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"[ABSTRAKLatar Belakang. SNP IL-28B mempunyai peran penting dalam pencapaian SVR pada pengobatan Hepatitis C kronik antarras manusia dan berpotensi untuk memprediksi keberhasilan terapi Peg-IFN/RBV maupun penyembuhan spontan Hepatitis C akut. Hingga saat ini, mekanisme molekular yang mendasari kaitan SNP IL-28B dengan respons terapi masih belum jelas meskipun diperkirakan terkait dengan ekspresi IFN-l3 dan reseptor IFN-l3 di jaringan hati.Tujuan. Mengetahui hubungan SNP IL-28B dan SVR serta ekspresi IFN-l3 dan reseptor IFN-l3 di jaringan hati serta mendapatkan kemaknaan klinis SNP IL-28B dan kovariat SVR dalam memprediksi respons terapi Peg-IFN/RBV.Metode. Penelitian ini terbagi menjadi dua bagian. Pertama, penelitian potong lintang pada pasien Hepatitis C kronik yang telah selesai menjalani terapi Peg-IFN/RBV dengan melakukan pengambilan data dasar dan sampel darah. Kedua, penelitian kasus kontrol pasien yang menjalani biopsi hati dan pewarnaan imunohistokimia.Hasil. Pencapaian SVR yang lebih tinggi ditemukan pada pasien dengan alel CC SNP IL28B (p=0,014). Alel CC SNP IL28B mempunyai ekspresi IFN-l3 lebih tinggi dibandingkan dengan alel non-CC (p = 0,018). Meskipun demikian, tidak ditemukan adanya perbedaan bermakna antara ekspresi IFN-l3 (p = 0,237) maupun reseptor IFN-l3 dengan SVR (p = 0,237). Pada penelitian ini, diformulasikan persamaan faktor risiko pencapaian SVR sebagai p = 1 / (1 + e-y); e = 2,7, y = -2,498 + 2,652 (SNP IL-28B) + 2,029 (trombosit) untuk praterapi dan sedangkan untuk masa terapi y = -0,223 + 2,621 (RVR).Simpulan. SNP IL-28B merupakan faktor risiko praterapi yang penting dalam pengobatan hep C kronik G1 menggunakan terapi dua kombinasi. Alel mayor IL28B mengekspresikan IFN-l3 dan reseptornya lebih banyak sebagai respons adanya VHC, namun tidak ditemukan adanya hubungan hal tersebut dengan pencapaian SVR. RVR merupakan faktor masa terapi terbaik untuk memprediksi SVR. Penelitian lanjutan diperlukan untuk membuktikan adanya faktor lain yang berperan dalam pencapaian SVR.;

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ABSTRACTBackground: SNP IL-28B played an important role in achieving sustained virological response (SVR) among different ethnics in chronic Hepatitis C patients and is considered potential in predicting treatment response of Pegylated interferon/ribavirin (Peg-IFN/RBV) combination and spontaneous clearance in acute hepatitis. Up to date, molecular mechanism underlying correlation between SNP IL28B and SVR has not been fully understood yet although it is predicted to be related to IFN-λ3 and IFN-λ3 receptor in liver tissues.Aim: Understanding the association between SNP IL-28B and SVR in chronic Hepatitis C treatment and expression of IFN-l3 and IFN-l3 receptor in liver tissues to evaluate clinical importance of SNP IL-28B examination in Hepatitis C treatment of Peg-IFN/RBV through SVR prediction model.Methods: This study consisted of two parts. First, a cross-sectional study on chronic Hepatitis C patients who completed Peg-IFN/RBV therapy. The second part was case control study on patients underwent liver biopsy and immunohistochemical staining.Results: Sustained virological response was significantly higher in CC allele of SNP IL-28B compared to non CC allele (p = 0.015). Higher expression of IFN-l3 was found in CC allele compared to non CC allele (p = 0.018). On the other hand, there is no significant difference between SVR and expression of IFN-l3 (p = 0.237) and IFN-l3 receptor (p = 0.237). Risk factor for SVR probability were formulated into p = 1 / (1 + e-y); e = 2.7, y = -2.498 + 2.652 (SNP IL-28B) + 2.029 (thrombocytes) for pretreatment while for on treatment risk factor y = -0.223 + 2.621 (RVR)Conclusion: SNP IL-28B was important pretreatment risk factor in genotype 1 chronic Hepatitis C treated with dual therapy. Major allele of IL-28B expressed more IFN-l3 and its receptor in response to HCV although no association between both factors was found. RVR was the best on treatment factor for SVR. Further evaluation study was required to find other possible factors affecting SVR achievement, Background: SNP IL-28B played an important role in achieving sustained virological response (SVR) among different ethnics in chronic Hepatitis C patients and is considered potential in predicting treatment response of Pegylated interferon/ribavirin (Peg-IFN/RBV) combination and spontaneous clearance in acute hepatitis. Up to date, molecular mechanism underlying correlation between SNP IL28B and SVR has not been fully understood yet although it is predicted to be related to IFN-λ3 and IFN-λ3 receptor in liver tissues.Aim: Understanding the association between SNP IL-28B and SVR in chronic Hepatitis C treatment and expression of IFN-l3 and IFN-l3 receptor in liver tissues to evaluate clinical importance of SNP IL-28B examination in Hepatitis C treatment of Peg-IFN/RBV through SVR prediction model.Methods: This study consisted of two parts. First, a cross-sectional study on chronic Hepatitis C patients who completed Peg-IFN/RBV therapy. The second part was case control study on patients underwent liver biopsy and immunohistochemical staining.Results: Sustained virological response was significantly higher in CC allele of SNP IL-28B compared to non CC allele (p = 0.015). Higher expression of IFN-l3 was found in CC allele compared to non CC allele (p = 0.018). On the other hand, there is no significant difference between SVR and expression of IFN-l3 (p = 0.237) and IFN-l3 receptor (p = 0.237). Risk factor for SVR probability were formulated into p = 1 / (1 + e-y); e = 2.7, y = -2.498 + 2.652 (SNP IL-28B) + 2.029 (thrombocytes) for pretreatment while for on treatment risk factor y = -0.223 + 2.621 (RVR)Conclusion: SNP IL-28B was important pretreatment risk factor in genotype 1 chronic Hepatitis C treated with dual therapy. Major allele of IL-28B expressed more IFN-l3 and its receptor in response to HCV although no association between both factors was found. RVR was the best on treatment factor for SVR. Further evaluation study was required to find other possible factors affecting SVR achievement]"

