Chronic blood-borne viral hepatitis in a tertiary hospital in Al-Baha, Saudi Arabia: epidemiology, liver enzyme correlations, and treatment outcomes

Abstract

Background

In Al-Baha viral hepatitis in clinical settings has not been adequately investigated. This study examined chronic HBV and HCV infections and their treatment outcomes among patients at King Fahd Hospital in Al-Baha.

Methods

Patients records were retrieved anonymously for clinical, demographic, virological and biochemical data from January 2019 to December 2022.

Results

Of 148 patients (mean age was 49.6 ± 13.2; 56.8% males) 80.4% had HBV, 18.2% had HCV while 1.4% had dual infection. HBV viral loads correlated with ALT levels (r = 0.317, p = 0.001) while HCV viral loads did not. (r = 0.246, p = 0.23). Among the 148 cases, 144 were clinically classified as chronic HBV infections (n = 117), chronic HCV infections (n = 25), acute HCV infection (n = 1). The remaining cases were unclassified HCV infections (n = 4) or dual HBV/HCV infection (n = 1). Cirrhosis was observed in 6% of HBV cases and 18.5% of HCV cases. Viral load suppression with ALT levels either maintained at baseline or normalized in most cases occurred in 93.3% of HBV patients (n = 15) treated with tenofovir alafenamide and in all those (n = 8) treated with entecavir with generally unchanging ALT levels. All HCV patients (n = 16) achieved viral clearance after 12 weeks treatment course; sofosbuvir–daclatasvir (n = 14) was highly effective though 2 showed elevated post-treatment ALT.

Conclusions

Chronic HBV and HCV infections remain clinical challenge in Al-Baha. Current antivirals showed strong efficacy. Cirrhosis and post- treatment liver abnormalities underscores the need for continuing monitoring, improved prevention and broadened hepatitis health care.

Background

The threat of hepatitis B virus (HBV) and hepatitis C virus (HCV) remains enormous owing to the life-threatening complications that result from their infections. According to WHO, 254 million people live with HBV and 50 million with HCV worldwide [1]. Viral hepatitis is the second leading infectious cause of death, causing 1.3 million deaths annually, 83% from HBV and 17% from HCV [1]. Currently there is a protective vaccine against HBV while vaccine to HCV infection is unavailable [2]. Even though direct-acting antiviral therapy (DAAs) to HCV infections can cure over 95% of HCV infections, yet access to diagnosis and treatment remains limited [3].

In Saudi Arabia the mass immunization program initiated in 1990 has led to a dramatic decline in prevalence HBsAg [4–6]. In 2017, the overall HBsAg prevalence was 1.7%, with 0.1% among 5-year-olds and under 0.1% among infants. Still, HBV caused 490 cases of decompensated cirrhosis, 1,500 hepatocellular carcinoma cases, and 1,740 liver-related deaths [7]. This suggests that HBV infection remains a significant health problem. Despite nearly four decades of control efforts and direct acting antiviral (DAA) therapy HCV still affects an estimate of 0.7% overall and roughly 100,000 live with active infection, majority untreated and therefore at risk of cirrhosis and hepatocellular carcinoma (HCC) [6–8]. This is likely due to gaps in early diagnosis and subsequent progress to advanced chronic infection and cirrhosis.

Previous research focused mainly on urban Saud Arabia leaving regional variation, particularly in Al-Baha region under- investigated. Assessing treatment outcomes in routine practice helps determine effectiveness, adherence and the burden of complications in everyday settings.

Methods

This retrospective cross-sectional study investigated chronic blood-borne viral hepatitis and treatment outcomes among patients who attended a major hospital in Al-Baha city between January 2019 and December 2022 for assessment, follow-up, and treatment. This study design enabled assessment of the regional burden of viral hepatitis utilizing existing clinical data, given the logistical constraints of a prospective study. Chronic HBV is defined by persistent HBsAg for ≥ 6 months or ongoing HBV DNA beyond the acute window, with or without biochemical or histological liver disease [9]. Chronic HCV is defined by the presence of anti-HCV antibodies and detectable HCV RNA with biochemical or histological evidence of chronic hepatitis beyond 4–6 months [10]. All serologically and molecularly confirmed HBV and HCV infected cases which attended during the study period were included in this study. While focusing on chronic infections, 4 unclassified HCV cases and 1 acute HCV case were analyzed for demographic purposes (Fig. 1). The unclassified cases were likely chronic but, due to incomplete documentation, were conservatively categorized as unclassified. We excluded these cases from analyses of chronic disease progression and treatment outcomes. Patients with liver diseases not caused by HBV or HCV were excluded. The four-year study period was chosen to capture consecutive patients with HBV and HCV infections who presented to the hospital within a sufficiently long and recent timeframe and to ensure an adequate number of cases for meaningful statistical analysis, maintain consistency in diagnostic and management practices, and reduce selection bias.

