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Journal articles on the topic 'Iron in chronic hepatitis C'

Author: Grafiati
Published: 4 June 2021
Last updated: 9 February 2022

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1

Hayashi, Hisao, and Motoyoshi Yano. "Iron Cytotoxicity in Chronic Hepatitis C." JOURNAL OF HEALTH SCIENCE 48, no. 3 (2002): 227–31. http://dx.doi.org/10.1248/jhs.48.227.

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2

Corengia, Chiara, Stefania Galimberti, Giorgio Bovo, Anna Vergani, Cristina Arosio, Raffaella Mariani, Alessandro Redaelli, et al. "Iron Accumulation in Chronic Hepatitis C." American Journal of Clinical Pathology 124, no. 6 (December 2005): 846–53. http://dx.doi.org/10.1309/x4uh5q68q4j3gdnv.

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3

Nozic, Darko, Bela Balint, Nebojsa Stankovic, Jovan Dimitrijevic, and Gorana Neskovic. "Significance of iron reduction for the therapy of chronic hepatitis C." Vojnosanitetski pregled 62, no. 2 (2005): 161–64. http://dx.doi.org/10.2298/vsp0502161n.

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Background. It has been established that many patients with chronic hepatitis C have elevated serum iron, feritin levels and iron deposits in the liver. Therefore, the liver damage due to hepatitis C virus may be aggravated with iron overload. In many studies higher levels of iron in the blood and the liver were connected with the decreased response to interferon-alfa therapy for chronic viral hepatitis C. Recent introduction of pegylated interferons plus ribavirin has improved the therapeutic response, so it is now possible to cure more than 50% of the patients. Case report. Three patients with chronic hepatitis C and iron overload were presented. Iron reduction therapy using phlebotomy or eritrocytapheresis with plasmapheresis was done at different times in regard to specific antiviral therapy or as a sole therapy. Conclusion. It has been shown that iron reduction, sole or combined with antiviral therapy, led to the deacreased aminotransferase serum activity and might have slow down the evolution of chronic hepatitis C viral infection.
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4

Fujita, Naoki, and Yoshiyuki Takei. "Iron, hepatitis C virus, and hepatocellular carcinoma: iron reduction preaches the gospel for chronic hepatitis C." Journal of Gastroenterology 42, no. 11 (November 22, 2007): 923–26. http://dx.doi.org/10.1007/s00535-007-2110-4.

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5

Price, Leslie, and Kris V. Kowdley. "The Role of Iron in the Pathophysiology and Treatment of Chronic Hepatitis C." Canadian Journal of Gastroenterology 23, no. 12 (2009): 822–28. http://dx.doi.org/10.1155/2009/290383.

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Increased hepatic iron content may be observed in patients with chronic hepatitis C infection, and may contribute to disease severity. The presence of hemochromatosis gene mutations is associated with increased hepatic iron accumulation and may lead to accelerated disease progression. Hepatic iron depletion has been postulated to decrease the risk of hepatocellular carcinoma in patients with cirrhosis due to chronic hepatitis C. It is possible that iron depletion stabilizes or improves liver histology and slows disease progression in these individuals. The present article reviews the prevalence and risk factors for hepatic iron overload in chronic hepatitis C, with emphasis on the available data regarding the efficacy of iron depletion in the treatment of this common liver disease.
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6

Ivashkin, V. T., E. Lukina, M. Majevskaja, A. Levina, E. Sysojeva, C. Pavlov, N. D. Khoroshko, and G. A. Frank. "Iron status of patients with chronic hepatitis C." Journal of Hepatology 28 (1998): 205. http://dx.doi.org/10.1016/s0168-8278(98)80996-3.

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7

BURT, MICHAEL J., and W. GRAHAM COOKSLEY. "The influence of iron on chronic hepatitis C." Journal of Gastroenterology and Hepatology 13, no. 3 (March 1998): 330–33. http://dx.doi.org/10.1111/j.1440-1746.1998.01549.x.

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8

Indrasari, Nuri Dyah, Ina Susianti Timan, and Pustika Amalia. "PERBEDAAN KOLAGEN IV DI KERUSAKAN HATI DAN INFEKSI HEPATITIS C PASIEN TALASEMIA DENGAN KELEBIHAN ZAT BESI (Diferrence of Collagen IV in Liver Damage and Hepatitis C Infection in Iron Overload Thalassemia Patients)." INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY 22, no. 1 (April 14, 2018): 1. http://dx.doi.org/10.24293/ijcpml.v22i1.1214.

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Thalassemia patients who receive repeated blood transfusions are at risk of iron overload and hepatitis C infection. Iron overload cancause iron deposit in many organs, including the liver. Iron deposits in the liver and hepatitis C infection can cause chronic inflammationof the liver and induce hepatic stellate cells to produce Extra Cellular Matrix (ECM) causing liver fibrosis. Laboratory diagnosis of liverfibrosis is based on direct and indirect markers. Collagen IV is a direct marker reflecting ECM degradation in liver fibrosis. AlanineTransaminase (ALT), Aspartate Transaminase (AST) and AST/ALT ratio are indirect markers reflecting liver cell damage due to liverfibrosis. The aim of this study was to investigate the difference of Collagen IV in liver damage and hepatitis C infection in thalassemiapatients with iron overload. Collagen IV was measured using ELISA, while ALT and AST were measured by enzymatic colorimetric assay.Fifty eight thalassemia patients with iron overload, 29 with hepatitis C and 29 without hepatitis C were studied. This study showed nosignificant difference in Collagen IV level, ALT, AST activity and AST/ALT ratio between subjects with and without hepatitis C(p 0.131,0.243, 0.256 and 0.726) and no significant correlation was found between collagen IV level and ALT activity, and between collagen IVand AST/ALT ratio (p 0.160 and 0.509). These findings indicate that Collagen IV showed no correlation with liver damage and hepatitisC infection in thalassemia patients with iron overload.
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9

Dostalikova-Cimburova, Marketa, Karolina Kratka, Jaroslav Stransky, Ivana Putova, Blanka Cieslarova, and Jiri Horak. "Iron Overload andHFEGene Mutations in Czech Patients with Chronic Liver Diseases." Disease Markers 32, no. 1 (2012): 65–72. http://dx.doi.org/10.1155/2012/790464.

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The aim of the study was to identify the prevalence ofHFEgene mutations in Czech patients with chronic liver diseases and the influence of the mutations on iron status. The presence ofHFEgene mutations (C282Y, H63D, and S65C) analyzed by the PCR-RFLP method, presence of cirrhosis, and serum iron indices were compared among 454 patients with different chronic liver diseases (51 with chronic hepatitis B, 122 with chronic hepatitis C, 218 with alcoholic liver disease, and 63 patients with hemochromatosis). Chronic liver diseases patients other than hemochromatics did not have an increased frequency ofHFEgene mutations compared to controls. Although 33.3% of patients with hepatitis B, 43% of patients with hepatitis C, and 73.2% of patients with alcoholic liver disease had elevated transferrin saturation or serum ferritin levels, the presence ofHFEgene mutations was not significantly associated with iron overload in these patients. Additionally, patients with cirrhosis did not have frequencies ofHFEmutations different from those without cirrhosis. This study emphasizes the importance, not only of C282Y, but also of the H63D homozygous genetic constellation in Czech hemochromatosis patients. Our findings show that increased iron indices are common in chronic liver diseases butHFEmutations do not play an important role in the pathogenesis of chronic hepatitis B, chronic hepatitis C, and alcoholic liver disease.
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10

MATSUMOTO, Masafumi, Shigeyoshi IMAMURA, Hitomi SATO, Masahiko TAKAMASU, Takeshi OKANOUE, and Kei KASHIMA. "Dietary iron reduction on patients with chronic hepatitis C." Kanzo 40, no. 8 (1999): 436–44. http://dx.doi.org/10.2957/kanzo.40.436.

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11

Lucariello, A., M. de Martino, E. Russo, D. Lombardini, F. D'Aria, G. Scherillo, M. Scotto di Vetta, and A. Cioffi. "Iron overload and HFE mutations in chronic hepatitis C." Journal of Hepatology 38 (April 2003): 135. http://dx.doi.org/10.1016/s0168-8278(03)80730-4.

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12

Valenti, Luca, Paola Dongiovanni, Silvia Fargion, and Anna Ludovica Fracanzani. "Iron genes, dysmetabolism and fibrosis in chronic hepatitis C." Journal of Hepatology 48, no. 3 (March 2008): 513–14. http://dx.doi.org/10.1016/j.jhep.2007.12.001.

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13

K. C, Sajeevan, Lyson Lonappan, Biju George, and Parvathi K. Warrier. "SERUM IRON PARAMETERS IN ALCOHOLIC CIRRHOSIS, CRYPTOGENIC CIRRHOSIS, CHRONIC HEPATITIS B AND CHRONIC HEPATITIS C." Journal of Evidence Based Medicine and Healthcare 3, no. 94 (November 24, 2016): 5157–61. http://dx.doi.org/10.18410/jebmh/2016/1078.

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14

Radicheva, Mariana Penkova, Albena Nikolaeva Andonova, Hristina Tancheva Milcheva, Nadejda Gospodinova Ivanova, Silviya Georgieva Kyuchukova, Mima Stefanova Nikolova, and Мagdalena Stefanova Platikanova. "Serum Markers of Iron Metabolism in Chronic Liver Diseases." Open Access Macedonian Journal of Medical Sciences 6, no. 6 (June 14, 2018): 1010–16. http://dx.doi.org/10.3889/oamjms.2018.251.

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BACKGROUND: Disorders in the metabolism of iron in the direction of iron overload are observed not only in primary hemochromatosis but also in some chronic liver diseases other aetiology. Elevation of serum iron, ferritin and transferrin saturation is reported in nonalcoholic fatty liver disease and alcohol, chronic hepatitis C and liver cirrhosis.AIM: Aim of the study was to evaluate and compare the frequency of the iron serum markers in patients with various chronic liver diseases.MATERIAL AND METHODS: The study included a total of 246 persons -186 patients with chronic liver disease without cirrhosis (-115 men, women -71; average age of 50.41 ± 12.85, from 23 to 77 years) and 60 healthy controls (-30 men, women -30, middle-aged 50.50 ± 11.31, from 29 to 83 years). Medical history, physical examination and demographic data including height, weight, laboratory and instrumental studies were performed.RESULTS: The highest incidence of elevated serum iron, transferrin saturation and ferritin and decreased serum hepcidin found in cases of alcoholic liver disease (ALD), nonalcoholic fatty liver disease (NAFLD) and chronic hepatitis C (CHC).CONCLUSION: Finally, analysis of the changes in serum markers of iron metabolism shows that the difference between healthy and sick with liver disease is primarily due to changes in alcoholic and nonalcoholic fatty liver disease, particularly steatohepatitis, and chronic hepatitis C.
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15

Pereira, Patricia da Silva Fucuta, Ivonete Sandra de Souza e. Silva, Silvia Naomi de Oliveira Uehara, Christini Takemi Emori, Valéria Pereira Lanzoni, Antonio Eduardo Benedito Silva, and Maria Lucia Gomes Ferraz. "Chronic hepatitis C: hepatic iron content does not correlate with response to antiviral therapy." Revista do Instituto de Medicina Tropical de São Paulo 51, no. 6 (December 2009): 331–36. http://dx.doi.org/10.1590/s0036-46652009000600004.

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The complex interaction between hepatitis C virus infection, iron homeostasis and the response to antiviral treatment remains controversial. The aim of this study was to evaluate the influence of hepatic iron concentration (HIC) on the sustained virological response (SVR) to antiviral therapy in patients with chronic hepatitis C. A total of 50 patients who underwent pretreatment liver biopsy with assessment of HIC by graphite furnace atomic absorption spectroscopy and were subsequently submitted to antiviral treatment with interferon/peginterferon and ribavirin were included in the study. Patients with alcoholism, history of multiple blood transfusion, chronic kidney disease, hemolytic anemia and parenteral iron therapy were excluded. The iron related markers and HIC were compared between those who achieved an SVR and non-responders (NR) patients. The mean age was 45.7 years and the proportion of patients' gender was not different between SVR and NR patients. The median serum iron was 138 and 134 µg/dL (p = 0.9), the median serum ferritin was 152.5 and 179.5 ng/mL (p = 0.87) and the median HIC was 9.9 and 8.2 µmol/g dry tissue (p = 0.51), for SVR and NR patients, respectively. Thus, hepatic iron concentration, determined by a reliable quantitative method, was not a negative predictive factor of SVR in patients with chronic hepatitis C presenting mild to moderate hepatic iron accumulation.
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16

Atta, AsmaaS, KhalidA Khalifa, OmaimaM Abbas, and NahlaO Shokri. "Do all chronic hepatitis C virus bleeders develop iron deficiency?" Menoufia Medical Journal 33, no. 1 (2020): 217. http://dx.doi.org/10.4103/mmj.mmj_168_18.

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17

Obando, Jorge, Kristina Tortorelli, Barbara Banner, Denise Stefancyk, and Herbert L. Bonkovsky. "Iron, the major HFE gene mutation and chronic hepatitis C." Gastroenterology 118, no. 4 (April 2000): A953. http://dx.doi.org/10.1016/s0016-5085(00)85954-5.

