bayi (Allen 1997). Dampak lanjutan di usia sekolah adalah

timbulnya Intelegent Quotion (IQ) yang rendah, penurunan kemampuan belajar, dan penurunan

angka pertumbuhan anak (Purwani dan Hadi 2002; Conrad 2003). Sedangkan dampak jangka

panjang dari anemia adalah penurunan kualitas sumber daya manusia, penurunan produktivitas

kerja, dan memberikan implikasi ekonomis yang negatif (Ross dan Horton 1998).

        Prevalensi ADB dilaporkan masih tinggi dan menyerang hampir seluruh kelompok umur di

masyarakat. Menurut Conrad (2003), wanita hamil merupakan salah satu kelompok dengan

prevalensi ADB yang cukup tinggi. Hal yang sama juga ditemukan di Indonesia yaitu masih

tingginya prevalensi ADB pada wanita hamil, walaupun data yang tersedia memiliki variasi yang

sangat lebar. Temuan Baker (2000) bahwa rata-rata 18% wanita hamil di negara maju mengalami

ADB sedangkan di Indonesia mencapai sekitar 63,5% (Muhilal dkk. 2004). Di Bali, disebutkan

bahwa prevalensi ADB pada wanita hamil sebesar 46,2% (Suega dkk. 2002). Khusus di

Kabupaten Bangli anemia pada ibu hamil ditemukan sebesar 45,8% (Sri Ekawati dkk. 2007).

       Pemerintah telah melakukan upaya penanggulangan ADB melalui pelaksanaan program

pemberian tablet besi pada wanita hamil yang diintegrasikan ke dalam program Kesehatan Ibu

dan Anak di puskesmas. Sayangnya, sampai saat ini upaya tersebut masih belum berjalan dengan

optimal, ditandai oleh masih tingginya angka kejadian anemia pada wanita hamil. Menurut Bakta

dkk (2006), salah satu faktor yang diduga menjadi penyebab adalah terbatasnya cadangan besi

dalam tubuh.

          Dalam kondisi hamil, seorang wanita membutuhkan 1000 mg besi selama kehamilan.

Apabila kebutuhan tersebut tidak dapat dipenuhi melalui diet harian maka akan terjadi mobilisasi

cadangan besi tubuh (Halberg 1992). Oleh karena itu, seorang wanita seharusnya memiliki

cadangan besi tubuh yang memadai untuk mencukupi kebutuhan selama kehamilan.

            Kenyataan yang berkembang justru berbeda dari yang diharapkan yakni wanita hamil

memiliki cadangan besi tubuh yang rendah bahkan kosong dari sejak masa prahamil. Hal ini

terjadi karena wanita-wanita di negara berkembang sering mengalami defisiensi zat besi laten

sejak masa prahamil. Peningkatan kebutuhan besi selama kehamilan semakin menguras

cadangan besi tubuh yang sudah mengalami defisiensi, sehingga menjadi kosong selama masa

kehamilan. Hal ini mengindikasikan bahwa cadangan besi tubuh seharusnya terisi penuh sejak

masa prahamil sehingga jika seorang wanita mengalami kehamilan, kebutuhan besi tubuh masih

tetap mampu dipenuhi.

           Terjadinya defisiensi zat besi laten tersebut disebabkan karena pola makan penduduk yang

lebih banyak mengkonsumsi besi non heme dibandingkan dengan besi heme. Diet harian

penduduk, khususnya di wilayah Bangli lebih banyak yang bersumber dari bahan nabati dengan

kandungan besi non heme yang lebih tinggi. Besi non heme memiliki kualitas yang lebih buruk

dan lebih sulit diserap dibandingkan dengan besi heme. Selain itu, wanita normal akan

mengalami menstruasi setiap bulannya, sehingga kehilangan besi sebesar 1 mg/dl. Kehilangan

ini memerlukan pengganti, bila tidak terpenuhi melalui diet harian maka kondisi ini akan

berlanjut pada penipisan cadangan besi tubuh. Pada masa ini, gagalnya pemenuhan besi oleh diet

harian seharusnya dapat digantikan dengan pemberian tablet besi. Ketidaktahuan akan informasi

tersebut menyebabkan wanita prahamil tidak melakukan upaya pencegahan sejak dini. Dengan

demikian, penyuluhan ADB menjadi sangat penting untuk menanggulangi permasalahan ADB

pada wanita prahamil ataupun pada saat mereka mengalami kehamilan.

            Sebelum memasuki masa kehamilan, seorang wanita tentu harus melewati fase prahamil.

Masa prahamil merupakan masa sebelum hamil bagi wanita usia subur (umur 15-35 tahun).

Berdasarkan penelitian yang dilakukan oleh Seri Ani dkk (2007) ditemukan bahwa prevalensi

ADB pada wanita prahamil adalah sebesar 38,6%. Tingginya prevalensi ADB pada wanita

prahamil mampu menggambarkan kemungkinan besarnya kejadian ADB yang akan terjadi pada

wanita hamil. Menyadari potensi permasalahan tersebut, tindakan pencegahan sangat perlu

dilakukan pada kelompok wanita prahamil untuk menurunkan kejadian ADB pada wanita

prahamil maupun pada saat mereka mengalami kehamilan.

          Salah satu kelompok tersebut adalah remaja-remaja putri di Sekolah Menengah Atas

Negeri 1 Bangli, yang merupakan bagian dari kelompok wanita prahamil. Tindakan pencegahan

secara primer diberikan kepada kelompok remaja putri tersebut melalui penyuluhan tentang

ADB dan dampak yang ditimbulkan. Materi yang diberikan juga dihubungkan dengan besarnya

kejadian ADB pada ibu hamil di Kabupaten Bangli yaitu sebesar 45,8%.

        Melalui penyuluhan ini diharapkan terjadi peningkatan pengetahuan kelompok remaja putri.

Peningkatan pengetahuan tentang ADB dan dampaknya merupakan kondisi yang memungkinkan

timbulnya perilaku sehat khususnya perilaku dalam pencegahan ADB sejak dini secara mandiri

oleh remaja putri tersebut. Upaya ini dalam jangka panjang diharapkan berkontribusi terhadap

penurunan kejadian ADB pada wanita prahamil sekaligus menurunkan ADB pada wanita hamil,

khususnya di wilayah Kabupaten Bangli.

METODE PEMECAHAN MASALAH

           Kegiatan yang dilakukan meliputi peningkatan pengetahuan dengan penyuluhan tentang

ADB, dampak yang ditimbulkan, serta upaya pencegahan yang dapat dilakukan. Penyuluhan ini

diikuti dengan pengenalan tablet besi kepada remaja putri sehingga mereka dapat mengakses

pada saat membutuhkan.

       Penyuluhan dilakukan di SMAN 1 Bangli pada Hari Sabtu, 26 September 2009 dengan

melibatkan 78 remaja putri dari kelas 1 dan kelas 2. Kegiatan diawali dengan pemberian pre test

untuk menilai pengetahuan dasar peserta sebelum dilakukan penyuluhan. Tahap selanjutnya

adalah memberikan penyuluhan yang bertujuan untuk meningkatkan pengetahuan remaja putri

terkait ADB, dampak, dan cara pencegahannya. Kegiatan ini dilanjutkan dengan pemberian post

test untuk mengukur peningkatan pengetahuan remaja putri terkait dengan ADB. Setelah itu,

kepada para siswa diperkenalkan contoh tablet besi, sehingga mereka dapat mengakses pada saat

membutuhkan.

