Hiperlipidemia I Definisi dan Etiologi Hiperlipidemia Penyakit hiperlipidemia (disebut juga hiperlipoproteinemia atau dislipidemia) merupakan kelainan metabolisme lipid yakni terjadinya peningkatan fraksi lipid dan lipoprotein dalam plasma. Beberapa kelainan fraksi lipid yang utama adalah kenaikan kadar kolesterol total, kolesterol LDL, triasilgliserol (TG), serta penurunan kolesterol HDL. Berdasarkan penyebabnya, hiperlipidemia dibagi menjadi 2, yaitu : hiperlipidemia primer, terjadi akibat kelainan genetik. Biasanya kelainan ini ditemukan pada waktu pemeriksaan laboratorium secara kebetulan. Pada umumnya tidak ada keluhan, kecuali pada keadaan yang agak berat tampak adanya xantoma adanya xantoma (penumpukan lemak di bawah jaringan kulit); hiperlipidemia sekunder terjadi akibat peningkatan kadar lipid darah yang disebabkan oleh suatu penyakit tertentu, misalnya diabetes melitus, gangguan tiroid, penyakit hepar & penyakit ginjal. Hiperlipidemia sekunder bersifat reversibel r eversibel (berulang). Beberapa obat-obatan yang dapat menyebabkan gangguan metabolisme lemak, seperti βbloker , diuretik, kontrasepsi oral (estrogen, gestagen). Menurut klasifikasi Fredrickson yang didasarkan pada pola lipoprotein pada elektroforesis atau ultrasentrifugasi, hiperlipidemia dibagi oleh Organisasi Kesehatan Dunia (WHO) sebagai berikut :
Tabel 1. Klasifikasi hiperlipidemia berdasarkan WHO Penyakit hiperlipidemia sekunder juga dapat disebabkan oleh beberapa faktor berikut : usia, di mana kadar lipoprotein, terutama kolesterol LDL, meningkat sejalan dengan bertambahnya usia;jenis kelamin, dalam keadaan normal, pria memiliki
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kadar yang lebih tinggi, tetapi setelah menopause kadarnya pada wanita mulai meningkat; obesitas atau kegemukan; penggunaan alkohol; mengonsumsi makanan yang mengandung asam lemak jenuh seperti mentega, margarin, whole milk , es krim, keju, daging berlemak; kurang melakukan aktivitas fisik; merokok; diabetes yang tidak terkontrol dengan baik; gagal ginjal; kelenjar tiroid yang kurang aktif; dan konsumsi obat-obatan tertentu yang dapat mengganggu metabolisme lemak seperti estrogen, pil KB, kortikosteroid, diuretik tiazid. B. Gejala Hiperlipidemia Penyakit hiperlipidemia ini memiliki potensi yang berbahaya, namun gejalagejala yang ditimbulkan sangat awam sehingga seringkali sulit didiagnosis lebih dini pada kasus-kasus tertentu. Biasanya penyakit ini diketahui tidak sengaja pada saat medical check up. up. Diagnosa kelainan lipid dapat dilakukan pemeriksaan darah untuk mengukur kadar kolesterol total. Untuk mengukur kadar kolesterol LDL, HDL dan trigliserida, sebaiknya penderita berpuasa dulu minimal selama 12 jam. Seorang pasien dinyatakan hiperlipidemia apabila kadar lemak darah menunjukkan nilai yang lebih tinggi dari yang tertulis pada tabel. Pemeriksaan Laboratorium Kolesterol total
Kisaran yang Ideal (mg/dL darah) 120-200
Kilomikron
negatif (setelah berpuasa selama 12 am)
VLDL LDL HDL Perbandingan LDL dengan HDL Trigliserida
1-30 60-160 35-65 < 3,5 10-160
Tabel 2. Kadar lemak darah normal pada manusia C. Definisi Hiperlipidemia Tipe 1 Hiperlipidemia tipe 1 atau hiperlipoproteinemia tipe 1 (hiperkolesterolemia murni) merupakan hiperlipidemia yang disebabkan oleh asupan lipid eksogen yang berlebihan ditandai dengan peningkatan kilomikron yang melebihi batas normal. Hiperlipidemia tipe ini dapat diatasi dengan diet rendah lipid, tidak memerlukan terapi farmakologi. D. Fisiologis Hiperlipidemia Tipe 1 Pada keadaan normal, lipid yang dikonsumsi dalam tubuh adalah kolesterol dan trigliserid. Pada kasus hiperlipidemia terjadi kelainan metabolisme lipid yang terjadi akibat kelainan produksi lipoprotein. Enzim lipase yang dihasilkan oleh pankreas menghidrolisis lemak di mana
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kilomikron remnan (sisa), asam lemak, gliserol dan kolesterol. Kilomikron remnan akan terikat dengan hepatosit dan mengalami degradasi oleh enzim lisosom. E. Patofisiologis Hiperlipidemia Tipe 1 Pada keadaan normal, gen LPL (Lipoprotein Lipase) akan memacu produksi enzim lipoprotein lipase dan membutuhkan bantuan apo C-II sebagai kofaktornya. Enzim lipoprotein lipase ini akan memecah lipoprotein dalam bentuk kilomikron yang membawa molekul lemak dari usus ke dalam darah. Ketika lipoprotein dipecah, lipoprotein akan melepaskan asam lemak yang disimpan dalam jaringan adiposa dan digunakan untuk energi dalam otot serta gliserol yang digunakan oleh hati untuk sintesis lemak lainnya. Pada penderita hiperlipidemia tipe 1 terjadi defisiensi enzim lipoprotein lipase dan apo C-II yang disebabkan karena adanya mutasi pada gen LPL. Akibatnya, lipoprotein tidak akan terurai secara efisien dan menyebabkan akumulasi drastis kilomikron dalam plasma, walaupun dalam keadaan puasa. Pada dasarnya, penderita hiperlipidemia tipe 1 mengalami kegagalan memecah kilomikron menjadi asam lemak dan gliserol, sehingga kadar kilomikron (triasilgliserida) meningkat drastis.