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18

Nakamuta, M., M. Kohjima, Y. Shimonaka, R. Yada, A. Taketomi, K. Gotoh, T. Yoshimoto, et al. "1171 ROLE OF IRON METABOLISM IN CHRONIC HEPATITIS C TREATMENT." Journal of Hepatology 54 (March 2011): S462—S463. http://dx.doi.org/10.1016/s0168-8278(11)61173-2.

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19

Katoh, Tomoko, Kazutomo Suzuki, Hiroshi Takada, Gordon Luk, and Hajime Kuwayama. "Effect of a low iron diet in chronic hepatitis C." Gastroenterology 124, no. 4 (April 2003): A384. http://dx.doi.org/10.1016/s0016-5085(03)81945-5.

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20

Rigamonti, C., S. Andorno, E. Maduli, S. Morelli, S. Pittau, G. Nicosia, R. Boldorini, and M. Sartori. "Iron, hepatic stellate cells and fibrosis in chronic hepatitis C." European Journal of Clinical Investigation 32 (March 2002): 28–35. http://dx.doi.org/10.1046/j.1365-2362.2002.0320s1028.x.

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21

Pirisi, Mario, Cathryn A. Scott, Claudio Avellini, Pierluigi Toniutto, Carlo Fabris, Giorgio Soardo, Carlo A. Beltrami, and Ettore Bartoli. "Iron Deposition and Progression of Disease in Chronic Hepatitis C." American Journal of Clinical Pathology 113, no. 4 (April 1, 2000): 546–54. http://dx.doi.org/10.1309/trb1-jxuj-l9r6-9nhx.

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22

CHANDRA, B. "Iron overload in chronic hepatitis C : How common is it?" Hepatology 22, no. 4 (October 1995): A275. http://dx.doi.org/10.1016/0270-9139(95)94823-6.

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23

López-Prieto, Javier, Emilio González-Reimers, M. Remedios Alemán-Valls, María José de la Vega-Prieto, Pedro Abreu-González, Ricardo Pelazas-González, Rubén Hernández-Luis, Carlos Jorge-Ripper, and Francisco Santolaria-Fernández. "Iron and Proinflammatory Cytokines in Chronic Hepatitis C Virus Infection." Biological Trace Element Research 155, no. 1 (July 28, 2013): 5–10. http://dx.doi.org/10.1007/s12011-013-9760-2.

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24

Isom, Harriet C., Emily I. McDevitt, and Mi Sun Moon. "Elevated hepatic iron: A confounding factor in chronic hepatitis C." Biochimica et Biophysica Acta (BBA) - General Subjects 1790, no. 7 (July 2009): 650–62. http://dx.doi.org/10.1016/j.bbagen.2009.04.009.

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25

Farid, Saadia, Sameh Mohamed, Lila Rashid, and Dina Sbry. "A Key Regulator For Iron Homeostasis in chronic hepatitis C." Egyptian Journal of Hospital Medicine 49, no. 1 (October 1, 2012): 615–27. http://dx.doi.org/10.21608/ejhm.2012.16203.

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26

Iqbal, Waheed, Mirza Rehan Baig, Mudassar Ali, Muhammad Zaid Iqbal, Ajmaal Jami, and Tarik Alam Solangi. "Assessing Responsiveness of Elevated Serum Ferritin for Treatment in Chronic Hepatitis C Infected Patients." Pakistan Journal of Medical and Health Sciences 15, no. 6 (June 30, 2021): 2149–52. http://dx.doi.org/10.53350/pjmhs211562149.

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Background: Hepatitis C virus (HCV) infection is a foremost community health issue globally. There is anoptimisticrelationamid iron accumulation in hepatocytes and high serum markers counting transferrin and ferritin. The purpose of this analysis was to examine the responsiveness of the treatment with elevated serum ferritin in patients with hepatitis C infection. Methods: The study included 200 HCV-infected patients from the department of Medicine, Divisional Headquarters teaching hospital, Mirpurand Isra Medical University, Karachi for six months duration from 16thJune 2020 to 15thDecember 2020. The clinical feature assesses HCV exposure in all patients, biochemical data, and iron status parameters. The results were quantified using Microsoft Excel 2013. Results: The obtained outcomes indicate that antiviral treatment significantly interferes the iron accumulation in hepatocytes in HCV positive patients. All positive iron values were calculated as 19.93 mol / L; and for all negative PCR, the value was calculated at 24.61 μmol / L prior to drug started. Our patients’ levels of iron were 62.77 μmol / L in patients whose PCR is positive for HCV which is within the normal range. Reduced ferritin levels have negative effects after drug administration. The increase in ALT was observed in 37.62% of cases. Conclusions: Patients with chronic HCV have strong association with serum iron concentration. Keywords: Ferritin levels, Drugs, Iron load, Hepatitis C Virus Infection, Serum and Liver Cells.
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27

Fabris, Carlo, Pierluigi Toniutto, Cathryn A. Scott, Edmondo Falleti, Claudio Avellini, Monica Del Forno, Martina Mattiuzzo, Barbara Branca, and Mario Pirisi. "Serum iron indices as a measure of iron deposits in chronic hepatitis C." Clinica Chimica Acta 304, no. 1-2 (February 2001): 49–55. http://dx.doi.org/10.1016/s0009-8981(00)00397-1.