"[Association between SNP IL-28B and Sustained Virological Response and Its Relation with Expression of Interferon Lambda-3 and Interferon Lambda-3 Receptor in Liver Tissues of Chronic Hepatitis C Patients Treated with Pegylated Interferon α2 and Ribavirin;Association between SNP IL-28B and Sustained Virological Response and Its Relation with Expression of Interferon Lambda-3 and Interferon Lambda-3 Receptor in Liver Tissues of Chronic Hepatitis C Patients Treated with Pegylated Interferon α2 and Ribavirin, Association between SNP IL-28B and Sustained Virological Response and Its Relation with Expression of Interferon Lambda-3 and Interferon Lambda-3 Receptor in Liver Tissues of Chronic Hepatitis C Patients Treated with Pegylated Interferon α2 and Ribavirin]"

"HIV coinfection in HCV-infected patients accelerates the course of disease and affects the outcome of Peg-IFN/RBV combination treatment. HCV-HIV coinfected patients are suspected to have HCV mutation in NS5A-ISDR/PKR-BD region that had a role to the successfulness of Peg-IFN/RBV therapy. SNP IL-28B polymorphism is predicted to have an effect on the HCV quasi-species evolution. However, until now the effect of HCV NS5A mutation and SNP IL-28B of the host to the response of treatment is still unclear.This study aimed to determine the presence and role of HCV NS5A-ISDR/PKR-BD region mutation and host SNP IL-28B on the succes of Peg-IFN/RBV combination treatment in HCV-HIV coinfected patients.Prospective cohort study design was conducted in this study. Plasma sample was collected from 22 monoinfected and 134 HCV-HIV coinfected patients prior to therapy. All of them were treated with Peg-IFN/RBV for 48 weeks. The examination of HCV RNA was performed 24 weeks after the end of therapy. PCR nucleotide sequencing was performed after the RNA virus extraction and cDNA synthesis had been performed. Analysis of secondary structure and prediction of mutation function were assessed by PredictProtein (PP) program.Sixteen from thirthy HCV-HIV co-infection patients and none from eight HCV patients achieved SVR. Nonneutral mutation ≥ 1 was found in 23/30 subjects with HCV-HIV co-infection. The presence of nonneutral mutation ≥ 1 was observed more frequent in SVR group than non-SVR group. Nonneutral mutation ≥ 1 was associated with SVR achievement, regardless the monoinfection or coinfection status (p = 0.04). Interaction of CC gene and nonneutral mutation was not associated with SVR. Secondary structure transformation of VHC NS5A was not associated with SVR in coinfected subjects. NS5A binding site structure was different from consensus in SVR group, while the structure was similar to consensus in non-SVR group.Nonneutral mutation ≥ 1 has the most important role on the SVR achievement in patients treated with Peg-IFN/RBV. The interaction of CC-gene and nonneutral mutation was not associated with SVR. The change of secondary structure was also not associated with SVR achievement, however, the changes of NS5A binding site structure were found in HCV-HIV coinfected patients who achieved SVR.