Gambar 1. Nasib kilomikron secara metabolik F. Parameter Klinis Hiperlipidemia Tipe 1
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LDL
100 mg/dL
Level kolesterol total
160-200 mg/dL
Trigliserida
150 mg/dL
↓
(mencapai mg/dL)
1000-10.000
Tabel 3. Kadar lipid pada penderita hiperlipidemia tipe 1 G. Gejala Klinis Hiperlipidemia Tipe 1 Gejala klinis penyakit hiperlipidemia tipe 1 antara lain : pankreasitis (peradangan pankreas, yang menyebabkan kerusakan kelenjar yang menetap), hepatomegali (pembesaran hati) akibat kerja hati yang berlebihan dalam membentuk triasilgliserida, dan lesi kulit berwarna kuning ( xanthoma xanthoma eruptif ). ). H. Pengobatan dan Terapi Hiperlipidemia Tipe 1 Pengobatan yang umum dilakukan untuk penderita hiperlipoproteinemia tipe 1 adalah diet rendah lemak (low-fat (low-fat diet ) yaitu dengan menghindari lemak baik lemak jenuh maupun lemak tak jenuh.Perawatan hiperlipoproteinemia tipe 1 ditujukan langsung untuk mengurangi kilomikron dari lemak makanan dengan juga pengurangan plasma trigliserida. Total asupan harian lemak sebaiknya tidak lebih dari 10-25 g/hari, atau sekitar 15% dari total kalori. Pengobatan juga dilakukan dengan cara mengubah gaya hidupseperti mengonsumsi makanan rendah lemak, meningkatkan intensitas olahraga, menurunkan stress, dan tidak mengonsumsi alkohol. Pada penderita hiperlipidemia tipe 1, terapi yang diberikan antara lain dengan mengonsumsi obat-obatan. Contohnya adalah obat statin (obat yang menurunkan kadar kolesterol atau triasilgliserol). Obat statin bekerja dengan caramenghalangi enzim yang dibutuhkan untuk membentuk kolesterol dalam hati. Selain itu obat yang sering digunakan adalah asam omega-3 atau fibrate tablets, tablets, di mana konsumsi obat digunakan jika hanya kadar triasilgliserol saja yang tinggi. 2.3.2 Hiperlipidemia II Penyakit hyperlipidemia 2A sama seperti penyakit hiperlipidemia pada umumnya, yaitu merupakan penyakit yang disebabkan karena kadar kolesterol tinggi di dalam darah. Hiperlipidemia biasa disebut dengan hiperkolesterolemia. Hiperkolesterolemia adalah salah satu gangguan kadar lemak dalam darah (dislipidemia) yang mana kadar kolesterol dalam darah lebih dari 240 mg/dl. (perkeni 2004). Penyakit ini sangat berhubungan erat dengan kadar kolesterol LDL (low
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·
Faktor genetik dan faktor sekunder adalah pembagian bagi etiologi hiperkolesterolemia. Penyebab penyakit ini antara lain berasal dari faktor genetik. Berdasarkan faktor genetiknya, hiperkolesterolemia dibagi menjadi : Hiperkolesterolemia familial Penyakit yang diturunkan segara genetis. berupa mutasi pada kromosom nomor 19 atau region ligan apo B-100 yang yang merupakan reseptor LDL di hati dan jaringan ekstrahepatik. Karena mengganggap mengganggap LDL tidak ada, hati kemudian memproduksi VLDL yang banyak ke dalam plasma hal ini menyebabkan penumpukan lemak di darah.
