International Journal of Hepatology
Volume 2018 (2018), Article ID 4136253, 8 pages
https://doi.org/10.1155/2018/4136253

Research Article

Sofosbuvir Based Regimens in the Treatment of Chronic Hepatitis C with Compensated Liver Cirrhosis in Community Care Setting

Vijay Gayam,¹ Amrendra Kumar Mandal,¹ Mazin Khalid,¹ Osama Mukhtar,¹ Arshpal Gill,¹ Pavani Garlapati,¹ Mowyad Khalid,² and Mohammed Mansour¹

¹Department of Medicine and Gastroenterology, Interfaith Medical Center, 1545 Atlantic Avenue, Brooklyn, NY 11213, USA
²Department of Medicine, Wayne State University/Detroit Medical Center, Detroit, Michigan, USA

Correspondence should be addressed to Vijay Gayam; vgayam@interfaithmedical.com

Received 9 April 2018; Accepted 19 July 2018; Published 1 August 2018

Academic Editor: Dirk Uhlmann

Copyright © 2018 Vijay Gayam et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract.

Background. Direct-acting antiviral (DAA) drugs have been highly effective in the treatment of chronic hepatitis C (CHC) infection. We aim to evaluate the treatment response of Sofosbuvir based DAA in CHC patients with compensated liver cirrhosis as limited data exists in the real-world community setting. Methods. All the CHC patients with compensated liver cirrhosis treated with Sofosbuvir based DAAs between January 2014 and December 2017 in a community clinic setting were retrospectively analyzed. Pretreatment baseline patient characteristics, treatment efficacy with the sustained virologic response at 12 weeks posttreatment (SVR12), and adverse reactions were assessed. Results. One hundred and twelve patients with CHC infection and concurrent compensated cirrhosis were included in the study. Black patients represented the majority of the study population (64%). Eighty-seven patients were treated with Ledipasvir/Sofosbuvir (LDV/SOF) ±Ribavirin and 25 patients were treated with Sofosbuvir/Velpatasvir (SOF/VEL). Overall, SVR 12 after treatment was achieved in 90% in patients who received one of the two DAA regimens (89.7% in LDV/SOF group and 92% in SOF/VEL group). SVR 12 did not vary based on age, sex, body mass index, baseline HCV viral load, HCV/HIV coinfection, type of genotype, and prior treatment status. Apart from a low platelet count, there were no other factors associated with a statistical difference in SVR 12(p=0.002) between the two regimens. Fatigue (35%) was the most common adverse effect and no patients discontinued treatment due to adverse effects. Conclusion. In the community care setting, Sofosbuvir based DAAs are safe, effective with high overall SVR, and well tolerated in patients with CHC patients with compensated liver cirrhosis.

1. Introduction

Anywhere between 3.2 and 5 million people in the United States have a chronic hepatitis C (CHC) infection which if untreated can develop into cirrhosis, hepatocellular carcinoma, and death [1, 2]. CHC is the most common indication for a liver transplantation and a more common cause of death than all other notifiable infectious etiologies combined in the United States [3, 4].

Successful treatment of CHC, also described as a sustained virological response (SVR), is defined as an absence of detectable HCV RNA 12 weeks after the completion of treatment. CHC patients who achieve SVR have both lower rates of complications and lower overall mortality [5]. Until recently, CHC treatment was primarily based on interferon-based regimens, but disappointing response rates, particularly amongst patients with advanced liver disease, necessitated the need for a new regimen [6].

Newer drugs that directly inhibit the virus replication cycle have led to the advent of oral HCV treatment regimens known as direct-acting antiviral (DAAs) [7]. In existing clinical trials, DAA regimens have demonstrated cures rates over 90% of patients who have chronic CHC infection and concurrent cirrhosis.