HASIL KEGIATAN

            Pengabdian masyarakat yang dilakukan di SMAN 1 Bangli berhasil melibatkan 78

remaja putri kelas 1 dan kelas 2. Pada awal kegiatan dilakukan perkenalan tim penyuluh

dilanjutkan dengan penjelasan tujuan dan manfaat kegiatan yang dilakukan. Tahap berikutnya

adalah membagikan lembar soal pre test untuk mengukur pengetahuan sebelum penyuluhan.

Lembar soal pre test yang telah terisi kemudian dikumpulkan. Kegiatan dilanjutkan dengan

memberikan penyuluhan yang terbagi menjadi tiga bagian utama yaitu 1) penjelasan tentang

ADB, 2) pemaparan tentang penyebab dan dampak, dan 3) pemaparan tentang upaya pencegahan

yang dapat dilakukan.

a. Partisipasi Peserta Penyuluhan

           Para peserta penyuluhan terlihat sangat antusias dalam mengikuti kegiatan penyuluhan.

Pada saat penyampaian materi penyuluhan seluruh peserta tampak tertib sehingga penyampaian

materi berlangsung dengan tertib. Pada saat dibuka sesi tanya jawab, banyak peserta yang

mengajukan pertanyaan yang kritis sekaligus berkaitan dengan kehidupan sehari-hari, misalkan

saja pertanyaan tentang pola makan dengan minum teh, makanan yang baik untuk meningkatkan

penyerapan besi. Pertanyaan lain yang cukup menarik adalah apakah donor darah dapat

menimbulkan anemia?, apa beda anemia dengan tensi rendah, dan beberapa pertanyaan lainnya.

b. Tanggapan Peserta terhadap Kegiatan Penyuluhan

Pihak sekolah sangat menyambut baik kegiatan penyuluhan dan memberikan tanggapan

yang positif. Hal ini terlihat dari kemudahan perijinan, persiapan ruangan yang dibantu oleh

pihak sekolah, sampai pada pengumpulan remaja putri yang akan diberikan penyuluhan. Kepala

Sekolah dan guru pembina mengharapkan kegiatan penyuluhan semacam ini dapat terus

dilakukan secara berkesinambungan, baik tentang anemia ataupun masalah kesehatan lainnya.

Para peserta penyuluhan mengaku mendapatkan banyak informasi yang baru dan

bermanfaat tentang anemia, karena selama ini sebagian besar dari peserta hanya mendapatkan

informasi tentang anemia yang sangat terbatas dari iklan produk komersial di televisi. Para

peserta mengaku bahwa informasi yang diperoleh sangat bermanfaat dan menginspirasi mereka

untuk menampilkan perilaku pencegahan terhadap anemia secara mandiri.

c. Tingkat Pengetahuan Peserta Penyuluhan

Tingkat keberhasilan dari kegiatan ini diukur dari hasil pre test dan post test. Untuk

melihat ada tidaknya peningkatan pengetahuan peserta terhadap ADB, dapat dilihat dari

perbandingan hasil pre test dan post test pada jawaban yang benar dan salah.

Dari hasil analisis pre test dan post test diperoleh data bahwa 78 responden yang

mengikuti pre test dan post test mengalami peningkatan rerata nilai pada saat post test sebanyak

3 poin. Rerata nilai pre test dan post test masing-masing adalah 3 dan 6, dengan range nilai pre

test yaitu 1-6, sedangkan range nilai post test 6-10. Jawaban responden pada masing masing

pertanyaan juga memperlihatkan peningkatan dimana pada hasil pre test ada sejumlah siswa

yang tidak mampu menjawab pertanyaan namun pada saat post test berhasil menjawab

pertanyaan tersebut dengan benar, seperti yang disajikan dalam tabel berikut ini: (tabel 1)

Berdasarkan analisis pre test dan post test yang dilakukan, terlihat bahwa tingkat

pengetahuan peserta penyuluhan mengalami peningkatan yaitu dari rerata sebesar 3,47

meningkat menjadi 6,14.

Tabel 1. Hasil Analisis Pre Test dan Post Test Pengetahuan Remaja Putri Terhadap Anemia

Nama Variabel Pre Test Post Test

Jawaban f % Jawaban f %Apa yang dimaksud dengan Anemia?

Benar 34 44,2 5 6,5

Salah 44 56,8 73 93,5

Apa saja penyebab anemia? Benar 4 5,1 47 60,3

Salah 74 94,9 31 39,7

Apakah perempuan lebih rentan untuk mengalami anemia?

Benar 69 88,5 77 98,7

Salah 8 11,5 1 1,3

Hal yang dapat dilakukan untuk mencegah anemia?

Benar 0 0 7 9,0

Salah 78 100 71 91,0

Makanan yang banyak mengandung zat besi?

Benar 22 28,6 23 29,5

Salah 56 71,4 55 70,5

Minuman yang menghambat penyerapan besi?

Benar 26 36,8 69 88,5

Salah 52 63,2 8 11,5

Perlukah kita minum tablet fe setiap hari?

Benar 39 52,0 43 55,8

Salah 38 48,0 35 44,2

Siapa saja yang memerlukan tablet Fe?

Benar 65 86,7 73 93,6

Salah 13 13,2 5 6,4

Buah yang dapat membantu penyerapan zat besi?

Benar 19 24,7 22 28,2

Salah 59 75,3 56 71,8

Berapa kadar Hb yang normal? Benar 18 24,0 60 76,9

Salah 60 76 18 23,1

Gambar 1. Grafik Perbandingan Jawaban Benar Pre dan Post Test

SIMPULAN DAN SARAN

Simpulan

        Dari kegiatan pengabdian masyarakat yang telah dilakukan tentang penyuluhan ADB pada

remaja putri di SMAN 1 Bangli pada Sabtu, 26 September 2009 dapat disimpulkan bahwa terjadi

peningkatan pengetahuan pada remaja putri yang mendapatkan penyuluhan yaitu mengalami

peningkatan rerata dari 3,47 pada saat pre test menjadi 6,14 pada saat post test. Semua peserta

terlihat sangat antusias dalam mengikuti kegiatan ini, serta sekolah memberikan dukungan kuat

dalam pelaksanaan kegiatan ini. Hampir semua peserta mengaku bahwa kegiatan ini sangat

bermanfaat dan berguna bagi remaja putri terutama berkaitan dengan perilaku pencegahan

anemia sejak dini secara mandiri. Para siswi mengharapkan suapay kegiatan seperti ini dapat

dilakukan secara berkesinambungan.

Saran

          Kegiatan penyuluhan ADB untuk remaja putri harus dilakukan di sekolah-sekolah lain

secara berkelanjutan dengan melakukan kerjasama dengan dinas terkait ataupun dalam bentuk

kerjasama dengan Fakultas Kedokteran Universitas Udayana sehingga mampu meningkatkan

pengetahuan siswi-siswi mengenai bahaya ADB dan cara-cara pencegahannya.

