Objective: To investigate the incidence of postoperative neurological complications among patients who underwent spinal deformity surgery and to determine the significant risk factors for postoperative neurological complications. Methods: Six databases PubMed, Web of Science, Scopus, MEDLINE, Embase, and Cochrane Library have been searched to identify observational studies from inception until January 2025. Inclusion criteria were patients aged ≥10 years with postoperative neurological complications after spinal deformity surgery. Stata/MP18.0 was used to conduct the meta-analysis in this review. The summary incidence estimates, proportion with 95% confidence intervals (CIs) and weights were pooled by the random-effects restricted maximum likelihood model. Results: The search strategy identified 53 articles with 40,958 patients for final review. Overall incidence of postoperative neurological complications was 7% (95% CI, 5.0%–9.0%; p < 0.001; I2 = 98.34%) in which incidence estimates for patients with adult spinal deformity and underwent 3-column spinal osteotomies were 12% (95% CI, 9%–16%; p < 0.001; I2 = 93.17%) and 18% (95% CI, 8%–31%; p < 0.001; I2 = 94.68%) respectively. Preoperative neurological deficit was the risk factor with highest overall odds ratio (OR, 2.86; 95% CI, 1.85–4.41; p = 0.01; I2 = 76.20%), followed by the presence of kyphosis (OR, 1.13; 95% CI, 0.75–1.70; p = 0.02; I2 = 81.80%) and age at surgery (OR, 1.04; 95% CI, 1.01–1.08; p = 0.04; I2 = 68.80%). Conclusion Preoperative neurological deficit, the presence of kyphosis and age at surgery were significant risk factors for postoperative neurological complications. Therefore, comprehensive preoperative assessment and surgical planning are crucial to minimize the risk of developing postoperative neurological complications or the deterioration of pre-existing neurologic deficits.

Objective: To investigate the incidence of postoperative neurological complications among patients who underwent spinal deformity surgery and to determine the significant risk factors for postoperative neurological complications. Methods: Six databases PubMed, Web of Science, Scopus, MEDLINE, Embase, and Cochrane Library have been searched to identify observational studies from inception until January 2025. Inclusion criteria were patients aged ≥10 years with postoperative neurological complications after spinal deformity surgery. Stata/MP18.0 was used to conduct the meta-analysis in this review. The summary incidence estimates, proportion with 95% confidence intervals (CIs) and weights were pooled by the random-effects restricted maximum likelihood model. Results: The search strategy identified 53 articles with 40,958 patients for final review. Overall incidence of postoperative neurological complications was 7% (95% CI, 5.0%–9.0%; p < 0.001; I2 = 98.34%) in which incidence estimates for patients with adult spinal deformity and underwent 3-column spinal osteotomies were 12% (95% CI, 9%–16%; p < 0.001; I2 = 93.17%) and 18% (95% CI, 8%–31%; p < 0.001; I2 = 94.68%) respectively. Preoperative neurological deficit was the risk factor with highest overall odds ratio (OR, 2.86; 95% CI, 1.85–4.41; p = 0.01; I2 = 76.20%), followed by the presence of kyphosis (OR, 1.13; 95% CI, 0.75–1.70; p = 0.02; I2 = 81.80%) and age at surgery (OR, 1.04; 95% CI, 1.01–1.08; p = 0.04; I2 = 68.80%). Conclusion Preoperative neurological deficit, the presence of kyphosis and age at surgery were significant risk factors for postoperative neurological complications. Therefore, comprehensive preoperative assessment and surgical planning are crucial to minimize the risk of developing postoperative neurological complications or the deterioration of pre-existing neurologic deficits.