Due to the relative novelty of DAA regimens, there is a paucity of literature establishing safety, tolerability, and efficacy of DAA in the real-world community care setting. As a result, we aim to analyze DAA’s safety, tolerability, and efficacy in an inner-city community care setting with an emphasis on the most commonly used DAA in patients with cirrhosis.

2. Materials and Methods

The study protocol was approved by the Institutional Review Board (IRB) and the patients were recruited from a community hospital: Interfaith Medical Center

2.1. Patients

The 112 consecutive patients with CHC treated between January 2015 and December 2017 were included in this retrospective cohort study and received at least twelve weeks of treatment with one of the recommended combination regimens in standard doses for chronic HCV infection. Two different treatment regimens were used in our study, Ledipasvir (LDV) 90 mg/day+ Sofosbuvir (SOF) 400 mg/day ±Ribavirin (RBV) 1000 mg/day if <75kg and 1200 mg/day if ≥75kg, and Sofosbuvir (SOF) 400 mg/day+ Velpatasvir (VEL) 100 mg/day. Duration of treatment ranged from 12 weeks (n=98) to 24 weeks (n=14) depending on prior treatment status and existing cirrhosis.

2.2. Study Assessments

Treatment safety and tolerability were assessed by reviewing documented adverse events, treatment completion rates, reduction in the dosage, and discontinuation of medications. Laboratory studies were conducted both pretreatment and posttreatment. Laboratory values were then compared to look for any abnormalities associated with antiviral therapy. A diagnosis of liver cirrhosis was based on the amalgamation of clinical symptoms, laboratory parameters including FibroSure score ≥ 0.75, imaging modalities (ultrasonography and or computed tomography scan), and histopathology when indicated. We included compensated cirrhosis, defined as the absence of ascites, jaundice, hepatic encephalopathy and variceal bleeding according to the American Association for the Study of Liver Diseases, in this study.

Treatment response was assessed with HCV RNA viral load (IU/ mL) at each of 4 weeks after initiation of treatment, completion of treatment, and 12 weeks after completion of treatment. Viral load was assessed using COBAS® AmpliPrep/COBAS® TaqMan® HCV Quantitative Test, v2.0 (Roche molecular diagnostics) with the lower limit of quantification (LLOQ) of HCV RNA 15 IU/ml. SVR 12 was defined as an undetectable viral load 12 weeks after the completion of treatment.

2.3. Statistical Analysis

The SPSS® statistics software package (IBM SPSS® statistics version 21, USA) was used for statistical analysis. Values were expressed as mean ± SD and mean quantitative values were analyzed using Student’s t-test. Differences in qualitative values were analyzed by Chi-square test. All p values were two-tailed and p-value < 0.05 was considered significant. One-way analysis of variance (ANOVA) was used to determine whether there were differences among the group means. Multivariable logistic regression was performed only in variables with a p-value < 0.05 in univariate analysis.

3. Results

3.1. Baseline Characteristics

Baseline characteristics are shown in Table 1. Mean age of the patients in the study was 60.7 years with age, ranging from 28 to 82 years. The majority of the patients were males 67 (75%), black 71(63.4%), and treatment-naive (76.8%). Genotype 1 was predominant, consisting of over 89.3% of the study population. Nine (23.2%) patients had received prior treatment. Thirty-five patients (31.3%) had a history of diabetes; 51 (45.5%) had hypertension; 12 (10.7%) patients had coronary artery disease, 24 patients had HCV/HIV coinfection. None of the patients had a hepatocellular carcinoma, previous liver transplant, or decompensated cirrhosis.

Table 1: Demographic and clinical characteristics of patients at baseline by treatment regimen.

