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"Penyakit hati merupakan masalah kesehatan yang sulit diobati. Adanya masalah dalam pengobatan penyakit ini sebagian disebabkan karena tidak tersedianya obat yang terbukti herkhasiat. Kurkumin, senyawa aktif dalam ke keluarga tanaman curcuma telah diteliti dalam berbagai peyakit termasuk penyakit hati. Efek terapi kurkramin diduga berdasarkan efek antioksidatifnya. Dalam penelitian ini, kami menyelidiki efek kurkumin lerhadap swelling mitochondria yang diinduksi oleh tert-butilhidroperoksida (t-BuOOH) Mitokondria hali diisolasi secara homogen dari tikus Sprague-Dawley (relative specific activity suksinat dehidrogenase adalah 35.73 ±2.78). Pemberian 90 }M t-BuOOH menyebabkan swelling 2 fase yang khas pada mitokondria. Pola swelling dipengaruhi oleh berbagai faktor seperti komposisi bufer, kadar t-BuOOH, jumlah bufer isolasi dan protein mitokondria serta temperatur inkubasi. Swelling dapat dihambat sebesar 85 ±3% oleh kurkumin 2.50 jjM. Pada kadar rendah (1.25 //MJ dan tinggi (5.00 fiM), efek proteksi kurkumin terhadap swelling berkurang (bertitrut-turut 41 ±3% and 77+6%). Swelling dapat terjadi akibat terbukanya mitochondrial transition pore dan dapat mempakan petunjuk awal dan proses kematian sel. Efek inhibisi kurkumin terhadap swelling mitokondria yang diindukxi oleh t-BuOOH diduga disebabkan karena efek antioksidannya. (MedJ Indones 2006; 15:131-6)

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Liver diseases have been a medical problem which is difficult to manage. Some of the problems in the treatment of these diseases lie in the lack of reliable drug available. Curcumin, an active ingredient of the rhizomes of plant Curcuma has been investigated in the treatment of various disorders incuding liver diseases. The therapeutic effects of curcumin on liver diseases have been thought to be associated to its antioxidative properties. In the present study, we investigated the effects of curcumin on mitochondrial swelling in vitro induced by tert-butylhydroperoxide (t-BuOOH). Liver mitochondria were homogeneously isolated from Sprague-Dawley rats (the relative specific activity of succinate dehydrogenase was 35.73 ±2.78). Addition of 90 fj.M oft-BuOOHcauseda typical 2-phase swelling of the mitochondria. The pattern of swelling was influenced by various factors such as buffer composition, concentrations of t-BuOOH, amount of isolation buffer and mitochondrial proteins and incubation temperature.The swelling could be reduced by as much as 85 ±3% by 2.50 uM of curcumin. At lower (1.25 ^M) or higher (5.00 fjM) concentrations, the protection against swelling by curcumin were less effective (respectively were 41 ±3% and 77 ±6%). Swelling might occur due to the opening of mitochondrial transition pore and could be an initial indication in the cascade process leading to cell death. The inhibition of t-BuOOH-induced mitochondrial swelling by curcumin might be because of the antioxidant effects of the compound. (Med JIndones 2006; 15:131-6)."

"Kurkumin, bahan aktif tanaman kurkuma diduga bermanfaat dalam pengobatan penyakit hati. Dalam penelitian terdahulu, diperlihatkan efek protektif kurkumin terhadap peroksidasi lipid dan swelling mitokondria yang diisolasi dari hati tikus karena pemberian t-butilhidroperoksida (t-BuOOH). Dalam penelitian ini, pemberian t-BuOOH 90 M menyebabkan mitokondria tidak dapat membentuk potensial transmembran (m). Kegagalan pembentukan potential transmembran diduga berhubungan dengan transisi permeabilitas dan apoptosis. Dari 3 dosis kurkumin yang dicoba (0,5 M, 2,5 M dan 5,0 M), ternyata kurkumin dosis 2,5 M dapat mencegah kegagalan pembentukan potensial transmembran akibat t-BuOOH (79,13 + 6,28%). Pemeriksaan elektroforesis protein mitokondria menunjukkan kurkumin 1000 M dapat mencegah agregasi protein yang terjadi akibat t-BuOOH. Dari penelitian ini diperlihatkan efek proteksi kurkumin terhadap kerusakan sistem pembentukan energi dan protein mitokondria yang disebabkan oleh t-BuOOH. (Med J Indones 2007; 16:139-45)