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Koinfeksi HIV pada pasien dengan infeksi VHC dapat memperberat perjalanan penyakit dan memengaruhi keberhasilan terapi kombinasi Peg-IFN/RBV. Pasien koinfeksi VHC-HIV diduga mengalami mutasi VHC pada regio NS5A-ISDR/PKR-BD yang mempunyai peran terhadap keberhasilan terapi Peg-IFN/RBV. Polimorfisme SNP IL-28B diprediksi berpengaruh terhadap evolusi quasi-spesies VHC, namun hingga saat ini keberadaan dan peran mutasi VHC NS5A serta SNP IL-28B pejamu pada koinfeksi VHC-HIV terhadap keberhasilan terapi masih belum diketahui secara jelas.Penelitian ini bertujuan untuk mengetahui keberadaan dan peran mutasi VHC NS5A-ISDR/PKR-BD serta SNP IL-28B pejamu terhadap keberhasilan terapi dengan kombinasi Peg-IFN/RBV pada pasien koinfeksi VHC-HIV.Penelitian ini menggunakan desain studi kohort prospektif. Sampel plasma dikumpulkan dari 22 subjek monoinfeksi dan 134 subjek koinfeksi sebelum menjalani terapi. Seluruh pasien mendapatkan terapi Peg-IFN/RBV selama 48 minggu. Pemeriksaan VHC RNA setelah 24 minggu dari akhir terapi dilakukan untuk menilai respons terapi (sustained virological response/SVR 24). Sekuensing nukleotida menggunakan PCR dilakukan setelah ekstraksi RNA virus dan sintesis cDNA dari sampel plasma. Analisis struktur sekunder dan prediksi fungsi mutasi menggunakan program PredictProtein (PP).Sebanyak 16 pasien dari 30 pasien koinfeksi VHC-HIV yang mengalami SVR serta tidak ada dari 8 pasien monoinfeksi VHC yang mengalami SVR. Mutasi nonnetral ≥ 1 ditemukan pada 23/30 pasien koinfeksi VHC-HIV. Keberadaan mutasi nonnetral ≥ 1 didapatkan lebih tinggi pada kelompok SVR (14 pasien) dibandingkan dengan non-SVR (9 pasien). Mutasi nonnetral ≥1 berhubungan dengan kejadian SVR, tanpa memandang status monoinfeksi dan koinfeksi (p = 0,04). Interaksi antara gen CC dan mutasi nonnetral tidak berhubungan dengan SVR. Perubahan struktur sekunder NS5A tidak berhubungan dengan SVR pada pasien koinfeksi. Struktur binding site NS5A pada kelompok SVR didapatkan berbeda dengan konsensus, sedangkan pada kelompok non-SVR mirip dengan konsensus.Mutasi nonnetral ≥ 1 berperan terhadap kejadian SVR pada pasien yang mendapat terapi Peg-IFN/RBV. Interaksi mutasi nonnetral dan gen CC tidak berhubungan dengan pencapaian SVR. Perubahan struktur sekunder juga tidak berhubungan dengan pencapaian SVR, akan tetapi perubahan struktur binding site NS5A-ISDR/PKR-BD ditemukan pada pasien koinfeksi VHC-HIV yang mencapai SVR dengan terapi Peg-IFN/RBV."

"Background: HIV infection in HCV-infected patients accelerates disease progression and reduces the success rate of Peg-IFN/RBV treatment. HCV mutation in NS5A-ISDR/PKR-BD region improved the outcome in HCV monoinfection treated with Peg-IFN/RBV. SNP-IL28B polymorphism is predicted to have an effect on HCV quasispecies evolution. However, the role of NS5A mutation and SNP IL-28B in HIV-HCV coinfection is still unclear. The aim of the study is to determine the role of HCV NS5A-ISDR/PKR-BD mutation and SNP IL-28 polymorphism on the successfulness of Peg-IFN/RBV therapy in HCV-HIV coinfection.Methods: prospective cohort was performed in this study. Plasma sample were obtained from 30 and 8 patients with HCV-HIV coinfection and HCV monoinfection, respectively. PCR nucleotide sequencing was performed after RNA virus extraction and cDNA synthesis. Protein secondary structure and prediction of mutation function were analyzed using PredictProtein (PP) program.Results: sixteen HCV-HIV coinfected patients and none from eight HCV patients achieved sustained virological response (SVR). ≥1 non-neutral mutation was found in 24/30 HCV-HIV coinfection and more frequent in SVR group (14 patients). ≥1 non-neutral mutation were found statistically significant for overall SVR achievement (p<0.05) in all patients regardless of coinfection or monoinfection status. Of the 27 HCV-HIV coinfected patients with CC-gene, 21 subjects had non-neutral mutation. The structure which was expected as NS5A binding site structure was different from consensus (wild type) in SVR group, while the structure was similar to consensus in non-SVR group.Conclusion: having ≥1 non-neutral mutation was associated with SVR achievement in Peg-IFN/RBV therapy, regardless of monoinfection and coinfection status."