Characteristics
All patients 
(n = 112)
Treatment Regimens
p-value

LDV/SOF
SOF/VEL

(n = 87)
(n = 25)

Sex

0.629

    Male
67 (59.8)
51 (58.6)
16 (64.0)

    Female
45 (40.2)
36 (41.4)
9 (36.0)

Age (years)
60.7 (28-82)
61.6 (28-82)
57.2 (34-73)
0.076

Age group (Years)

0.234

    < 65
74 (66.1)
55 (63.2)
19 (76.0)

    ≥ 65
38 (33.9)
32 (36.8)
6 (24.0)

BMI (Kg/m²)
29.0 (18.5-47.0)
28.7 (18.5-47.0)
30.2 (20-43)
0.242

BMI (Kg/m²)

0.488

    < 30
65 (58.0)
52 (59.8)
13 (52.0)

    ≥ 30
47 (42.0)
35 (40.2)
12 (48.0)

HCV Genotype

0.131

    1a
66 (58.9)
52 (59.8
14 (56.0)

    1b
34 (30.4)
28 (32.2)
6 (24.0)

    2
5 (4.5)
4 (4.6)
1 (4.0)

    3
3 (2.7)
2 (2.3)
1 (4.0)

    4
4 (3.6)
1 (1.1)
3 (12.0)

HCV RNA (IU/mL)

0.330

    < 800,000
31 (27.7)
26 (29.9)
5 (20.0)

    ≥ 800,000
81 (72.3)
61 (70.1)
20 (80.0)

Prior treatment

0.086

    Naïve
86 (76.8)
70 (80.5)
16 (64.0)

    Experienced
26 (23.2)
17 (19.5)
9 (36.0)

Comorbidities

    Diabetes
35 (31.3)
25 (28.7)
10 (40.0)
0.284

    Hypertension
51 (45.5)
37 (42.5)
14 (56.0)
0.233

    Coronary artery disease
12 (10.7)
9 (10.3)
3 (12.0)
0.728

    Kidney disease
9 (8.0)
8 (9.2)
1 (4.0)
0.681

    Chronic anemia
5 (4.5)
2 (2.3)
3 (12.0)
0.073

    HIV seropositive
24 (21.4)
21 (24.1)
3 (12.0)
0.192

MELD score

0.195

    < 10
62 (55.4)
51 (58.6)
11 (44.0)

    ≥ 10
50 (44.6)
36 (41.4)
14 (56.0)

Laboratory tests

    Hemoglobin (g/dL)
13.4 (9.2-17.5)
13.5 (9.2-17.5)
13.0 (10.0-16.0)
0.278

    Platelets (x1000/mL)
140.7 (23-316)
143.4 (43-316)
131.5 (23-216)
0.371

    Albumin (g/dL)
3.5 (1.3-4.7)
3.5 (1.3-4.7)
3.5 (2.2-4.5)
0.899

    AST (IU/L)
82.3 (16-210)
83.3 (16-210)
78.9 (20-179)
0.639

    ALT (IU/L)
77.8 (12-264)
79.5 (12-264)
72.1 (13-200)
0.510

    Bilirubin (mg/dL)
1.2 (0.3-4.9)
1.2 (0.3-4.9)
1.1 (0.5-3.2)
0.752

Data are presented as mean (range) or number (percentage).

BMI, body mass index; HCV, hepatitis C virus; RNA, ribonucleic acid; APRI, AST-to-platelet ratio index; MELD, model for end-stage liver disease; AST, aspartate transaminase; and ALT, alanine transaminase.

3.2. Treatment Regimens

Among the 112 patients with CHC infection, 87(77.7%) patients were treated with Ledipasvir/Sofosbuvir, and 25 (22.3%) were treated with Sofosbuvir/Velpatasvir (Figure 1).

Figure 1: Treatment regimens.

3.3. Overall Virologic Response to Treatments

The overall sustained virological response (SVR) on completion of treatment was 90 %. SVR 12 in the two treatment groups is depicted in Figure 2. In the univariate analysis, there were characteristics noted in the patients who achieved SVR12 as compared to those who did not achieve SVR. Higher mean BMI, higher Child-Pugh score, low mean platelet count, low mean albumin, and low mean bilirubin level were all more likely to be seen in patients who achieved SVR 12 in the univariate analysis. After adjusting baseline characteristics in multivariable logistic regression models, only low platelet count was found as a significant predictor of treatment response (p-value =0.020). Interestingly, SVR was not affected by HCV RNA levels or previous treatment status (Table 2).