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Curcumin, an active ingredient of curcuma plant has been thought to be beneficial in the treatment of liver diseases. In the previous studies, we have shown the protective effects of curcumin against lipid peroxidation and swelling of the rat liver mitochondrial preparation induced by tert-butylhydroperoxide (t-BuOOH). In the present study, the administration of t-BuOOH of 90 M caused the mitochondria failed to generate a transmembrane potential (m). Of 3 doses of curcumin administered (0.5 M, 2.5 M dan 5.0 M) the maximum protective effect against failure to generate a transmembrane potential caused by t- BuOOH was obtained by 2.5 M of curcumin (79.13 + 6.28%). Further, curcumin of 1000 M could prevent protein aggregation formation caused by t-BuOOH in the electrophoretogram. This study shows the protective effects of curcumin against damaged of energy production system and protein of the mitochondria caused by t-BuOOH. (Med J Indones 2007; 16:139-45"

"Alkohol merupakan senyawa yang paling sering disalahgunakan (abuse), dan akhirnya menimbulkan berbagai permasalahan, bukan hanya di bidang kesehatan, melainkan juga di bidang sosial dan ekonomi, di seluruh dunia. Hati merupakan salah satu organ yang paling banyak dipengaruhi oleh toksisitas etanol. Hepatotoksisitas intrinsik etanol timbul akibat oksidasi etanol oleh enzim alkohol dehidrogenase (ADH) dan sistem enzim yang mengoksidasi etanol di mikrosom (MEOS), yang terutama melibatkan CYP2E1. Metabolit toksik etanol (akibat oksidasi etanol oleh ADH dan CYP2E1), yaitu asetaldehid, serta induksi aktivitas CYP2E1 akibat pemberian etanol kronik, dapat meningkatkan stres oksidatif terutama pada mitokondria, yang merupakan organel target intoksikasi alkohol. Styes oksidatif yang mengakibatkan gangguan fungsi mitokondria, mengawali berbagai gangguan metabolik maupun aktivasi sistem makrofag hepatik, yang akhimya menuju kematian sel hati (hepatosit), balk secara nekrosis ataupun apotosis; dan dianggap memainkan peranan panting dalam patogenesis dan progresi penyakit hati alkoholik. Oleh karena itu, antioksidan dapat menjadi salah satu terapi yang potensial dalam penanganan penyakit had alkoholik di masa mendatang. Likopen, sebagai salah satu senyawa karotenoid non pro-vitamin A yang memiliki aktivitas antioksidan yang sangat kuat, secara in vide terbukti dapat mencegah sties oksidatif pada mitokondria dan apoptosis yang diinduksi oleh etanol pada kultur set HepG2 yang mengekspresikan CYP2E1. Namun demikian, sampai scat ini belum ada penelitian yang mengkonflr nasi efek protektif likopen in vivo terhadap gangguan fungsi mitokondria akibat stres oksidatif oleh pemberian etanol kronik. Penelitian ini merupakan penelitian in vivo yang menggunakan model hewan untuk mempelajari hal tersebut. Model hewan yang digunakan adalah tikus jantan (120-180 g), strain Sprague Dawley. Hewan uji dibagi ke dalam 6 kelompok @ 4 ekor. Diet standar untuk tikus yang diperoleh dari Badan POM, Jakarta, diberikan ad libitum. Untuk menimbulkan induksi gangguan fungsi mitokondria, pemberian etanol dilakukan pada tikus percobaan dilakukan selama 4 minggu, dengan dosis 1 mL etanol 25%I100 g BB. Suplementasi likopen diberikan dalam 3 dosis yang berbeda (masing-masing 25, 50 dan 100 mg/kg BB/hari) dan dimulai sejak 2 minggu sebetum pemberian etanol kronik, dan tetap dilanjutkan selama etanol diberikan. Tikus dimatikan dengan dislokasi leper, dan segera dilakukan isolasi mitokondria. Stres oksidatif dan gangguan fungsi mitokondria akibat pemberian etanol kronik pada tikus dikuantifikasi menggunakan beberapa parameter, seperti: tingkat peroksidasi lipid (kadar MDA) mitokondria dan homogenat had, kadar GSH mitokondria (mGSH), dan aktivitas beberapa enzim mitokondria, seperti suksinat dehidrogenase dan NADH-sitokrom c oksido-reduktase serta FO-Fl-ATPase. Pengukuran parameter-parameter tersebut dilakukan dengan metode spektrofotometri menggunakan cahaya visibel (kolorimetri).Mitokondria diisolasi dengan kemumian sedang (RSA SDH = 11.01). Dibandingkan dengan kelompok kontrol, pemberian etanol kronik secara bermakna meningkatkan stres oksidatif pada mitokondria, yang ditunjuklcan oleh peningkatan kadar MDA mitokondria (100%) maupun homogenat hati (55%), serta penurunan kadar mGSH (30%) dan rasio GSH/GSSG mitokondria (40%). Pemberian etanol kronik juga menyebabkan gangguan fungsi mitokondria, seperti menurunkan SA SDH mitokondria (40%), meningkatkan aktivitas NADH-sitokrom c oksido-reduktase (76%) dan meningkatkan aktivitas hidrolisis F1-ATPase (30%). Enzim NADH-sitokrom c oksido-reduktase tidak sensitif terhadap inhibitor rotenon. Pemberian rotenon hanya sedikit meningkatkan atau tidak mempengaruhi aktivitas enzim tersebut, dan tidak mengubah perbandingan aktivitas enzim anlar kelompok. Enzim FI-ATPase sens"itif terhadap inhibitor oligomisin. Pada kelompok etanol kronik, pemberian oligomisin menurunkan aktivitas enzim FO-FI-ATPase sebesar 82%. Nilai ini lebih tinggi secara bermakna dibandingkan dengan penurunan akitivitas pada kelompok kontrol (72%). Suplementasi likopen pada ketiga dosis yang diberikan mampu mengembalikan aktivitas SDH, NADH-sitokrom c reduktase, kadar MDA mitokondria dan homogenat hati, serta kadar mGSH, sampai setara dengan kelompok kontrol. Peningkatan dosis Iikopen tidak menimbulkan perbedaan berrnakna pada parameter-parameter tersebut. Namun demikian, hanya likopen dosis 100 mg/kg BB/hari yang dapat mengembalikan rasio GSH/GSSG, aktivitas hidrolisis FOFI-ATPase dan sensitivitasnya terhadap oligomisin, sampai setara dengan kelompok kontrol. Secara umum dapat disimpulkan bahwa likopen memiliki efek proteksi terhadap gangguan fungsi mitokondria hati tikus akibat pemberian etanol kronik. Namun demikian, suplementasi likopen tanpa induksi gangguan fungsi mitokondria tidak memperlihatkan manfaat yang berarti.