"Latar Belakang. Salah satu terapi standar hepatitis C kronik adalah terapi kombinasi interferon alfa (IFN) dan ribavirin (RIB). Namun terapi kombinasi tersebut dapat menimbulkan efek samping anemia. Anemia menyebabkan dosis ribavirin harus diturunkan atau dihentikan sementara yang mengakibatkan penurunan keberhasilan terapi hepatitis C kronik. Oleh karena itu perlu diketahui prevalensi dan faktor risiko anemia pada pasien yang menjalani terapi kombinasi agar anemia dapat diantipasi dan diawasi lebih cermat pada pasien dengan faktor risiko tersebut. Penelitian semacam ini belum pernah dipublikasi di Indonesia.Tujuan. Mengetahui prevalensi dan faktor risiko terjadinya anemia pada pasien hepatitis C kronik yang menjalani terapi interferon alfa dan ribavirin serta mengetahui frekuensi pasien anemia yang mengalami penurunan dan penghentian ribavirin.Metodologi. Pasien hepatitis C kronik yang mendapat pengobatan berupa terapi kombinasi interferon alfa-ribavirin oleh staf divisi Hepatologi FKUIIRSCM diikutsertakan dalam penelitian. Data yang dikumpulkan meliputi anamnesis, pemeriksaan fisik dan pemeriksaan darah tepi pada minggu ke 8 terapi kombinasi. Penelitian menggunakan desain cross sectional dengan variabel yang diteliti adalah umur, jenis kelamin, genotip, dosis ribavirin dan, kadar hemoglobin awal terapi.Hasil. Enam puluh satu subyek penelitian terdiri dari pria 47 (77%), wanita 14 (23%) dan usia rerata 38,9 tahun, 23 (71,9 %) subyek mempunyai genotip 1 dan 4, dan 44 (72,1 %) subyek mendapat dosis ribavirin 1000 mg. Prevalensi anemia sebesar 52,5 % (32 subyek). Dari analisis multivariat hanya kadar hemoglobin awal terapi yang rendah yang berhubungan bermakna dengan anemia.. Jumlah pasien anemia yang mengalami penurunan dosis ribavirin adalah 8 dari 32 pasien anemia.Kesimpulan. Prevalensi anemia pada terapi kombinasi 52,5 %. Kadar hemoglobin awal terapi < 14 gldl merupakan faktor risiko terjadinya anemia sehingga pengawasan lebih ketat dan intervensi terhadap anemia dapat dilakukan pada pasien dengan faktor risiko tersebut. Meskipun umur ? 50 tahun, dan wanita belum terbukti sebagai faktor risiko anemia namun harus tetap menjadi perhatian. Delapan subyek (25 %) Ban 32 pasien anemia memerlukan penurunan dosis ribavirin dan tidak ada yang mengalami penghentian ribavirin.

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Background. Interferon alfa and ribavirin combination therapy is one of effective standard therapy for chronic hepatitis C. However, anemia is a common side effect of this therapy. Therefore, patients have to reduce or discontinue ribavirin therapy and this can reduce the effectivity of the therapy. Hence, it is important to know the prevalence of anemia and to determine the factors associated with anemia.

Objective. To determine the prevalence of anemia and some risk factors associated with anemia caused by combination therapy in chronic hepatitis C, also to know frequencies of anemia patients who received dose reduction or discontinuation ribavirin therapy.

Method. Sixty one patient of chronic hepatitis C received combination therapy from staff of Hepatology Division FKUIfRSCM were included in the study. Data were obtained by anamnesis, physical examination, and measured complete blood count on 8`h week of therapy. This study was conducted by using cross sectional design.