UCAPAN TERIMA KASIH

            Kegiatan ini dapat terlaksana dengan baik berkat dukungan semua pihak. Pada

kesempatan ini penulis ingin menyampaikan ucapan terima kasih kepada Ketua LPM Universitas

Udayana beserta staf, Dekan Fakultas Kedokteran Universitas Udayana, Kepala Bagian IKK IKP

FK Unud beserta staf dosen, Kepala SMAN 1 Bangli beserta staf guru, serta siswi-siswi SMAN

1 Bangli yang telah berpartisipasi secara aktif, serta pihak-pihak lain yang tidak dapat disebutkan

satu per satu.

DAFTAR PUSTAKA

Allen, L.H. 1997. Pregnancy and Iron Deficiency: Unresolved Issues. Nutr Revs 55 (4): 91-101

Baker, W.F. 2000. Iron Deficiency in Pregnancy. Hematol One Clin North Am 14 (5): 1061-77

Bakta, I.M. 2006. Hematologi Klinik Ringkas. Penerbit Buku Kedokteran EGC. Jakarta

Conrad, M.E. 2003. Iron Deficiency Anemia. E-Med.com.Inc. (17): 267-69

Hallberg, L. 1992. Iron Balance in Pregnancy and Lactation in: Nutritional Anemias. edited by Formon, S.J. and Zlotkin, S. Nestle Nutrition Workshop Series Vol.30: 13-28

Muhilal, Sumaryono I., Komari. 2004. Review of Survey and Supplementation Studies of Anemia in Indonesia. Pen Gizi dan Makanan (24): 34-39

Purwani RD dan Hadi H. 2002. Pengaruh Pemberian Pil Besi Folat dan Pil Vitamin C Terhadap Perubahan Kadar Hemoglobin Anak Sekolah Dasar yang Anemia di Desa Nelayan Kabupaten Rembang. J. Kedokt Yarsi: 10 (3): 8-15

Ross J and Horton S. 1998. Economic Consequence of Iron Deficiency. ISBN pp 544

Seri Ani Luh, Bakta IM, Suryadhi INT, Bagiada N. 2007. Pengaruh Pemberian Tablet Besi Terhadap Kadar Feritin dan Hemoglobin Pada Wanita Prahamil di Bali (Disertasi). Universitas Udayana. Bali

Sri Ekawati LP., Ayu Trisnadewi N., Setiani P. 2007. Prevalensi Anemia Pada Ibu Hamil di Wilayah Kerja Puskesmas Susut I Bangli (Skripsi). Universitas Udayana. Bali

Suega K., Dharmayuda TG., Sutarga IM., Bakta IM. 2002. Iron Deficiency Anemia in Pregnant Women in Bali, Indonesia: A Profile of Risk Factor and Epidemiology. Southeast Asian J Trop Med Public Health 32 (2): 128-130

[IRON DEFICIENCY ANEMIA]. In severe iron deficiency characteristic morphologic changes include microcytosis (low MCV), hypochromasia (low MCHC), anisocytosis (high RDW), and poikilocytosis (abnormal shaped RBCs) with elliptocytes (arrowheads) and target cells. Reticulocytes are decreased. Other microcytic anemias such as thalassemia, sideroblastic anemia, anemia of chronic diseases and certain hemoglobin disorders should be excluded based on clinical history and laboratory tests.

Iron Deficiency Anemia

SHERSTEN KILLIP, M.D., M.P.H., JOHN M. BENNETT, M.D., M.P.H., and MARA D. CHAMBERS, M.D., University of Kentucky, Lexington, Kentucky

Am Fam Physician. 2007 Mar 1;75(5):671-678.

  Patient information: See a related handouts on this topic at http://familydoctor.org/751.xml.

The prevalence of iron deficiency anemia is 2 percent in adult men, 9 to 12 percent in non-Hispanic white women, and nearly 20 percent in black and Mexican-American women. Nine percent of patients older than 65 years with iron deficiency anemia have a gastrointestinal cancer when evaluated. The U.S. Preventive Services Task Force currently recommends screening for iron deficiency anemia in pregnant women but not in other groups. Routine iron supplementation is recommended for high-risk infants six to 12 months of age. Iron deficiency anemia is classically described as a microcytic anemia. The differential diagnosis includes thalassemia, sideroblastic anemias, some types of anemia of chronic disease, and lead poisoning. Serum ferritin is the preferred initial diagnostic test. Total iron-binding capacity, transferrin saturation, serum iron, and serum transferrin receptor levels may be helpful if the ferritin level is between 46 and 99 ng per mL (46 and 99 mcg per L); bone marrow biopsy may be necessary in these patients for a definitive diagnosis. In children, adolescents, and women of reproductive age, a trial of iron is a reasonable approach if the review of symptoms, history, and physical

examination are negative; however, the hemoglobin should be checked at one month. If there is not a 1 to 2 g per dL (10 to 20 g per L) increase in the hemoglobin level in that time, possibilities include malabsorption of oral iron, continued bleeding, or unknown lesion. For other patients, an endoscopic evaluation is recommended beginning with colonoscopy if the patient is older than 50.

Iron deficiency anemia (IDA) is the most common nutritional deficiency worldwide. It can cause reduced work capacity in adults1 and impact motor and mental development in children and adolescents.2 There is some evidence that iron deficiency without anemia affects cognition in adolescent girls3 and causes fatigue in adult women.4 IDA may affect visual and auditory functioning3 and is weakly associated with poor cognitive development in children.4

SORT: KEY RECOMMENDATIONS FOR PRACTICE

Clinical recommendationEvidence rating ReferencesComment

High-risk infants six to 12 months of age should be given routine iron supplementation.

B 14 Infants are considered high risk if they are living in poverty; are black, Native American, or Alaskan Native; are immigrants from developing countries; are preterm or low birth weight; or if their primary dietary intake is unfortified cow's milk.

Blood donors should take 20 mg elemental iron daily with vitamin C.

C 13,17,18 Blood donors lose iron; 20 mg per day replaces lost iron with minimal constipation or gastroesophageal reflux disease; vitamin C potentiates iron absorption.

Patients of either sex who are older than 65 and have iron deficiency anemia should be screened for occult gastrointestinal cancers.

B 30 In a population-based cohort, 9 percent of adults older than 65 years (95% CI, 0.02 to 0.25) had gastrointestinal cancer, and older adults with anemia had gastrointestinal cancer 31 times as often as adults without anemia.

In men and nonmenstruating women younger than 65 years, screening for occult gastrointestinal cancer should be undertaken in the absence of another explanation for iron deficiency.

B 30 In a population-based cohort, 6 percent of adults with anemia (95% CI, 0.01 to 0.16) had gastrointestinal cancer on investigation.

Hemoglobin and ferritin tests are the best for diagnosing iron deficiency anemia.

C 25–27,29 See Table 4 for likelihood ratios.

CI = confidence interval.

A = consistent, good-quality patient-oriented evidence; B = inconsistent or limited-quality patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, see page 603 or http://www.aafp.org/afpsort.xml.

Prevalence

The prevalence of IDA in the United States varies widely by age, sex, and race (Table 1).5 The Healthy People 2010 goals are to reduce the occurrence of IDA to less than 5 percent in toddlers; 1 percent in preschool-age children; and 7 percent in women of reproductive age, regardless of race.6

[corrected]

TABLE 1Prevalence of Iron Deficiency Anemia in Selected Populations in the United States

Group/age (years)*1988 to 1994 (%)1999 to 2000 (%)Both SexesOne to two 3 2Women (nonpregnant)12 to 49 4 350 to 69 2 370 and older 2 1†

*—Data for all racial/ethnic groups.

