Abstract
Background and Aim
The GALAD score (Gender, Age, AFP, AFP-L3, and Des-gamma- carboxy prothrombin) is a mathematical model that incorporates gender, age, alpha-fetoprotein (AFP), the lens culinaris agglutinin-reactive fraction of AFP (AFP-L3), and des-gamma-carboxy prothrombin (DCP). It has been developed to assess the presence of hepatocellular carcinoma (HCC) in patients with chronic liver disease. This study aimed to evaluate the efficacy of the GALAD score in predicting HCC and assessing its prognosis in patients with hepatitis C–related HCC who had received prior direct-acting antiviral (DAA) treatment.
Materials and Methods
This case-control study included patients with hepatitis C virus (HCV)-related liver cirrhosis who had been treated with DAAs, with or without HCC, recruited from the HCC clinic at Kasr Al-Ainy Hospital, Cairo University. Patients were followed until death or the end of the study period. Collected data included clinical and laboratory parameters, levels of DCP, AFP, and AFP-L3, imaging findings, treatment response, and survival outcomes. Logistic regression analysis was used to identify independent predictors of HCC, mortality, and recurrence.
Results
Eighty-eight patients with HCV-related HCC following DAA treatment and 88 patients without HCC were recruited, with no significant differences in gender or age between the two groups. Participants with HCC had a higher mean GALAD score than those without HCC (4.32±2.47 vs. 1.32±1.46, p<0.001). The area under the receiver operating characteristic (ROC) curve (AUC) for the GALAD score in diagnosing HCC at a cut-off value of 3.805 was 0.849 (95% confidence interval [CI]: 0.794–0.905, p<0.001), with a sensitivity of 59.3% and a specificity of 97.7%. Multivariate logistic regression identified liver stiffness (odds ratio [OR]=1.140, 95% CI: 1.007–1.291, p=0.038) and the GALAD score (OR=2.378, 95% CI: 1.171–4.831, p=0.017) as independent predictors of HCC. The GALAD score demonstrated low prognostic value for mortality, with an AUC of 0.564 (95% CI: 0.434–0.693). Patients with HCC recurrence had a slightly higher baseline GALAD score than those without recurrence (6.16 vs. 4.18, p=0.032).
Conclusion
The GALAD score demonstrated adequate diagnostic performance for predicting HCC following DAA therapy but showed low prognostic value.
Keywords: Hepatitis C virus, direct-acting antivirals, hepatocellular carcinoma, GALAD score
Highlights & Insights
Scientific Gap: HCC may still occur or recur after successful DAA therapy for hepatitis C. This study assessed whether the GALAD score can help diagnose HCC and predict outcomes in these patients.
Key Finding: The GALAD score showed good diagnostic accuracy for HCC (AUC=0.849). Liver stiffness and GALAD were independent predictors, but GALAD poorly predicted mortality.
linical Impact: GALAD may support post-DAA HCC diagnosis, but better tools are needed for mortality prediction.
Introduction
Hepatocellular carcinoma (HCC) is the fourth most prevalent malignancy in Egypt and the sixth most common malignancy worldwide.[1] Because chronic hepatitis B and C infections are more prevalent in Africa than in most other regions, the incidence of HCC is higher in Africa, reaching 8.9 cases per 100,000 person-years.[2] Despite advancements in treatment, the global incidence of HCC continues to rise, with no corresponding improvement in survival.[3] The Barcelona Clinic Liver Cancer (BCLC) classification is widely used to stage HCC and guide treatment decisions.[4] Treatment of chronic hepatitis C infection with direct-acting antivirals (DAAs) has demonstrated excellent efficacy.[5] However, regardless of whether sustained virologic response (SVR) is achieved, several recent studies have reported unexpected rates of de novo and recurrent HCC following DAA treatment.[6–8]
Several research trials have investigated potential molecular pathways through which DAAs may contribute to hepatocarcinogenesis. These mechanisms include the stimulation of angiogenesis, cytokine imbalance, and immune cell dysfunction.[9] The aim of HCC surveillance programs is to detect cancer at an early stage to allow curative treatment and thereby improve survival rates.[10] In the context of screening and surveillance, the GALAD model (Gender, Age, Alpha-fetoprotein, AFP-L3, and Des-gamma-carboxy prothrombin) has the potential to serve as a cost-effective tool.[11] Its high sensitivity and specificity have been demonstrated in several studies across diverse ethnic populations.[12] The diagnostic accuracy of the GALAD score has been evaluated across various underlying etiologies of chronic liver disease, with adequate performance reported in patients with nonalcoholic fatty liver disease (NAFLD)-related HCC, as well as hepatitis B- and C-related HCC.[13–15] The present study aimed to evaluate the role of the GALAD score in predicting the occurrence of HCC following DAA treatment and in assessing HCC treatment outcomes, survival, and mortality.