Result. Subjects were 47 males (77%), females 14 (23%) with mean age 38.9 years. Twenty three subjects had genotype 1 and 4 (71.9%) and 44 subject (72.1) received 1000 mg ribavirin. Prevalence of anemia was found to be 52.5 % (32 subjects). It was concluded that risk factors of anemia are: age > 50 years, females, low pretreatment hemoglobin concentration (<14 gldl) were risk factors of anemia. On multivariate analysis only pretreatment hemoglobin concentration < 14 g/dl was determined to be the risk factor of anemia There were 8 subjects from 32 anemia patients had ribavirin reduction, and no patient had discontinuation treatment on Bch week of therapy.

Conclusion. Prevalence anemia was 52,5 % and pretreatment hemoglobin concentration <14 gldl were found to be the risk factors of anemia. Although age > 50 years and female were not yet found to be risk factors of anemia, we should be careful of these risk factors. Therefore patient with these risk factors should be carefully monitored and intervention to prevent anemia should be considered. Eight subjects from 32 anemia patients had ribavirin reduction, and no patient had discontinuation treatment on 8`h week of therapy."

"ABSTRAKLatar Belakang: Penyakit hepatitis C kronik merupakan masalah kesehatan global yang dapat menyebabkan morbiditas serta mortalitas yang tinggi pada kondisi sirosis dan karsinoma hepatoseluler. Adanya terapi sofosbuvir-daclatasvir yang bersifat pangenotipik diharapkan dapat mengatasi penyakit ini. Namun, didapatkan hasil pencapaian SVR 12 yang bervariasi dan lebih rendah pada genotipe 3 dibandingkan genotipe 1. Di Indonesia sendiri belum ada data mengenai pencapaian SVR 12 pada kedua genotipe ini yang menggunakan terapi sofosbuvir-daclatasvir. Tujuan: Mengetahui pencapaian SVR 12 pasien hepatitis C Kronik genotipe 3 dibandingkan genotipe 1 yang mendapatkan terapi sofosbuvir-daclatasvir.Metode: Penelitian ini merupakan studi kohort retrospektif dengan menggunakan data sekunder yang melibatkan 209 pasien hepatitis C kronik genotipe 3 dan 1. Dilakukan analisis dengan membagi pasien menjadi dua kelompok yaitu genotipe 3 dan 1 serta dibandingkan dengan pencapaian keberhasilan SVR 12 menggunakan uji chi-square. Faktor sirosis hepatis dan usia yang dianggap dapat memengaruhi keberhasilan SVR 12 dianalisis dengan menggunakan uji chi-square kemudian dilanjutkan dengan analisis regresi logistik.Hasil: Sampel berjumlah 209 pasien yang terdiri dari 45 pasien genotipe 3 dan 164 pasien genotipe 1. Pencapaian keberhasilan SVR 12 pada genotipe 3 dan 1 yaitu 84,4% dan 98,8%. Kelompok pasien genotipe 3 memiliki keberhasilan SVR 12 lebih rendah dibandingkan kelompok pasien genotipe 1 dengan adjusted OR=0,065 (IK95% 0,013-0,330) dan ARR 14,4%. Sirosis hepatis dan usia tidak memengaruhi keberhasilan SVR 12 (p=1,00 dan p=0,72). Sejumlah 5 dari 9 pasien yang mengalami kegagalan memiki koinfeksi dengan HIV. Simpulan: Pasien hepatitis C kronik genotipe 3 yang menggunakan terapi sofosbuvir-daclatasvir memiliki keberhasilan SVR 12 lebih rendah dibandingkan genotipe 1.

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ABSTRACTBackground. Chronic hepatitis C is a global health problem with high morbidity and mortality in the condition of cirrhosis and hepatocellular carcinoma. sofosbuvir-daclatasvir is pangenotypic therapy that expected to overcome this disease. However, the achievement of SVR 12 was varied and lower in genotype 3 compared to genotype 1. In Indonesia, there is no data about achievement SVR 12 in both genotypes using sofosbuvir-daclatasvir.Objectives. To know SVR 12 achievement between genotype 3 and 1 chronic hepatitis C patients that using sofosbuvir-daclatasvir therapy.Methods. This study is a retrospective cohort using secondary data of 209 hepatitis C chronic genotype 3 and 1. Samples were divided into two groups according to its genotype and compared with achievement of SVR 12 then analyzed using chi-square test. Hepatic cirrhosis and age factors that are considered to affect the achievement SVR 12 were analyzed using chi-square test and logistic regression test.Results. 209 patients participated in this study consisting of 45 genotype 3 and 164 genotype 1. Achievement of SVR 12 succeed in genotypes 3 and 1 were 84,4% and 98,8%. Genotype 3 patients had lower SVR 12 achievement compared to genotype 1 patients with adjusted OR=0,065 (95% CI 0,013-0,330) and ARR 14,4. Hepatic cirrhosis and ages did not affect SVR 12 (p= 1.00 and 0,72, respectively). Five from nine patients who failed have co-infection with HIV.Conclusions. Chronic hepatitis C patients using sofosbuvir-daclatasvir theraphy had lower SVR 12 achievement in genotype 3 than genotype 1."