Fig. 1.

Patient clinical classification and antiviral therapy

King Fahd Hospital is designated as a tertiary care center by the Ministry of Health (MOH), with a capacity of over 400 beds, and serves as the main referral hospital for the seven governorates of the Al-Baha region. The Al-Baha region is located in the southwest of the Kingdom of Saudi Arabia, between the holy city of Makkah and the Aseer region. It has a population of 461,360 and covers an area of 10,362 square kilometers [11]. The region consists of mountainous governorates, characterized by cold winters and mild summers, as well as lowland coastal governorates in Tehama, which experience mild winters and hot summers.

Patient records were retrieved in anonymized form and reviewed for demographic, clinical, and laboratory data, including HBsAg, HBeAg, Anti-HBe, anti-HCV, HBV and HCV viral load and liver function tests. Treatment-related data was inconsistently available. Records of antiviral regimen and baseline laboratory values were complete for the treated patients. Nonetheless, data on treatment duration, adherence, and follow-up viral load for sustained virological response (SVR) were incomplete in a number of cases because of the retrospective nature of the study and lack of follow-up data after treatment course completion. The study protocol was approved by the Ethics Research Committee (ERC) of the Faculty of Medicine, Al-Baha University, in accordance with the Declaration of Helsinki (approval number: REC/MIC/BU-FM/2022/63R). Access to patient records was granted with written authorization from King Fahd Hospital.

Whole blood samples were collected in a plain tube for serological testing and in an EDTA tube when plasma was required for nucleic acid testing. Serum or plasma were separated and tested immediately. All testing was performed according to the instructions of the manufacturer.

HBsAg primary and confirmatory testing was performed using a commercial ELISA (DS-ELA-0.01 HBsAg, Diagnostic system, Germany), HBeAg and anti-HBe testing were accomplished using a commercial Monolisa HBe Ag-Ab PLUS ELISA (Bio-Rad, France), while primary anti-HCV testing was carried out using a commercial fourth generation (EIAgen HCV Ab (v.4), ADALTIS, Italy Y) and confirmatory testing was achieved using a third-generation immune assay INNO-LIA HCV Score (Fujirebia, Belgium).

Levels of total and direct bilirubin, alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), gamma-glutamyl transferase (GGT) were measured using a quantitative enzymatic colorimetric assay (Beckman Coulter ALT Assay Kit, Beckman Coulter-Ireland Y).

The HBV viral load was determined using a commercial real-time PCR-based assay (Abbott Real Time Viral Load Assay, Abbott, Germany Y). The assay is an in vitro real-time PCR for the quantification of hepatitis B virus DNA in human plasma or serum from HBV-infected individuals with 100% specificity and a limit of detection of 10 IU/mL for the 0.5mL sample preparation procedure.

The HCV viral load was determined using a commercial real-time PCR-based assay (Abbott Real Time Viral Load Assay, Abbott, Germany Y). The assay is an in vitro reverse transcription polymerase chain reaction (RT-PCR) for the quantitation HCV-RNA in human plasma or serum from HCV-infected individuals. The assay has 100% specificity and a 30 IU/mL limit of detection for the 0.2mL sample preparation procedure. Both assays were performed according to the manufacturer’s instructions.

Data was coded, entered, and analyzed using IBM SPSS Statistics for Windows, Version 25.0 (IBM Corp., Armonk, NY, USA, 2017). Continuous variables were summarized as means with standard deviations using independent-samples t-tests, with p < 0.05 considered statistically significant. Categorical variables were expressed as absolute and relative frequencies. Associations between independent and dependent variables were evaluated using the chi-square test, with statistical significance defined as p < 0.05. Correlation analyses were conducted following logarithmic transformation of values to normalize distributions and reduce skewness.

Results

A total of 148 patients with HBV and/or HCV infection attended the hospital during the four-year study period, corresponding to a mean annual incidence of 37.5 cases. The patients mean age was 49.6 ± 13.2 years (range: 20–88), distributed across three age groups: 20–40, 41–60, and > 60 years and included 84 males (56.8%) and 64 females (43.2%) (Fig. 2).