Patients and Methods
Study Design and Patient Selection Criteria
This case-control study included adult patients (≥18 years) with hepatitis C virus (HCV)-related liver cirrhosis who had been treated with DAAs, with or without HCC. Patients were recruited from the multidisciplinary HCC clinic between January 2016 and January 2022 and were followed until death or the end of the study period in June 2023. All procedures were conducted after approval by the Faculty of Medicine, Cairo University Ethics Committee and in accordance with the Declaration of Helsinki (1975), as revised in 2008 (MS-524-2021/27.02.2022). Patients were excluded if they had recurrent HCC, had not received DAAs for HCV before developing HCC, had concomitant malignancies other than HCC, or had concomitant hepatitis B virus or human immunodeficiency virus (HIV) infection.
Data Collection
After providing written informed consent, all participants underwent a comprehensive clinical evaluation, including a full medical history and complete physical examination. Basic demographic data, manifestations of liver decompensation, history of DAA treatment, sustained virological response, and retreatment history were recorded. Laboratory investigations included complete blood count, liver function tests, international normalized ratio (INR), serum creatinine, alpha-fetoprotein (AFP), HCV antibodies, the Lens culinaris agglutinin–reactive fraction of alpha-fetoprotein (AFP-L3), and des-gamma-carboxy prothrombin (DCP). These markers were measured using enzyme-linked immunosorbent assay (ELISA) kits supplied by SinoGeneClon Biotech Co., Ltd., and readings were obtained using the STAT FAX 2000 ELISA Reader. HCV RNA was assessed by reverse transcriptase real-time polymerase chain reaction (PCR) using the QIAGEN Rotor-Gene Q RT-PCR System. HCV RNA levels were measured before treatment and three months after completion of DAA therapy. All laboratory analyses were conducted at the Clinical and Chemical Pathology Department, Kasr Al-Ainy Hospital, Cairo University. The Child-Turcotte-Pugh score and Model for End-Stage Liver Disease (MELD) score were calculated, and performance status was assessed using the Eastern Cooperative Oncology Group (ECOG) performance status scale.[16]
Hepatocellular carcinoma was diagnosed according to American Association for the Study of Liver Diseases (AASLD) guidelines using triphasic computed tomography (CT), with or without magnetic resonance imaging (MRI). Tumor site, size, number of focal lesions, and the presence of vascular or nodal metastases were recorded. Participants with HCC were treated according to international guidelines and followed to assess treatment outcomes, recurrence, and survival. Overall survival was calculated from the date of HCC diagnosis to the date of death or the end of the study. All procedures were conducted in compliance with the Declaration of Helsinki (1975), as revised in 2008, and the ethical standards of the national and institutional committees responsible for human experimentation. The GALAD score was calculated using the following formula:
GALAD = –10.08 + 0.09 × age + 1.67 × gender + 2.34 log10 (AFP) + 0.04 × AFP-L3 + 1.33 × log10 (DCP),
where gender is coded as 0 for female and 1 for male.[17] HCC was staged according to the Barcelona Clinic Liver Cancer classification.[4] Response to therapy in patients with HCC was evaluated using the mRECIST criteria (modified Response Evaluation Criteria in Solid Tumors).[18]
Statistical Analysis
Data were entered and analyzed using the Statistical Package for the Social Sciences (SPSS), version 28 (IBM Corp., Armonk, NY, USA). Quantitative data were expressed as mean ± standard deviation, whereas categorical data were expressed as frequency and percentage. The non-parametric Mann-Whitney test was used to compare quantitative variables. The chi-square (χ2) test was used to compare categorical variables; however, when the expected frequency was less than five, an exact test was applied. The Spearman correlation coefficient was used to assess associations between quantitative variables. Logistic regression analysis was performed to identify independent predictors of HCC, mortality, and recurrence. To determine the optimal GALAD score cut-off value for identifying HCC and predicting mortality, a receiver operating characteristic (ROC) curve was constructed using the area under the curve analysis. A p value <0.05 was considered statistically significant.