·
Hiperkolesterolemia poligenik Merupakan hiperkolesterolemia yang paling ditemukan namun tidak disertai xantoma ( penumpukan lemak pada jaringan ). Sesuai dengan namanya, penyakit hiperkolesterolemia poligenik merupakan interaksi antara kelainan genetik yang multipel, nutrisi dan faktor-faktor lingkungan lainnya serta memiliki lebih dari satu dasar metabolik. Faktor sekunder membawahi pola hidup serta penyakit lain sehingga hiperkolesterolemia dapat terjadi. Gaya hidup yang sering mengonsumsi makanan berlemak, kegemukan serta kurangnya olah raga ternyata diduga dapat menyebabkan penyakit hiperkolesterolemia, sedangkan diabetes mellitus adalah penyakit yang dianggap memperparah hiperkolesterolemia. Diagnosis penyakit ini, dapat berupa pemeriksaan fisik yang dilakukan adalah antropometri, frekuensi denyut nadi, tekanan darah, auskultasi irama jantung, serta EKG. Pemeriksaan laboratorium darah yaitu kadar kolesterol total, kolesterol LDL, Trigliserida dan kolesterol HDL dalam plasma. Pengobatan dan terapi farmakologi dapat dilakukan untuk mencegah penyakit hiperkolesterolemia, antara lain secara farmakologi adalah dengan meminum obat kolestiramin, kolestipol, lovastatin atau mevastatin. Sedangkan secara non farmakologi atau tIdak menggunakan obat ada cara cara mencegah penyakit ini seperti menurunkan berat badan jika mereka mengalami kelebihan berat badan, badan , berhenti merokok, mengurangi jumlah lemak dan kolesterol dalam m akanannya, dan menambah porsi olah raga. Hiperlipidemia tipe IIB adalah suatu kondisi dimana kadar lipid dalam darah melebihi kadar normal. Hiperlipidemia tipe IIB seringkali disebut juga sebagai Familial Combined Hypercholesterolemia, yaitu merupakan suatu penyakit genetik yang dapat mempercepat terjadinya aterosklerosis, serta kematian dini yang sering terjadi akibat serangan jantung. Hiperlipidemia IIB ini ditandai dengan tingginya kadar kolesterol dan trigliserida akibat peningkatan LDL dan VLDL. Tingginya LDL dan VLDL dapat menimbulkan endapan lemak dan menyebabkan adanya pertumbuhan xantoma di lapisan kulit. Peningkatan LDL dan VLDL ini dapat terjadi karena adanya mutasi pada reseptor apolipoprotein B-100 dimana apolipoprotein B100 ini merupakan komponen utama dari LDL dan VLDL.
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disregulasi dari 3-hidroksi-3-metilglutaril A reduktase (HMG-CoA reductase) yang merupakan enzim pengendali dalam biosintesis kolesterol. Parameter klinis dari penyakit hiperlipidemia IIB ini yaitu kadar LDL dan VLDL yang tinggi, trigliserida dengan kadar 250-750 mg/dL dan kolesterol dengan kadar 250-500 mg/dL. Gejala dari penyakit hiperlipidemia IIB ini tidak muncul secara signifikan, hanya saja kondisi pasien menunjukkan adanya penyumbatan arteri yang dapat menyebabkan serangan jantung, struk, dan lain lain. Hiperlipidemia IIB tidak menular, hanya perlu dilakukan screening kolesterol secara rutin untuk memantau kadar kolesterol dalam tubuh. Dalam mendiagnosis penyakit ini dapat dilihat dari riwayat keluarga yang hasil testnya menunjukkan kadar kolesterol dan triasilgliserolnya tinggi. Selain itu, dapat juga dilakukan pemantauan lewat screening kadar kolesterol. Hiperlipidemia IIB dapat disebabkan oleh hipotiroidism, penyakit obstruktif hati, sindrim Nefrotik, anorexia nervosa, porphyria akut, serta penyalahgunaan alkohol. Pencegahan terhadap penyakit hiperlipidemia IIB ini dapat dilakukan dengan cara monitoring serta memberikan konseling kepada pasien. Apabila sudah terkena penyakit hiperlipidemia IIB ini, pasien diharuskan menurunkan berat badan dengan cara menyusun diet rendah kalori, rendah lemak, serta berolahraga. Pencegahan lainnya dapat dilakukan dengan cara menghindari rokok dan obesitas. Penyakit hiperlipidemia tipe IIB ini dapat disembuhkan dengan terapi, baik terapi non farmakologis maupun terapi farmakologis. Terapi non farmakologi yang dapat dilakukan yaitu menurunkan berat badan, berhenti merokok, mengurangi jumlah lemak dalam makanan, rutin berolahraga, mengkonsumsi mengkonsumsi obat penurun kadar lemak, serta menambahkan bekatul gandum pada makanan yang dapat membantu mengikat lemak di usus. Terapi farmakologi dapat dilakukan dengan cara memberikan obat-obat seperti, Nama Obat Contoh Cara Kerja Obat penyerap asam Kolestiramin, kolestipol Mengikat asam empedu empedu di usus dan meningkatkan pembuangan LDL dalam aliran darah Obat penghambat Niasin Mengurangi kecepatan sintesa lipoprotein sintesis VLDL yang merupakan prekursor dari LDL
Obat penghambat HMG Adrenalin, Fluvastatin, Menghambat Ko-A Reduktase Lovastatin, Sinvastatin pembentukan kolesterol, meningkatkan
dan
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Obat probukol
dapat meningkatkan katabolisme lipoprotein. Menurunkan LDL.
