Wednesday, January 27, 2010

Jangan Ragu Memberi ASI



Produksi ASI sangat dipengaruhi kondisi psikis si ibu. Bila hati ibu tenang, bahagia, maka produksi ASI-nya bakal berlimpah. ASI diproduksi sesuai dengan permintaan. Bila bayi Anda butuh 100 cc maka ASI yang bakal diproduksi pun 100 cc. Jadi, jangan takut ASI-nya tidak mencukupi kebutuhan bayi. Kemungkinan hanya 1 dari 1.000 wanita yang benar-benar tidak dapat menyusui. Oleh karena itu setiap ibu harus yakin dapat menyusui bayinya. Teorinya, ASI itu akan semakin banyak mengalir apabila payudara semakin sering dihisap oleh bayi. Karena itu, kiat sederhana yang perlu diikuti demi berhasilnya ASI eksklusif adalah: Sodorkan payudara setiap kali bayi menangis. Minggu-minggu pertama melahirkan, sebaiknya ibu mengikuti prosedur standar sebagai berikut, untuk menanggapi jika bayi menangis:

1. Sodorkan payudara
2. Jika tidak berhasil menenangkan bayi, periksa popoknya
3. Jika tidak berhasil juga, gendong bayi sambil tepuk tepuk atau tengkurapkan bayi sambil tepuk tepuk
4. Jika tidak berhasil juga, kembali ke langkah 1
Namun, sewaktu waktu, ada saatnya bayi mengalami lonjakan pertumbuhan (growth spurts), selama kira-kira 2-3 hari. Growth spurts itu seringkali terjadi umur 3 minggu, 6 minggu, 3 bulan, dan 6 bulan. Saat itu, bayi akan membutuhkan lebih banyak susu dari sebelumnya, sehingga dia akan meminta ASI lebih sering bahkan setiap setengah jam, selama 2-3 hari itu. Tidak apa apa, turuti saja kemauan bayi itu seberapa seringnya pun, karena payudara anda akan beradaptasi dengan membuat ASI lebih banyak lagi. Setelah beberapa hari, jarak antar menyusui akan menjadi lebih jarang kembali. Intinya, kalau nangis, sodorkan payudara!

Selain itu banyak ibu yang merasa ASI sedikit, karena tidak tahu apakah bayinya sudah cukup minum. Berikut adalah cara mengetahui bahwa ASI cukup banyak dan cukup mengenyangkan bayi:
• Kalau bayi melepaskan payudara dengan sendirinya ketika kenyang, berarti dia cukup minum ASI
• Kalau bayi kelihatan kenyang setelah minum ASI, berarti dia cukup minum ASI. (Bayi saya bertampang ‘mabok’ kalau kenyang ASI, dan langsung tidur lagi)
• Kalau bayi cukup banyak berak dan pipis, berarti dia cukup minum ASI.
Jika tanda-tanda sederhana ini diikuti, ibu tidak perlu khawatir lagi.


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ISPA pada Anak

Penyakit infeksi dan kurang gizi masih termasuk penyebab kematian balita (bayi di bawah lima tahun) di Indonesia. Angka kematian bayi (AKB) saat ini masih dirasa tinggi: 52 per 1.000 kelahiran hidup dalam setahun. Jika dibandingkan 1970 yang mencapai AKB 145, angka 52 itu jelas menurun jauh. Maklum, penurunan itu didapat berkat program imunisasi dari pemerintah kepada balita secara gratis di Puskesmas sejak 1977. Program imunisasi meliputi BCG (antituberkulosis), tetanus, polio, campak, dipteri (antiinfeksi saluran pernapasan), pertusis (antibatuk rejan), dan hepatitis B, serta didukung pemberian gizi cukup, seperti air susu ibu, makanan bervitamin dan buah-buahan. ISPA sendiri sempat dijuluki sebagai pembunuh utama kematian bayi serta balita di Indonesia.

ISPA (Infeksi Saluran Pernapasan Akut) masih merupakan masalah kesehatan yang penting karena menyebabkan kematian bayi dan balita yang cukup tinggi yaitu kira-kira 1 dari 4 kematian yang terjadi. Setiap anak diperkirakan mengalami 3-6 episode ISPA setiap tahunnya. 40 % - 60 % dari kunjungan diPuskesmas adalah oleh penyakit ISPA. Dari seluruh kematian yang disebabkan oleh ISPA mencakup 20 % - 30 %. Kematian yang terbesar umumnya adalah karena pneumonia dan pada bayi berumur kurang dari 2 bulan.



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Etiologi ISPA



ISPA (infeksi saluran pernafasan akut) yang diadaptasi dari istilah dalam bahasa Inggris Acute Respiratory Infections (ARI) mempunyai pengertian sebagai berikut:
• Infeksi adalah masuknya kuman atau mikroorganisma ke dalam tubuh manusia dan berkembang biak sehingga menimbulkan gejala penyakit.
• Saluran pernafasan adalah organ mulai dari hidung hingga alveoli beserta organ adneksanya seperti sinus-sinus, rongga telinga tengah dan pleura. ISPA secara anatomis mencakup saluran pernafasan bagian atas, saluran pernafasan bagian bawah (termasuk jaringan paru-paru) dan organ adneksa saluran pernafasan. Dengan batasan ini, jaringan paru termasuk dalam saluran pernafasan (respiratory tract)
• Infeksi akut adalah infeksi yang berlangsung sampai dengan 14 hari. Batas 14 hari diambil untuk menunjukkan proses akut meskipun untuk beberapa penyakit yang dapat digolongkan dalam ISPA proses ini dapat berlangsung lebih dari 14 hari.

Adapun etiologi ISPA terdiri lebih dari 300 jenis bakteri, virus dan riketsia. Bakteri penyebabnya antara lain dari genus Streptokokus, Stafilokokus, Pnemokokus, Hemofilus, Bordetella dan Korinebakterium. Virus penyebabnya antara lain golongan Miksovirus, Adenovirus, Koronavirus, Pikornavirus, Mikoplasma, Herpesvirus.

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Eklampsia

Pengertian

Eklampsia adalah kelainan akut pada wanita hamil, dalam persalinan atau masa nifas yang ditandai dengan timbulnya kejang (bukan timbul akibat kelainan neurologik) dan/atau koma dimana sebelumnya sudah menunjukkan gejala-gejala pre eklampsia.

Patofisiologi
Sama dengan pre eklampsia dengan akibat yang lebih serius pada organ-organ hati, ginjal, otak, paru-paru dan jantung yakni terjadi nekrosis dan perdarahan pada organ-organ tersebut.

Gejala Klinis

- Kehamilan lebih 20 minggu atau persalinan atau masa nifas
- Tanda-tanda pre eklampsia (hipertensi, edema dan proteinuria)
- Kejang-kejang dan/atau koma
- Kadang-kadang disertai gangguan fungsi organ.
Pemeriksaan dan diagnosis
1. Berdasarkan gejala klinis di atas
2. Pemeriksaan laboratorium
- Adanya protein dalam urin
- Fungsi organ hepar, ginjal, dan jantung
- Fungsi hematologi / hemostasis.

Penatalaksanaan
Tujuan pengobatan :
1. Untuk menghentikan dan mencegah kejang.
2. Mencegah dan mengatasi penyulit, khususnya hipertensi krisis
3. Sebagai penunjang untuk mencapai stabilisasi keadaan ibu seoptimal mungkin
4. Mengakhiri kehamilan dengan trauma ibu seminimal mungkin.

Pengobatan Medisinal
Sama seperti pengobatan pre eklampsia berat kecuali bila timbul kejang-kejang lagi maka dapat diberikan MgSO4 2 gram intravenous selama 2 menit minimal 20 menit setelah pemberian terakhir. Dosis tambahan 2 gram hanya diberikan 1 kali saja. Bila setelah diberi dosis tambahan masih tetap kejang maka diberikan amobarbital / thiopental 3-5 mg/kgBB/IV perlahan-lahan.
Perawatan bersama : konsul bagian saraf, penyakit dalam / jantung, mata, anestesi dan anak.
Perawatan pada serangan kejang : di kamar isolasi yang cukup terang / ICU

Pengobatan Obstetrik
1. Sikap dasar : Semua kehamilan dengan eklampsia harus diakhiri dengan tanpa
memandang umur kehamilan dan keadaan janin.
2. Bilamana diakhiri, sikap dasar : Kehamilan diakhiri bila sudah terjadi stabilisasi
(pemulihan) hemodinamik dan metabolisme ibu. Stabilisasi ibu dicapai dalam 4-
8 jam setelah salah satu atau lebih keadaan dibawah :
- Setelah pemberian obat anti kejang terakhir.
- Setelah kejang terakhir
- Setelah pemberian obat-obat antihipertensi terakhir
- Penderita mulai sadar (responsif dan orientasi)

Terminasi Kehamilan
1. Apabila pada pemeriksaan, syarat-syarat untuk mengakhiri persalinan per
vaginam dipenuhi maka persalinan tindakan dengan trauma yang minimal.
2. Apabila penderita sudah inpartu pada fase aktif, langsung dilakukan amniotomi
lalu diikuti partograf. Bila ada kemacetan dilakukan seksio sesar.
3. Tindakan seksio sesar dilakukan pada keadaan :
- Penderita belum inpartu
- Fase laten
- Gawat janin
Tindakan seksio sesar dikerjakan dengan mempertimbangkan keadaan atau
kondisi ibu.


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Efek Nagatif Obesitas


Siapa yang tidak kenal dengan obesitas. Tidak sedit orang yang bermasalah dengan obesitas, baik di dalam maupun di luar negeri . OBESITAS atau kegemukan didefinisikan sebagai suatu kelainan atau penyakit, ditandai dengan penimbunan jaringan lemak tubuh secara berlebihan. Organisasi Kesehatan Dunia (WHO) telah mendeklarasikan, obesitas sebagai epidemik global. Prevalensinya meningkat tidak saja di negara-negara maju, tetapi juga di negara-negara berkembang, termasuk Indonesia.

Obesitas tidak memberikan manfaat apapun selain memberikan efek negative yang banyak. Dampak yang disebabkan obesitas, pertama ,gangguan psikososial, misalnya, rendah diri karena diolok-olok teman akibat berbagai perbedaan dengan sesama. Kedua, pertumbuhan fisik yang lebih cepat. Usia tulang juga menjadi lebih cepat dibanding umur biologiknya. Ketiga, gangguan pernapasan, umpamanya tidur mendengkur, sering mengantuk di siang hari, atau infeksi saluran napas.


Keempat, obesitas berlanjut sampai usia dewasa terutama apabila dimulai pada masa prapubertas. Lima, adanya penyakit degeneratif maupun metabolik, seperti darah tinggi, jantung koroner, kencing manis, dan kelebihan kolesterol maupun lemak protein. Keenam, penyempitan pembuluh darah karena timbunan lemak yang berlebihan. Ketujuh, potensi paling sering terjadi pada anak obesitas adalah infeksi pernapasan atas (ISPA).

Oleh karena banyaknya efek negative yang ditimbulkan oleh obesitas tersebut, amak perlu penanganan khusus. Penanganan obesitas yang bisa dilakukan adalah, pengobatan hanya diberikan kepada anak yang sudah dipastikan memenuhi kriteria obesitas.
Mencegah gemuk pada bayi, tetapi jangan menjalankan diet ketat. Mengurangi masukan kalori atau energi. Jangan menghilangkan seluruh kelebihan berat badan. Dipertahankan saja agar tidak bertambah karena pertumbuhan pada fase anak masih berlangsung. Memodifikasi pola perilaku anak maupun keluarga khususnya pola makan. Menambah pengeluaran atau penggunaan energi dengan mengajak anak untuk aktif bergerak.


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What Is Diabetes?

Diabetes occurs either because of a lack of insulin or because of the presence of factors that oppose the action of insulin. The result of insufficient action of insulin is an increase in blood glucose concentration (hyperglycaemia). Many other metabolic abnormalities occur, notably an increase in ketone bodies in the blood when there is a severe lack of insulin.

There are the types of diabetes: Type 1 diabetes (previously insulin dependent diabetes) is due to B-cell destruction, usually leading to absolute insulin deficiency). It can be immune mediated or idiopathic. Type 2 diabetes (previously non-insulin dependent diabetes) ranges from those with predominant insulin resistance associated with relative insulin deficiency, to those with a predominantly insulin secretory defect with insulin resistance.

Type 1 and Type 2 diabetes are the commonest forms of primary diabetes mellitus. The division is important both clinically in assessing the need for treatment, and also in understanding the causes of diabetes which are entirely different in the two groups.


• Type 1 diabetes
Type 1 diabetes is due to destruction of B-cells in the pancreatic islets of Langerhans with resulting loss of insulin production. A combination of environmental and genetic factors that trigger an autoimmune attack on the B-cells is responsible, occurring in genetically susceptible individuals.
Thus, among monozygotic identical twins only about one-third of the pairs are concordant for diabetes in contrast to the situation in Type 2 diabetes where almost all pairs are concordant. The process of islet destruction probably begins very early in life and is known to start several years before the clinical onset of diabetes.
• Type 2 diabetes
There are numerous causes of Type 2 diabetes, which is now known to include a wide range of disorders with differing progression and outlook. The underlying mechanism is due either to diminished insulin secretion—that is, an islet defect, associated with increased peripheral resistance to the action of insulin resulting in decreased peripheral glucose uptake, or increased hepatic glucose output.
Probably as many as 98% of Type 2 diabetic patients are “idiopathic”—that is, no specific causative defect has been identified. Whether decreasing insulin secretion or increasing insulin resistance occurs first is still uncertain, but the sequence of events may vary in different individuals. Obesity is the commonest cause of insulin resistance. Some adults (especially those not overweight) over 25 years of age who appear to present with Type 2 diabetes may have latent autoimmune diabetes of adulthood (LADA) and become insulin dependent. Autoantibodies are often present in this group of patients.
Type 2 diabetes is a slowly progressive disease: insulin secretion declines over several decades, resulting in an insidious deterioration of glycaemic control which becomes increasingly difficult to achieve


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Friday, January 22, 2010

Cara Menghitung Masa Kehamilan



Hari pertama haid terakhir
Di sini, daur haid yang jadi patokan. Berdasarkan tanggal itu, dokter memperkirakan usia kehamilan dan tanggal kelahiran si kecil yang dihitung berdasarkan rumus Naegele, yakni (hari+7), (bulan–3), (tahun+1). Contohnya, bila haid terakhir tanggal 1 Juni 2003, diperkirakan persalinan tanggal 8 Maret 2004.
Catatan:
 Rumus ini hanya bisa diterapkan pada wanita yang daur haidnya teratur, yakni antara 28-30 hari.
 Perkiraan tanggal persalinan sering meleset antara 7 hari sebelum atau setelahnya. Hanya sekitar 5% bayi yang akan lahir sesuai perhitungan ini.
 Untuk mengurangi kemungkinan terlalu melesetnya perhitungan pada wanita yang daur haidnya pendek, akan ditambahkan beberapa hari dari hari-H. Sedang yang daur haidnya panjang, akan dikurangi beberapa hari.
 Untuk bulan yang tidak bisa dikurangi 3, misalnya Januari, Februari, dan Maret, maka bulannya ditambah 9, tapi tahunnya tetap.

Gerakan janin
Pada kehamilan pertama, gerakan janin mulai terasa sesudah usia kehamilan 18-20 minggu. Pada kehamilan ke-2 dan seterusnya, gerakan janin sudah terasa pada usia kehamilan 16-18 minggu. Memasuki trimester ke-3 usia kehamilan, gerakan janin akan semakin kuat dan sering. Namun, tak jarang janin justru kurang aktif bergerak. Perkiraan ini dilakukan bila Anda lupa hari pertama haid terakhir.
Tinggi puncak rahim
Pada pengukuran ini, dokter akan meraba puncak rahim (fundus uteri) yang menonjol di dinding perut. Di sini, usia kehamilan dihitung dengan 3 cara yang dimulai dari tulang kemaluan.
• Memakai satuan cm
• Kalau jarak dari tulang kemaluan sampai puncak rahim sekitar 28 cm, ini berarti usia kehamilan sudah mencapai 28 minggu.
• Tinggi maksimal puncak rahim adalah 36 cm, dan ini menunjukkan usia kehamilan 36 minggu.
Catatan: Ukuran ini tidak akan bertambah lagi, meski usia kehamilan mencapai 40 minggu. Kalaupun tingginya bertambah, kemungkinan bayi Anda besar, kembar, atau cairan tubuh Anda berlebih.
Menggunakan 2 jari tangan
o Jika jarak antara tulang kemaluan dengan puncak rahim masih di bawah pusar, setiap penambahan 2 jari berarti penambahan usia kehamilan sebanyak 2 minggu.
o Bila jarak tadi sudah di atas pusar, setiap penambahan 2 jari sama dengan bertambahnya usia kehamilan 4 minggu.
o Membandingkan tinggi puncak rahim dan tinggi pusar
o Kalau sama-sama tinggi, ini berarti usia kehamilan mencapai 5 bulan.
o Tinggi puncak rahim yang melewati pusar dan hampir di tengah-tengah dada menunjukkan usia kehamilan sudah sekitar 7 bulan.
o Jika tinggi puncak rahim sudah mencapai dada, dapat dipastikan usia kehamilan 9 bulan.
Catatan: Cara ini agak sulit dilakukan pada wanita yang bertubuh gemuk.
Ultrasonografi (USG)
USG dapat menentukan usia kehamilan dan memperkirakan waktu kelahiran si kecil berdasarkan “gambar” janin yang muncul pada layar monitor dengan bantuan transducer Catatan: USG sering digunakan untuk melengkapi kepastian usia kehamilan. Meski biaya pemeriksaannya agak mahal, tapi tingkat akurasinya tinggi, yakni sekitar 95%


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ASI Eksklusif



ASI eksklusif adalah pemberian ASI tanpa makanan dan minuman tambahan lain pada bayi berumur nol sampai enam bulan. Bahkan air putih tidak diberikan dalam tahap ASI eksklusif ini.

Pada tahun 2001 World Health Organization / Organisasi Kesehatan Dunia menyatakan bahwa ASI eksklusif selama enam bulan pertama hidup bayi adalah yang terbaik. Dengan demikian, ketentuan sebelumnya (bahwa ASI eksklusif itu cukup empat bulan) sudah tidak berlaku lagi

WHO dan UNICEF merekomendasikan langkah-langkah berikut untuk memulai dan mencapai ASI eksklusif:
• Menyusui dalam satu jam setelah kelahiran
• Menyusui secara ekslusif: hanya ASI. Artinya, tidak ditambah makanan atau minuman lain, bahkan air putih sekalipun.
• Menyusui kapanpun bayi meminta (on-demand), sesering yang bayi mau, siang dan malam.
• Tidak menggunakan botol susu maupun empeng.
• Mengeluarkan ASI dengan memompa atau memerah dengan tangan, disaat tidak bersama anak.
• Mengendalikan emosi dan pikiran agar tenang

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Apakah Anda Kelebihan Berat Badan ?



Kelebihan berat badan terjadi bila makanan yang dikonsumsi mengandung energi melebih kebutuhan tubuh. Kelebihan energi tersebut akan disimpan tubuh sebagai cadangan dalam bentuk lemak sehingga mengakibatkan seseorang menjadi lebih gemuk. Sama halnya dengan badan kurus. Orang yang berbadan gemuk atau kelebihan berat badan pun memiliki efek negative. Bahkan resiko orang yang kelebihan berat badan jauh lebih banyak disbanding yang bertubuh kurus.
Berikut adalah beberapa kerugian bagi yang memiliki berat badan berlebih:

• Penampilan kurang menarik
• Gerakan tidak gesit dan lambat
• Merupakan faktor resiko penyakit:
• Jantung dan pembuluh darah
• Kencing manis (diabetes mellitus)
• Tekanan darah tinggi
• Gangguan sendi dan tulang
• Gangguan ginjal
• Gangguan kandungan empedu
• Kanker
• Pada wanita dapat mengakibatkan gangguan haid (haid tidak teratur, perdarahan yang tidak teratur), factor penyulit pada persalinan.

Bagi Anda yang telah memiliki berat badan berlebih, anda tetap dapat menurunkan berat badan hingga mencapai ideal. Berikut adalah cara menurunkan berat badan yang dianjurkan:
1. Diet
• Makan teratur (2 atau 3 kali sehari) dengan gizi seimbang.
• Kurangi jumlah makanan terutama sumber energi
• Kurangi makanan yang berminyak, berlemak atau bersantan karena memberikan energi yang tinggi.
• Kurangi konsumsi gula dan makanan yang manis, karena makanan tersebut juga menghasilkan energi yang tinggi.
• Makan banyak sayuran dan buah-buahan karena makan tersebut banyak mengandung serat.
• Hindari minuman beralkohol karena merupakan sumber kalori dan berpotensi menimbulkan gangguan kesehatan.
2. Olah raga dan kegiatan fisik
• Olahraga secara teratur selama ½ - 1 jam minimal 3 kali seminggu.
• Pilihlah olah raga yang sesuai dengan usia dan kondisi kesehatan.
• Tingkatkan kegiatan fisik sesuai yang dilakukan sehari-hari.
Berikut adalah cara menurunkan berat badan yang tidak dianjurkan:
• Mengurangi jumlah konsumsi makanan sehari –hari secara drastis sehingga mengakibatkan pusing, lemas, keringat dingin atau gejala lainnya yang membahayakan kesehatan.
• Menurunkan berat badan secara cepat, lebih dari 2 kg perbulan.
• Mengandalkan makanan formula saja untuk menurunkan berat badan.
• Menggunakan obat-obatan atau bahan penurun berat badan tanpa pengawasan tenaga medis. Beberapa obat dan bahan tersebut hanya menurunkan berat badan sementara dengan mengeluarkan cairan tubuh.


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4 Vitamin Kecantikan Kulit



Setiap wanita pasti mendambakan kulit yang indah, halus, dan lembut. Namun terkadang karena ingin cepat memiliki kulit indah, banyak wanita melakukan hal instan. Mereka akhirnya mengunakan produk kosmetik yang banyak mengandung zat kimia yang terkadang sangat berbahaya bagi kulit. Namun sebenarnya ada cara mudah, murah, aman dan sehat untuk memperoleh kulit sehat tersebut. Cukup dengan mengkonsumsi vitamin A, B Kompleks, C dan Vitamin E yang banyak disediakan oleh alam dalam bentuk buah-buahan dan sayuran. Empat vitamin ini sangat berguna sebagai antioksidan dan menyehatkan kulit. Gunakan secara teratur untuk mendapatkan hasil terbaik.

VITAMIN A Sumber antioksidan yang sangat kuat untuk mengusir radikal bebas dan racun. Juga efektif mengurangi kerut dan garis halus. Bagus untuk mencegah jerawat dan mengurangi produksi sebum. Dosis yang dianjurkan untuk mengatasi jerawat adalah 10.000 IU.

VITAMIN B KOMPLEKS Memperbaiki sirkulasi dan metabolisme kulit. Penting juga untuk fungsi kekebalan tubuh dan produksi antibodi. Bagus untuk memerangi jerawat.

VITAMIN C Antioksidan yang penting dalam penyembuhan luka karena membantu stabilisasi kolagen. Vitamin yang penting untuk membuat Anda terlihat cerah. Jika dioleskan secara topikal, vitamin C bagus untuk mengurangi garis halus dan keriput. Vitamin C adalah antioksidan yang sangat kuat yang juga memperkuat antioksidan lain seperti vitamin E. Karena larut dalam air, ia mudah menetralisir Radikal Bebas dalam cairan tubuh. Banyak penelitian ynag telah menunjukkan bahwa Vitamin C adalah pertahanan pertama dalam pertahanan antioksidan, terutama untuk sel otak dan tulang belakang
VITAMIN E Sumber antioksidan yang punya efek antiperadangan pada kulit. Vitamin E adalah antioksidan yang sangat kuat yang menjaga dari terjadinya oksidasi lemak, yang mengarah ke atheroschelrosis. Karena larut dalam lemak, dan kebanyakan sel terbentuk dari lemak, Vitamin E sangat ampuh dalam melindungi sel. Vitamin E juga meningkatkan penggunaan oksigen, memperkuat respon imun, membantu mencegah katarak dan menurunkan resiko penyakit arteri koroner.
Vitamin E yang alami (d-alpha tocopherol) jauh lebih ampuh dari yang sintetis (dl-alpha tocopherol). Penelitian terbaru menunjukkan bahwa zinc dibutukan untuk menjaga konsentrasi Vitamin E dalam darah. Selenium meningkatkan aktifitas Vitamin E dan bekerja bersama di dalam tubuh. Jika dioleskan ke kulit bagus untuk memperbaiki kelembaban, kelembutan, dan melindungi kulit dari sinar yang merugikan.


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Thursday, January 14, 2010

EPIDEMIOLOGY OF HEART FAILURE

Studies of the epidemiology of heart failure have been complicated by the lack of universal agreement on a definition of heart failure, which is primarily a clinical diagnosis. National and international comparisons have therefore been difficult, and mortality data, postmortem studies, and hospital admission rates are not easily translated into incidence and prevalence.

Several different systems have been used in large population studies, with the use of scores for clinical features determined from history and examination, and in most cases chest radiography, to define heart failure.

The Task Force on Heart Failure of the European Society of Cardiology has recently published guidelines on the diagnosis of heart failure, which require the presence of symptoms and objective evidence of cardiac dysfunction. Reversibility of symptoms on appropriate treatment is also desirable.

Echocardiography is recommended as the most practicable way of assessing cardiac function, and this investigation has been used in more recent studies. In the Framingham heart study a cohort of 5209 subjects has been assessed biennially since 1948, with a further cohort (their offspring) added in 1971. This uniquely large dataset has been used to determine the incidence and prevalence of heart failure, defined with consistent clinical and radiographic criteria.

Several recent British studies of the epidemiology of heart failure and left ventricular dysfunction have been conducted, including a study of the incidence of heart failure in one west London district (Hillingdon heart failure study) and large prevalence studies in Glasgow (north Glasgow MONICA study) and the West Midlands ECHOES (echocardiographic heart of England screening) study. It is important to note that epidemiological studies of heart failure have used different levels of ejection fraction to define systolic dysfunction.

The Glasgow study, for example, used an ejection fraction of 30% as their criteria, whereas most other epidemiological surveys have used levels of 40-45%. Indeed, prevalence of heart failure seems similar in many different surveys, despite variation in the levels of ejection fraction, and this observation is not entirely explained.


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Energy Intake

Analysis of the dietary factors associated with obesity is confounded by the difficulties in assessing food intake and eating behaviour. Dietary surveys are increasingly beset by the problem of underreporting, probably related to the increased awareness of nutrition issues and concern over body weight, which leads individuals to consciously or sub-consciously mis-report their food intake.