Results
This study included 88 patients with HCV-related HCC following DAA treatment and 88 patients without HCC. The two groups were matched for age and gender. Patients with HCC exhibited significantly higher median liver stiffness values, as measured by FibroScan. SVR was achieved in all patients without HCC and in 89.4% of patients with HCC (p=0.001) (Table 1). Median levels of AFP, DCP, and the GALAD score were significantly higher in patients with HCC (Table 2). The median duration between the end of DAA therapy and the development of HCC was one year.
Table 1.
Basic characteristics of studied groups
| HCC group (n=88) Mean (SD) |
HCV group (n=88) Mean (SD) |
p | |||
|---|---|---|---|---|---|
| Age | 62.20±8.12 | 62.86±8.43 | 0.338 | ||
| Duration between DAAs intake and HCC development in months | 19.93±16.01 | ||||
| Count | % | Count | % | ||
| Sex | 0.748 | ||||
| Male | 58 | 65.9 | 60 | 68.2 | |
| Female | 30 | 34.1 | 28 | 31.8 | |
| DAA | |||||
| Yes | 88 | 100 | 88 | 100 | |
| SVR | 0.001 | ||||
| Yes | 76 | 89.4 | 88 | 100 | |
| No | 8 | 9.4 | 0 | 0.0 | |
| Unknown | 1 | 1.2 | 0 | 0.0 | |
| CHILD score | 0.012 | ||||
| A | 64 | 72.7 | 72 | 81.8 | |
| B | 20 | 22.7 | 8 | 9.1 | |
| C | 4 | 4.5 | 8 | 9.1 | |
| Performance status | |||||
| 0 | 53 | 64.6 | – | – | |
| 1 | 24 | 29.3 | – | – | |
| 2 | 4 | 4.9 | – | – | |
| 3 | 1 | 1.2 | – | – | |
| Variables with normal values | HCC group | HCV group | p | ||
| Mean | SD | Mean | SD | ||
| Hb | 12.18 | 2.08 | 12.30 | 2.26 | 0.501 |
| Albumin | 3.68 | 0.58 | 3.84 | 0.63 | 0.037 |
| Creatinine | 0.96 | 0.23 | 1.00 | 0.63 | 0.214 |
| INR | 1.18 | 0.19 | 1.19 | 0.20 | 0.859 |
| CHILD score | 6.55 | 5.40 | 6.13 | 2.35 | 0.215 |
| MELD score | 9.67 | 3.2 | 9.83 | 3.41 | 0.904 |
| Total Bilirubin | 1.21 | 1.10 | 1.20 | 1.45 | 0.269 |
| ALT | 37.23 | 27.91 | 30.83 | 32.20 | 0.001 |
| AFP | 806.58 | 2343.22 | 4.62 | 3.21 | <0.001 |
| GALAD score | 4.32 | 2.47 | 1.32 | 1.46 | <0.001 |
| Median | Median | ||||
| AFP-L3 | 7.25 | 9.50 | <0.001 | ||
| DCP | 551.00 | 277.00 | <0.001 | ||
| HCC group (n=88) | HCV group (n=88) | p | |||
| Count | % | Count | % | ||
| Portal vein thrombosis | <0.001 | ||||
| Thrombosis | 17 | 19.3 | 1 | 1.1 | |
| Patent | 71 | 80.7 | 74 | 84.1 | |
| Dilated | 0 | 0.0 | 8 | 9.1 | |
| Attenuated | 0 | 0.0 | 5 | 5.7 | |