Fig. 2.

Demographic characteristics of patients with HBV and HCV infections

Of all patients, 117 (80.4%) had HBV infection, 30 (18.2%) had HCV infection while 1 (1.4%) patient had dual HBV/HCV infections. The rate of infection varied, although insignificantly (p = 0.20), between males and females and age groups (Fig. 2).

HBV infection was significantly more common than HCV among males across age groups (p = 0.02), particularly in the 41–60-year age group (91.7%). Among females, HBV and HCV prevalence did not differ significantly (p = 0.32) (Fig. 3).

Fig. 3.

HBV and HCV infection rates by age and sex. * One patient had dual HBV/HCV infection not included in analysis

With progress of age, HBV infection rates increased, albeit insignificantly (p > 0.05) among males but decreased among females, while HCV infection rates significantly decreased (p = 0.02) among males and insignificantly (p > 0.05) increased among females (Fig. 3).

Of all patients, 111 (75.5%) had complete data of ALT, AST and HBV viral load. Among these, 28 (25.2%) exhibited elevated ALT levels with higher mean log₁₀ viral load, albeit insignificantly (p = 0.16), than those with normal ALT levels while patients with elevated AST levels had a significantly higher mean log₁₀ viral load (p = 0.001), than those with normal AST (Table 1). Additionally, 25 (92.3%) patients had complete ALT, AST and HCV viral load data. Of these 15 (57.7%) had elevated ALT with significantly (p = 0.03) higher log₁₀ viral load than those with normal ALT levels, while 15 (60.0%) exhibited abnormal AST levels had significantly (p = 0.003) higher log₁₀ viral load (Table 1).

Table 1.

Correlation between mean log₁₀ viral load and ALT/AST log₁₀ enzyme levels among HBV and HCV patients

Virus	Liver enzyme (Type)	Log10 levels (IU/L)	No (%)	Viral load range (IU/ml)	Log10 viral load Mean ± SD (Log10)	t	p	95% CI
HBV (n = 111)	ALT	≤ 40	83 (74.7)	9.0 × 10⁰- 1 × 109	2.72 ± 1.25	1.4	0.16	-0.25- 1.44
	ALT	> 40	28 (25.2)	1.9 × 101- 5.61 × 10⁸	3.32 ± 2.10
	AST	≤ 40	99 (89.2)	9.0 × 101 − 1 × 109	2.70 ± 1.28	3.7	< 0.001	0.07–3.18)
	AST	> 40	12 (10.8)	2.0 × 101 − 5.61 × 10⁸	4.32 ± 2.43
HCV (n = 25)	ALT	≤ 40	11 (42.3)	1.40 × 104 − 3.07 × 106	5.6 ± 0.65	2.2	0.04	0.04–1.14
	ALT	> 40	14 (57.7)	4.34 × 104- 9.79 × 106	5.96 ± 0.67
	AST	≤ 40	10 (40.0)	1.40 × 104 − 3.07 × 106	5.2 ± 0.66	3.1	0.006	0.25–1.32
	AST	> 40	15 (60.0)	1.69 × 105 − 9.79 × 106	6.01 ± 0.57

Bivariate analysis of logarithmic values of HBV viral loads with ALT and AST have shown a moderate correlation with ALT (r = 0.317, p = 0.001) and a stronger correlation with AST levels (r = 0.369, p < 0.001) (Table 2). In contrast HCV viral loads showed no significant association with ALT levels (r = 0.246, p = 0.23) but were significantly associated with higher AST levels (r = 0.473, p = 0.02) (Table 2).

Table 2.

Correlation between log₁₀ ALT and log₁₀ AST with log₁₀ viral load among patients with chronic HBV and HCV infections

Log10 viral load		Log10 AST levels	Log 10 ALT levels
HBV	r	0.369	0.317
	p	0.000	0.001
	N	111	111
HCV	r	0.506	0.346
	p	0.01	0.09
	N	25	25