Background: s/Aims: Plasma pregenomic hepatitis B virus RNA (pgRNA) is a novel biomarker in chronic hepatitis B infection (CHB). We aimed to describe the longitudinal profile of pgRNA and factors influencing its levels in CHB patients on nucleoside analogue (NUC). Methods: Serial plasma samples from 1,354 CHB patients started on first-line NUC were evaluated. Time of NUC initiation was taken as baseline (year 0), followed by 1-year, 3-year and 5-year of NUC therapy. pgRNA was measured by Research Use Only RealTime HBV RNA v2.0 (0.2 mL) (Abbott Diagnostics) with lower limit of detection of 0.8 log U/mL (~20 copies/mL). Results: Among 1,354 subjects (median age at baseline 49.8 [interquartile range, IQR 40.2–57.3]) years, 65.2% male, 16.1% hepatitis B e antigen (HBeAg)-positive, 28.6% cirrhotic), baseline median HBV RNA was 3.68 (IQR 2.42–5.19) log U/mL. Upon NUC therapy, median pgRNA levels were 2.45 (IQR 1.82–3.62), 2.23 (IQR 1.67–3.05) and 2.14 (IQR 1.48–2.86) log U/mL at 1, 3 and 5 years, respectively, with the corresponding log U/mL reductions of 0.82, 1.20 and 1.54. Undetectable/ unquantifiable pgRNA was achieved in 13.5%, 15.9% and 20.1% of patients at 1, 3 and 5 years, respectively. Older age, male sex, HBeAg-negativity and high PAGE-B score were associated with lower pgRNA. Conclusions Plasma pgRNA declines are modest under NUC therapy, with only 16.3% achieving RNA undetectability after 5 years of first-line NUC indicating cccDNA silencing has not been achieved in the majority of patients. Clinical characteristics should be taken into consideration when interpreting the plasma pgRNA level.

Functional cure, defined as sustained hepatitis B surface antigen (HBsAg) seroclearance with unquantifiable hepatitis B virus (HBV) DNA at 24 weeks off treatment, is a favorable treatment endpoint in chronic hepatitis B (CHB). Nonetheless, functional cure is rarely attained with the current treatment modalities of nucleos(t)ide analogues (NUCs) and pegylated interferon alpha. Multiple novel virus-targeting agents and immunomodulators are under development for HBV with functional cure as the treatment goal. Among virus-targeting agents, antisense oligonucleotides and small-interfering RNAs are the most advanced in the developmental pipeline, and can induce potent and sustainable HBsAg suppression. The other virus-targeting agents have varying effects on HBsAg and HBV DNA, depending on the drug mechanism. In contrast, immunomodulators have modest effects on HBsAg and have limited roles in monotherapy. Multiple combination regimens incorporating RNA interference agents with immunomodulators have been studied through many ongoing clinical trials. These combination strategies demonstrate synergistic effects in inducing functional cure, and will likely be the future direction of development. Despite the promising results, research is warranted to optimize treatment protocols and to establish criteria for NUC withdrawal after novel therapies. Functional cure is now an attainable target in CHB, and the emerging novel therapeutics will revolutionize CHB management.

Chronic hepatitis B (CHB) poses a major global public health challenge and is a leading cause of cirrhosis and liver cancer. Hepatic steatosis is common in individuals with CHB compared to the non-CHB population and is particularly prevalent in hepatitis B virus (HBV)-endemic regions, affecting about one-third of CHB patients. The interaction between hepatic steatosis and CHB-related disease progression is complex and still under debate. Evidence demonstrates that co-existing steatosis may worsen liver fibrosis while paradoxically increasing the likelihood of achieving better HBV control. In particular, despite the association of steatotic liver disease (SLD) with lower HBV viral loads and higher rates of HBsAg seroclearance, the coexistence of CHB and SLD can potentially accelerate liver disease progression. Factors such as fat deposition, lipotoxicity, oxidative stress, and chronic inflammation in SLD may foster a pro-fibrotic and pro-carcinogenic environment, accelerating the disease progression. Additionally, loss of global DNA methylation, changes in the immune microenvironment, and genetic susceptibility further contribute to the development of CHB-related cirrhosis and hepatocellular carcinoma (HCC). This review examines the mechanisms driving liver disease progression and the heightened risk of cirrhosis and HCC in patients with concurrent CHB and steatotic liver disease, underscoring the importance of prioritizing antiviral therapy for CHB in addition to addressing SLD.

Objective: To investigate the incidence of postoperative neurological complications among patients who underwent spinal deformity surgery and to determine the significant risk factors for postoperative neurological complications. Methods: Six databases PubMed, Web of Science, Scopus, MEDLINE, Embase, and Cochrane Library have been searched to identify observational studies from inception until January 2025. Inclusion criteria were patients aged ≥10 years with postoperative neurological complications after spinal deformity surgery. Stata/MP18.0 was used to conduct the meta-analysis in this review. The summary incidence estimates, proportion with 95% confidence intervals (CIs) and weights were pooled by the random-effects restricted maximum likelihood model. