case_images: PMC7292374_01
case_images: Course of disease and treatment (Case 1).
case_images: IJNRD-13-139-g0002.jpg
case_images: PMC7292374_01_IJNRD-13-139-g0002.jpg
case_images: F0001
case_images: The rise in ALT and AST levels was later revealed to be caused by HCV seroconversion (Figure 1). HCV infection (viral load 3.75 x 105 IU/mL, 5.57 log IU/mL of serum HCV RNA) (Figure 1). HCV RNA genotype testing was conducted using hybridization probe (The Versant HCV Genotype 2.0 Assay (LiPA), Siemens), which revealed HCV genotype 1a. A 7.3-kPa liver stiffness was observed with transient elastography (fibroscan), which was categorized as F1-F2 (mild-moderate liver fibrosis) (Figure 1). Evaluation immediately after (March 2019), at 12 weeks (June 2019), and at 24 weeks (October 2019) following treatment cessation showed no HCV recurrence (Figure 1).
case_images: PMC7292374_02
case_images: Course of disease and treatment (Case 2).
case_images: IJNRD-13-139-g0003.jpg
case_images: PMC7292374_02_IJNRD-13-139-g0003.jpg
case_images: F0002
case_images: ALT 133 IU/L, GGT 142 U/L) in September 2015 (Figure 2). HCV RNA genotype testing was conducted using hybridization probe (The Versant HCV Genotype 2.0 Assay (LiPA), Siemens), revealing HCV genotype 1a. A 4.8-kPa liver stiffness was observed with transient elastography (fibroscan), which was categorized as F0-F1 (mild liver fibrosis) (Figure 2). HCV RNA with real-time PCR immediately after, at 12 weeks, and at 24 weeks after treatment initiation showed no HCV RNA (Figure 2).