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Alcohol is the most frequently abused substance worldwide, which will eventually bring about lots of health, social and economical problems. Of many other organs, alcohol exerts its toxicity mostly in the liver. Ethanol intrinsic hepatotoxidty results mainly from its oxidation by alcohol dehydrogenase (ADH) and microsomal ethanol oxidizing system (MEOS) which involves mainly CYP2E1. Acetaldehyde, a toxic metabolite of ethanol (results from its oxidation by ADH and CYP2E1), and the induction of CYP2EI enzyme due to chronic alcohol consumption will raise oxidative stress on mitochondria, the target organelle of ethanol intoxication. Oxidative stress, which results in mitochondria) dysfunction, initiates various metabolic disorders, activates hepatic macrophageal system, and contributes to enhanced cell death, either by apoptosis or necrosis. Mitochondrial oxidative stress plays a critical role in the pathogenesis and progression of alcoholic liver disease (ALD). Hence, antioxidants may be a potential therapy in the future management of ALD. To date, lycopene, a non-provitamin A carotenoid with a potent antioxidant activity, attenuated mitochondrial oxidative stress and ethanol-induced apoptosis in HepG2 cell expressing CYP2EI. Yet, there has no in vivo study been done in order to confirm the protective effect of lycopene against mitochondrial dysfunction due to chronic ethanol intake. Thus, the current in vivo study was designed to answer -at least partly- the question. The animal models used were male Sprague Dawley rats (120-180 g), which were divided into 6 groups @ 4 rats. Standard diet for rodents, produced by BPOM, Jakarta, was administered ad libitum every day. Ethanol at a concentration of 25%v/v (1 mL/100 g BW) was administered orally for 4 weeks, in order to induce mitochondrial injury. Lycopene supplementation was given orally in 3 dosage regimens, 25, 50 and 100 mg/kg BW/ day, since 2 weeks before and continued for 4 weeks during ethanol treatment. The rats were all terminated by cervical dislocation and then mitochondrial isolation was performed immediately. The ethanol-induced oxidative stress and mitochondria) injury were quantified by measuring the following parameters: degree of lipid peroxidation (mitochondria) and liver homogenate MDA levels), mitochondria) GSH level (mGSH) and the activity of some mitochondrial enzymes, such as sucdnate dehydrogenase, NADH-cytochrome c oxido-reductase, and FO-F1-ATPase. All parameters were measured by using the method of visible spectrophotometry (colorimetry).The liver mitochondria was adequately purified (RSA SDH = 11.01). Compared to the control group, chronic ethanol treatment significantly increased mitochondria) oxidative stress, as exhibited by the increased levels of mitochondria) and liver homogenate MDA (by 100% and 55%, respectively), depressed level of mGSH (by 30%) and lowered ratio of mitochondrial GSH/GSSG (by 40%). Chronic ethanol treatment also induced mitochondria) dysfunction, as measured by the reduced specific activity of mitochondria) SDH (by 40%), increased activity of NADH-cytochrome c oxido-reductase (by 76%), and increased hydrolysis activity of FO-F1-ATPase (by 30%). NADH-cytochrome c oxido-reductase was insensitive to rotenone, as addition of the inhibitor to the reaction mixture slightly increased or did not affect the enzyme activity, nor changed the ratio of its activity between groups. FO-FI-ATPase was sensitive to oligomycin. In chronic ethanol group, addition of oligomydn to the reaction mixture reduced the enzyme activity by 82%, which was significantly greater than the reduction showed by control group (72%). Lycopene supplementation was able to normalize the activity of SDH, NADH-cytochrome c oxido-reductase, the levels of mitochondrial and liver homogenate MDA and mGSH level, back to the levels of control group. Higher doses of lycopene did not provide significantly better results to those parameters. However, only the highest dose of lycopene (100 mg of /kg BW/day) could normalize mitochondria) GSH/GSSG ratio, the activity of FO-FIATPase and its sensitivity to oligomydn to the levels of control group. Generally, this study concluded that lycopene has protective effect against ethanol-induced hepatic mitochondria) injury in rats. However, without ethanol-induced mitochondrial injury, lycopene supplementation does not provide any additional benefit."