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28

Di Marco, Vito, Marcello Capra, Emanuele Angelucci, Caterina Borgna-Pignatti, Paul Telfer, Paul Harmatz, Antonis Kattamis, et al. "Management of chronic viral hepatitis in patients with thalassemia: recommendations from an international panel." Blood 116, no. 16 (October 21, 2010): 2875–83. http://dx.doi.org/10.1182/blood-2009-11-248724.

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AbstractChelation therapy with new drugs prevents cardiac damage and improves the survival of thalassemia patients. Liver diseases have emerged as a critical clinical issue. Chronic liver diseases play an important role in the prognosis of thalassemia patients because of the high frequency of viral infections and important role of the liver in regulating iron metabolism. Accurate assessment of liver iron overload is required to tailor iron chelation therapy. The diagnosis of hepatitis B virus– or hepatitis C virus–related chronic hepatitis is required to detect patients who have a high risk of developing liver complications and who may benefit by antiviral therapy. Moreover, clinical management of chronic liver disease in thalassemia patients is a team management issue requiring a multidisciplinary approach. The purposes of this paper are to summarize the knowledge on the epidemiology and the risks of transmission of viral infections, to analyze invasive and noninvasive methods for the diagnosis of chronic liver disease, to report the knowledge on clinical course of chronic viral hepatitis, and to suggest the management of antiviral therapy in thalassemia patients with chronic hepatitis B or C virus or cirrhosis.
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29

Girelli, Domenico, Michela Pasino, Julia Goodnough, Elizabeta Nemeth, Annalisa Castagna, Fabiana Busti, Natascia Campostrini, et al. "Hepcidin Suppression Relative to Iron Status in Patients with Chronic Hepatitis C." Blood 112, no. 11 (November 16, 2008): 1860. http://dx.doi.org/10.1182/blood.v112.11.1860.1860.

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Abstract Patients with chronic hepatitis C (CHC) often have increased liver iron deposits, a condition associated with reduced sustained response to antiviral therapy, more rapid progression to cirrhosis, and development of hepatocellular carcinoma. The hepatic hormone hepcidin is a major regulator of iron metabolism that inhibits iron absorption and recycling from erythrophagocytosis. Hepcidin decrease is a possible pathophysiological mechanism of iron overload in CHC, but studies in humans have been hampered so far by the lack of reliable quantitative assays for the 25-amino acid bioactive peptide in serum (s-hepcidin). Using a recently validated immunoassay (Ganz T, Blood 2008, epub Aug 8), we measured s-hepcidin levels in 82 CHC naïve patients and 57 sex-matched healthy controls with rigorous definition of normal iron status. All CHC patients underwent liver biopsy with histological iron score (according to Deugnier YM, Gastroenterology 1992). S-hepcidin was much lower in CHC than in controls (geometric means with 95% CIs: 33.7, 21.5–52.9 versus 90.9, 76.1–108.4 ng/ml, respectively; P<0.001), while both serum ferritin and transferrin saturation were significantly higher in CHC than in controls, as expected. S-hepcidin strongly correlated with serum ferritin in both controls (r=0.741; P<0.001) and CHC patients (r = 0.718; P<0.001). In CHC patients, s-hepcidin also correlated with histological total iron score (r = 0.46; P<0.001), but not with serum interleukin-6 (r = −0.042; P = n.s.). After stratification for serum ferritin quartiles, s-hepcidin levels increased significantly across quartiles in both controls and CHC patients (chi for trend, P<0.001). However, in the latter group s-hepcidin levels were significantly lower than in controls for each corresponding quartile (ANOVA, P<0.001). In the lowest ferritin quartile, s-hepcidin was significantly inversely correlated with viral loading (e.g. serum HCV-RNA IU/ml; r = −0.526; P=0.036), while this association gradually disappeared with increasing ferritin quartiles. These results, together with very recent studies in animal and cellular models (Nishina S, Gastroenterology 2008; Miura K, Hepatology 2008), indicate that though hepcidin regulation by iron stores is maintained in CHC, the suppression of this hormone by HCV is likely an important factor in liver iron accumulation in this condition.
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30

Arber, N., F. M. Konikoff, M. Moshkowitz, M. Baratz, A. Hallak, M. Santo, Z. Halpern, H. Weiss, and T. Gilat. "Increased serum iron and iron saturation without liver iron accumulation distinguish chronic hepatitis C from other chronic liver diseases." Digestive Diseases and Sciences 39, no. 12 (December 1994): 2656–59. http://dx.doi.org/10.1007/bf02087705.