Table 2: Demographic and clinical characteristics of patients at baseline by treatment response.

Characteristics
All patients 
(N =112)
Treatment Response
Univariate Analysis 
p-value
Multivariate Analysis 
p-value

SVR
No SVR

(n =101)
(n =11)

Age (years)
60.7 (28-82)
60.7 (28-82)
60.0 (45-67)
0.797
NA

Age group

0.747
NA

    < 65
74 (66.1)
66 (65.3)
8 (72.7)

    ≥ 65
38 (33.9)
35 (34.7)
3 (27.3)

Sex

0.194
NA

    Male
67 (59.8)
58 (57.4)
9 (81.8)

    Female
45 (40.2)
43 (42.6)
2 (18.2)

BMI (Kg/m²)
29.0 (18.5-47.0)
29.4 (19.0-47.0)
25.8 (18.5-32.5)
0.050
0.085

BMI (Kg/m²)

0.353
NA

    < 30
65 (58.0)
57 (56.4)
8 (72.7)

    ≥ 30
47 (42.0)
44 (43.6)
3 (27.3)

HCV Genotype

0.150
NA

    1a
66 (58.9)
57 (56.4)
9 (81.8)

    1b
34 (30.4)
34 (33.7)
0

    2
5 (4.5)
4 (4.0)
1 (9.1)

    3
3 (2.7)
3 (3.0)
0

    4
4 (3.6)
3 (3.0)
1 (9.1)

HCV RNA (IU/mL)

1.000
NA

    < 800,000
31 (27.7)
28 (27.7)
3 (27.3)

    ≥ 800,000
81 (72.3)
73 (72.3)
8 (72.7)

Prior treatment

1.000
NA

    Naïve
86 (76.8)
77 (76.2)
9 (81.8)

    Experienced
26 (23.2)
24 (23.8)
2 (18.2)

Comorbidities

    Diabetes
35 (31.3)
31 (30.7)
4 (36.4)
0.738
NA

    Hypertension
51 (45.5)
46 (45.5)
5 (45.5)
0.995
NA

    Coronary artery disease
12 (10.7)
12 (11.9)
0
0.604
NA

    Kidney disease
9 (8.0)
8 (7.9)
1 (9.1)
1.000
NA

    Chronic anemia
5 (4.5)
4 (4.0)
1 (9.1)
0.410
NA

    HIV Seropositive
24 (21.4)
20 (19.8)
4 (36.4)
0.245
NA

MELD score

0.060
NA

    < 10
62 (55.4)
59 (58.4)
3 (27.3)

    ≥ 10
50 (44.6)
42 (41.6)
8 (72.7)

Laboratory tests

    Hemoglobin (g/dL)
13.4 (9.2-17.5)
13.3 (9.2-17.5)
13.9 (11.6-15.9)
0.276
NA

    Platelets (x1000/mL)
140.7 (23-316)
146.4 (23-316)
88.6 (43-177)
0.002
0.020

    Albumin (g/dL)
3.5 (1.3-4.7)
3.6 (1.3-4.7)
3.2 (2.2-4.1)
0.042
0.873

    AST (IU/L)
82.3 (16-210)
81.6 (16-198)
88.7 (42-210)
0.585
NA

    ALT (IU/L)
77.8 (12-264)
77.2 (12-204)
83.9 (27-264)
0.666
NA

    Bilirubin (mg/dL)
1.2 (0.3-4.9)
1.1 (0.3-3.9)
1.6 (0.8-4.9)
0.043
0.821

Data are presented as mean (range) or number (percentage).

Only variables with the p-value < 0.05 in univariate analysis were assessed.

