Hasil Pencarian  ::  Simpan CSV :: Kembali

"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."

"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.

---

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."

"[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]"

"Latar 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.

---

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."

"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.

---

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."

"Background: Tuberculosis and its resistance are a major global health problem in the world. The increased incidence and mortality of tuberculosis in Indonesia remain a big public health issue especially in Jakarta Province. No published studies have focused on assessing the outcome treatment of tuberculosis resistance both in success and death. We aimed this study to assess the survival of cured and death outcomes as well as the determinant factors which might influence drugs resistant tuberculosis in Jakarta between 2010 and 2015. Methods: this study analyzed the national electronic tuberculosis register (e-TB Manager) of Jakarta province in 2010 to 2015. All adult patients who lived in Jakarta province and were diagnosed with multidrug-resistant tuberculosis (MDR-TB) and extensively drug-resistant tuberculosis (XDR-TB) were eligible for the study. Kaplan Meier survival curve was used, together with log-rank test and Chi-Square (X2) test for descriptive analysis. Cox regression analysis helped determine the potential risk factors. Several risk factors were analyzed in this study, including age, gender, residency, HIV status, resistance status, and history of previous treatment. Results: we analyzed 553 samples in this study. The drug-resistant tuberculosis cases increased gradually from 2010 to 2015. Of all cases, 248 and 67 patients were cured and death, respectively. There was a difference in survival rate between patients diagnosed with MDR-TB and XDR-TB with successful treatment. Poor treatment outcome (death) among patients was predicted by age greater than 60 years old (HR 3.48; 95% CI 1.48 - 8.38, p-value = 0.004). Conclusion: there was a difference survival rates between success treatment (cured) and poor treatment outcome (death) during six years of observation. Age of patients is a single-predictor in survival of death. While, HIV status and resistance status were predictors in survival of cured."

"Chronic hepatitis C virus : lessons from the past, promise for the future documents the monumental advances that have been made in our understanding of chronic HCV during the past decade. The first section reviews the natural history of chronic HCV, how this virus can affect other organs in addition to the liver, and whether treating chronic HCV alters the natural history of this disease. Section 2 reviews the advances that have been made in the treatment of chronic HCV during the past decade with interferon based therapy. Separate chapters on response guided therapy and how to manage the adverse events associated with these medications provide the physician with the concepts required to more effectively treat chronic HCV now and in the future. As the genetics of virologic response have recently been elucidated, a chapter is devoted to helping the clinician understand how genes that modulate disease processes and their treatment are identified and utilized in clinical care. Section 3 deals with the future of HCV treatment and specific inhibitors of HCV. Specific chapters explain how targets for drugs are identified and how drugs are then developed and tested; how mutations of HCV develop and how anti-viral agents will affect this process; the most up to date data regarding the treatment of chronic HCV with peginterferon, ribavirin and anti-viral agents; and the potential to treat chronic HCV with just oral anti-viral agents and without peginterferon and ribavirin in the future. The final section of this book covers issues related to liver transplantation in patients with chronic HCV. Separate chapters review the natural history of chronic HCV in liver transplant recipients and the impact of utilizing HCV positive donors. The volume concludes with chapters that cover the treatment of chronic HCV both prior to and after liver transplantation with potent anti-viral agents. Chronic hepatitis C virus : lessons from the past, promise for the future is a valuable resource for all physicians caring for patients with chronic HCV."

"Currently, we reported results of a nested polymerase chain reaction (PCR) assay specific 5` untranslated region (UTR) region of hepatitis C virus (HCV) genome that showed three different patterns of deoxyribonucleic acid (DNA) fragments (single expected specific DNA band, single DNA band higher in size than an expected band, and multiple DNA bands). Three isolates (Isolate A, B, and C), representing all the three DNA bands, were analyzed by using phylogenetic trees. The results showed that the Isolate A, B, and C were classified into HCV genotypes 2, 1, and 3, respectively. The Isolate A and B were very closely related to viral isolates from Madagascar and Brazil, respectively and were not closely related to other Indonesia isolates. In contrast with the Isolate A and B, the Isolate C was very closely related to another Indonesia isolate. Among all there isolates, the Isolate C was very closely related to an Indonesia isolate detected from a cirrhosis patient, indicating that the Isolate C might be more virulence than the Isolate B and C. However, a complete genome-based comprehensive genetic characterization for all the three isolates needs to be conducted in future research to confirm all findings in this study."

"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.

---

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."