2.3.3 HIPERLIPIDEMIA TIPE III Salah satu penyakit hiperlipidemia yang masih jarang terjadi adalah adalah hiperlipidemia tipe III. Hiperlipidemia tipe III merupakan suatu penyakit yang ditandai dengan gangguan kemampuan tubuh dalam memecah lemak tertentu, seperti lemak kaya trigliserida, yang mengakibatkan penumpukan lipoprotein sisa dalam darah dan berisiko pada perkembangan aterosklerosis dini. Hiperlipidemia tipe III ini disebabkan karena adanya kecacatan akibat terjadinya mutasi pada gen Apolipoprotein E (Apo E) yang berperan penting dalam metabolisme normal lipoprotein kaya trigliserida. Adanya kesalahan pada Apo E ini dapat mengakibatkan akumulasi partikel kaya trigliserida dalam plasma. Penyakit ini diawali dengan terjadinya mutasi pada genotip Apo E-3 menjadi Apo E-2. Mutasi ini menyebabkan Apo memiliki defek dan tidak dapat berikatan dengan reseptor lipoprotein. Pada keadaan metabolisme yang normal, VLDL remnans atau IDL yang mengandung trigliserida, kolestrol, Apo B, dan Apo E akan masuk ke hati melalui reseptor LDL (reseptor Apo B-100/Apo-E). Akan tetapi, Apo E yang telah mengalami mutasi tidak dapat berikatan dengan reseptor lipoprotein ini sehingga IDL (VLDL remnant ) tidak dapat masuk ke hati. Hal ini akan menyebabkan terjadinya penumpukan kilomikron dan VLDL remnant dalam dalam darah, sehingga berisiko terkena stroke, aterosklerosis, dan penyakit lainnya. Penyakit hiperlipidemia III ini menunjukkan beberapa gejala, seperti nyeri perut, xanthoma (penimbunan lemak tertentu di bawah permukaan kulit), dan aterosklerosis yang berkembang pada usia dini, yang ditandai dengan terjadinya nyeri dada awal (angina) atau penurunan aliran darah ke bagian tertentu dari tubuh. Pada penderita pria, pertumbuhan lemak di bawah kulit akan tampak pada masa dewasa awal, sedangkan pada penderita wanita, pertumbuhan lemak ini akan terlihat 10-15 tahun kemudian. Namun, jika penderitanya mengalami obesitas, baik pada pria maupun wanita, pertumbuhan lemak akan muncul lebih awal. Pada pemeriksaan, penyakit hiperlipidemia tipe III ditandai dengan meningkatnya kadar kolestrol, serta triasilgliserol yang berkisar antara 250-750
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a.
Hipertrigliseridemia primer Disebabkan oleh hasil dari berbagai cacat genetik yang menyebabkan metabolisme trigliserida tidak teratur. b. Hipergliseridemia sekunder Disebabkan oleh diet tinggi lemak, obesitas, diabetes, hipotiroidisme, dan obatobatan tertentu. Gejala Gejala umum hiperlipidemia : › Tanpa gejala, ini biasanya terjadi pada saat-saat awal terjadinya hiperlipidemia › Nyeri abdomen berat › Pankreatitis › Xanthomas eruptif › Polineuropati perifer › Hipertensi Patofisiologi Kadar VLDL meningkat, meningkat, sedangkan sedangkan kadar LDL normal normal atau berkurang, berkurang, mengakibatkan kolesterol kolesterol normal atau meningkat dan peningkatan peningkatan kadar gliserol yang berbeda. Peningkatan kadar triasilgliserol yang terkandung di dalam VLDL dan kemungkinan akan berkembang menjadi aterosklerosis. Kondisi berhubungan dengan abnormalitas toleransi glukosa (resisten insulin) dan obesitas. Diagnosis Hiperlipidemia Tipe IV ditandai oleh peningkatan VLDL dan kadar trigliserida hampir selalu kurang dari 1000 mg / dL. Kadar kolesterol serum normal. Tipe IV Penyakit ini ditandai dengan keruhnya serum dan tingkat kolesterol normal atau hanya sedikit lebih tinggi dari kadar normal. Hyperlipoproteinemia dapat bersifat primer, yang dihasilkan dari karakteristik diwariskan, atau sekunder, yang disebabkan oleh diabetes yang kurang terkontrol, alkoholisme, sindrom nefrotik, gagal ginjal kronis, dan dysgammaglobulinemia. Disebut juga dengan Familial Hyperlipemia. Cacat metabolik utama berasal dari familial hypertriglyceridemia (FHTG) yang meningkatkan sintesis trigliserida di hati disertai dengan akumulasi trigliserida kaya VLDL dalam plasma, akibat dari kejenuhan proses katabolik.