BMI, body mass index; HCV, hepatitis C virus; RNA, ribonucleic acid; APRI, AST-to-platelet ratio index; MELD, model for end-stage liver disease; AST, aspartate transaminase; and ALT, alanine transaminase.

Figure 2: Treatment response in both groups by overall SVR 12.

3.4. Virologic Response in LDV/SOF Group

In this group, 78(89.7%) achieved SVR 12. HCV viral load and type of HCV genotype did not have any impact on overall SVR. Additional comorbidities including diabetes mellitus, chronic kidney disease, and HIV seropositivity did not impact SVR rates as shown in Table 3.

Table 3: SVR 12 rates in patients receiving LDV/SOF by population subgroup.

Response
SVR 12 Rate
Univariate Analysis 
p-value
Multivariate Analysis 
p-value

Overall
78/87 (89.7)

Age group

1.000
NA

    < 65
49/55 (89.1)

    ≥ 65
29/32 (90.6)

Sex

1.000
NA

    Male
44/51 (86.3)

    Female
34/36 (94.4)

BMI (Kg/m²)

0.304
NA

    < 30
45/52 (86.5)

    ≥ 30
33/35 (94.3)

HCV Genotype

0.009
0.983

    1a
45/52 (86.5)

    1b
28/28 (100)

    2
3/4 (75.0)

    3
2/2 (100)

    4
0/1 (0)

HCV RNA (IU/mL)

1.000
NA

    < 800,000
23/26 (88.5)

    ≥ 800,000
55/61 (90.2)

Prior treatment

0.682
NA

    Naïve
62/70 (88.6)

    Experienced
16/17 (94.1)

Comorbidities

    Diabetes
21/25 (84.0)
0.272
NA

    Hypertension
33/37 (89.2)
1.000
NA

    CAD
9/9 (100)
0.589
NA

    Kidney disease
7/8 (87.5)
1.000
NA

    Chronic anemia
2/2 (100)
1.000
NA

    HIV Seropositive
18/21 (85.7)
0.681
NA

MELD Score

0.154
NA

    < 10
48/51 (94.1)

    ≥ 10
30/36 (83.3)

ALT (IU/L)

0.678
NA

    < 40
17/18 (94.4)

    ≥ 40
61/69 (88.4)

Data presented as number/total number (percent).

Only variables with the p-value < 0.05 in univariate analysis were assessed.

BMI, body mass index; HCV, hepatitis C virus; RNA, ribonucleic acid; APRI, AST-to-platelet ratio index; MELD, model for end-stage liver disease; and ALT, alanine transaminase

3.5. Virologic Response in SOF/VEL Group

In this treatment group, 23 (92%) achieved SVR (Table 4). Although this value is encouraging, it may not be truly significant due to a small sample size. HCV viral load and type of HCV genotype did not have any impact on overall SVR. Additional comorbidities including diabetes mellitus, chronic kidney disease, and HIV seropositivity did not impact SVR rates as shown in Table 4.

Table 4: SVR 12 rates in patients receiving SOF/VEL by population subgroup.

Response
SVR 12 Rate
Univariate Analysis 
p-value
Multivariate Analysis 
p-value

Overall
23/25 (92.0)

Age group

1.000
NA

    < 65
17/19 (89.5)

    ≥ 65
6/6 (100)

Sex

0.520
NA

    Male
14/16 (87.5)

    Female
9/9 (100)

BMI (Kg/m²)

1.000
NA

    < 30
12/13 (92.3)

    ≥ 30
11/12 (91.7)

HCV Genotype

0.789
NA

    1a
12/14 (85.7)

    1b
6/6 (100)

    2
1/1 (100)

    3
1/1 (100)

    4
3/3 (100)

HCV RNA (IU/mL)

1.000
NA

< 800,000
5/5 (100)

≥ 800,000
18/20 (90.0)

Prior treatment

1.000
NA

    Naïve
15/16 (93.8)