†—Unreliable; relative standard error (i.e., standard error/prevalence estimate) is greater than 30 percent.

Adapted from the Centers for Disease Control and Prevention. Iron deficiency—United States, 1999–2000. MMWR Morb Mortal Wkly Rep. 2002;51(40):899.

Etiology

Iron metabolism is unusual in that it is controlled by absorption rather than excretion. Iron is only lost through blood loss or loss of cells as they slough. Men and nonmenstruating women lose about 1 mg of iron per day. Menstruating women lose from 0.6 to 2.5 percent more per day. An average 132-lb (60-kg) woman might lose an extra 10 mg of iron per menstruation cycle, but the loss could be more than 42 mg per cycle depending on how heavily she menstruates.7 A pregnancy takes about 700 mg of iron, and a whole blood donation of 500 cc contains 250 mg of iron.

Iron absorption, which occurs mostly in the jejunum, is only 5 to 10 percent of dietary intake in persons in homeostasis. In states of overload, absorption decreases. Absorption can increase three- to fivefold in states of depletion. Dietary iron is available in two forms: heme iron, which is found in meat; and nonheme iron, which is found in plant and dairy foods. Absorption of heme iron is minimally affected by dietary factors, whereas nonheme iron makes up the bulk of consumed iron. The bioavailability of non-heme iron requires acid digestion and varies by an order of magnitude depending on the concentration of enhancers (e.g., ascorbate, meat) and inhibitors (e.g., calcium, fiber, tea, coffee, wine) found in the diet.7

Iron deficiency results when iron demand by the body is not met by iron absorption from the diet. Thus, patients with IDA presenting in primary care may have inadequate dietary intake, hampered absorption, or physiologic losses in a woman of reproductive age. It also could be a sign of blood loss, known or occult. IDA is never an end diagnosis; the work-up is not complete until the reason for IDA is known.

Risk factors

Table 2 8 –13 lists risk factors associated with IDA. Low socioeconomic status is not a risk factor for IDA in women who never get pregnant, but it is a risk factor when coupled with the increased iron demands imposed by pregnancy. Black women have a lower mean hemoglobin and a wider standard deviation than white women, even after adjustment for iron status.8 There is a high rate of IDA among Mexican women living in the United States that is not accounted for by dietary intake or parity, suggesting there may be an unidentified, possibly racial factor predisposing these women to iron deficiency.11

TABLE 2Risk Factors for Iron Deficiency Anemia in the United States

Risk factor StatisticsBlack8 Prevalence in white women: 7.1 percent;

prevalence in black women: 25.1 percentBlood donation more than two units per year in women and three units per year in men9

No statistics given

Low socioeconomic status and postpartum status10

Zero to six months postpartum: OR, 4.1; seven to 12 months postpartum: OR, 3.1

Mexican ethnicity living in the United States11 OR, 1.8Child and adolescent obesity12BMI ≥ 85% and < 95% percentile OR, 2.0 (95% CI, 1.2 to 3.5)BMI ≥ 95% percentile OR, 2.3 (95% CI, 1.4 to 3.9)Vegetarian diet13 40 percent of vegans 19 to 50 years of age

were iron deficient

OR = odds ratio; BMI = body mass index; CI = confidence interval

Information from references 8 through 13.

Screening and Primary Prevention

The U.S. Preventive Services Task Force (USPSTF) recommends screening pregnant women for IDA, but found insufficient evidence to recommend for or against routine screening in other asymptomatic persons. However, the guidelines did recommend routine iron supplementation in asymptomatic infants six to 12 months of age who are at high risk of IDA. Infants are considered to be at high risk if they are living in poverty; are black, Native American, or Alaskan Native; are immigrants from a developing country; are preterm or low birth weight; or if their primary dietary intake is unfortified cow's milk.14

Encouraging mothers to breastfeed their infants and to include iron-enriched foods in the diet of infants and young children also is recommended. Although the USPSTF found insufficient evidence to recommend for or against the routine use of iron supplements in healthy infants or pregnant women,15 a recent study showed a significant decline in the number of newborns weighing less than 5 lbs 8 oz (2.5 kg) (number needed to treat = 7) when the mothers used routine prenatal iron supplementation.16 This supports prescribing prenatal vitamins with iron to all pregnant women, which is the current standard of care in the United States.

The U.S. Food and Nutrition Board publishes Dietary Reference Intakes (DRI) for many vitamins and minerals, including iron. DRI replaced Recommended Daily Allowance. The DRI for iron is 8 mg per day for healthy, nonmenstruating adults; 18 mg per day for menstruating women; and 16 mg per day for vegetarians because of their differential absorption of nonheme iron.17 For blood donors, a daily dose of 20 mg of elemental iron is recommended.18

Diagnosis

The definition of anemia varies by sex and age. The most commonly used definitions of anemia come from the Centers for Disease Control and Prevention (CDC) and the World Health Organization (WHO) (Table 3 15 ).

TABLE 3Definition of Anemia by Hemoglobin Value

Population

Hemoglobin levelWorld Health Organization

Centers for Disease Control and Prevention

Infants 0.5 to 4.9 years — <11 g per dL (110 g per L)Children 5.0 to 11.9 years — <11.5 g per dL (115 g per L)Menstruating women <12 g per dL (120 g per

L)—

Pregnant women in first or third trimester

<11 g per dL <11 g per dL

Pregnant women in second trimester

<11 g per dL <10.5 g per dL (105 g per L)

Men <13 g per dL (130 g per L)

—

Information from reference 15.

DIFFERENTIAL DIAGNOSIS

IDA is classically described as a microcytic anemia. The differential diagnosis for microcytic anemia includes iron deficiency, thalassemia, sideroblastic anemias, some types of anemia of chronic disease, and lead poisoning (rare in adults).19 Patients with sideroblastic anemia will have almost complete saturation of the serum transfer-rin,20 which can differentiate them from patients with iron deficiency. Differentiating between iron deficiency and anemia of chronic disease can sometimes be difficult, especially in early iron deficiency or when the conditions coexist. Patients with lead poisoning will have characteristic signs and symptoms of lead poisoning.

CLINICAL PRESENTATION

Anemia cannot be reliably diagnosed by clinical presentation. Fatigue, the most common reason to check hemoglobin, was caused by anemia in only one out of 52 patients in a primary care practice.21 In a hospital setting, pallor predicted anemia with a likelihood ratio (LR) of 4.5. However, absence of pallor was less helpful at ruling out anemia, giving an LR of 0.6 even when anemia was defined as less than 9 g per dL (90 g per L), a lower diagnostic level than that of the WHO or CDC.22 Other classic symptoms such as koilonychia (spoon nails), glossitis, or dysphagia are not common in the developed world.23

DIAGNOSTIC TESTS

The diagnosis of IDA requires that a patient be anemic and show laboratory evidence of iron deficiency. Red blood cells in IDA are usually described as being microcytic (i.e., mean corpuscular volume less than 80 μm3 [80 fL]) and hypochromic, however the manifestation of iron deficiency occurs in several stages.24  Patients with a serum ferritin concentration less than 25 ng per mL (25 mcg per L) have a very high probability of being iron deficient. The most accurate initial diagnostic test for IDA is the serum ferritin measurement. Serum ferritin values greater than 100 ng per mL (100 mcg per L) indicate adequate iron stores and a low likelihood of IDA (Table 4 25 ,26).25 In some populations, such as those with inflammatory disease or cirrhosis, these tests must be interpreted slightly differently because ferritin is an acute-phase reactant. Cutoffs for abnormality in these patients generally are higher.27