"Multiple Liver AbscessLiver abscess is a public health problem in few countries in Asia, Africa, and South America. As time goes, there were only few cases of amebic liver abscess found in developed countries, on the contrary more pyogenic liver abscess are found in those countries. Liver abscess could be caused by bacteria, parasite, or fungus J. The common symptoms among the liver' abscess are fever; chill, fatigue, loss of appetite, weight loss, right upper' abdominal pain,? in a few cases have symptoms like coughing, hiccup, pain in low right chest, or' pain on the shoulder: We reported a male patient 38 years batak ethnic was admitted with major symptoms such as high lever follow by chill, right upper abdominal pain, nausea, vomiting, appetite loss, fatigue and sometimes coughing. Based on clinical, laboratory data, and abdominal USG found this patient suspected suffered from pyogenic liver abscess. Treatment of this pattern consist of antibiotic (cefotaxime 29x1 IV metronidazol 3x500mg orally and aspiration of the liver' abscess). Aspiration was done 2 times with the interval l week, extracted 260cc totally yellow greenish watery fluid with no smell. On the follow up abdominal USG was repeated on January 8, 2003 found enlarge of the liver; 3 small abscesses on the right lobe liver and so recovery process and then patient left the hospital in good condition after 3 weeks hospitalized."

"Ultrasonography examination is an one of examination that can be used to see the abnormality of portal vein system. The technology of ultrasonography examination has further developed especially after using of Doppler ultrasonography which could portray haemodynamic changes from portal vein in liver cirrhosis patient. From this examination we also could predict bleeding."