In 1986 Prentice et al. demonstrated that obese women under-reported energy intake relative to energy needs by a mean of 3.5MJ/day, while among lean women the two measures agreed to within 0.14 MJ/day (Prentice et al., 1986). This observation has been repeatedly reconfirmed, although it is now recognized that there is a spectrum of mis-reporting of food intake across the population, the nature of which is not easily predicted on the basis of individual phenotype or demographic statistics. Others may alter their dietary habits during periods of food recording, usually leading to a record of undereating (Goris et al., 2000)

Analysis of the dietary determinants of obesity is also confounded by the problems of post-hoc changes in consumption in response to increasing body weight. This makes it difficult to draw quantitative conclusions from crosssectional or even prospective studies of food intake and body weight. Nonetheless increasingly refined recording tools and statistical analysis are seeking to understand more about the broader context of eating behaviour with targeted questions about the location and social context of eating episodes and using factor analysis to identify types of dietary patterns, which may inform future strategies to prevent and treat obesity (Whichelow and Prevost, 1996).

Instead much of our understanding of the relationship between dietary factors and the risk of obesity comes from experimental studies in the laboratory or highly controlled intervention studies in the community. These may not truly mimic eating behaviour in a naturalistic setting, but they provide useful insights into the response to imposed dietary manipulations under standardized conditions.
(Written By: Susan A. Jebb and Jeremy Krebs in The Book Of Obesity And Diabets)


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ENERGY DENSITY

Energy density is a critical component in the regulation of human appetite and plays an important role in determining total energy intake. In one of the most robust experimental studies Stubbs et al showed that lean, young healthy men, allowed to eat ad libitum, consumed significantly more energy as the fat content of the food was increased (Stubbs et al., 1995a, b). Careful measurements of fat balance over one week in a whole body indirect calorimeter showed that body fat decreased by 0.86 ± 0.61 kg on the 20 per cent fat diet, while increasing by 0.39 ± 0.59 kg and 2.24 ± 0.94 kg on the 40 and 60 per cent fat diets respectively. These studies provided no evidence of any physiological compensation or cognitive ‘learning’ associated with sustained consumption of foods of differing fat content even after a week or more of sustained over-consumption.

Importantly, when the energy density of the food was equalized, through careful experimental manipulation of the recipes, the high fat hyperphagia was abolished (Stubbs et al., 1996) (Figure 3.1). This strongly suggests that excess energy was consumed by a process of ‘passive over-consumption’, in which changes in food quality, not quantity, were the driving force beyond the disruption in the previously accurate regulation of body weight. This phenomenon implies that the bulk of food consumed is an important determinant of energy intake.


In the ‘real world’ energy-dense diets are frequently high in fat, since fat (37 kJ/g) contains more than twice as much energy gram-for-gram as protein (17 kJ/g) or carbohydrate (16 kJ/g). Many low-fat foods, especially dairy products, contain substantially less energy than their full-fat equivalent, allowing consumers to maintain the bulk of food in the diet, while constraining energy intake. However, recent advances in food technology have resulted in some food ranges that are low in fat but where the energy content is similar to traditional equivalents. These foods, such as biscuits, cakes and desserts often contain large quantities of added sugars and might be expected to lead to similar passive over-consumption as high-fat foods of similar energy density.

Foods served in most ‘fast-food’ chains such as burger and chicken outlets are characterized by a particularly high energy density. These foods are frequently high in fat and have a low water content. A recent analysis has shown that the energy density of foods offered in a selection of these outlets has an energy density of over 1000 kJ/100 g relative to the typical energy density of the diet of a woman in the UK of 670 kJ/100 g (Prentice and Jebb, 2003). This implies that for regular consumers the total quantity of food which can be consumed without exceeding energy needs must be constrained to accommodate this increase in the energy density of the diet in regular consumers. The high energy density of these foods provides a plausible biological explanation for the epidemiological associations between ‘fast-food’ consumption and obesity. However this is likely to be compounded by large portion size and specific marketing strategies to encourage further consumption of these products.

(Written By: Susan A. Jebb and Jeremy Krebs in The Book Of Obesity And Diabets)

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Educational Inequalities In Cardiovascular Disease

Educational inequalities in cardiovascular disease are evident in many countries, especially those in northern Europe. Cardiovascular disease also strongly contributes to overall health inequalities in these countries due to its relatively high prevalence. However, much less is known about biological mechanisms accounting for these inequalities. The metabolic syndrome is one potential factor behind educational and other socioeconomic inequalities in cardiovascular disease.

The metabolic syndrome is a metabolic state characterized by many classical risk factors of cardiovascular disease, i.e. abdominal obesity, low high-density lipoprotein (HDL) cholesterol, elevated triglycerides, hyperinsulinaemia, and hyperglycaemia. The causes of the metabolic syndrome are not yet well understood. In addition to behavioural factors, such as diet and physical activity, previous research indicates a strong genetic influence. It has also been suggested that undernutrition during fetal life and early childhood may cause permanent changes in human metabolism and thus affect the development of the metabolic syndrome in later life.6 Thus, the metabolic syndrome may mediate the effect of early material resources on later cardiovascular disease risk.

Inequalities in the prevalence of the metabolic syndrome by occupational status or education have been examined by three previous studies. In the Whitehall II Study with a large sample of British civil servants, a clear negative association was found between occupational status and the prevalence of the metabolic syndrome. Among men, the prevalence of the metabolic syndrome decreased across the six categories of the occupational scale, but among women a higher prevalence was found only in the three lowest categories. In a follow-up study in the UK, negative, but statistically insignificant, associations were found between the metabolic syndrome and socioeconomic class in childhood or in adulthood.

However, the sample size was smaller than in the Whitehall II study, which may explain the statistically insignificant results. In a study of Swedish women, an inverse gradient in the prevalence of the metabolic syndrome was found across categories of education.9 In this study, the age-adjusted prevalence of the metabolic syndrome was 2.6 times higher among women with basic education compared with women who had college or university level education. Adjustment for other risk factors only slightly decreased the occupational gradient in the Whitehall II study and the educational gradient in the Swedish study.

The social gradient in the metabolic syndrome could help explain socioeconomic inequalities in coronary heart disease (CHD). If so, then factors that cause the metabolic syndrome may also be important in the formation of social inequalities in CHD risk. Further, the metabolic syndrome may offer a simple screening tool to find sub-groups and individuals at high risk for CHD. If educational variation is found in the metabolic syndrome, then interventions to prevent and treat metabolic abnormalities, especially in people with low social position, may help to narrow socioeconomic inequalities in CHD. In this study, we examined educational disparities in the metabolic syndrome in a cohort of Finnish middle-aged men and women.

Education is a good indicator of social position in epidemiological studies because it precedes other indicators, such as occupational based social position or income, is comparable between men and women, does not usually change in adulthood, and shapes health behaviours through attitudes, values, and knowledge. First, we investigated whether there were educational differences in the prevalence of the metabolic syndrome and whether adjusting for other risk factors attenuated these differences. Second, we investigated whether the educational differences in the prevalence of the metabolic syndrome at baseline explained educational inequalities in CHD incidence.


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Diagnosis of Diabetes



Diabetes once diagnosed is for life. The perseverance and self discipline needed over a lifetime can often tax even the most robust of people to the limit. Those caring for them also require perseverance and an understanding of humanity combined with a cautious optimism, to guide those with diabetes through the peaks and troughs of their lives.

Definition of Diabetes
Diabetes occurs either because of a lack of insulin or because of the presence of factors that oppose the action of insulin. The result of insufficient action of insulin is an increase in blood glucose concentration (hyperglycaemia). Many other metabolic abnormalities occur, notably an increase in ketone bodies in the blood when there is a severe lack of insulin.

Diagnosis of diabetes

The diagnosis of diabetes must always be established by a blood glucose measurement made in an accredited laboratory.

Glucose tolerance test
The glucose tolerance test is not normally needed in routine clinical practice, and then only if uncertainty exists in younger patients, or to establish an exact diagnosis in pregnancy. For reliable results, glucose tolerance tests should be performed in the morning after an overnight fast, with the patient sitting quietly and not smoking; it is also important that the patient should have normal meals for the previous three days and should not have been dieting.

False results may also occur if the patient has been ill recently or has had prolonged bed rest. Blood glucose concentrations are measured fasting and then one and two hours after a drink of 75 g of glucose in 250-350 ml water (in children 1•75 g/kg to a maximum of 75 g), preferably flavoured, for example, with pure lemon juice. Urine tests should be performed before the glucose drink and at one and two hours. Interpretation of blood glucose values according to WHO criteria is shown in the table.

Adapted from Diabetes Care 1997;20:1183-119


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Coronary Artery Disease And Its Risk Factors



Coronary heart disease is the commonest cause of heart failure in Western countries. In the studies of left ventricular dysfunction (SOLVD) coronary artery disease accounted for almost 75% of the cases of chronic heart failure in male white patients, although in the Framingham heart study, coronary heart disease accounted for only 46% of cases of heart failure inmen and 27% of chronic heart failure cases in women. Coronary artery disease and hypertension (either alone or in combination) were implicated as the cause in over 90% of cases of heart failure in the Framingham study. Recent studies that have allocated aetiology on the basis of non invasive investigations—such as the Hillingdon heart failure study—have identified coronary artery disease as the primary aetiology in 36% of cases of heart failure. In the Hillingdon study, however, researchers were not able to identify the primary aetiology in 34% of cases; this methodological failing has been addressed in the current Bromley heart failure study, which uses coronary angiography as well as historical and non invasive findings.