    Experienced
8/9 (88.9)

Comorbidities

    Diabetes
10/10 (100)
0.500
NA

    Hypertension
13/14 (92.9)
1.000
NA

    CAD
3/3 (100)
1.000
NA

    Kidney disease
1/1 (100)
1.000
NA

    Chronic anemia
2/3 (66.7)
0.230
NA

    HIV Seropositive
2/3 (66.7)
0.230
NA

MELD Score

0.487
NA

    < 10
11/11 (100)

    ≥ 10
12/14 (85.7)

ALT (IU/L)

1.000
NA

    < 40
4/4 (100)

    ≥ 40
19/21 (90.5)

Data presented as number/total number (percent).

BMI, body mass index; HCV, hepatitis C virus; RNA, ribonucleic acid; APRI, AST-to-platelet ratio index; MELD, model for end-stage liver disease; and ALT, alanine transaminase.

3.6. Safety

Only a small percentage of patients developed minor side effects from DAA treatment, and none required discontinuation of therapy. Fatigue, headache, rash, and thrombocytopenia were the most common adverse events observed. Anemia was seen only in patients treated with LDV/SOF + Ribavirin combination. There were no serious adverse events seen amongst all regimens. There was no statistically significant difference of adverse events noted between the two treatment groups. A complete list of adverse events is shown in Table 5.

Table 5: Treatment adverse events.

Adverse event
Treatment Regimen
p-value

LDV/SOF
SOF/VEL

Fatigue
26 (29.9)
9 (36.0)
0.561

Insomnia
1 (1.1)
1 (4.0)
0.398

Headache
6 (6.9)
0
0.335

Nausea
5 (5.7)
3 (12.0)
0.374

Abdominal pain
1 (1.1)
0
1.000

Skin rash
7 (8.0)
0
0.346

Arthralgia
3 (3.4)
2 (8.0)
0.310

Thrombocytopenia
6 (6.9)
2 (8.0)
1.000

Data presented as number (percent).

4. Discussion

Antiviral therapy has rapidly evolved for the treatment of chronic HCV infection. The primary endpoint is to achieve SVR 12, which in turn diminishes the risk of decompensation, hepatocellular carcinoma, and death.

DAAs offer the most effective regimens for the majority of HCV infected patients. Selection of regimens is primarily based on the genotype, cirrhosis status, and other various individual patient factors. The efficacy of DAAs for patients with compensated cirrhosis is now well validated [8–10]. We studied the two most commonly used regimens, LDV/SOF and SOF/VEL.

We noted an SVR of 89.7% in LDV/SOF group which is comparable to ION-2 trial where SVR of 86% was reported in patients with cirrhosis [8]. Another trial (SIRIUS trial) reported a higher SVR of 97% (HCV genotype 1) in compensated cirrhosis. This discrepancy may be explained by the difference in duration of therapy; the SIRIUS trial patients each received 24 weeks of therapy versus our study in which patients received only 12 weeks of therapy [11].

Our second regimen was SOF/VEL which is currently approved for the treatment of all genotypes (as per AASLD guidelines). In the present study, 23 patients (92%) achieved SVR in SOF/VEL which is similar to the study by Asselah et al. They reported SVR in 96% of patients with HCV related cirrhosis after 12 weeks of treatment [12]. Our study also showed SVR rates consistent with ASTRAL-3 and ASTRAL-1 trial. These trials also used SOF/VEL regimen in a similar group of patients with overall SVR rate of 88% and 98%, respectively [12, 13]. Our study also exhibited similar response rates to the recent POLARIS-3 trial in which cirrhotic patients were given SOF/VEL for 12 weeks. They demonstrated an excellent SVR of 96 % in HCV genotype 3 infections [14].