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Merupakan penyakit keturunan yang jarang terjadi, dimana tubuh tidak mampu memetabolisme dan membuang kelebihan trigliserida sebagaimana mestinya. II.
Penyebab
Terkadang dipengaruhi oleh faktor keluarga, terkait dengan ketidaksempurnaan pembersihan trigliserida eksogen maupun endogen yang tidak sempurna dapat dan ancaman resiko pankreatitis seumur hidup. Selain diturunkan, penyakit ini juga bisa terjadi akibat : a. Penyalahgunaan alkohol b. Diabetes yang tidak terkontrol dengan baik c. Gagal ginjal d. Obesitas III.
Gejala
· Diturunkan, biasanya penyakit ini muncul pada masa dewasa awal. · Ditemukan sejumlah besar pertumbuhan lemak (xantoma) di kulit, pembesaran hati dan limpa serta nyeri perut. · Biasanya terjadi diabetes ringan dan peningkatan asam urat. · Banyak penderita yang mengalami kelebihan berat badan. IV.
Patofisiologi
Kadar VLDL dan kilomikron serum meningkat. LDL normal atau berkurang.Ini menyebabkan kadar kolesterol meningkat dan triasilgliserol sangat m eningkat. Penyebabnya adalah peningkatan produksi atau penurunan bersihan VLDLdan kilomikron. Biasanya suatu kelainan genetic.Paling sering terjadi pada orang dewasa yang gemuk dan/atau diabetic. V.
Pemeriksaan dan Parameter Klinis
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b.
VI. · ·
Parameter Klinis VLDL Levels
High
LDL Levels
Usually low
Chylomicron
Increase
Appearance of Plasma
Creamy layer over infranatant on standing
The triglycerides
are invariably greater than 1000 mg/dL, and total cholesterol levels are always elevated
Lipoprotein Lipase
Decrease
turbid
Pengobatan Penurunan berat (jika terjadi) sangat penting. Diet harus mengandung protein, rendah lemak dan karbohidrat yang terkontrol serta tidak boleh mengkonsumsi alcohol. Jika perlu, terapi obat termasuk niasin,
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2.3.6 HIPERLIPIDEMIA SEKUNDER I. PENGERTIAN HIPERLIPIDEMIA SEKUNDER Hiperlipidemia sekunder adalah kondisi abnormal yang disebabkan oleh faktor tertentu seperti obat – obat –obatan obatan dan penyakit. II. HIPERLIPIDEMIA SEKUNDER AKIBAT GOLONGAN OBAT Hiperlipidemia sekunder ini dapat disebabkan karena penggunaan obat golongan tertentu. 1. Golongan diuretik ( obat antihipertensi) golongan diuretik thiazid dan loop diuretik dapat menyebabkan hiperlipidemia dengan cara meningkatkan VLDL (Very Low Density Lipid) dan LDL (Low Density Lipid). 2. Golongan Kortikostetorid pengaruh pemberian glukokortikoid pada kadar lemak sudah terbukti dengan melakukan penelitian pada pasien asma, rematoid artritis dan gangguan jaringan ikat. Hasil penelitian tersebut didapatkan bahwa pengobatan dengan prednisolon ternyata dapat meningkatkan kadar LDL dalam tubuh 3. ß-blocker ß-blocker mempengaruhi metabolisme yang dampaknya dapat menaikan kadar trigliserida dan menurunkan HDL tetapi tidak mempengaruhi LDL. 4. Obat Pil KB (Kontrasepsi Oral), esterogen dan progesteron bersifat mineralkortikoid dan glukokortikoid yang menyebabkan hipertensi dan diabetes mellitus. Efek kedua hormon tersebut bersifat berlawanan. Esterogen sedikit menaikkan VLDL dan HDL, serta menurunkan LDL terutama pada wanita menopause. Sebaliknya progesteron menaikkan LDL dan menurunka VLDL dan HDL. 5.
Siklosporin
siklosporin adalah suatu obat penekan imunitas terutama digunakkan untuk menekan penolakan transplantasi organ, Obat golongan ini dapat meningkatkan LDL.