Coronary risk factors, such as smoking and diabetes mellitus, are also risk markers of the development of heart failure. Smoking is an independent and strong risk factor for the development of heart failure in men, although the findings in women are less consistent. In the prevention arm of SOLVD diabetes was an independent risk factor (about twofold) for mortality, the development of heart failure, and admission to hospital for heart failure, whereas in the Framingham study diabetes and left ventricular hypertrophy were the most significant risk markers of the development of heart failure. Body weight and a high ratio of total cholesterol concentration to high density lipoprotein cholesterol concentration are also independent risk factors for heart failure. Clearly, these risk factors may increase the risks of heart failure through their effects on coronary artery disease, although diabetes alone may induce important structural and functional changes in the myocardium, which further increase the risk of heart failure.
(Source: ABC of Heart Failure)

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Controlling STI (Sexually Transmitted Infections)



The approach to controlling STIs and the emphasis placed on different components will depend on the local pattern and distribution of STIs in the community and whether one is working in a setting that is resource rich or resource poor.
However, the same general principles will apply. Prevention can be aimed at uninfected people in the community to prevent them from acquiring infection (primary prevention) or at infected people to prevent the onward transmission of the infection to their sexual partners (secondary prevention).

Although effective primary prevention can theoretically reduce the prevalence of viral and bacterial STIs, secondary prevention is much more effective at reducing the prevalence of bacterial STIs, which all are curable with antibiotics. In fact, the population prevalence of a bacterial STI can be reduced entirely through effective secondary prevention activities without any reduction in risky sexual behavior occurring.

Countries that combine primary and secondary prevention approaches, at the individual and population levels, have managed substantially to reduce the burden of infection in their population. Effective implementation of prevention programmes requires strong political leadership and genuine commitment, without which the most well designed and appropriate programmes are likely to founder. Countries such as Thailand, Brazil, Uganda, and Senegal have seen a dramatic impact on their rates of STIs and HIV, which has been facilitated greatly by political support at the highest level.

Interventions that reduce the rate of STI can be aimed at the entire community or targeted at specific groups who are at high risk of, or are particularly vulnerable to, infection. One to one prevention interventions can take place in clinic settings, such as:

Primary Prevention

Primary prevention interventions aim to keep people uninfected. These approaches are obviously not mutually exclusive. Individual behaviour change probably will be best sustained in a community that is broadly supportive. In addition, the broader cultural mores of the community will influence greatly the feasibility of delivering education in that community and will also affect how people respond to it.
• Behavioural interventions are aimed at enhancing knowledge, skills, and attitudes to help people protect themselves against infection (for example, health promotion to decrease partner change and increase condom use)
• Structural interventions are aimed at broader societal and economic issues that drive the spread of STIs
• Biomedical interventions include condoms, vaccines, vaginal microbicides, or male circumcision to prevent the acquisition of infection

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CHRONIC OBSTRUCTIVE PULMONARY DISEASE

Chronic obstructive pulmonary disease (COPD) is a growing health problem in women. The major causative agent behind the disease is smoking, but there are few longitudinal studies concerning women’s health problems in this field.
In 1968, a population study of women in Göteborg, Sweden, was initiated; engaging 1462 women aged 38–60, representative of the female population of Göteborg. Subsequently, four follow-up examinations have been performed, the latest in
2000-2001, i.e. 32 years after the initial examination.

Lung function was measured as peak expiratory flow (PEF) by a peak flow meter in 1968-1969 and as PEF, vital capacity (VC) and forced expiratory volume in one second (FEV1) at the 2000-2001 examination. A 12-year follow-up study on lung function has previously been presented from this population, in which reduced PEF increased the risk of cardiovascular disease (CVD) and death twelve years later, independent of the presence of risk factors for CVD.

In this paper, we present data concerning lung function, airway symptoms and health status in those women who were 38 years old at the initial examination and 70 years old at the 32-year follow up in 2000-2001. As there are only a few longitudinal studies concerning women’s health problems in this field and epidemiological studies of lung function impairment in women and risk factors in a long-term perspective are scarce we aimed to assess the possible association between selected risk factors among women and lung function, health status as well as airway symptoms in a 32-year perspective.

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CHILDHOOD SOCIOECONOMIC STATUS AND THE METABOLIC SYNDROME

Research on social inequalities has demonstrated a clear relationship between socioeconomic status (SES) and health. Individuals of lower SES experience higher rates of all-cause morbidity and mortality than do more advantaged individuals. This relationship is not attributable solely to poor health among the most deprived individuals, but reflects a gradient of health risk extending across the full distribution of socioeconomic position existing within populations (Adler et al., 1994).

Despite the recognition of this well-established association, the underlying mechanisms by which social inequalities impair health are not well understood. Measures of socioeconomic status indicate one’s position within a broader society, and this position might affect health in various ways. Social position can determine both the availability of preventative and health promoting resources, as well as the amount of one’s exposure to health-damaging environments (Lynch & Kaplan, 2000). SES may also influence health through its association with psychological and lifestyle-associated risk factors, such as smoking prevalence and subjective distress due to more frequent stressful life events (Anderson & Armstead, 1995). In the latter regard, chronic stressors associated with social position may conceivably alter neuroendocrine functioning, resulting in later health consequences (Brunner et al., 1997).


In the following sections, several aspects of SES and health will be reviewed. First, a conceptual basis for SES research will be presented, along with information concerning the relationship of SES to cardiovascular health. The metabolic syndrome and its association with adult SES will then be discussed. Next, research on childhood SES as a predictor of adult CHD will be presented. Finally, a review of the current study will be provided, and implications of the findings will be discussed.

A conceptualization of socioeconomic status itself is necessary when attempting to explain the relationship between socioeconomic status and health. Socioeconomic status (SES) has been defined as one’s relative “position” in society, as reflected in access to or the accumulation of material resources or prestige (Lynch & Kaplan, 2000). Measures of socioeconomic position indicate particular structural locations within society (Lynch & Kaplan, 2000) and attempt to quantify an individual’s probability of success, i.e. “life chances”. Current conceptualization of socioeconomic status relies heavily on the Marxist, Weberian and Functionalist sociological traditions, as summarized by Lynch & Kaplan (2000).

A discussion of socioeconomic status must first address the concept of social class. Social class refers to groups defined by interdependent economic and legal relationships, based on an individual’s position within the economy (Krieger, Williams & Moss, 1997). Relationships between classes co-define each other, and are determined by a society’s connections through production, consumption and distribution of goods (Krieger et al., 1997). Conceptualizing class as a social relationship emphasizes how members of different social classes advance their economic and social well-being, and how the well-being of one class is linked to the deprivation of another (Krieger et al., 1997). Measures of social class attempt to capture these economic interactions among people, rather than identify the personal characteristics that determine an individual’s position within a hierarchy.
Each sociological tradition approaches social class in a slightly different way. The Marxian definition of social class reflects stratification in relation to the means of production in society. A social class is a group within a society that is relatively similar in political, economic, educational, occupational, and prestige status (Lynch & Kaplan, 2000).

According to the Weberian tradition, one's class position yields certain probabilities (or life-chances) of success. Society is stratified by class, status, and political power, and a lack of resources (i.e. goods, skills) places certain groups at a competitive disadvantage. The functionalist approach to stratification suggests that complex societies require stratification into sectors that are more or less valuable to social maintenance and progress. This position maintains that social inequality is necessitated by the need to preferentially reward, by money and power, individuals best qualified to occupy the positions of highest responsibility (Lynch & Kaplan, 2000). The sociological schools of thought described here maintain that macrosocial processes determine the socioeconomic prospects of individuals, with prevailing political and economic conditions generating hierarchies of social position.

Ignored here, however, are individual attributes, such as cognitive abilities and dimensions of personality, that covary with indices of socioeconomic status (Tomlinson-Keasey & Little, 1990). Although such individual characteristics are affected by a wide range of variables, including macrosocial factors, both personality and intelligence also have genetic bases and are influenced by idiosyncratic developmental experiences unrelated to social class (i.e. “nonshared” environmental effects). Individual differences in educational attainment, occupation, and earnings are themselves moderately heritable, and there is significant genetic covariation of SES and intelligence (Lichtenstein & Pedersen, 1997; Rowe, Vesterdal & Rodgers, 1998). Therefore, it is likely that relative socioeconomic position results from a complex interplay of the political and economic structures described in sociological thought, along with individuals’ intellectual and personality characteristics.

Although the concept of socioeconomic status has built upon these sociological traditions of social class, it is important to differentiate these two terms. Whereas social class refers strictly to social groups arising from interdependent economic relationships (i.e. “working class”, “managerial class”), current measures of SES aim to quantify an individual’s life chances of success in a social hierarchy by including both resource-based (material resources and assets) and prestige-based measures (rank or status in a hierarchy) (Krieger et al, 1997).

For example, epidemiological research in England and many other countries draws upon social class data based on the Registrar-General’s grouping of occupations, and categorizes individuals’ structural location within the economy (Marmot, Kogevinas & Elston, 1987). Because social class in this sense is conceptualized as an ordinal variable, it cannot provide a meaningful measure of distance between adjacent occupational categories, and is therefore less precise. Measures of socioeconomic status, based on composites of resource-based and prestige-based measures at an individual, household, or childhood level, in contrast, provide a more continuous measure of one’s standing in a social structure (Krieger, et al., 1997)

Most commonly, SES is assessed at the level of the individual, although household and neighborhood-level indicators are also used. The SES indicators described here are related, but not fully overlapping, and they may affect health through disparate pathways (Gallo & Matthews, 2000). Yet interestingly, disparities in health outcomes persist independently of the measure of socioeconomic status used.