TABLE 4Diagnosis of Iron Deficiency

Adults with anemia* Adults older than 65

TestLikelihood ratio Test

Likelihood ratio

Mean corpuscular volume Mean corpuscular volumeLess than 70 μm3 (70 fL) 12.5 Less than 75 μm3 8.82

Adults with anemia* Adults older than 65

TestLikelihood ratio Test

Likelihood ratio

70 to 74 μm3 (74 fL) 3.3 75 to 85 μm3 1.3575 to 79 μm3 (75 to 79 fL) 1.0 86 to 91 μm3 (86 to 91 fL) 0.6480 to 84 μm3 (80 to 84 fL) 0.91 92 to 95 μm3 (92 to 95 fL) 0.3485 to 89 μm3 (85 to 89 fL) 0.76 More than 95 fL 0.1190 μm3 (90 fL) or more 0.29Ferritin FerritinLess than 15 ng per mL (15 mcg per L)

51.8 Less than 19 ng per mL (19 mcg per L)

41.0

15 to 24 ng per mL (15 to 24 mcg per L)

8.8 19 to 45 ng per mL (19 to 45 mcg per L)

3.1

25 to 34 ng per mL (25 to 34 mcg per L)

2.5 46 to 100 ng per mL (46 to 100 mcg per L)

0.46

35 to 44 ng per mL (35 to 44 mcg per L)

1.8 More than 100 ng per mL 0.13

45 to 100 ng per mL (45 to 100 mcg per L)

0.54

More than 100 ng per mL 0.08Transferrin saturation Transferrin saturationLess than 5 percent 10.5 Less than 5 percent 16.515 to 9 percent 2.5 5 to 8 percent 1.4310 to 19 percent 0.81 More than 8 to 21 percent 0.5720 to 29 percent 0.52 More than 21 percent 0.2830 to 49 percent 0.4350 percent or more 0.15

*Hemoglobin less than 13 g per dL [130 g per L] for men and less than 12 g per dL [120 g per L] for women

Adapted with permission from Guyatt GH, Oxman AD, Ali M, Willan A, McIlroy W, Patterson C. Laboratory diagnosis of iron-deficiency anemia: an overview. J Gen Intern Med 1992;7:145–53, with additional information from reference 26.

Another laboratory change that occurs in patients with IDA is an increase in the iron-carrying protein transferrin. The amount of iron available to bind to this molecule is reduced, causing a decrease in the transferrin saturation and an increase in the total iron-binding capacity. The serum transferrin receptor assay is a newer approach to measuring iron status at the cellular level. Increased levels are found in patients with IDA, and normal levels are found in patients with anemia of chronic disease.28

RECOMMENDED DIAGNOSTIC STRATEGY

Figure 1 29 shows a suggested diagnostic algorithm to determine if a patient has IDA. This algorithm is adapted from a clinical guideline, with the primary modification that serum iron, total iron-binding capacity, and transferrin saturation are recommended as follow-up tests in patients with an intermediate ferritin level as a strategy to reduce the need for bone marrow biopsy.29 If these blood tests are indeterminate, an elevated serum transferrin receptor level is recommended to distinguish IDA from anemia of chronic disease. The choice of a ferritin level of less than 45 ng per mL (45 mcg per L) is to allow for a higher sensitivity, despite the fact that most laboratories' normal range for ferritin includes 45 ng per mL.

Diagnosis of Iron Deficiency Anemia

Figure 1.

Diagnostic algorithm for iron deficiency anemia. (MCV = mean corpuscular volume; LR+ = positive likelihood ratio; TIBC = total iron-binding capacity; FE = serum iron; TfR = serum transferrin receptor.)

Adapted with permission from Ioannou GN, Spector J, Scott K, Rockey DC. Prospective evaluation of a clinical guideline for the diagnosis and management of iron deficiency anemia. Am J Med 2002;113:281–7.

Because IDA has physiologic and pathophysiologic causes, a cause for IDA must be established or serious disease may be overlooked. In a population-based study of more than 700 adults with IDA, 6 percent were diagnosed with a gastrointestinal malignancy. The risk of malignancy was 9 percent in patients older than 65 years with IDA. None of the 442 premenopausal women with iron deficiency, 92 of whom also were anemic, had a gastrointestinal malignancy detected.30

Figure 2 4 ,21,29,31,32 shows the authors' suggested evaluation for underlying causes of IDA. The general approach is to separate groups by risk of underlying disease. Patients with a high risk of underlying disease (e.g., men of all ages and postmenopausal women) should be evaluated endoscopically for occult bleeding unless the history and physical examination strongly indicate a known benign cause for IDA.

Whether to begin with endoscopy or colonoscopy should be indicated by symptoms or age. In a patient older than 50 years who lacks symptoms, the diagnostic work-up should begin with colonoscopy.31 Some disease-oriented evidence by specialty researchers suggests that esophagogastroduodenoscopy may be valuable in women of reproductive age.33 However, in the absence of symptoms, a therapeutic trial of oral iron therapy is the recommended initial approach.29

Evaluation and Treatment of Iron Deficiency Anemia

Figure 2.

Algorithm for evaluation and treatment of iron deficiency anemia.

Information from references 4,21,29,31, and 32.

Treatment

Transfusion should be considered for patients of any age with IDA complaining of symptoms such as fatigue or dyspnea on exertion. It also should be considered for asymptomatic cardiac patients with hemoglobin less than 10 g per dL (100 g per L). However, oral iron therapy is usually the first-line therapy for patients with IDA.34 As noted in the etiology section, iron absorption varies widely based on type of diet and other factors. Bone marrow response to iron is limited to 20 mg per day of elemental iron. An increase in the hemoglobin level of 1 g per dL (10 g per L) should occur every two to three weeks on iron therapy; however, it may take up to four months for the iron stores to return to normal after the hemoglobin has corrected.35 Ferrous sulfate in a dose of 325 mg provides 65 mg of elemental iron, whereas 325 mg of ferrous gluconate provides 38 mg of elemental iron. Sustained-release formulations of iron are not recommended as initial therapy because they reduce the amount of iron that is presented for absorption to the duodenal villi.

Gastrointestinal absorption of elemental iron is enhanced in the presence of an acidic gastric environment. This can be accomplished through simultaneous intake of ascorbic acid (i.e., vitamin C).36 Although iron absorption occurs more readily when taken on an empty stomach, this increases the likelihood of stomach upset because of iron therapy. Increased patient adherence should be weighed against the inferior absorption. Foods rich in tannates (e.g., tea)37 or phytates (e.g., bran, cereal),38 or medications that raise the gastric pH (e.g., antacids, proton pump inhibitors, histamine H2 blockers)39 reduce absorption and should be avoided if possible. Some persons have difficulty absorbing the iron because of poor dissolution of the coating.40 A liquid iron preparation would be a better choice for these patients. Laxatives, stool softeners, and adequate intake of liquids can alleviate the constipating effects of oral iron therapy.