Of all patients (n = 148), 143 had chronic infections, the majority of which were due to HBV. Of these 69, (47.2%) were HBeAg undesignated chronic HBV infection, due to unknown HBeAg status, 47 (32.6%) were HBeAg-negative chronic HBV infections (Table 3). Among these, 33 (70.2%) patients were HBeAg-negative/anti-HBe-positive with viral loads between < 2,000 and < 20,000 IU/ml. One patient had immune-tolerance chronic HBV infection while 7 (6.0%) had compensated cirrhosis; 6 (85.7%) male and 1 (14.3%) female. Of 30 HCV patients; 25 had chronic, 1 acute and 4 had unclassified infections (Table 3). Of the 25 patients with chronic HCV, 5 (20%) had cirrhosis, of which 2 (40.0%) had decompensated cirrhosis. Of the patients treated with tenofovir alafenamide (n = 15), 7 (46.7%) achieved undetectable HBV viral load, 7 (46.7%) had a > 2 log₁₀ reduction in post-treatment viral load, and 1 (6.7%) showed < 1 log₁₀ difference between pre- and post-treatment viral load. Normal ALT levels were observed both pre- and post-treatment in 8 patients (47.1%), while 5 patients (29.4%) had elevated ALT before treatment that normalized after treatment.

Table 3.

Clinical characteristics of patients (n = 143) with HBV and HCV infections

Clinical characteristic	No (%)
HBeAg -ve/anti-HBe + ve chronic HBV infection	47 (32.9%)
HBeAg -undesignated chronic HBV infections	69 (48.3%)
Immune tolerant chronic HBV infections	1 (0.7)
Acute HCV	1 (0.7)
Chronic HCV	25 (17.4)
Unclassified HCV infection	4 (2.8)

Among the 8 HBV patients treated with entecavir, 4 (50.0%) achieved undetectable viral load with normalized ALT, 2 (25.0%) achieved undetectable viral load with ALT that was normal or only slightly elevated both pre- and post-treatment, and 2 (25.0%) had a 5 log₁₀ reduction in viral load with ALT remaining normal pre- and post-treatment (Fig. 4 and 5).

Fig. 4.

HBV versus HCV infection rates among males and females of various age groups. * One patient had dual HBV/HCV infection not included in analysis

Fig. 5.

Age- and sex-specific infection rates with HBV and HCV. * One patient had dual HBV/HCV infection not included in analysis

Of 16 chronic HCV patients treated, 14 received sofosbuvir–daclatasvir, 1 received glecaprevir/pibrentasvir, and 1 received elbasvir/grazoprevir. All patients treated with sofosbuvir–daclatasvir achieved undetectable viral load at the end of treatment. Among these, 11 achieved normalizations of ALT, 1 had persistently normal ALT pre- and post-treatment, and 2 had higher ALT levels post-treatment than before treatment. The patient treated with glecaprevir/pibrentasvir achieved undetectable viral load with ALT remaining normal both pre- and post-treatment. The patient treated with elbasvir/grazoprevir also achieved undetectable viral load and had a normal pretreatment ALT level; however, post-treatment ALT data were not available. Sustained virological response data 12 weeks (SVR12) post treatment for HCV infected patients was not available. That was primarily because patients were referred to primary healthcare for follow-up and became inaccessible to the study.

Discussion

This study was limited by its retrospective design, sample size, and the inconsistent availability of treatment-related data including duration, adherence, and follow-up viral-load measurements for SVR. Nevertheless, the study offers region-specific insight into epidemiology and treatment outcomes of chronic HBV and HCV infection in Al-Baha and highlights geographical regions requiring further public health attention.

Since the inclusion of HBV vaccine in EPI in 1989 [12] Saudi Arabia have accomplished a marked decline in HBsAg prevalence, reaching overall rate of 1.7% [7]. Similarly, control efforts have maintained the HCV seroprevalence between 0.4% and 1.7% [13]. Despite these accomplishments the findings of this study revealed that HBV and HCV infections remain a major challenge in Al-Baha region. Supporting this is several national reports which have consistently demonstrated substantial incidence of HBV and HCV infections with considerable mortality and morbidity [7, 8, 14–16]. Consistent with previous reports, the present findings confirm that hepatitis B is the predominant blood-borne viral hepatitis in Saudi Arabia [1, 15] while HCV infection is less detected due to its nonspecific symptoms [17], or asymptomatic nature [17, 18] posing a major obstacle to achieving HCV elimination by 2030 [19].

A considerable proportion of our HBV cases occurred among those > 40 years reflecting the pre-vaccination era where most of the Saudi public of this age were unlikely to have been immunized. The small proportion of HBV infected young adults likely to have received the vaccine as were born during the era of HBV vaccination. These may have remained susceptible due to a likely missed vaccination opportunity because of low vaccination coverage or were vaccine non-responders.