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31

El Hefni, AshrafM, RedaA Kamel Salem, and Huda Ebian. "Iron status and erythropoiesis in chronic hepatitis C patients on hemodialysis." Egyptian Journal of Haematology 40, no. 2 (2015): 80. http://dx.doi.org/10.4103/1110-1067.161293.

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32

Haque, S., B. Chandra, M. A. Gerber, and A. S. F. Lok. "Iron overload in patients with chronic hepatitis C: A clinicopathologic study." Human Pathology 27, no. 12 (December 1996): 1277–81. http://dx.doi.org/10.1016/s0046-8177(96)90337-8.

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33

Chino, S. "Clinical pathological significance of iron metabolism with chronic hepatitis C patients." Hepatology Research 24, no. 3 (November 2002): 245–55. http://dx.doi.org/10.1016/s1386-6346(02)00110-9.

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34

Kugelmas, M., W. D. Carey, and C. J. McClain. "Serum cytokine response to iron reduction in chronic hepatitis C patients." Journal of Trace Elements in Experimental Medicine 13, no. 4 (2000): 327–31. http://dx.doi.org/10.1002/1520-670x(2000)13:4<327::aid-jtra1>3.0.co;2-r.

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35

BOUCHER, E. "Reduction of liver iron content following tratment of chronic hepatitis C." Hepatology 22, no. 4 (October 1995): A397. http://dx.doi.org/10.1016/0270-9139(95)95309-4.

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36

Franchini, Massimo, Giovanni Targher, Franco Capra, Martina Montagnana, and Giuseppe Lippi. "The effect of iron depletion on chronic hepatitis C virus infection." Hepatology International 2, no. 3 (May 8, 2008): 335–40. http://dx.doi.org/10.1007/s12072-008-9076-z.

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37

Mascitelli, L., F. Pezzetta, and M. R. Goldstein. "Insulin resistance and iron perturbation in patients with chronic hepatitis C." Internal Medicine Journal 40, no. 2 (February 2010): 168–69. http://dx.doi.org/10.1111/j.1445-5994.2009.02128.x.

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38

Hino, Keisuke, Sohji Nishina, and Yuichi Hara. "Iron metabolic disorder in chronic hepatitis C: insights from recent evidence." Clinical Journal of Gastroenterology 5, no. 4 (July 31, 2012): 251–56. http://dx.doi.org/10.1007/s12328-012-0323-4.

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39

Hayashi, H. "Iron removal as premedication for treatment of chronic active hepatitis C." Hepatology 19, no. 4 (April 1994): I72. http://dx.doi.org/10.1016/0270-9139(94)90455-3.

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40

Kaito, Masahiko. "Molecular mechanism of iron metabolism and overload in chronic hepatitis C." Journal of Gastroenterology 42, no. 1 (January 2007): 96–99. http://dx.doi.org/10.1007/s00535-006-1983-y.

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41

Indrawanto, Wingsar, Adi Koesoema Aman, and Alwi Thamrin. "THE CORRELATION OF ANEMIA AND HEPCIDIN SERUM LEVELS IN REGULAR HEMODIALYSIS PATIENTS WITH CHRONIC HEPATITIS C IN HAJI ADAM MALIK HOSPITAL MEDAN." INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY 25, no. 2 (April 13, 2019): 218. http://dx.doi.org/10.24293/ijcpml.v25i2.1464.