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Klasifikasi Tingkat normal
TG level (dalam mg/dL) < 150
Perbatasan
150 - 199
Tingkat TG tinggi
200 - 499
Tingkat TG sangat >500 tinggi
Hiperlipidemia dapat diwariskan dan meningkatkan risiko terkena kelainan pembuluh darah, kelainan tersebut akan mengarah kepada penyakit stroke dan penyakit jantung. Hiperlipidemia terbagi menjadi dua macam, yaitu hiperlipidemia primer dan hiperlipidemia sekunder. Hiperlipidemia primer adalah salah satu jenis hiperlipidemia yang terjadi karena perihal genetik atau keturunan. Di samping terdapat hiperlipidemia primer, terdapat pula hiperlipidemia sekunder. Hiperlipidemia sekunder adalah salah satu jenis hiperlipidemia yang terjadi bukan karena hal-hal yang diterkait dengan pewarisan gen dari orangtua ke anaknya. Dengan kata lain, hiperlipidemia sekunder adalah acquired condition dan bukan merupakan inherited condition. condition. Hiperlipidemia sekunder ini timbul disebabkan oleh beberapa penyebab seperti diabetes atau obesitas. Pada lembar tugas mandiri ini, saya akan membahas lebih dalam tentang hiperlipidemia sekunder ditinjau dari patofisiologi, gejala, pemeriksaan lab, dan terapi. Penyebab
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sekunder pula. Akan tetapi, pengembangan penyakit jantung koroner tetaplah bahaya dan juga harus diwaspadai. · Disfungsi endotelial Hipotesa respon terhadap cedera menyatakan bahwa faktor risiko seperti LDL teroksidasi, cedera mekanik kepada endothelium, hoomosistein berlebih, atau perubahan endotelial yang terinfeksi akan mengakibatkan tubuh menuju keadaan disfungsi endotelial dan akan mengarah pula kepada aterosklerosis (yang terbentuk oleh kumpulan interaksi seluler di endotelium yang tidak berfungsi). · Lesi aterosklerosis Lesi aterosklerosis ini disebabkan oleh transpor plasma LDL-C melalui lapisan sel endotelial seperti yang telah dijelaskan sebelumnya. Ketika berada di dinding arteri, LDL diubah secara kimia melalui oksidasi dan glikasi non-enzimatik. LDL yang sedikit ini teroksidasi dan menarik monosit ke dinding arteri, lalu selanjutnya monosit ini berubah menjadi makrofag menimbulkan oksidasi pada LDL. · Respon Inflamasi Peristiwa oksidasi pada LDL yang sedikit tadi menimbulkan respon inflamasi yang dimediasi oleh chemoattractant dan chemoattractant dan sitoleukin. Tahap ini merupakan kontrol genetik dari hiperlipidemia (namun cenderung lebih spesifik pada hiperlipidemia primer). Gejala Tidak ada gejala khusus dan spesifik (terutama gejala fisik dan psikis) yang dapat menandakan bahwa seseorang terkena hiperlipidemia sekunder. Namun, apabila seseorang telah memiliki kadar trigliserida dalam level yang tinggi jumlahnya, lemaknya akan terdeposit di kulit dan membentuk benjolan yang disebut dengan xanthoma. Selain itu, apabila seseorang telah memiliki kadar trigliserida
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ü
Tes LDL Tes LDL ini menunjukkan banyak atau sedikit kadar LDL dalam darah. Semakin banyak kadar LDL dalam darah, maka kemungkinan seseorang terkena hiperlipidemia sekunder akan besar karena banyaknya LDL akan menimbulkan penumpukan pada saluran pembuluh darah dan dapat membahayakan tubuh. Sebaliknya, apabila seseorang memiliki kadar LDL sedikit di dalam darah, maka seseorang tersebut akan mendapat kemungkinan sangat kecil terkena hiperlipidemia sekunder. Tingkatan jumlah LDL dalam darah dapat dilihat pada tabel di bawah ini:
ü
Tes trigliserida Tes trigliserida ini menunjukkan banyak atau sedikit kadar trigliserida dalam darah. Kemungkinan terjadinya hiperlipidemia sekunder pada tes trigliserida ini dapat dinyatakan dalam tabel di bawah ini:
Klasifikasi
TG level
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Pengobatan dan Pencegahan Hiperlipidemia sekunder dapat diatasi atau dicegah dengan melakukan beberapa cara, yaitu: · Diet lemak jenuh dan kolesterol Diet lemak jenuh dan kolesterol dapat menurunkan kadar LDL yang berlebih dalam tubuh. Beberapa ahli merekomendasikan untuk membatasi lemak dalam makanan agar makanan tersebut tidak mengandung lebih dari 25-30 % dari jumlah kalori total. Hal tersebut dapat direalisasikan dengan cara mengurangi pengonsumsian daging merah, kelapa, kuning telur, produk susu, dan beberapa kacang-kacang. Selain itu, kita juga dapat menggantikannya dengan makanan yang memiliki lemak jenuh yang rendah, contohnya seperti margarine, serta dapat mengonsumsi buah-buahan, buah-buahan, ikan, dan ayam (tanpa kulit). · Pengonsumsian obat Hiperlipidemia sekunder dapat diobati dengan obat-obatan yang bersifat lipidlowering drugs, drugs, seperti niacin, statin, derivat asam fibrat, pengikat asam empedu, penghambat absorpsi kolesterol, dan suplemen dari lemak omega-3 (akan dijelaskan dalam gambar tabel). Setiap obat yang telah disebutkan sebelumnya memiliki mekanisme kerja yang berbeda. Obat-obat ini dapat bekerja lebih banyak daripada tingkat lipid rendah itu sendiri. Sehingga, obat-obat ini dapat mengobati hiperlipidemia sekunder.