Indications for the use of intravenous iron include chronic uncorrectable bleeding, intestinal malabsorption, intolerance to oral iron, nonadherence, or a hemoglobin level less than 6 g per dL (60 g per L) with signs of poor perfusion in patients who would otherwise receive transfusion (e.g., those who have religious objections).41 Until recently, iron dextran (Dexferrum) has been the only parenteral iron preparation available in the United States. The advantage of iron dextran is the ability to administer large doses (200 to 500 mg) at one time.42 One major drawback of iron dextran is the risk of anaphylactic reactions that can be fatal. There also is a delayed reaction, which consists of myalgias, headache, and arthralgias, that can occur 24 to 48 hours after infusion. Nonsteroidal anti-inflammatory drugs will usually relieve these symptoms, but they may be prolonged in patients with chronic inflammatory joint disease.

Sodium ferric gluconate (Ferrlecit), a safer form of parenteral iron, was approved by the U.S. Food and Drug Administration in 1999. The risk of anaphylaxis is drastically reduced using sodium ferric gluconate. In a study of 2,534 patients on hemodialysis, 0.04 percent receiving sodium ferric gluconate had life-threatening reactions compared with 0.61 percent receiving iron dextran.43 Sodium ferric gluconate is usually administered intravenously in eight weekly doses of 125 mg for a total dosage of 1,000 mg. No test dose is required.

Another intravenous preparation, approved for use in the United States in 2000, is iron sucrose (Venofer). In iron deficiency not associated with hemodialysis, 200 mg is administered intravenously five times over a two-week period. Safety profiles are similar to sodium ferric gluconate, although published experience is more limited.28

Iron Deficiency Anemia

SHERSTEN KILLIP, M.D., M.P.H., JOHN M. BENNETT, M.D., M.P.H., and MARA D. CHAMBERS, M.D., University of Kentucky, Lexington, Kentucky

Am Fam Physician. 2007 Mar 1;75(5):671-678.

  Patient information: See a related handouts on this topic at http://familydoctor.org/751.xml.

The prevalence of iron deficiency anemia is 2 percent in adult men, 9 to 12 percent in non-Hispanic white women, and nearly 20 percent in black and Mexican-American women. Nine percent of patients older than 65 years with iron deficiency anemia have a gastrointestinal cancer when evaluated. The U.S. Preventive Services Task Force currently recommends screening for iron deficiency anemia in pregnant women but not in other groups. Routine iron supplementation is recommended for high-risk infants six to 12 months of age. Iron deficiency anemia is classically described as a microcytic anemia. The differential diagnosis includes thalassemia, sideroblastic anemias, some types of anemia of chronic disease, and lead poisoning. Serum ferritin is the preferred initial diagnostic test. Total iron-binding capacity, transferrin saturation, serum iron, and serum transferrin receptor levels may be helpful if the ferritin level is between 46 and 99 ng per mL (46 and 99 mcg per L); bone marrow biopsy may be necessary in these patients for a definitive diagnosis. In children, adolescents, and women of reproductive age, a trial of iron is a reasonable approach if the review of symptoms, history, and physical examination are negative; however, the hemoglobin should be checked at one month. If there is not a 1 to 2 g per dL (10 to 20 g per L) increase in the hemoglobin level in that time, possibilities include malabsorption of oral iron, continued bleeding, or unknown lesion. For other patients, an endoscopic evaluation is recommended beginning with colonoscopy if the patient is older than 50.

Iron deficiency anemia (IDA) is the most common nutritional deficiency worldwide. It can cause reduced work capacity in adults1 and impact motor and mental development in children and adolescents.2 There is some evidence that iron deficiency without anemia affects cognition in adolescent girls3 and causes fatigue in adult women.4 IDA may affect visual and auditory functioning3 and is weakly associated with poor cognitive development in children.4

SORT: KEY RECOMMENDATIONS FOR PRACTICE

Clinical recommendationEvidence rating ReferencesComment

High-risk infants six to 12 months of age should be given routine iron supplementation.

B 14 Infants are considered high risk if they are living in poverty; are black, Native American, or Alaskan Native; are immigrants from developing countries; are preterm or low birth weight; or if their primary dietary intake is unfortified cow's milk.

Blood donors should take 20 mg elemental iron daily with vitamin C.

C 13,17,18 Blood donors lose iron; 20 mg per day replaces lost iron with minimal constipation or gastroesophageal reflux disease; vitamin C potentiates iron absorption.

Patients of either sex who are older than 65 and have iron deficiency anemia should be screened for occult gastrointestinal cancers.

B 30 In a population-based cohort, 9 percent of adults older than 65 years (95% CI, 0.02 to 0.25) had gastrointestinal cancer, and older adults with anemia had gastrointestinal cancer 31 times as often as adults without anemia.

In men and nonmenstruating women younger than 65 years, screening for occult gastrointestinal cancer should be undertaken in the absence of another explanation for iron deficiency.

B 30 In a population-based cohort, 6 percent of adults with anemia (95% CI, 0.01 to 0.16) had gastrointestinal cancer on investigation.

Hemoglobin and ferritin tests are the best for diagnosing iron deficiency anemia.

C 25–27,29 See Table 4 for likelihood ratios.

CI = confidence interval.

A = consistent, good-quality patient-oriented evidence; B = inconsistent or limited-quality patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, see page 603 or http://www.aafp.org/afpsort.xml.

Prevalence

The prevalence of IDA in the United States varies widely by age, sex, and race (Table 1).5 The Healthy People 2010 goals are to reduce the occurrence of IDA to less than 5 percent in toddlers;

1 percent in preschool-age children; and 7 percent in women of reproductive age, regardless of race.6

[corrected]

TABLE 1Prevalence of Iron Deficiency Anemia in Selected Populations in the United States

Group/age (years)*1988 to 1994 (%)1999 to 2000 (%)Both SexesOne to two 3 2Women (nonpregnant)12 to 49 4 350 to 69 2 370 and older 2 1†

*—Data for all racial/ethnic groups.

†—Unreliable; relative standard error (i.e., standard error/prevalence estimate) is greater than 30 percent.

Adapted from the Centers for Disease Control and Prevention. Iron deficiency—United States, 1999–2000. MMWR Morb Mortal Wkly Rep. 2002;51(40):899.

Etiology

Iron metabolism is unusual in that it is controlled by absorption rather than excretion. Iron is only lost through blood loss or loss of cells as they slough. Men and nonmenstruating women lose about 1 mg of iron per day. Menstruating women lose from 0.6 to 2.5 percent more per day. An average 132-lb (60-kg) woman might lose an extra 10 mg of iron per menstruation cycle, but the loss could be more than 42 mg per cycle depending on how heavily she menstruates.7 A pregnancy takes about 700 mg of iron, and a whole blood donation of 500 cc contains 250 mg of iron.

Iron absorption, which occurs mostly in the jejunum, is only 5 to 10 percent of dietary intake in persons in homeostasis. In states of overload, absorption decreases. Absorption can increase three- to fivefold in states of depletion. Dietary iron is available in two forms: heme iron, which is found in meat; and nonheme iron, which is found in plant and dairy foods. Absorption of heme iron is minimally affected by dietary factors, whereas nonheme iron makes up the bulk of consumed iron. The bioavailability of non-heme iron requires acid digestion and varies by an order of magnitude depending on the concentration of enhancers (e.g., ascorbate, meat) and inhibitors (e.g., calcium, fiber, tea, coffee, wine) found in the diet.7

Iron deficiency results when iron demand by the body is not met by iron absorption from the diet. Thus, patients with IDA presenting in primary care may have inadequate dietary intake,

hampered absorption, or physiologic losses in a woman of reproductive age. It also could be a sign of blood loss, known or occult. IDA is never an end diagnosis; the work-up is not complete until the reason for IDA is known.