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Background : End stage renal disease patients who undergo hemodialysis therapy are the high-risk populations who are infected by hepatitis C virus. Some studies have been reported that hepcidin levels decreased in patients with chronic hepatitis C. Hepcidin serum concentrations were also reported to increase in patients with renal failure in the line with increased severity of renal failure, which can cause the accumulation of hepcidin which culminates in anemia because iron deficiency. This Study was to analyze the correlation of anemia and hepcidin serum levels in patients end stage renal disease who undergoing regular hemodialysis with chronic hepatitis C.Methods : This study was an analytic observational with cross sectional design which was conduted on 24 patients end stage renal disease (ESRD) with chronic hepatitis C and 24 patients with ESRD without hepatitis who are undergoing regular hemodialysis theraphy in Haji Adam Malik Hospital, Medan in July – September 2016. All study subjects were examined for full blood count and hepcidin serum levels. The result of the iron status were recorded from the patient’s medical record.Result : In this study, the mean hemoglobin was 8,15±1,44 g/dL, mean hematocrit 25,42±4,53%, median hepcidin levels 29,75 (4,92-359,49) in the patients ESRD with chronic hepatitis C and mean hemoglobin 8,21±1,50 g/dL, mean hematocrit 25,25±4,37%, median hepcidin levels 30,33 (11,65-141,53) in the patients ESRD without hepatitis. In Spearman’s rho test was showed a positive correlation that significant between hepcidin and hemoglobin (r = 0,439, p = 0,032), hepcidin and hematocrit (r = 0,021, p = 0,024) in patients ESRD with chronic hepatitis C.Conclusion : This study showed there was a positive correlation between anemia and hepcidin serum levels in patients ESRD who undergoing regular hemodialysis with chronic hepatitis C.
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Mitsuyoshi, Hironori, Kohichiroh Yasui, Kanji Yamaguchi, Masahito Minami, Takeshi Okanoue, and Yoshito Itoh. "Pathogenic Role of Iron Deposition in Reticuloendothelial Cells during the Development of Chronic Hepatitis C." International Journal of Hepatology 2013 (2013): 1–8. http://dx.doi.org/10.1155/2013/686420.

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Aim. Chronic hepatitis C (CHepC) is frequently associated with hepatic iron overload, yet mechanisms underlying iron-induced liver injury have not been elucidated. We examined the significance of iron deposition in hepatocytes (HC) and reticuloendothelial cells (REC) in CHepC.Methods. Stainable hepatic iron was scored according to the iron deposition pattern in 373 patients. The levels of serum soluble TNF-αreceptor (sTNFR2) and hepatic hepcidin mRNA and the efficacy of phlebotomy were compared among patients with different iron deposition patterns.Results. Serum transaminase levels and hepatic scores of stage, grade, and steatosis were higher in patients with REC iron staining than in those without. REC iron scores were independently associated with advanced stage. Serum sTNFR2 levels were significantly higher in patients with REC iron than in those without. REC iron scores were independently correlated with sTNFR2 levels. Compared with patients without stainable iron, those with iron overload had decreased ratios of hepcidin mRNA to serum ferritin. The efficacy of phlebotomy was greater in patients with REC iron than in those without REC iron.Conclusions. The present results show the importance of REC iron for the development of CHepC and the therapeutic effect of phlebotomy in CHepC.
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43

Kamal, Sanaa, Sara Abdelhakam, Dahlia Ghoraba, Mohamad Amer Mohsen, Ahmed Abdelsalam, Huda Hassan, and Leila Nabeigh. "THE COURSE OF HEPATITIS C INFECTION AND RESPONSE TO ANTI-VIRAL THERAPY IN PATIENTS WITH THALASSEMIA MAJOR AND HEPATITIS C INFECTION: A LONGITUDINAL, PROSPECTIVE STUDY." Mediterranean Journal of Hematology and Infectious Diseases 11, no. 1 (October 30, 2019): e2019060. http://dx.doi.org/10.4084/mjhid.2019.060.

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Background/Aims: The course of hepatitis C infection (HCV) in patients with thalassemia has not been adequately studied and management has not been optimized. The current prospective longitudinal study assessed the clinical course, outcome, progression and management of recently acquired HCV in patients with transfusion dependent thalassemia major versus acute HCV without thalassemia. Methods: A well-characterized cohort of patients with thalassemia and recent HCV infection or recent HCV without thalassemia were enrolled and prospectively followed. The blood transfusion needs and chelating agents were determined. Liver functions tests, HCV-RNA, iron and ferritin levels were measured. Patients with chronic HCV evolution received treatment for HCV. The fibrosis progression rate was determined in chronic HCV patients with or without thalassemia by paired liver biopsies or serial transient elastography (TE), or serum markers of liver fibrosis. Liver iron content (LIC) was assessed by R2 MRI. Results: Self-limited acute HCV was observed in 17% of patients with acute HCV and thalassemia versus 35% of patients without thalassemia (P=0.031). The fibrosis progression rates were significantly higher in patients with chronic HCV and thalassemia compared to those with chronic HCV alone (1.14±0.48) and (0.35±0.14) (P < 0.0001) respectively. A direct linear correlation was observed between the fibrosis progression rate and each of LIC (R=+0.67; P=0.01) and ferritin (R=0.77; P<0.01). In patients with chronic HCV and thalassemia, the sustained virologic response (SVR) to pegylated interferon based therapy and direct antiviral agents (DAAS) were 33% and 82% respectively (P=), while in chronic HCV patients without thalassemia, the SVR rates to PEG-IFN/RBV and DAAs were 51% and 92% respectively. Five patients with concomitant HCV and thalassemia died during the study due to cardiac causes (n=3) and liver cancer (n=2). Conclusions: Patients with acute HCV and thalassemia have low rates of spontaneous resolution of HCV infection and the majority develop chronic HCV. Direct acting antiviral combinations are associated with high SVR rates and low adverse event in treatment naïve and experienced patients with chronic HCV and thalassemia. Liver fibrosis is accelerated in thalassemia patients with chronic HCV, therefore, early diagnosis, treatment with DAAs, adequate iron chelation and non-invasive monitoring liver status are recommended to prevent cirrhosis and hepatocellular carcinoma.
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44