Thrombocytopenia was associated with a lower SVR (p=0.02) in our study. Several studies have documented that chronic HCV infection is strongly associated with thrombocytopenia. Between 64% and 76% of patients with fibrosis and cirrhosis related to chronic HCV infections exhibited thrombocytopenia, as compared to only 6% in noncirrhotic patients [15, 16]. Thrombocytopenia is strongly related to the degree of liver fibrosis owing to low thrombopoietin levels and splenic sequestration of blood cells as a direct result of elevated portal pressure, especially among patients with advance fibrosis or cirrhosis [17–19]. Thrombocytopenia has also been associated with a higher risk for cirrhosis-related morbidity and mortality [20, 21]. Thus, early treatment of HCV infection before the development of thrombocytopenia may improve overall treatment outcomes.

Our study was supported by Suwantarat et al. who reported that thrombocytopenia was associated with lower SVR (P=0.05) [22]. In contrast to our study, they used interferon-based therapy and greater cytopenia was hypothesized to be a marker for greater TNF activity, which translated into a significant SVR variation. Importantly, several studies including Coverdale et al. and Taniguchi et al. reported that improvement in platelet count correlated with the regression of hepatic fibrosis following SVR 12 among patients with chronic HCV infection [23, 24].

The present study had a high HIV/HCV coinfection rate of 21.4%, but there was still a high overall SVR. This is consistent with the literature, as Osinusi et al. also demonstrated an overall high SVR (97%) in patients with HIV/HCV coinfection [25].

There were no major adverse effects in our study leading to a discontinuation of therapy, which was also noted in the ION-1 trial in which no patient discontinued LDV/SOF. Common adverse events in the present study were fatigue, headache, insomnia, and nausea. ASTRAL-1, 2, and 3 with SOF/VEL also had similar adverse effects [12, 13].

We noted an excellent sustained virological response rate in patients with compensated cirrhosis irrespective of genotypes in both treatment groups, and these results are consistent with the landmark literature described above. Our study is distinct from most studies in current literature as it establishes real-world effectiveness, tolerability, and safety of Sofosbuvir based regimens in CHC patients with compensated cirrhosis. This is in contrast to the literature, which still relies heavily on clinical trials. Limitations of the study are the small sample size and retrospective nature.

5. Conclusion

In the community care setting, Sofosbuvir based DAAs remain a safe, effective, and well tolerated in patients with chronic CHC patients with compensated liver cirrhosis.

Abbreviations

CHC: | Chronic hepatitis C
HCV: | Hepatitis C virus
HCC: | Hepatocellular cancer
DAAs: | Direct-acting antivirals
GT: | Genotype
SOF: | Sofosbuvir
RBV: | Ribavirin
LDV: | Ledipasvir
VEL: | Velpatasvir
SVR12: | Sustained virologic response at 12 weeks posttreatment
APRI: | Aspartate aminotransferase-to-platelet ratio index
ESLD: | End stage liver disease.

Data Availability

The Excel sheet data used to support the findings of this study have not been made available because of the hospital policy. Institutional Review Board does not allow the authors to share data with any journal.

Disclosure

An abstract of this article is presented as a poster at NY Department of Health Viral Hepatitis Symposium, May 2018.

Conflicts of Interest

The authors declare no conflicts of interest.

Authors’ Contributions

Vijay Gayam, M.D., made substantial contribution to conception and design of the study, data acquisition, analysis, interpretation of the data, and drafting of the manuscript, performed critical reviews, communicated with the journal, and addressed comments from the reviewers. Amrendra Kumar Mandal, M.D., and Mazin Khalid, M.D., performed data acquisition and provided assistance with interpretation of data and drafting of the manuscript. Osama Mukhtar, M.D., and Mowyad Khalid, M.D., made substantial contribution to statistical data analysis and interpretation of the data. Pavani Garlapati and Arshpal Gill have contributed in the acquisition of the patient data. Dr. Mohammed Mansour made substantial contribution to critical review of the abstract. All the authors vouch for the veracity and completeness of the data presented and agreed to submit the manuscript for publication.

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