"Latar Belakang: Saat ini hubungan antara kejadian SVR12 pasien hepatitis C, profil lipid, dan steatosis hati masih belum jelas. Hasil publikasi yang ada saat ini masih tidak konsisten mengenai perubahan nilai parameter tersebut pasca SVR12. Di Indonesia sendiri, belum ada penelitian yang mengevaluasi kejadian steatosis hati pasca SVR12, padahal karakteristik populasi di Indonesia berbeda dengan populasi negara lain. Penelitian ini bertujuan untuk meneliti perubahan derajat steatosis hati dan profil lipid pada pasien hepatitis C saat SVR12 dan mencari hubungannya.Metode: Penelitian dengan desain longitudinal, before and after study yang dilakukan di Rumah Sakit Cipto Mangunkusumo (RSCM). Penelitian dilakukan selama 1 tahun di Poliklinik Hepatobilier, Ruang Prosedur Terpadu (RPT) Divisi Hepatobilier. Pasien yang memenuhi kriteria inklusi akan diikutsertakan dan diperiksa profil lipid dan nilai controlled attenuated parameter sebelum dan sesudah terapi.Hasil: Rerata SD sampel penelitian adalah 45±8.78 tahun. Subjek sebagian besar (62%) berjenis kelamin laki-laki. Nilai rerata SD CAP meningkat, sebelum terapi 196±49.36 dB/m dan setelah terapi 227±47.11 dB/m. Nilai rerata SD kolesterol total meningkat, sebelum terapi 166±40.30 mg/dL dan setelah terapi 190±42.58 mg/dL. Nilai rerata SD trigliserida, sebelum terapi 94±45.39 mg/dL dan setelah terapi 109±49.83 mg/dL. Nilai rerata SD HDL meningkat, sebelum terapi 44.4±15.02 mg/dL dan setelah terapi 47.0±17.20 mg/dL. Nilai rerata SD LDL meningkat, sebelum terapi 109.48±39.57 mg/dL dan setelah terapi 130.88±34.32 mg/dL. Tidak ditemukan korelasi korelasi delta berbagai jenis kolesterol dengan delta CAP. Ditemukan adanya korelasi negatif antara nilai CAP pada pasien hepatitis C sebelum terapi dan perubahan nilai CAP sesudah terapi DAA. Terdapat penurunan nilai rerata SD kekakuan hati, sebelum terapi 6.90±2.34 kPa dan setelah terapi 5.35±1.79 kPa. Terdapat penurunan nilai median APRI, sebelum terapi 0.50 (0.3 – 0.7) dan setelah terapi 0.20 (0.20 – 0.30).Simpulan: 1) Terdapat perbedaan derajat steatosis hati sebelum terapi dan saat SVR12 pada pasien hepatitis C yang mendapat terapi DAA. 2) Terdapat perbedaan kadar kolesterol total, kolesterol HDL, kolesterol LDL, dan trigliserida sebelum terapi dan saat SVR12 pada pasien hepatitis C yang mendapat terapi DAA. 3) Tidak terdapat korelasi perubahan kadar kolesterol total, kolesterol HDL, kolesterol LDL, dan trigliserida terhadap derajat steatosis hati saat SVR12.

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Background: Currently, the relationship between hepatitis C patients' SVR12 events, lipid profiles and liver steatosis remains unclear. Current publications are inconsistent regarding the changes in these parameters after SVR12. In Indonesia alone, there are no studies evaluating the incidence of liver steatosis after SVR12, even though the characteristics of the population in Indonesia are different from those in other countries. This study aims to examine changes in the degree of hepatic steatosis and lipid profile in hepatitis C patients during SVR12 and find out the relationship.

Method: Longitudinal design, before and after study conducted at Cipto Mangunkusumo Hospital (RSCM). The study was conducted for 1 year at the Hepatobiliary Polyclinic, Integrated Procedure Room of the Hepatobiliary Division. Patients who met the inclusion criteria were included and examined for lipid profile and controlled attenuated parameter values before and after therapy.