The most widely reported measures of SES are educational attainment, occupational status, income, or some combination of these measures. In studying social inequalities, each measure may be seen to have both advantages and disadvantages. Individual or family income is commonly used to index SES, and can be quantified continuously or divided into categories. Income measures at any one point in time predict various health outcomes, and mortality is strongly and inversely associated with income (Kreiger et al., 1997).

Limitations of using income alone as an indicator of SES include income’s imperfect correlation with accumulated wealth and insensitivity to fluctuations in life circumstances over time. Level of education is an important marker of socioeconomic position in that it provides information about the likelihood of future success, and is also frequently an indicator of prestige.

Potential limitations of using education as a sole measure of SES include variation in the “value” of differing educational experiences defining putatively similar levels of attainment, or in how particular educational accomplishments are rewarded in a given society or economic circumstance (Lynch & Kaplan, 2000). Occupational status is useful in reflecting the prestige, income level and educational requirements associated with various positions in the economic structure, as well as in providing information about job characteristics (such as environmental and working conditions), decision-making latitude, and psychological demands of the job (Lynch & Kaplan, 2000).

Various measures of occupation categorize job types in order to reflect a particular occupational hierarchy, such as Rose and Marmot’s (1981) Occupational Grade and the Registrar General’s Classification (Szreter, 1984). One difficulty of using occupational status as a marker of social position, though, is that of quantifying change in occupational status over the life course (Krieger et al., 1997).

In sum, the intellectual traditions of Marx, Weber and the Functionalists provide a framework for research into social inequalities, and describe structural positions within society that can be measured in several ways. Interest in the associations between socioeconomic position and health has increased in recent years (Lynch & Kaplan, 2000). Most notably, the Whitehall study of mortality (Marmot et al., 1991) demonstrated a clear SES-health gradient among occupational grades of British Civil Servants. This gradient has been shown in U.S. studies as well, using both years of education (Kitagawa & Hauser, 1973) and income (Pappas, Queen, Hadden & Fisher, 1993). Advances in this body of research continue to spur efforts toward the understanding and measurement of socioeconomic variables in relation to health.

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Causes Of Heart Failure

These are some cause of Heart Failure:
a) Coronary artery disease:
•Myocardial infarction
•Ischaemia
b) Hypertension
c) Cardiomyopathy
•Dilated (congestive)
•Hypertrophic/obstructive
•Restrictive—for example, amyloidosis, sarcoidosis, haemochromatosis
•Obliterative
d) Valvar and congenital heart disease
•Mitral valve disease
•Aortic valve disease
•Atrial septal defect, ventricular septal defect

e) Arrhythmias
•Tachycardia
•Bradycardia (complete heart block, the sick sinus syndrome)
•Loss of atrial transport—for example, atrial fibrillation
f) Alcohol and drugs
•Alcohol
•Cardiac depressant drugs (â blockers, calcium antagonists)
g) “High output” failure
•Anaemia, thyrotoxicosis, arteriovenous fistulae, Paget’s disease
h) Pericardial disease
•Constrictive pericarditis
•Pericardial effusion
i) Primary right heart failure
•Pulmonary hypertension—for example, pulmonary embolism, cor

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Sunday, January 10, 2010

Osteoporosis

Osteoporosis, or porous bone, is a disease characterized by low bone mass and structural deterioration of bone tissue, leading to bone fragility and an increased risk of fractures of the hip, spine, and wrist. It is often called a “silent” disease because it has no discernable symptoms until there is a bone fracture. Like other tissues in the body, bone tissue is in a state of constant flux – remodeling and rebuilding. There are many influences on bone mass and strength, such as genetics, hormones, physical exercise and diet (especially intake of calcium, phosphate, vitamin D, and other nutrients). Osteoporosis occurs when there are problems with these factors, resulting in more bone loss than bone rebuilding. Osteoporosis can strike at any age and affects both men and women. One out of every two women and one in four men over 50 will have an osteoporosis-related fracture in their lifetime. In the U.S. today, 10 million individuals already have osteoporosis and 34 million more have low bone mass, placing them at increased risk for this disease.

Osteoporosis is a disease that is characterized by low bone mass and a deterioration in the microarchitecture of bone that increases its susceptibility to fracture.

Normal bone mineral density (BMD) measured using dual x-ray absorptiometry is a T-score that falls within 1 standard deviation (SD) of the reference mean for healthy, young white women. Based on epidemiologic studies, the World Health Organization (WHO) defines osteoporosis as a BMD (hip, spine, or wrist) that is 2.5 SDs or more below the reference mean for healthy, young white women (corresponding to a T-score below –2.5) and defines osteopenia as a BMD that is between 1 and 2.5 SDs below the reference mean.

Men generally have 20 percent greater BMD than women. Blacks have 20 percent greater bone density than whites. Therefore, neither men nor blacks are affected with osteoporosis as frequently as white women, although they can develop the disease. Glucocorticoids can induce osteoporosis in any of these groups.

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Impact of Osteoporosis

Osteoporosis is twice as common in white and Hispanic women as in black women. In white women 50 years and older, the lifetime risk of osteoporotic fractures approaches 40 percent.4 More than 90 percent of hip and vertebral fractures in elderly white women are attributed to osteoporosis.

Osteoporosis is responsible for almost 1 million vertebral and hip fractures annually. In 1995, osteoporotic fractures resulted in 2.5 million physician visits, 432,000 hospitalizations, and 180,000 nursing home admissions. In the United States alone, annual medical expenditures for the management of osteoporotic fractures may be as high as $15 billion.

Vertebral fractures trigger back pain, limit activity, and confine patients to bed. Multiple vertebral fractures cause kyphosis and loss of height. Fracture at any site increases the risk for subsequent fracture: up to 20 percent of women who have an incident vertebral fracture incur another fracture within one year. One analysis found that postmenopausal women with hip or clinical (i.e., symptomatic) vertebral fractures had an age-adjusted increased risk of death (greater than sixfold risk after hip fracture, greater than eightfold risk after vertebral fracture) during the next four years.

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How to Do Breast Feeding



Breastfeeding is the natural, physiologic way of feeding infants and young children milk, and human milk is the milk made specifically for human infants. Formulas made from cow’s milk or soy beans (most of them) are only superficially similar, and advertising which states otherwise is misleading. Breastfeeding should be easy and trouble free for most mothers. A good start helps to assure breastfeeding is a happy experience for both mother and baby.

The vast majority of mothers are perfectly capable of breastfeeding their babies exclusively for four to six months. In fact, most mothers produce more than enough milk. Unfortunately, outdated hospital routines based on bottle feeding still predominate in many health care institutions and make breastfeeding difficult, even impossible, for some mothers and babies. For breastfeeding to be well and properly established, a good early few days can be crucial. Admittedly, even with a terrible start, many mothers and babies manage.

The trick to breastfeeding is getting the baby to latch on well. A baby who latches on well, gets milk well. A baby who latches on poorly has difficulty getting milk, especially if the supply is low. A poor latch is similar to giving a baby a bottle with a nipple hole which is too small—the bottle is full of milk, but the baby will not get much. When a baby is latching on poorly, he may also cause the mother nipple pain. And if he does not get milk well, he will usually stay on the breast for long periods, thus aggravating the pain. Here are a few ways breastfeeding can be made easy:

1. The baby should be at the breast immediately after birth. The vast majority of newborns can be put to breast within minutes of birth. Indeed, research has shown that, given the chance, babies only minutes old will often crawl up to the breast from the mother’s abdomen, and start breastfeeding all by themselves. This process may take up to an hour or longer, but the mother and baby should be given this time together to start learning about each other. Babies who "self-attach" run into far fewer breastfeeding problems. This process does not take any effort on the mother’s part, and the excuse that it cannot be done because the mother is tired after labour is nonsense, pure and simple. Incidentally, studies have also shown that skin to skin contact between mothers and babies keeps the baby as warm as an incubator.

2. The mother and baby should room in together. There is absolutely no medical reason for healthy mothers and babies to be separated from each other, even for short periods. Health facilities which have routine separations of mothers and babies after birth are years behind the times, and the reasons for the separation often have to do with letting parents know who is in control (the hospital) and who is not (the parents). Often bogus reasons are given for separations. One example is the baby passed meconium before birth. A baby who passes meconium and is fine a few minutes after birth will be fine and does not need to be in an incubator for several hours’ "observation".

3. Artificial nipples should not be given to the baby. There seems to be some controversy about whether "nipple confusion" exists. Babies will take whatever method gives them a rapid flow of fluid and may refuse others that do not. Thus, in the first few days, when the mother is producing only a little milk (as nature intended), and the baby gets a bottle (as nature intended?) from which he gets rapid flow, he will tend to prefer the rapid flow method. You don’t have to be a rocket scientist to figure that one out, though many health professionals, who are supposed to be helping you, don’t seem to be able to manage it. Nipple confusion includes not just the baby refusing the breast, but also the baby not taking the breast as well as he could and thus not getting milk well and /or the mother getting sore nipples. Just because a baby will "take both" does not mean that the bottle is not having a negative effect. Since there are now alternatives available if the baby needs to be supplemented.