The differences in HBV and HCV infection rates by sex and age reflect patterns reported previously, though some discrepancies exist, possibly due to sample size or cohort characteristics. Age- and sex-related variations suggest differing transmission dynamics, historical vaccination coverage, and exposure risks, highlighting the need for further investigation with larger, representative samples to clarify these trends. The lower HBV infection rates in females in the current study align with previous reports [20–22]. The higher HCV rate in females contradicts previous reports [19, 23] likely due to the small female sample size. HBV is more common in Saudi males due to horizontal exposure in older, unvaccinated generation, whereas regions where common vertical transmission occur show higher HBV rates in younger populations [24]. Increasing HBV infection rates in males but declining in females reflect age and sex- associated variations requiring further verification. The age associated declined HCV infection rates in male but not in females contrast a previous report of higher female clearance [23] while female age- associated infection rates warrant further investigation with a larger sample.

This study’s finding of a moderate correlation between ALT and HBV viral load, although underestimated by the sample size, aligns with previous reports in both HBeAg-positive and HBeAg-negative patients [25–29]. This further emphasizes that in chronic HBV infection, elevated viral load is closely associated with increased ALT levels highlighting viral replication as a key contributor to liver injury. The incomplete HBeAg data among our HBV-infected cohort limits deeper interpretation. On the other hand, in the ALT levels elevation associated with higher HCV viral loads, albeit no clear bivariate correlation, reflects non-linear relationship between ALT and viral replication. This aligns with prior reports demonstrating inconsistent ALT- viral load correlation [25, 26, 30–32]. This is reasonable given that the immune response varies across patients and serum viral load does not necessarily reflect that of the liver. The moderate correlation of ALT with HBV but not with HCV infected patients likely reflects the different mechanisms of the immune mediated liver injury triggered by each virus [33, 34] as the two viruses differ biologically. Chronic HBV is a dynamic infection developing over transition through phases marked by fluctuating ALT, and viral load which are important predictors of long-term outcomes and guide treatment initiation and response assessment [9, 35]. On the other hand HCV chronic infection tends to generate a low-grade or variable inflammation independent of viral load level [36]. Additionally, variation in age and sex, disease stage and level of treatment response may also be reasons of ALT levels variation.

The positive correlation between AST and viral load in HBV infections in this study aligns with earlier findings [25] and its link to liver pathology, disease stage [25] and severity of liver injury [26], is likely true here as well. However, our cohort lacks additional virological and clinical data essential to substantiate this inference. On the other hand, the HCV patients significant AST- viral load correlation concurs with a prior report [37] although other reports correlation vary from weak to significant according to the viral genotype, stage of the diseases and individual immune status [28, 29, 38]. Arriving in clear inferences on the significance of ALT and AST in our patients merits further investigation.

In the present study HCV accounted for a higher proportion of cirrhosis cases than HBV contrasting some global trends mirroring impact of HBV vaccination leading to replacement with HCV [39].This may suggest slower progress of chronic HBV infection as compared to that of HCV. Around one third of patients of our cohort were HBeAg negative/anti-HBe positive. This profile is consistent with that commonly observed in the Saudi HBV-infected populations and linked to the predominance of genotype D [40, 41] which had low to moderate viral load suggesting low to moderate liver pathology. Nevertheless, the large proportion of patients in our cohort with unknown HBeAg status and the small sample size restricted firm inference highlighting the need for mor comprehensive studies.

Moreover, the higher cirrhosis proportion among our HCV-infected patients despite the larger overall prevalence of HBV resembles observations in other regions [39]. This pattern may reflect cohort effects such as metabolic or lifestyle [42], older age groups with historical HCV exposure, cofactors, and perhaps referral biases that concentrate more advanced HCV disease to tertiary care centers. These findings support reinforcement of HBV vaccination, expanding targeted HCV screening in older adults, and integrating fibrosis assessment and metabolic risk management into regional liver-disease control programs. In addition, the highly effective therapies of HCV will further enhance the feasibility of achieving national HCV elimination goals through comprehensives screening, linkage to care, and timely treatment.

The occurrence of decompensated cirrhosis among our HCV patients but not among those with HBV infections aligns with what has been previously reported [43]. Although HCV has a higher annual rate of hepatic decompensation than HBV, antiviral therapy significantly improves long-term outcomes [44]. The finding that the majority of our HBV cirrhotic patients, albeit small in number, were male is in accordance with previous reports identifying male sex as a risk factor for cirrhosis [21, 22].