| Hepatic focal lesion number | |||||
| Single | 51 | 58.0 | 0 | 0.0 | |
| Two | 15 | 17.0 | 0 | 0.0 | |
| Multiple | 22 | 25.0 | 0 | 0.0 | |
| BCLC stage | |||||
| 0 | 4 | 4.9 | 0 | 0.0 | |
| A | 20 | 24.4 | 0 | 0.0 | |
| B | 36 | 43.9 | 0 | 0.0 | |
| C | 18 | 22.0 | 0 | 0.0 | |
| D | 4 | 4.9 | 0 | 0.0 | |
DAA: Direct-acting antiviral; SVR: Sustained virologic response; Hb: Hemoglobin; INR: International normalized ratio; CHILD score: Child-Turcotte-Pugh score; MELD score: Model for End-Stage Liver Disease score; AFP: Alpha-fetoprotein; GALAD score: Gender, Age, AFP, AFP-L3, and Des-gamma-carboxy prothrombin; AFP-L3: The lens culinaris agglutinin-reactive fraction of AFP; DCP: Des-gamma-carboxy prothrombin; BCLC: Barcelona Clinic Liver Cancer; HCC: Hepatocellular carcinoma; HCV: Hepatitis C virus.
Table 2.
Baseline characteristics of patients with HCC according to survival status (alive vs dead)
| Alive (n=49) | Dead (n=35) | p | |||
|---|---|---|---|---|---|
| Mean | SD | Mean | SD | ||
| Age | 62.57 | 8.77 | 61.77 | 7.61 | 0.467 |
| Duration between DAAs intake and HCC development in months | 21.86 | 16.56 | 18.02 | 15.71 | 0.354 |
| Count | % | Count | % | ||
| Sex | 0.817 | ||||
| Male | 32 | 65.3 | 22 | 62.9 | |
| Female | 17 | 34.7 | 13 | 37.1 | |
| DAA | |||||
| Yes | 48 | 100.0 | 35 | 100.0 | ----- |
| SVR | 0.691 | ||||
| Yes | 41 | 89.1 | 31 | 88.6 | |
| No | 5 | 10.9 | 3 | 8.6 | |
| Unknown | 0 | 0.0 | 1 | 2.9 | |
| CHILD score | 0.317 | ||||
| A | 38 | 77.6 | 22 | 62.9 | |
| B | 9 | 18.4 | 11 | 31.4 | |
| C | 2 | 4.1 | 2 | 5.7 | |
| Performance status | 0.026 | ||||
| 0 | 28 | 63.6 | 23 | 65.7 | |
| 1 | 16 | 36.4 | 7 | 20.0 | |
| 2 | 0 | 0.0 | 4 | 11.4 | |
| 3 | 0 | 0.0 | 1 | 2.9 | |
| Variables | Alive | Dead | p | ||
| Mean | SD | Mean | SD | ||
| Hb | 12.22 | 2.36 | 12.09 | 1.67 | 0.530 |
| Albumin | 3.78 | 0.59 | 3.53 | 0.56 | 0.033 |
| Creatinine | 0.96 | 0.21 | 0.95 | 0.26 | 0.852 |
| INR | 1.15 | 0.16 | 1.22 | 0.23 | 0.296 |
| MELD score | 9.11 | 3.04 | 10.56 | 3.38 | 0.028 |
| CHILD Score | 6.76 | 7.15 | 6.37 | 1.50 | 0.025 |
| Total Bilirubin | 1.21 | 1.33 | 1.26 | 0.74 | 0.116 |
| ALT | 34.29 | 31.26 | 40.76 | 24.44 | 0.116 |
| AFP | 396.93 | 1045.35 | 1457.29 | 3430.82 | 0.087 |
| GALAD | 4.13 | 2.32 | 4.65 | 2.68 | 0.327 |
| Median | Median | ||||