4. Supplements of water, sugar water, or formula are rarely needed. Most supplements could be avoided by getting the baby to take the breast properly and get the milk that is available. If you are being told you need to supplement without someone having observed you breastfeeding, ask for someone to help who knows what they are doing. There are rare indications for supplementation, but usually supplements are suggested for the convenience of the hospital staff. If supplements are required, they should be given by lactation aid, not cup, finger feeding, syringe or bottle. The best supplement is your own colostrum. It can be mixed with sugar water if you are not able to express much at first. Formula is hardly ever necessary in the first few days.

5. Free formula samples and formula company literature are not gifts. There is only one purpose for these "gifts" and that is to get you to use formula. It is very effective, and very unethical, marketing. If you get any from any health professional, you should be wondering about his/her knowledge of breastfeeding and his/her commitment to breastfeeding. "But I need formula because the baby is not getting enough!". Maybe, but, more likely, you weren’t given good help and the baby is simply not getting your milk well. Get good help. Formula samples are not help.
6. A proper latch is crucial to success. This is the key to successful breastfeeding. Unfortunately, too many mothers are being "helped" by people who don’t know what a proper latch is. If you are being told your two day old’s latch is good despite your having very sore nipples, be skeptical, and ask for help from someone who knows.

7. No restriction on length or frequency of breastfeedings. A baby who drinks well will not be on the breast for hours at a time. Thus, if he is, it is usually because he is not latching on well and not getting the milk which is available. Get help to fix the baby’s latch, and use compression to get the baby more milk. This, not a pacifier, not a bottle, not taking the baby to the nursery, will help.

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ETOLOGY OF ANAEMIA



Anaemia is the result of a wide variety of causes that can be isolated, but more often coexist. Globally, the most significant contributor to the onset of anaemia is iron deficiency so that IDA and anaemia are often used synonymously, and the prevalence of anaemia has often been used as a proxy for IDA. It is generally assumed that 50% of the cases of anaemia are due to iron deficiency, but the proportion may vary among population groups and in different areas according to the local conditions.

The main risk factors for IDA include a low intake of iron, poor absorption of iron from diets high in phytate or phenolic compounds, and period of life when iron requirements are especially high (i.e.growth and pregnancy).

Among the other causes of anaemia, heavy blood loss as a result of menstruation, or parasite infections such as hookworms, ascaris, and schistosomiasis can lower blood haemoglobin (Hb) concentrations. Acute and chronic infections, including malaria, cancer, tuberculosis, and HIV can also lower blood Hb concentrations. The presence of other micronutrient deficiencies, including vitamins A and B12, folate, riboflavin, and copper can increase the risk of anaemia. Furthermore, the impact of haemoglobinopathies on anaemia prevalence needs to be considered within some populations.

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Diet During Lactation



Body image is among the greatest concerns of women during the first year after childbirth. The desire to lose weight and tone muscles in the postpartum period is common concern after child birth in today's society. Weight reduction can be difficult for anyone at anytime, but a mother who is trying to return to her pre-pregnancy weight is also challenged with additional stresses of increased child care commitments, less rest and sleep, household responsibilities, and, possibly, returning to work outside the home. A woman trying to be successful at weight management while breastfeeding will need the support of her family, friends, employer, and medical caregiver.

This article provides preliminary recommendations for diet and exercise programming for breastfeeding women who have the desire and, in consultation with their health care provider, have determined that weight management is necessary.

Lactation places significant energy demands upon the mother, causing the additional expenditure of more that 500 calories per day. The recommended diet is at least 1,800 calories per day, the minimum recommended intake for lactating women. The food eaten should consists largely of complex carbohydrates, low in fat and sugar, and contains the necessary meat and dairy products to meet minimum safe nutritional intake guidelines (United States Department of Agriculture [USDA], 1995). No effort should be made to deliberately restrict total calorie intake, and women should feel free to eat to satiety when they are hungry but to refrain from becoming overly full.

There is a need to make use of dietary exchange list to simplify meal planning and facilitates eating and recording food intake. The exchange list represented below consists of six groups of foods classed together because of similar calorie content and percentage of carbohydrates, protein, and fat. The numbers and types of exchanges eaten should be recorded after each meal in a daily food log to keep a written track of the daily food intake. The strength of this type of dietary recommendation, which uses exchange lists, is that it allows the woman to plan and prepare her own menus based on the type of foods she and her family prefer.
The diet should be composed of approximately 60% of carbohydrate (<=10% of which is composed of refined sugars), 20% protein, and 20-25% fat (<=33% of which is composed of saturated fats.) Eat three or more meals per day, and eat snacks of fruit, vegetables, and grains whenever hungry.

It is important to dispel the myth that it is acceptable to eat as much as desired of any food touted by manufacturers as low- or non-fat. Foods in this category (particularly snacks and desserts) are often found to be high in refined sugar and calories. This diet is also nutritionally sound and conducive to a lifelong pattern of healthful eating by the woman and her family. Vitamin and mineral supplements are not necessary but may be taken at the discretion of the woman and her health care provider, especially if her food choices provide marginal dietary intake of calcium, magnesium, zinc folate, and vitamins B6 and B12. Excessive drinking of beverages with high sugar, caffeine, or alcohol content is discouraged.

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Calcium



Calcium is one of the micronutrients that we need for growth. Here is a simple explanation about Calcium. Calcium is a mineral that plays an important role in the development and maintenance of the bones. Calcium is also needed in tooth formation and is important in other body functions. Calcium is one of the most important and most abundant minerals in the human body. The main function of Calcium in the bloodstream plays an important role in blood clotting, transmission of nerve impulses, muscle contraction, and other metabolic activities. In the bloodstream, calcium maintains a constant balance with phosphate.

We can get Calcium from some foods source of calcium such as Eggs, green leafy vegetables, broccoli, legumes, nuts, and whole grains provide calcium but in smaller amounts than dairy products.
Our body just absorbs of Calcium Only about 10-30% of the calcium in food is absorbed into the body. Calcium must be broken down by the digestive system before the body can use it. Calcium is absorbed into the body in the small intestine. The absorption of calcium is influenced by such factors as the amount of vitamin D hormone in the body and the level of calcium already present in the bloodstream. The "fizz" in fizzy drinks like soda and Champagne inhibits the absorption of calcium and takes calcium out of the bones. Thus about 99% of the body's calcium is stored in bone tissue. The remaining 1% of the body's calcium circulates in the blood and other body fluids.

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Breast Feeding

Feelings about how to parent seem to shift with every generation. A new way of parenting, sometimes called attachment parenting, has emerged and it challenges many of the rigid teachings of our mother's generation. Although breastfeeding is on the rise now, women are still dealing with the repercussions of previous generations. Not too long ago mainstream women did not breastfeed at all and the ones that did were taught to follow strict schedules.

Some thought of breastfeeding as primitive. Formula was touted as being equal to or superior to breast milk. Only recently, has the fact that "breast is best" been acknowledged. Other women were in the workforce. They may have felt that breastfeeding was not an option for them. They did not have the modern breast pump available to them. The medical community may not have encouraged breastfeeding at the time. It is not hard to imagine. After all, even with all the knowledge about the benefits of breastfeeding there are still many health professionals today that are uneducated and unsupportive of breastfeeding. With all the challenges in the way of breastfeeding, it is understandable why many women of yesterday did not choose to breastfeed

Breastfeeding has come a long way but still many of the old thinking still carries on. Women are more educated on the subject; however, even with the many books and other information available, people are often most influenced by their immediate family and friends. Having the support of friends and family can boost the chances of having a successful breastfeeding experience. On the other hand, having to deal with criticism and misinformation from the people you are close to can sabotage a new mom trying to breastfeed.

There are many ways to deal with the negativity of others. One of the best things you can do is to try to understand why the person feels the way they do. Is it because they were taught differently about breastfeeding? Were they indoctrinated with the ideas that breastfeeding is primitive or inferior? Or is it that they feel breasts are a sexual object? Maybe they have never seen someone breastfeed and it makes them uncomfortable. This is the case with a lot of people. Once breastfeeding in public becomes more commonplace, perhaps, this will become less of a problem. Whatever the case, finding out the root of the person's issues with breastfeeding may help to resolve the tension.

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ASSESSING ANAEMIA

Hb concentration is the most reliable indicator of anaemia at the population level, as opposed to clinical measures which are subjective and therefore have more room for error. Measuring Hb concentration is relatively easy and inexpensive, and this measurement is frequently used as a proxy indicator of iron deficiency. However, anaemia can be caused by factors other than iron deficiency.

In addition, in populations where the prevalence of inherited haemoglobinopathies is high, the mean level of Hb concentration may be lowered. This underlines that the etiology of anaemia should be interpreted with caution if the only indicator used is Hb concentration. The main objective for assessing anaemia is to inform decision-makers on the type of measures to be taken to prevent and control anaemia. This implies that in addition to the measurement of Hb concentration, the causes of anaemia need to be identified considering that they may vary according to the population.