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· Olahraga Memperbanyak olahraga dapat mencegah hiperlipidemia sekunder. · Mengurangi berat badan Mengurangi berat badan merupakan salah satu cara efektif yang dapat dilakukan untuk mencegah hiperlipidemia sekunder, terutama untuk orang yang mengalami obesitas.
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HIPERLIPIDEMIA 1. A.
Definisi
Hiperlipidemia adalah suatu kondisi kadar lipid darah darah yang melebihi kadar normalnya. Hiperlipidemia disebut juga peningkatan lemak dalam darah dan karena sering disertai peningkatan beberapa fraksi lipoprotein, disebut juga hiperlipoproteinemia. Hiperlipidemik dapat berupa hiperkolesterolemia dan hipertrigliseridemia (Kumalasari, 2005). Lemak (disebut juga lipid ) adalah zat yang kaya energi, yang berfungsi sebagai sumber energi utama untuk proses metabolisme tubuh. Lemak diperoleh dari makanan atau dibentuk di dalam tubuh, terutama di hati dan bisa disimpan di dalam sel-sel lemak untuk digunakan di kemudian hari. Sel -sel lemak juga melindungi tubuh dari dingin dan membantu melindungi tubuh terhadap cedera. Lemak merupakan komponen penting dari selaput sel, selubung saraf yang membungkus sel-sel saraf serta empedu. Dua lemak l emak utama dalam darah adalah kolesterol dan trigliserida. trigliserida. Lemak mengikat dirinya pada protein tertentu sehingga bisa larut dalam darah; gabungan antara lemak dan protein ini disebut lipoprotein. lipoprotein. Lipoprotein yang utama adalah : 1. Kilomikron
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Katabolisme LDL terutama terjadi didalam hepatosit dan dalam sebagian besar sel bernukleus melibatkan endositosis yang diperantarai oleh reseptor berafinitas tinggi. Ester kolesteril dari inti LDL kemudian dihidrolisis, yang menghasilkan kolesterol bebas untuk sintesis membrane sel. Ses-sel juga mendapatkan kolesterol dari sintesis de-novo melalui suatu jalur yang melibatkan pembentukan asam mevalonat yang dikatalisis oleh HMG koA reduktase. Hati memainkan m emainkan peran utama dalam pengolahan kolesterol tubuh. Tidak seperti sel lainnya, hepatosit mampu mengeliminasi kolesterol dari tubuh melalui sekresi kolesterol dalam empedu dan mengkonversikan mengkonversikan kolesterol menjadi asam empedu yang juga disekresikan dalam empedu.
d. Lipoprotein Berdensitas Tinggi (HDL) Apolipoprotein disekresi oleh hati dan usus. Sebagian besar besar lipid dari permukaan satu lapis kilomikron dan VLDL selama liposis. HDL juga mendapatkan kolesterol dari jaringan perifer dari suatu jalur yang melindungi homeostasis kolesterol sel. HDL juga dapat membawa ester ester kolestril langsung ke hati melalui suatu reseptor reseptor pengait/ docking (reseptor scavenger, SR-BI) yang tidak melakukan endositosis terhadap
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kilomikron yang tersisa (yang lemaknya telah diambil) dibuang dari aliran darah oleh hati. Tubuh mengatur kadar lipoprotein melalui beberapa cara : 1. Mengurangi pembentukan lipoprotein dan mengurangi m engurangi jumlah lipoprotein yang masuk ke dalam darah. 2. Meningkatkan atau menurunkan kecepatan pembuangan lipoprotein dari dalam darah. Kadar lemak yang abnormal dalam sirkulasi darah (terutama kolesterol) bisa menyebabkan masalah jangka panjang. Resiko terjadinya aterosklerosis dan penyakit dan penyakit arteri koroner atau penyakit atau penyakit arteri karotis meningkat pada seseorang yang memiliki kadar kolesterol total yang tinggi. Kadar kolesterol rendah biasanya lebih baik dibandingkan dengan kadar kolesterol yang tinggi, tetapi kadar yang terlalu rendah juga tidak baik. Kadar kolesterol total yang ideal adalah 140-200 mg/dL atau kurang. Jika kadar kolesterol total mendekati 300 mg/dL, maka resiko terjadinya serangan jantung adalah lebih dari 2 kali. Tidak semua kolesterol meningkatkan resiko terjadinya penyakit jantung. Kolesterol yang dibawa oleh LDL (disebut juga kolesterol jahat ) menyebabkan meningkatnya resiko; kolesterol yang dibawa oleh HDL (disebut juga kolesterolbaik ) menyebabkan menurunnya resiko dan menguntungkan. Idealnya, kadar kolesterol LDL tidak boleh