Risk factors

Table 2 8 –13 lists risk factors associated with IDA. Low socioeconomic status is not a risk factor for IDA in women who never get pregnant, but it is a risk factor when coupled with the increased iron demands imposed by pregnancy. Black women have a lower mean hemoglobin and a wider standard deviation than white women, even after adjustment for iron status.8 There is a high rate of IDA among Mexican women living in the United States that is not accounted for by dietary intake or parity, suggesting there may be an unidentified, possibly racial factor predisposing these women to iron deficiency.11

TABLE 2Risk Factors for Iron Deficiency Anemia in the United States

Risk factor StatisticsBlack8 Prevalence in white women: 7.1 percent;

prevalence in black women: 25.1 percentBlood donation more than two units per year in women and three units per year in men9

No statistics given

Low socioeconomic status and postpartum status10

Zero to six months postpartum: OR, 4.1; seven to 12 months postpartum: OR, 3.1

Mexican ethnicity living in the United States11 OR, 1.8Child and adolescent obesity12BMI ≥ 85% and < 95% percentile OR, 2.0 (95% CI, 1.2 to 3.5)BMI ≥ 95% percentile OR, 2.3 (95% CI, 1.4 to 3.9)Vegetarian diet13 40 percent of vegans 19 to 50 years of age

were iron deficient

OR = odds ratio; BMI = body mass index; CI = confidence interval

Information from references 8 through 13.

Screening and Primary Prevention

The U.S. Preventive Services Task Force (USPSTF) recommends screening pregnant women for IDA, but found insufficient evidence to recommend for or against routine screening in other asymptomatic persons. However, the guidelines did recommend routine iron supplementation in asymptomatic infants six to 12 months of age who are at high risk of IDA. Infants are considered to be at high risk if they are living in poverty; are black, Native American, or Alaskan Native; are immigrants from a developing country; are preterm or low birth weight; or if their primary dietary intake is unfortified cow's milk.14

Encouraging mothers to breastfeed their infants and to include iron-enriched foods in the diet of infants and young children also is recommended. Although the USPSTF found insufficient evidence to recommend for or against the routine use of iron supplements in healthy infants or pregnant women,15 a recent study showed a significant decline in the number of newborns weighing less than 5 lbs 8 oz (2.5 kg) (number needed to treat = 7) when the mothers used routine prenatal iron supplementation.16 This supports prescribing prenatal vitamins with iron to all pregnant women, which is the current standard of care in the United States.

The U.S. Food and Nutrition Board publishes Dietary Reference Intakes (DRI) for many vitamins and minerals, including iron. DRI replaced Recommended Daily Allowance. The DRI for iron is 8 mg per day for healthy, nonmenstruating adults; 18 mg per day for menstruating women; and 16 mg per day for vegetarians because of their differential absorption of nonheme iron.17 For blood donors, a daily dose of 20 mg of elemental iron is recommended.18

Diagnosis

The definition of anemia varies by sex and age. The most commonly used definitions of anemia come from the Centers for Disease Control and Prevention (CDC) and the World Health Organization (WHO) (Table 3 15 ).

TABLE 3Definition of Anemia by Hemoglobin Value

Population

Hemoglobin levelWorld Health Organization

Centers for Disease Control and Prevention

Infants 0.5 to 4.9 years — <11 g per dL (110 g per L)Children 5.0 to 11.9 years — <11.5 g per dL (115 g per L)Menstruating women <12 g per dL (120 g per

L)—

Pregnant women in first or third trimester

<11 g per dL <11 g per dL

Pregnant women in second trimester

<11 g per dL <10.5 g per dL (105 g per L)

Men <13 g per dL (130 g per L)

—

Information from reference 15.

DIFFERENTIAL DIAGNOSIS

IDA is classically described as a microcytic anemia. The differential diagnosis for microcytic anemia includes iron deficiency, thalassemia, sideroblastic anemias, some types of anemia of chronic disease, and lead poisoning (rare in adults).19 Patients with sideroblastic anemia will have almost complete saturation of the serum transfer-rin,20 which can differentiate them from

patients with iron deficiency. Differentiating between iron deficiency and anemia of chronic disease can sometimes be difficult, especially in early iron deficiency or when the conditions coexist. Patients with lead poisoning will have characteristic signs and symptoms of lead poisoning.

CLINICAL PRESENTATION

Anemia cannot be reliably diagnosed by clinical presentation. Fatigue, the most common reason to check hemoglobin, was caused by anemia in only one out of 52 patients in a primary care practice.21 In a hospital setting, pallor predicted anemia with a likelihood ratio (LR) of 4.5. However, absence of pallor was less helpful at ruling out anemia, giving an LR of 0.6 even when anemia was defined as less than 9 g per dL (90 g per L), a lower diagnostic level than that of the WHO or CDC.22 Other classic symptoms such as koilonychia (spoon nails), glossitis, or dysphagia are not common in the developed world.23

DIAGNOSTIC TESTS

The diagnosis of IDA requires that a patient be anemic and show laboratory evidence of iron deficiency. Red blood cells in IDA are usually described as being microcytic (i.e., mean corpuscular volume less than 80 μm3 [80 fL]) and hypochromic, however the manifestation of iron deficiency occurs in several stages.24  Patients with a serum ferritin concentration less than 25 ng per mL (25 mcg per L) have a very high probability of being iron deficient. The most accurate initial diagnostic test for IDA is the serum ferritin measurement. Serum ferritin values greater than 100 ng per mL (100 mcg per L) indicate adequate iron stores and a low likelihood of IDA (Table 4 25 ,26).25 In some populations, such as those with inflammatory disease or cirrhosis, these tests must be interpreted slightly differently because ferritin is an acute-phase reactant. Cutoffs for abnormality in these patients generally are higher.27

TABLE 4Diagnosis of Iron Deficiency

Adults with anemia* Adults older than 65

TestLikelihood ratio Test

Likelihood ratio

Mean corpuscular volume Mean corpuscular volumeLess than 70 μm3 (70 fL) 12.5 Less than 75 μm3 8.8270 to 74 μm3 (74 fL) 3.3 75 to 85 μm3 1.3575 to 79 μm3 (75 to 79 fL) 1.0 86 to 91 μm3 (86 to 91 fL) 0.6480 to 84 μm3 (80 to 84 fL) 0.91 92 to 95 μm3 (92 to 95 fL) 0.3485 to 89 μm3 (85 to 89 fL) 0.76 More than 95 fL 0.1190 μm3 (90 fL) or more 0.29Ferritin FerritinLess than 15 ng per mL (15 mcg per L)

51.8 Less than 19 ng per mL (19 mcg per L)

41.0

15 to 24 ng per mL (15 to 24 mcg per L)

8.8 19 to 45 ng per mL (19 to 45 mcg per L)

3.1

Adults with anemia* Adults older than 65

TestLikelihood ratio Test

Likelihood ratio

25 to 34 ng per mL (25 to 34 mcg per L)

2.5 46 to 100 ng per mL (46 to 100 mcg per L)

0.46

35 to 44 ng per mL (35 to 44 mcg per L)

1.8 More than 100 ng per mL 0.13

45 to 100 ng per mL (45 to 100 mcg per L)

0.54

More than 100 ng per mL 0.08Transferrin saturation Transferrin saturationLess than 5 percent 10.5 Less than 5 percent 16.515 to 9 percent 2.5 5 to 8 percent 1.4310 to 19 percent 0.81 More than 8 to 21 percent 0.5720 to 29 percent 0.52 More than 21 percent 0.2830 to 49 percent 0.4350 percent or more 0.15

*Hemoglobin less than 13 g per dL [130 g per L] for men and less than 12 g per dL [120 g per L] for women

Adapted with permission from Guyatt GH, Oxman AD, Ali M, Willan A, McIlroy W, Patterson C. Laboratory diagnosis of iron-deficiency anemia: an overview. J Gen Intern Med 1992;7:145–53, with additional information from reference 26.