"Latar Belakang: Berbagai penelitian terdahulu telah membuktikan bahwa kurkumin memiliki sifat hepatoprotektif sehingga memungkinkannya untuk mengobati banyak jenis penyakit hepar. Meskipun kurkumin aman dan mempunyai banyak aktifitas biologis, penggunaan kurkumin belum dapat digunakan secara komersil sebagai obat terapeutik karena tingkat absorbsi, stabilitas, dan bioavailabilitas yang rendah serta metabolisme kurkumin yang cepat. Berhubung studi mengenai efek pengurangan ukuran partikel untuk meningkatkan distribusi jaringan belum dilakukan sepenuhnya, penelitian ini bertujuan untuk mengetahui apabila peningkatan konsentrasi kurkumin di jaringan hepar dapat dilakukan dengan menggunakan nanopartikel.Metode: Penelitian ini merupakan penelitian in vivo pada tikus. Tikus dirandomisasi menjadi 2 kelompok, masing-masing 5 ekor yang mendapatkan kurkumin konvensional 500 mg/kgBB atau nanokurkumin 500 mg/kgBB dosis tunggal secara oral. Sampel hati diambil setelah 3 atau 4 jam setelah pemberian obat dan konsentrasi kurkuminnya dikuantifikasi menggunakan UPLC-MS/MS.Hasil: Konsentrasi nanokurkumin lebih tinggi daripada konsentrasi kurkumin konvensional di jaringan hepar setelah 3 jam dan relatif lebih tinggi setelah 4 jam. Pada 3 jam, konsentrasi rerata nanokurumin (33.1934 ng/mg) adalah lebih dari 7 kali lipat dibandingkan konsentrasi rerata kurkumin (4.5189 ng/mg) dan bermakna secara statistik (p = 0.047). Pada 4 jam, konsentrasi rerata nanokurumin (11.8725 ng/mg) hanya sedikit lebih tinggi dibandingkan konsentrasi rerata kurkumin (11.6352 ng/mg) dan tidak bermakna secara statistik (p = 0.251).Konklusi: Pemberian nanokurkumin secara oral menghasilkan konsentrasi kurkumin yang lebih tinggi di hati tikus setelah 3 dan 4 jam daripada kurkumin konvensional.Background: Many previous researches have proven that curcumin possesses potent hepatoprotective propertiy which enables it to treat and prevent the progression of different hepatic disorders. However, despite its superior safety profile and biological activity, curcumin has not been commercially used as a therapeutic drug due to its extremely poor absorption and stability, low bioavailability and rapid metabolism. As the effect of decreasing its particle size to improve its tissue distribution have yet to be studied thoroughly, this research aims to find out if higher curcumin concentrations in liver tissue can be achieved by using nanoparticles.Method: This research is an in vivo research in rats. The rats are randomized into 2 groups, each with 5 rats which were given either single doses of 500 mg/kgBW conventional curcumin or 500 mg/kgBW nanocurcumin orally. The liver samples were obtained after 3 or 4 hours, followed by curcumin concentration measurement using the UPLC-MS/MS method. Results: Nanocurcumin concentrations were higher than curcumin concentrations in the liver tissue at 3 hours and relatively higher at 4 hours. At three hours, the mean nanocurcumin concentration (33.1934 ng/mg) is over 7 times higher than mean curcumin concentration (4.5189 ng/mg) and is statistically significant (p = 0.047). At 4 hours, the mean nanocurcumin concentration (11.8725 ng/mg) is slightly higher than mean curcumin concentration (11.6352 ng/mg) not statistically significant (p = 0.251)Conclusion: Oral administration of nanocurcumin results in higher curcumin concentrations in rat liver tissue after 3 and 4 hours compared to conventional curcumin."

"Hipoksia pada ketinggian diketahui menyebabkan stress oksidatif. Dilakukan penelitian mengenai aktivitas spesifik katalase pada jaringan hati tikus dengan metode spektrofotometri untuk mengukur pemecahan hidrogen peroksida. Tikus dipajankan pada hipoksia hipobarik akut berulang dengan simulasi ketinggian 35,000 kaki yang diturunkan bertahap ke ketinggian 25,000 kaki, 20,000 kaki, lalu 18,000 kaki. Hewan uji dibagi ke dalam 4 kelompok: 1) diberi 1 kali perlakuan, 2) diberi 2 kali perlakuan, 3) diberi 3 kali perlakuan, 4)diberi 4 kali perlakuan, dengan setiap prosedur diselingi periode normoksia selama 7 hari. Hipoksia menyebabkan penurunan aktivitas spesifik katalase pada semua kelompok uji. Penurunan bermakna didapatkan pada kelompok 2 (p = 0.008), 3 (p = 0.008), dan 4 (p = 0.008). Hasil pada kelompok 1 tidak menunjukkan perbedaan bermakna dibandingkan kontrol (p = 0.548). Hipoksia hipobarik menginduksi penurunan aktivitas spesifik katalase hati.