| AFP-L3 | 7.50 | 7.00 | 0.471 | ||
| DCP | 564.00 | 544.50 | 0.430 | ||
| Alive | Dead | p | |||
| Count | % | Count | % | ||
| Portal vein thrombosis | 0.001 | ||||
| Thrombosis | 4 | 8.2 | 13 | 37.1 | |
| Patent | 45 | 91.8 | 22 | 62.9 | |
| BCLC stage | 0.022 | ||||
| 0 | 4 | 9.1 | 0 | 0.0 | |
| A | 12 | 27.3 | 7 | 20.0 | |
| B | 21 | 47.7 | 13 | 37.1 | |
| C | 7 | 15.9 | 11 | 31.4 | |
| D | 0 | 0.0 | 4 | 11.4 | |
DAA: Direct-acting antiviral; SVR: sustained virologic response; Hb: Hemoglobin; INR: International normalized ratio; CHILD score: Child-Turcotte-Pugh score; MELD score: Model for End-Stage Liver Disease score; AFP: Alpha-fetoprotein; GALAD score: Gender, Age, AFP, AFP-L3, and Des-gamma-carboxy prothrombin; AFP-L3: The lens culinaris agglutinin-reactive fraction of AFP; DCP: Des-gamma-carboxy prothrombin; BCLC: Barcelona Clinic Liver Cancer; HCC: Hepatocellular carcinoma; HCV: Hepatitis C virus.
Table 3 shows the diagnostic accuracy of the GALAD score and each of the studied markers independently using ROC curve analysis. The area under the ROC curve of the GALAD score for diagnosing HCC following DAA treatment at a cut-off value of 3.805 was 0.849 (95% confidence interval [CI]: 0.794–0.905, p<0.001), with a sensitivity of 59.3% and specificity of 97.7% (Fig. 1). Independent predictors of HCC following DAA treatment identified by multivariate logistic regression were liver stiffness (odds ratio [OR]=1.140, 95% CI: 1.007–1.291, p=0.038) and GALAD score (OR=2.378, 95% CI: 1.171–4.831, p=0.017) (Table 4).
Table 3.
Diagnostic accuracy of GALAD score in early prediction of HCC
| Test result variable(s) | Area under curve | p | 95% CI | Cut-off value | Sensitivity % | Specificity % | |
|---|---|---|---|---|---|---|---|
| Lower bound | Upper bound | ||||||
| AFP | 0.854 | <0.001 | 0.794 | 0.915 | 7.9 | 74.4 | 94.3 |
| DCP | 0.860 | <0.001 | 0.800 | 0.920 | 366 | 82.6 | 86.4 |
| AFP-LP3 | 0.796 | <0.001 | 0.730 | 0.862 | 8.25 | 68.2 | 77.3 |
| GALAD | 0.849 | <0.001 | 0.794 | 0.905 | 3.805 | 59.3 | 97.7 |
AFP: Alpha-fetoprotein; CI: Confidence interval; DCP: desgamma-carboxy prothrombin; GALAD: Gender, Age, AFP, AFP-L3, and Des-gammacarboxy prothrombin.
Figure 1.
ROC curve for testing the diagnostic accuracy of GALAD score in early detection of HCC in comparison with AFP, AFP-L3, DCP.