Results: The mean age SD is 45±8.78 years. Subjects were mostly (62%) male. The mean SD value of CAP increased, before therapy 196±49.36 dB/m and after therapy 227±47.11 dB/m. The mean SD value of total cholesterol increased, before therapy 166±40.30 mg/dL and after therapy 190±42.58 mg/dL. The SD mean value of triglycerides, before therapy 94±45.39 mg/dL and after therapy 109±49.83 mg/dL. The mean SD value of HDL increased, before therapy 44.4±15.02 mg/dL and after therapy 47.0±17.20 mg/dL. The mean SD value of LDL increased, before therapy 109.48±39.57 mg/dL and after therapy 130.88±34.32 mg/dL. There was no correlation between the delta of various types of cholesterol and the delta of CAP. There was a negative correlation between CAP values in hepatitis C patients before therapy and changes in CAP values after DAA therapy. There was a decrease in the mean SD value of liver stiffness, before therapy 6.90±2.34 kPa and after therapy 5.35±1.79 kPa. There was a decrease in the median APRI value, before therapy 0.50 (0.3 - 0.7) and after therapy 0.20 (0.20 - 0.30).

Conclusion: 1) There is a difference in the degree of liver steatosis before therapy and after SVR12 in hepatitis C patients who received DAA therapy. 2) There are differences in total cholesterol, HDL cholesterol, LDL cholesterol, and triglyceride levels before therapy and after SVR12 in hepatitis C patients who received DAA therapy. 3) There is no effect of changes in total cholesterol, HDL cholesterol, LDL cholesterol, and triglycerides before therapy and after SVR12 on the degree of liver steatosis after SVR12."

"Latar belakang: Insidensi dan faktor risiko karsinoma hepatoseluler (KSH) pada pasien hepatitis C virus (HCV) yang sudah mencapai sustained virological response (SVR) pasca terapi direct acting antiviral (DAA) belum banyak diketahui. Mengingat terdapat perbedaan jenis DAA, genotype virus, dan profil pasien di Indonesia, dilakukan studi untuk menilai insidensi dan faktor-faktor yang memengaruhi KSH pada pasien HCV pasca SVR post terapi DAA.Tujuan: Mengetahui insidensi dan faktor-faktor yang memengaruhi kejadian KSH pada pasien HCV yang mencapai SVR pasca pengobatan DAA.Metode: Desain penelitian kohort retrospektif di RSUPN Cipto Mangunkusumo, sampel pasien HCV yang SVR pasca DAA tahun 2017 – 2019, diikuti hingga 2024. Pasien dilakukan skrining USG abdomen, alpha-fetoprotein (AFP) dan CT Scan abdomen 3 fase apabila terdapat indikasi. Dilakukan analisis deskriptif, bivariat dengan Fisher’s exact, dan multivariat dengan regresi logistik bila terdapat faktor risiko di analisis bivariat (p <0,25).Hasil: Dari 180 subjek penelitian, insidensi dan rasio insidensi KSH pada seluruh populasi mencapai 4,4% (rasio insidens 0,91/100PY). Terdapat hubungan signifikan dari analisis bivariat variabel sirosis hepatis (RR 10,5; IK 95% (1,32 – 83,5); p =0,0073) dan DM tipe 2 (RR 8,47; IK 95% (2,3 – 31,1) p = 0,0048). Terdapat hubungan signifikan dari analisis multivariat variabel DM tipe 2 (aRR 3,1; IK 95% (0,86 – 3,83); p=0,002).Kesimpulan: Insidensi KSH mencapai 4,4% dari total populasi. DM tipe 2 memiliki hubungan yang signifikan terhadap kejadian KSH pada pasien HCV yang mencapai SVR pasca pengobatan DAA.

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Background: The incidence and risk factors for hepatocellular carcinoma (HCC) in hepatitis C (HCV) patients who have achieved sustained virological response (SVR) after direct-acting antiviral (DAA) therapy are not well established. Considering there are differences in DAA types, virus genotypes, and patient profiles in Indonesia, this study was conducted to assess the incidence and factors influencing HCC in HCV patients after SVR post DAA therapy.

Objective: To determine the incidence and factors influencing HCC in HCV patients achieving SVR after DAA treatment.

Method: Retrospective cohort study conducted at Cipto Mangunkusumo National General Hospital, sample of HCV patients had SVR after DAA therapy in 2017 – 2019, followed until 2024. Patients were screened for abdominal ultrasound, alpha-fetoprotein (AFP) and 3-phase abdominal CT scan, if indicated. Descriptive, bivariate analysis with Fisher's exact, and multivariate analysis with logistic regression were conducted.