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Hypoxia at high altitude is known as a cause of oxidative stress. Specific activity of catalase in rat liver submitted to recurrent acute hypobaric hypoxia were studied by means of measuring the breakdown of hydrogen peroxide spectrophotometrically. Animals were submitted to simulated altitudes of 35,000 ft lowered gradually to 25,000 ft, 20,000, and 18,000 ft. The experimental groups were as follows: 1) rats exposed to one procedure, 2) exposed to two procedures, repeatedly, 3) exposed to three-times of procedures, and 4) exposed to four-times of procedures, each procedure was interrupted with 7 days period of normoxia. Hypoxia produced a decrease in specific activity of liver catalase in all experimental groups. Significant decreases were showed in group 2 (p = 0.008), 3 (p = 0.008), and 4 (p = 0.008). Group 1 showed no significant difference compared to control group (p = 0.548). Hypobaric hypoxia induces a decrease in the specific activity of catalase in rat liver."

"Pendahuluan: Volume hati sangat penting diketahui untuk menentukan kesesuaian graft pada Living Donor Liver Transplant (LDLT) dan untuk menentukan resektabilitas organ. Salah satu kunci kesuksesan dari LDLT adalah dengan diketahuinya volume parenkim hati yang adekuat baik untuk donor maupun resipien. CT Volumetri merupakan gold standard dalam menghitung volume hati non invasif. Namun pada pelaksanannya terdapat keterbatasan fasilitas, terbatasnya ketersediaan piranti lunak, dan membutuhkan waktu yang lama. Sampai saat ini belum disepakati formula biometrik yang sesuai dalam memprediksi volume hati pasien donor hati di Indonesia.Metode: Desain penelitian ini cross sectional untuk mengetahui formula yang mendekati prediksi volume hati pada pasien donor transplantasi dewasa di Indonesia. Penelitian dilakukan di Rumah Sakit dr. Cipto Mangunkusumo berdasarkan data pasien dari 1 Januari 2010 – 3 Oktober 2019.Hasil: Perbedaan antara ELV dengan CLV didapatkan paling kecil pada formula Poovatumkadavil dkk dengan perbedaan -24.484cm3, kemudian Vauthey dkk dengan nilai perbedaan -27.153 dan disusul Yoshizumi dkk dengan hasil beda -44.253. Pada grafik Bland-Altman dapat dilihat bahwa perbedaan terkecil ada pada formula yang diusulkan oleh Poovatumkadavil disertai dengan limit of agreement paling kecil dibandingkan formula lainnya.Kesimpulan: Formula biometrik yang diajukan oleh Poovatumkadavil dkk didapatkan paling akurat dalam memprediksi volume hati dewasa di RSCM berdasarkan prediksi volume hati dengan CT volumetrik.

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Liver volume calculation is very important in living donor liver transplant (LDLT) in assessing the compatibility and resectability of the graft. Accurate liver volume calculation to estimate adequate liver volume is one of the predictors of successful LDLT. CT volumetry is the gold standart for liver volume estimation, although there are some limitation in the software and facility availability and time. There are still no biometric formula agreed to predict liver volume in Indonesia. This study is conducted to acquire the best biometric formula for liver volume estimation in Indonesian population. The design of this study is cross-sectional study conducted in dr. Cipto Mangunkusumo General Hospital on 1st January 2010 – 3rd October 2019. The result of this study shows formuls by Poovatumkadavil has the least difference between estimated liver volume (ELV) and CT liver volume (CLV) with -24.4 cm3 difference. Formula by Vauthey and Yoshizumi also shows minute volume difference with -27.14cm3 and -44.25cm3 respectively. Bland-Altman graph shows the narrowest limit of agreement in Poovatumkadavil formula compared to the others. In conclusion, biometric formula by Poovatumkadavil is shown to be the most accurate in estimating liver volume in Indonesian population compared with CT volumetry.

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