ROC: Receiver operating characteristic; GALAD score: Gender, Age, AFP, AFP-L3, and Des-gamma-carboxy prothrombin; AFP-L3: The lens culinaris agglutinin-reactive fraction of AFP; DCP: Des-gamma-carboxy prothrombin.
Table 4.
Multivariate logistic regression for factors associated with the development of HCC
| p | OR | 95% CI | ||
|---|---|---|---|---|
| Lower | Upper | |||
| HCC | ||||
| GALAD | 2.378 | 1.171 | 4.831 | |
| Liver stiffness by fibroscan | 0.038 | 1.140 | 1.007 | 1.291 |
OR: Odd ratios; CI: Confidence interval; HCC: Hepatocellular carcinoma; GALAD: Gender, Age, AFP, AFP-L3, and Des-gammacarboxy prothrombin.
HCC Treatment and Outcomes
Transarterial chemoembolization (TACE) was the most frequently used treatment modality, applied in 39 patients (44.3%), followed by transarterial radioembolization (TARE) and best supportive care, each used in nine patients (10.11%). According to the modified RECIST criteria, 38 patients (45.0%) had progressive disease, 20 patients (23.8%) had a partial response, and five patients (6.0%) had stable disease. By the end of the study, the mortality rate was 41.7% (n=35). Hepatic encephalopathy was the most common cause of death (n=27, 79.4%). Recurrence of HCC was identified in eight patients (9.5%) (Table 5). The GALAD score demonstrated poor predictive ability for mortality, with an area under the curve (AUC) of 0.564 (95% CI: 0.434–0.693). Factors affecting mortality in univariate analysis included ECOG performance status, portal vein status, BCLC stage, serum albumin level, MELD score, and liver stiffness measured by FibroScan (Table 6). Multivariate regression analysis identified portal vein thrombosis (OR=7.366, 95% CI: 2.022–26.835, p=0.002) and MELD score (OR=1.198, 95% CI: 1.027– 1.398, p=0.022) as independent predictors of mortality.
Table 5.
Multivariate logistic regression for predictors of recurrence
| p | OR | 95% CI | ||
|---|---|---|---|---|
| Lower | Upper | |||
| Recurrence | ||||
| CHILD score (B) | 0.815 | 0.764 | 0.080 | 7.284 |
| CHILD score (C) | 0.020 | 13.750 | 1.513 | 124.989 |
OR: Odd ratios; CI: Confidence interval; CHILD score: Child-Turcotte-Pugh score.
Table 6.
Prediction of recurrence using GALAD score
| Area under the curve | p | 95% CI | Cut-off | Sen. (%) | Spe. (%) | |
|---|---|---|---|---|---|---|
| Lower bound | Upper bound | |||||
| 0.746 | 0.002 | 0.590 | 0.901 | 4.485 | 85.7 | 65.3 |
GALAD score: Gender, Age, AFP, AFP-L3, and Des-gamma-carboxy prothrombin; CI: Confidence interval; Sen: Sensitivity; Spe: Specificity
Univariate analysis of parameters influencing HCC recurrence is presented in Supplementary Table 1. These parameters included diabetes mellitus, Child-Pugh score, and GALAD score. The baseline GALAD score was significantly higher in patients who experienced HCC recurrence (6.16 vs. 4.18, p=0.032).
Discussion
Hepatocellular carcinoma is a major global health concern, with chronic viral hepatitis B and C being the most frequently reported causes due to a variety of direct and indirect carcinogenic mechanisms.[19] Over the past several years, debate has emerged regarding the impact of DAAs on HCC development. Several studies have suggested that treatment of chronic HCV infection with direct-acting antivirals may be associated with an increased risk of de novo and recurrent HCC.[20] In the current study, the median levels of AFP and DCP were higher among patients with HCC compared to those without HCC, which is consistent with the findings of Dating et al.[21] (p<0.0001). However, in contrast to the findings of Dating et al.[21] and Best et al.,[22] who reported elevated AFP-L3 levels in patients with HCC, our study demonstrated a significantly lower median AFP-L3 level among patients with HCC.[21,22] Furthermore, liver stiffness measured by FibroScan was significantly higher among patients with HCC following DAA therapy compared with HCV patients without HCC following DAA therapy (32.63±24.3 vs. 11.24±4.71, p=0.001). This may be explained by the presence of tumor masses, which likely contribute to increased liver stiffness.