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Disebut juga hiperkolesterolemia familial , merupakan suatu penyakit keturunan yang mempercepat terjadinya aterosklerosis dan kematian dini, biasanya karena serangan jantung. Kadar kolesterol LDLnya tinggi. Endapan lemak membentuk pertumbuhan xantoma pertumbuhan xantoma di dalam tendon dan kulit. 1 diantara 6 pria penderita penyakit ini mengalami serangan jantung pada usia 40 tahun dan 2 diantara 3 pria penderita penyakit ini mengalami serangan jantung pada usia 60 tahun. Penderita wanita juga memiliki resiko, tetapi terjadinya lebih lambat. 1 dari 2 wanita penderita penyakit ini akan mengalami serangan jantung pada usia 55 tahun. Orang yang memiliki 2 gen dari penyakit ini (jarang terjadi) bisa memiliki kadar kolesterol total sampai 500-1200 mg/dL dan seringkali meninggal karena penyakit karena penyakit arteri koroner pada masa kanak-kanak. Tujuan pengobatan adalah untuk menghindari faktor resiko, seperti merokok, dan obesitas, obesitas, serta mengurangi kadar kolesterol darah dengan mengkonsumsi obat-obatan. Penderita diharuskan menjalani diet rendah lemak atau tanpa lemak, terutama lemak jenuh dan kolesterol serta melakukan olah raga secara teratur. Menambahkan Menambahkan bekatul gandum pada makanan akan membantu mengikat lemak di usus. Seringkali diperlukan obat penurun lemak. 3. Hiperlipoproteinemia tipe III Merupakan penyakit keturunan yang jarang terjadi, yang menyebabkan tingginya kadar kolesterol VLDL dan trigliserida. Pada penderita pria, tampak pertumbuhan
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Jika diturunkan, biasanya penyakit ini muncul pada masa dewasa awal. Ditemukan sejumlah besar pertumbuhan lemak (xantoma) di kulit, pembesaran hati dan limpa serta nyeri perut. Biasanya terjadi diabetes ringan dan peningkatan asam urat. Banyak penderita yang mengalami kelebihan berat badan. Komplikasi utamanya adalah pankreatitis, yang seringkali terjadi setelah penderita makan lemak dan bisa berakibat fatal. Pengobatannya berupa penurunan berat badan, menghindari lemak dalam makanan dan menghindari alkohol. Bisa diberikan obat penurun kadar lemak.(http://www.medicastore.com) lemak.(http://www.medicastore.com).. Tabel 2. Klasifikasi Hiperproteinuremia menurut Fredrickson-Levy-Less Tipe
Evaluasi Lipoprotein
I
Kilomikron
IIa
LDL
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hiperlipoprotein sekunder dapat disebabkan oleh endokrinopati (hipotiroid, hipopituitari, diabetes melitus) dan biasanya dapat pulih dengan terapi hormon.
Tipe II terdiri atas 2 t ipe yaitu hiperlipidemia tipe IIa dan IIb : 1. Tipe IIa, ditandai dengan tingginya kadar LDL di dalam darah tapi kadar VLDLnya normal. Tipe ini dapat disebabkan beberapa kondisi genetik yaitu hiperkolesterol familial,defectiv familial,defectiv e apolipoprotein e apolipoprotein B familial, hiperkolesterolemia poligenik. 2. Tipe IIb, ditandai dengan tingginya kadar LDL dan VLDL, kolesteroldan trigliserida
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Penderita NIDDM umumnya akan menyebabkan terjadinya hipertrigliseridemia. Penyebabnya pada glukosa darah tinggi akan menginduksi sintesis kolesterol dan glukosa akan dimetabolisme menjadi Acetyl Co A. Acetyl Co A ini merupakan prekusor utama dalam biosintesis kolesterol. Sehingga akan menyebabkan produksi VLDL-trigliserida yang berlebihan oleh hati dan adanya pengurangan proses lipolisis pada lipoprotein yang kaya trigliserida.
2. Hipotiroidisme
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penyakit
Hipotiroidisme, penyakit hati obstruktif, sindrom nefrotik, anorexia
Obat-obatan Progestin, diuretik tiazid, glukokortikoid, ββbloker, isotretionin, inhibitor protease,siklosforin,
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3.Berkeringat 4.Cemas 5.Nafas pendek 6.Hilangnya kesadaran atau kesulitan berbicara atau bergerak 7.Sakit abdominal 8.Kematian mendadak
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Kolesterol total Diinginkan
< 200 mg/dL
Cukup tinggi
200-239 mg/dL
Tinggi
≥ 240 mg/dL
Kolesterol LDL Optimal
<100 mg/dL
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7)
Diabetes yang tidak terkontrol dengan baik
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Farmakokinetik : niasin diberikan per oral. Zat ini diubah dalam tubuh menjadi
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c. Keganasan
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c)
Interaksi Obat : kolestiramin dan kolestipol mengganggu absorbsi beberapa
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