Virological and biochemical response to tenofovir/alafenamide and entecavir therapy of HBV patients concur with previous reports [45–48]. However, interpretation of our findings is constrained by the absence of data on treatment duration and lack of follow-up confirming sustained virological response. This lack of data is mainly due to non-adherence to scheduled visits, inconsistent documentation, fragmented medical records and limited resources for longitudinal tracking. Future studies in our region are needed to confirm these outcomes ideally using larger sample sizes and more robust data on treatment duration and follow-up. Given that both entecavir and tenofovir/alafenamide have high barriers to resistance, they are considered first-line options for long-term antiviral therapy [49]. Therefore, it is reasonable to expect favorable long-term treatment outcomes in our patient population.

A high treatment efficacy shown by sofosbuvir/ daclatasvir in HCV patients in the current study. However, the absence of data on sustained virological response limits definitive conclusion. Previously reported treatment outcomes have shown sustained virologic response rates with sofosbuvir and daclatasvir in > 90% of non-cirrhotic and up to 92% for cirrhotic patients [50–53], > 90% of treatment-naïve patients [50, 52], and up to 87% in treatment-experienced patients [50]. The limited number of HCV patients treated with glecaprevir/pibrentasvir and elbasvir/grazoprevir although achieved undetectable viral loads with variably normal ALT levels was not considered significant due to the very limited sample size. The pangenotypic efficacy trials of glecaprevir/pibrentasvir have demonstrated consistently > 95% SVR rate of various in across cirrhosis status, genotypes, and risk groups [54–57]. Only small number of patients were treated with grazoprevir/elbasvir restricting clear inference. Overall, 95–96% SVR12 rates in treatment-naive cirrhotic and noncirrhotic patients with genotype 1, 4, or 6 infections [27, 53] have been reported for grazoprevir/elbasvir. In light of this robust external evidence, favorable long-term treatment outcomes may reasonably be anticipated in our patient population.

However, the absence of data on sustained virological response left a gap in our study. That was primarily because patients were referred to primary healthcare for follow-up and became inaccessible to the study. This may have implications for longitudinal outcome assessment and for planning and evaluating hepatitis elimination programs. Therefore, enhancing linkage-to-care systems, follow-up monitoring, and patient retention strategies may contribute to the success of national viral hepatitis control programs. Nevertheless, combined with relatively low HCV viraemia prevalence reported across Saud Arabia this highly effective therapies of HCV enhance the feasibility of achieving national HCV elimination goals through comprehensives screening, effective linkage to care, and timely treatment.

Conclusions

Despite control programs, chronic HBV and HCV infections remain clinical challenges in Al-Baha. Levels of ALT correlated with HBV viral load, while no such correlation was observed for HCV. This correlation may have been underestimated due to the limited sample size. Current antivirals demonstrated strong efficacy against both HBV and HCV chronic infections; however, interpretation of the findings is restricted by the absence of data on treatment duration and lack of follow-up to confirm SVR. Further research is needed to address these gaps.

Abbreviations

HBV

Hepatitis B virus

HCV

Hepatitis C virus

ALT

Alanine Aminotransferase

AST

Aspartate Aminotransferase

ALP

alkaline phosphatase

GGT

gamma-glutamyl transferase

HCC

Hepatocellular carcinoma

RES

Research Ethics Committee

EDTA

Ethylenediaminetetraacetic acid

ELISA

Enzyme linked immunosorbent assay

RT-PCR

reverse transcription polymerase chain reaction

SVR12

Sustained Virological Response at 12 weeks post completing antiviral therapy

Author contributions

Concept and design: TAS, RME, Analysis and interpretation of data: TAS, RME. Drafting of the manuscript: TAS, HHA. Assistance in interpretation of results, formulation of methodology and critical review of the manuscript for important intellectual content: RME, THA, HHA, MAH, KIA, MAA Supervision: TAS, THA, RME. Actively engaged in the data collection process, ensuring comprehensive and accurate gathering of relevant patient information. All authors approved the final manuscript.

Funding

The authors did not receive support from any organization for the submitted work.

Data availability

No datasets were generated or analysed during the current study.

Declarations

Ethical approval

In accordance with the Declaration of Helsinki the study protocol was approved by the Ethics Research Committee (ERC) of the Faculty of Medicine, Al-Baha University (Ethical approval number: REC/MIC//BU-FM/2022/63R). Data was obtained on written consent to the King Fahd Hospital, and no consent was required from participants as the study is retrospective.

Consent for publication

This manuscript does not contain any individual person’s data in any form either individual details, images or videos.

Competing interests

The authors declare no competing interests.