In our study, the GALAD score demonstrated poor prognostic performance for predicting mortality among patients with HCC (AUC=0.564, 95% CI: 0.434–0.693).
Our study also evaluated the diagnostic accuracy of the GALAD score using ROC curve analysis, yielding an AUC of 0.849 (95% CI: 0.794– 0.905, p<0.001), with a sensitivity of 59.3% and specificity of 97.7%. These findings are consistent with those of Best et al.,[22] who reported an area under the receiver operating characteristic curve (AUROC) of 0.9242 (95% CI: 0.8925–0.9559, p<0.0001) for the GALAD score. Similarly, a study by Huang et al.[23] demonstrated good diagnostic performance of the GALAD score, with an AUC of 0.869 (95% CI: 0.845–0.891), sensitivity of 85.6%, and specificity of 93.3%. The adequate diagnostic accuracy of the GALAD score may be attributed to its incorporation of multiple biomarkers (AFP, AFP-L3, and DCP), which reflect intratumoral heterogeneity, in addition to demographic factors (age and sex) associated with increased HCC risk. Thus, the GALAD score offers higher sensitivity and specificity compared to the use of individual markers alone.
Kushner et al.[24] proposed that modifications in the interferon gene expression environment and natural killer cell activity resulting from HCV eradication may underlie tumor recurrence following DAA therapy. Interferon genes may be suppressed by DAA therapy, potentially leading to enhanced cell proliferation and subsequent tumor growth. Furthermore, DAA therapy eliminates the inflammatory response associated with chronic HCV infection, which may increase the risk of liver carcinogenesis.[24]
The primary limitation of this study is its relatively small sample size. Additionally, all participants were of Egyptian ethnicity, which may limit the generalizability of the results to other populations. The high mortality rate observed in this study may be attributed to several factors, including the frequent diagnosis of HCC at advanced stages (BCLC B or C), the advanced age of many patients, and recurrent episodes of hepatic encephalopathy, all of which adversely affected survival.
Conclusion
The GALAD score demonstrated adequate diagnostic performance for predicting de novo HCC following DAA therapy and was associated with HCC recurrence. However, it showed limited ability to predict mortality.
Footnotes
How to cite this article: Abdelaziz AO, Nabeel MM, Atef M, Kamel MH, Elbaz TM, Hatem A, et al. Assessment of GALAD score as a diagnostic and prognostic factor of de novo hepatitis C–related hepatocellular carcinoma post treatment with direct-acting antivirals. Hepatology Forum 2026; 7(2):101–107.
Ethics Committee Approval
All procedures were conducted after approval by the Faculty of Medicine, Cairo University Ethics Committee and in accordance with the Declaration of Helsinki (1975), as revised in 2008 (MS-524-2021/27.02.2022).
Informed Consent
After providing written informed consent, all participants underwent a comprehensive clinical evaluation, including a full medical history and complete physical examination.
Conflict of Interest
The authors have no conflict of interest to declare.
Financial Disclosure
The authors declared that this study has received no financial support.
Use of AI for Writing Assistance
The authors declared that they did not use artificial intelligence (AI)– assisted technologies.
Author Contributions
Concept: AOA, TME; Design: MMN; Supervision: HIS, AHK, AHA; Funding: AH; Materials: MHK; Data Collection and/ or Processing: MA, AH; Analysis and/or Interpretation: SAAM, AOA; Literature Search: RM; Writing: AR; Critical Reviews: AOA, EM, RL.
Peer-review
Externally peer-reviewed.
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