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ANAEMIA

Anaemia is a public health problem that affects populations in both rich and poor countries. Although the primary cause is iron deficiency, it is seldom present in isolation.

More frequently it coexists with a number of other causes, such as malaria, parasitic infection, nutritional deficiencies, and haemoglobinopathies.
Given the importance of this pathology in the world, numerous countries conduct interventions to reduce anaemia; particularly in the groups most susceptible to its devastating effects: pregnant women and young children. In order to assess the impact of these interventions, the adequacy of the strategies implemented, and the progress made in the fight against anaemia, information on anaemia prevalence must be collected. This is the primary objective of the WHO Global Database on Anaemia.
However, estimates of anaemia prevalence by themselves are only useful if they are associated with a picture of the various causal factors that contribute to the development of anaemia in specific settings. Indeed these factors are multiple and complex, and it is critical to collect accurate information about them to provide the basis for developing the best interventions for anaemia control.


In the last three decades, there have been various attempts to produce estimates of the prevalence of anaemia at different levels including at the global level, but until the present time, there has never been a systematic review of all of the data collected and published with the objective of deriving regional and global estimates.
The WHO Global Database on Anaemia has filled this gap: data from 93 countries, representing as much as 76% of the population in the case of preschool-age children, were analysed and used to develop statistical models to generate national prevalence estimates for countries with no data within the time frame specified.

It is surprising that given the public health importance of anaemia, there are numerous countries lacking national prevalence data. Moreover, most survey data are related to the three population groups: preschool-age children, pregnant women, and non-pregnant women of reproductive age, which is why the report focuses on these groups.

The data available for school-age children, men, and the elderly were not sufficient to generate regional or countrylevel estimates for these groups, and therefore only global estimates for these groups are presented.

In addition, despite the fact that iron deficiency is considered to be the primary cause of anaemia, there are few data on the prevalence of this deficiency. The likely reason is that iron assessment is difficult because the available indicators of iron status do not provide sufficient information alone and must be used in combination to obtain reliable information on the existence of iron deficiency.
Furthermore, there is no real consensus on the best combination of indicators to use. Another reason is that the role of factors other than iron deficiency in the development of anaemia has been underestimated by public health officials, because for a long time anaemia has been confused with iron deficiency anaemia, and this has influenced the development of strategies and programmes designed to control anaemia.
In this report, the prevalence of anaemia is presented by country and by WHO regions. Because these prevalence data may be used to identify programme needs by other United Nations agencies, we have presented the estimates classified by United Nations regions in the annexes. In addition, one chapter is dedicated to the criteria used to identify, revise, and select the surveys, and the methodology developed to generate national, regional, and global estimates.

A lesson learned from producing this report is that in order for the database to reach its full potential, data should be collected on other vulnerable population groups such as the elderly and school-age children, and surveys should be more inclusive and collect information on iron status and other causes of anaemia.
This report is written for public health officials, nutritionists, and researchers. We hope that readers find it useful and feel free to share any comments with us.

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What is the cervix?



The cervix is part of a woman's reproductive system. It's in the pelvis. The cervix is the lower, narrow part of the uterus (womb).
The cervix is a passageway:
• The cervix connects the uterus to the vagina. During a menstrual period, blood flows from the uterus through the cervix into the vagina. The vagina leads to the outside of the body.
• The cervix makes mucus. During sex, mucus helps sperm move from the vagina through the cervix into the uterus.
• During pregnancy, the cervix is tightly closed to help keep the baby inside the uterus. During childbirth, the cervix opens to allow the baby to pass through the vagina.

What is cancer?

Cancer begins in cells, the building blocks that make up tissues. Tissues make up the organs of the body.

Normal cells grow and divide to form new cells as the body needs them. When normal cells grow old or get damaged, they die, and new cells take their place.
Sometimes, this process goes wrong. New cells form when the body does not need them, and old or damaged cells do not die as they should. The buildup of extra cells often forms a mass of tissue called a growth or tumor.

Growths on the cervix can be benign or malignant. Benign growths are not cancer. They are not as harmful as malignant growths (cancer).
• Benign growths (polyps, cysts, or genital warts):
o are rarely a threat to life
o don't invade the tissues around them
• Malignant growths (cervical cancer):
o may sometimes be a threat to life
o can invade nearby tissues and organs
o can spread to other parts of the body
Cervical cancer begins in cells on the surface of the cervix. Over time, the cervical cancer can invade more deeply into the cervix and nearby tissues. The cancer cells can spread by breaking away from the original (primary) tumor. They enter blood vessels or lymph vessels, which branch into all the tissues of the body. The cancer cells may attach to other tissues and grow to form new tumors that may damage those tissues. The spread of cancer is called metastasis. See the Staging section for information about cervical cancer that has spread.
(source: http://emedicine.medscape.com/article/)

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Risk factors and causes of cervical cancer



When you get a diagnosis of cancer, it's natural to wonder what may have caused the disease. Doctors cannot always explain why one woman develops cervical cancer and another does not. However, we do know that a woman with certain risk factors may be more likely than others to develop cervical cancer. A risk factor is something that may increase the chance of developing a disease.
Studies have found a number of factors that may increase the risk of cervical cancer. For example, infection with HPV (human papillomavirus) is the main cause of cervical cancer. HPV infection and other risk factors may act together to increase the risk even more:

• HPV infection: HPV is a group of viruses that can infect the cervix. An HPV infection that doesn't go away can cause cervical cancer in some women. HPV is the cause of nearly all cervical cancers.
HPV infections are very common. These viruses are passed from person to person through sexual contact. Most adults have been infected with HPV at some time in their lives, but most infections clear up on their own.
Some types of HPV can cause changes to cells in the cervix. If these changes are found early, cervical cancer can be prevented by removing or killing the changed cells before they can become cancer cells. The NCI fact sheet Human Papillomaviruses and Cancer: Questions and Answers has more information.
A vaccine for females ages 9 to 26 protects against two types of HPV infection that cause cervical cancer. The NCI fact sheet Human Papillomavirus (HPV) Vaccines: Questions and Answers has more information.
• Lack of regular Pap tests: Cervical cancer is more common among women who don't have regular Pap tests. The Pap test helps doctors find abnormal cells. Removing or killing the abnormal cells usually prevents cervical cancer.
• Smoking: Among women who are infected with HPV, smoking cigarettes slightly increases the risk of cervical cancer.
• Weakened immune system (the body's natural defense system): Infection with HIV (the virus that causes AIDS) or taking drugs that suppress the immune system increases the risk of cervical cancer.
• Sexual history: Women who have had many sexual partners have a higher risk of developing cervical cancer. Also, a woman who has had sex with a man who has had many sexual partners may be at higher risk of developing cervical cancer. In both cases, the risk of developing cervical cancer is higher because these women have a higher risk of HPV infection.
• Using birth control pills for a long time: Using birth control pills for a long time (5 or more years) may slightly increase the risk of cervical cancer among women with HPV infection. However, the risk decreases quickly when women stop using birth control pills.

• Having many children: Studies suggest that giving birth to many children (5 or more) may slightly increase the risk of cervical cancer among women with HPV infection.
• DES (diethylstilbestrol): DES may increase the risk of a rare form of cervical cancer in daughters exposed to this drug before birth. DES was given to some pregnant women in the United States between about 1940 and 1971. (It is no longer given to pregnant women.)
Having an HPV infection or other risk factors does not mean that a woman will develop cervical cancer. Most women who have risk factors for cervical cancer never develop it

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AIDS

The first recognised cases of the acquired immune deficiency syndrome (AIDS) occurred in the summer of 1981 in America. Reports began to appear of Pneumocystis carinii pneumonia and Kaposi’s sarcoma in young men, who it was subsequently realised were both homosexual and immunocompromised.

Even though the condition became known early on as AIDS, its cause and modes of transmission were not immediately obvious. The virus now known to cause AIDS in a proportion of those infected was discovered in 1983 and given various names. The internationally accepted term is now the human immunodeficiency virus (HIV). Subsequently a new variant has been isolated in patients with West African connections.

The definition of AIDS has changed over the years as a result of an increasing appreciation of the wide spectrum of clinical manifestations of infection with HIV. Currently, AIDS is defined as an illness characterised by one or more indicator diseases. In the absence of another cause of immune deficiency and without laboratory evidence of HIV infection (if the patient has not been tested or the results are inconclusive), certain diseases when definitively diagnosed are indicative of AIDS. Also, regardless of the presence of other causes of immune deficiency, if there is laboratory evidence of HIV infection, other indicator diseases that require a definitive, or in some cases only a presumptive, diagnosis also constitute a diagnosis of AIDS.

In 1993 the Centers for Disease Control (CDC) in the USA extended the definition of AIDS to include all persons who are severely immunosuppressed (a CD4 count <200 _ 106/1) irrespective of the presence or absence of an indicator disease. For surveillance purposes this definition has not been accepted within the UK and Europe. In these countries AIDS continues to be a clinical diagnosis defined by one or more of the indicator diseases mentioned. The World Health Organisation (WHO) also uses this clinically based definition for surveillance within developed countries. WHO, however, has developed an alternative case definition for use in sub-Saharan Africa. This is based on clinical signs and does not require laboratory confirmation of infection. Subsequently this definition has been modified to include a positive test for HIV antibody.

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