Liang, Quan. "Role of transferrin receptor in hepatitis C viral infection." Infection International 7, no. 2 (June 29, 2018): 33–37. http://dx.doi.org/10.2478/ii-2018-0016.

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Abstract Hepatitis C virus (HCV) is the main pathogen causing chronic hepatitis and primary liver cancer. Various viral proteins and host cell molecules are involved in the HCV cell entry, but the mechanism of infection has not been completely elucidated. The transferrin receptor can act as a receptor for many viruses during cell entry. The transferrin receptor is not only closely related to HCV-induced iron metabolism disorders but also mediates the fusion of HCV with the host cell membrane as a specific receptor for CD81-dependent viral adhesion.
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Yano, Motoyoshi, Hisao Hayashi, Shinya Wakusawa, Toshikuni Takikawa, and Ritsuko Ikeda. "Hepatotoxic iron storage in patients with chronic hepatitis C but no hepatic iron detectable histochemically." Medical Electron Microscopy 30, no. 2 (June 1997): 70–75. http://dx.doi.org/10.1007/bf01545084.

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46

Hasan, Yazan, and Kyle Brown. "Viral eradication restores normal iron status in chronic hepatitis C patients with abnormal iron studies." Annals of Hepatology 19, no. 4 (July 2020): 422–26. http://dx.doi.org/10.1016/j.aohep.2020.03.002.

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47

Association for Study of the Liver (CASL). "Hepatitis C Infection: Its Sequelaie and Outcomes – State-of-the-Art Workshop, September 24 to 25, 1998." Canadian Journal of Gastroenterology 14, suppl b (2000): 49B—59B. http://dx.doi.org/10.1155/2000/176345.

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This report summarizes a state-of the- art workshop held in September 1998 on the “Natural History and Outcome of Hepatitis C Infection”. Sixteen Canadian and two internationally renowned hepatologists were invited. A practical classification of HCV infection served as a framework for the meeting. The concepts of modelling of chronic disease, the epidemiology of HCV infection before the introduction of anti-HCV testing, and the outcome of various forms of chronic hepatitis C in adults and children were presented. Lectures on the outcome of HCV cirrhosis, hepatocellular carcinoma, the role of liver transplantation, the influence of host factors on outcome, iron overload in chronic hepatitis C and possible modification of the natural history by antiviral therapy were followed by discussion and consensus statements pertaining to each presentation. “The European Experience in Assessing Chronic Hepatitis C” was presented by Prof G Dusheiko from the United Kingdom, and Prof Leonard Seeff from the National Institutes of Health (United States) presented “The Epidemiology and Outcome of Hepatitis C Infection in the United States and the World”.
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Sartori, Massimo. "Phlebotomy improves histology in chronic hepatitis C males with mild iron overload." World Journal of Gastroenterology 16, no. 5 (2010): 596. http://dx.doi.org/10.3748/wjg.v16.i5.596.

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49

Sikorska, Katarzyna, and Agnieszka Bernat. "Iron homeostasis and its regulators over the course of chronic hepatitis C." Future Virology 9, no. 9 (September 2014): 831–46. http://dx.doi.org/10.2217/fvl.14.63.

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Calinas, F., M. Oliveira, J. Coimbra, M. Alves, M. Sampaio, C. E. Santo, I. Medeiros, and J. Peneda. "Iron status in chronic hepatitis C and response to treatment with interferon." Journal of Hepatology 28 (1998): 201. http://dx.doi.org/10.1016/s0168-8278(98)80981-1.

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