Results: Among 180 subjects, the incidence and incidence ratio of HCC is 4.4% (0.91/100PY). Significant correlation in bivariate analysis from the variables liver cirrhosis (RR 10.5; CI 95% (1. 32 – 83.5); p = 0.0073) and type 2 DM (RR 8.47; CI 95% (2, 3 – 31.1) p = 0.0048). In multivariate analysis, there was significant correlation from type 2 DM variable (aRR 3.1; CI 95% (0.86 – 3.83); p=0.002).

Conclusion: The incidence of HCC reaches 4.4% of the total population. Type 2 DM has significant correlation with the incidence of HCC in HCV patients who achieve SVR after DAA treatment."

"Pasien uveitis tanpa etiologi yang jelas (idiopatik) dengan kriteria klinis peradangan yang tidak spesifik namun memiliki status IGRA positif kerap menyebabkan dilema dalam pengobatan. Kelompok pasien tersebut diterapi sebagai kelompok suspek ekstrapulmonari TB dan mendapatkan pengobatan Obat Anti Tuberkulosis (OAT). Berbagai penelitian menunjukan bahwa profil ekspresi transkriptomik Interferon-stimulated Genes (ISG) tipe 1 ditemukan meningkat pada pasien aktif TB dan diketahui berpotensi sebagai biomarker diagnosa dan monitoring efikasi terapi. Selain itu level protein C1q ditemukan meningkat pada pasien TB aktif dibandingkan kelompok kontrol sehat serta kadarnnya menurun signifikan seiring dengan durasi pengobatan OAT. Pada penelitian ini dilakukan pemeriksaan ekspresi mRNA menggunakan RT-qPCR terhadap Interferon Stimulated Genes (ISG) tipe 1 (MyD88, FCG1R1B, IL1B, IFIT2, GBP1, IRF7, TLR8, STAT1, SERPING1, UBE2L6) dan protein C1q menggunakan ELISA pada pasien uveitis idiopatik dengan IGRA positif dari 20 pasien dengan time-point follow up pada minggu ke-0 (M0) dan minggu ke-2 (M2). Ekspresi gen GBP1 (p=0,001), UBE2L6 (p=0,0012) dan SERPING1 (p=0,03) berbeda bermakna pada kelompok perbaikan okular, dengan 8/10 gen menunjukan tren penurunan ekspresi pada M2. Hanya GBP1 (p=0,03) yang ekspresinya berbeda bermakna pada kelompok tanpa perbaikan okular, dengan 9/10 menunjukan tren peningkatan ekspresi gen pada M2. Perubahan ekspresi gen (M0-M2) MyD88, FCGR1B, GBP1, TLR8, STAT1 berkorelasi dengan outcome okular. Perubahan ekspresi gen GBP1 dan TLR8 berbeda bermakna sebagai biomarker diagnosis dengan AUC 88,1% dan 90,5%. Pada penelitian ini, level C1q sebelum dan setelah pengobatan ditemukan tidak berbeda bermakna (p=0,87) dan tidak terdapat hubungan berbeda bermakna antara perubahan klinis okular dengan level C1q.

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Uveitis patients without a clear etiology (idiopathic) with non-specific inflammation clinical criteria but who have a positive IGRA status often cause dilemmas in treatment. This group of patients was treated as a group of suspected extrapulmonary TB and received anti-tuberculosis drug (ATT) treatment. Various studies have shown that the transcriptomic expression profile of type 1 Interferon Stimulated Genes (ISG) was found to be increased in active TB patients and is known to have potential as a diagnostic biomarker and monitoring of therapy efficacy. In addition, the C1q protein level was found to be increased in active TB patients compared to the healthy control group and its levels decreased significantly with the duration of OAT treatment. In this study, mRNA expression was examined using RT-qPCR on Interferon Stimulated Genes (ISG) type 1 (MyD88, FCG1R1B, IL1B, IFIT2, GBP1, IRF7, TLR8, STAT1, SERPING1, UBE2L6) and C1q protein using ELISA in idiopathic uveitis patients. with positive IGRA of 20 patients with time-point follow-up at week 0 (W0) and week 2 (W2). GBP1 (p=0.001), UBE2L6 (p=0.0012), and SERPING1 (p=0.03) genes differentially expressed significantly in the group with ocular improvement, which 8/10 genes were downregulated in W2. In the non-improvement ocular group, only the GBP1 gene was significantly expressed differentially (p=0.03), with 9/10 genes expression upregulated in W2. Changes in expression of the MyD88, FCGR1B, GBP1, TLR8, and STAT1 genes correlated with ocular improvement. Changes in GBP1 and TLR8 gene expression were significantly different as a biomarker diagnosis with AUC of 88.1% and 90.5%. In this study, C1q levels before and after treatment were not significantly different (p=0.87) and there was no significant correlation between ocular clinical changes and C1q levels."