Another laboratory change that occurs in patients with IDA is an increase in the iron-carrying protein transferrin. The amount of iron available to bind to this molecule is reduced, causing a decrease in the transferrin saturation and an increase in the total iron-binding capacity. The serum transferrin receptor assay is a newer approach to measuring iron status at the cellular level. Increased levels are found in patients with IDA, and normal levels are found in patients with anemia of chronic disease.28

RECOMMENDED DIAGNOSTIC STRATEGY

Figure 1 29 shows a suggested diagnostic algorithm to determine if a patient has IDA. This algorithm is adapted from a clinical guideline, with the primary modification that serum iron, total iron-binding capacity, and transferrin saturation are recommended as follow-up tests in patients with an intermediate ferritin level as a strategy to reduce the need for bone marrow biopsy.29 If these blood tests are indeterminate, an elevated serum transferrin receptor level is recommended to distinguish IDA from anemia of chronic disease. The choice of a ferritin level of less than 45 ng per mL (45 mcg per L) is to allow for a higher sensitivity, despite the fact that most laboratories' normal range for ferritin includes 45 ng per mL.

Diagnosis of Iron Deficiency Anemia

Figure 1.

Diagnostic algorithm for iron deficiency anemia. (MCV = mean corpuscular volume; LR+ = positive likelihood ratio; TIBC = total iron-binding capacity; FE = serum iron; TfR = serum transferrin receptor.)

Adapted with permission from Ioannou GN, Spector J, Scott K, Rockey DC. Prospective evaluation of a clinical guideline for the diagnosis and management of iron deficiency anemia. Am J Med 2002;113:281–7.

Because IDA has physiologic and pathophysiologic causes, a cause for IDA must be established or serious disease may be overlooked. In a population-based study of more than 700 adults with IDA, 6 percent were diagnosed with a gastrointestinal malignancy. The risk of malignancy was 9 percent in patients older than 65 years with IDA. None of the 442 premenopausal women with iron deficiency, 92 of whom also were anemic, had a gastrointestinal malignancy detected.30

Figure 2 4 ,21,29,31,32 shows the authors' suggested evaluation for underlying causes of IDA. The general approach is to separate groups by risk of underlying disease. Patients with a high risk of underlying disease (e.g., men of all ages and postmenopausal women) should be

evaluated endoscopically for occult bleeding unless the history and physical examination strongly indicate a known benign cause for IDA.

Whether to begin with endoscopy or colonoscopy should be indicated by symptoms or age. In a patient older than 50 years who lacks symptoms, the diagnostic work-up should begin with colonoscopy.31 Some disease-oriented evidence by specialty researchers suggests that esophagogastroduodenoscopy may be valuable in women of reproductive age.33 However, in the absence of symptoms, a therapeutic trial of oral iron therapy is the recommended initial approach.29

Evaluation and Treatment of Iron Deficiency Anemia

Figure 2.

Algorithm for evaluation and treatment of iron deficiency anemia.

Information from references 4,21,29,31, and 32.

Treatment

Transfusion should be considered for patients of any age with IDA complaining of symptoms such as fatigue or dyspnea on exertion. It also should be considered for asymptomatic cardiac patients with hemoglobin less than 10 g per dL (100 g per L). However, oral iron therapy is

usually the first-line therapy for patients with IDA.34 As noted in the etiology section, iron absorption varies widely based on type of diet and other factors. Bone marrow response to iron is limited to 20 mg per day of elemental iron. An increase in the hemoglobin level of 1 g per dL (10 g per L) should occur every two to three weeks on iron therapy; however, it may take up to four months for the iron stores to return to normal after the hemoglobin has corrected.35 Ferrous sulfate in a dose of 325 mg provides 65 mg of elemental iron, whereas 325 mg of ferrous gluconate provides 38 mg of elemental iron. Sustained-release formulations of iron are not recommended as initial therapy because they reduce the amount of iron that is presented for absorption to the duodenal villi.

Gastrointestinal absorption of elemental iron is enhanced in the presence of an acidic gastric environment. This can be accomplished through simultaneous intake of ascorbic acid (i.e., vitamin C).36 Although iron absorption occurs more readily when taken on an empty stomach, this increases the likelihood of stomach upset because of iron therapy. Increased patient adherence should be weighed against the inferior absorption. Foods rich in tannates (e.g., tea)37 or phytates (e.g., bran, cereal),38 or medications that raise the gastric pH (e.g., antacids, proton pump inhibitors, histamine H2 blockers)39 reduce absorption and should be avoided if possible. Some persons have difficulty absorbing the iron because of poor dissolution of the coating.40 A liquid iron preparation would be a better choice for these patients. Laxatives, stool softeners, and adequate intake of liquids can alleviate the constipating effects of oral iron therapy.

Indications for the use of intravenous iron include chronic uncorrectable bleeding, intestinal malabsorption, intolerance to oral iron, nonadherence, or a hemoglobin level less than 6 g per dL (60 g per L) with signs of poor perfusion in patients who would otherwise receive transfusion (e.g., those who have religious objections).41 Until recently, iron dextran (Dexferrum) has been the only parenteral iron preparation available in the United States. The advantage of iron dextran is the ability to administer large doses (200 to 500 mg) at one time.42 One major drawback of iron dextran is the risk of anaphylactic reactions that can be fatal. There also is a delayed reaction, which consists of myalgias, headache, and arthralgias, that can occur 24 to 48 hours after infusion. Nonsteroidal anti-inflammatory drugs will usually relieve these symptoms, but they may be prolonged in patients with chronic inflammatory joint disease.

Sodium ferric gluconate (Ferrlecit), a safer form of parenteral iron, was approved by the U.S. Food and Drug Administration in 1999. The risk of anaphylaxis is drastically reduced using sodium ferric gluconate. In a study of 2,534 patients on hemodialysis, 0.04 percent receiving sodium ferric gluconate had life-threatening reactions compared with 0.61 percent receiving iron dextran.43 Sodium ferric gluconate is usually administered intravenously in eight weekly doses of 125 mg for a total dosage of 1,000 mg. No test dose is required.

Another intravenous preparation, approved for use in the United States in 2000, is iron sucrose (Venofer). In iron deficiency not associated with hemodialysis, 200 mg is administered intravenously five times over a two-week period. Safety profiles are similar to sodium ferric gluconate, although published experience is more limited.28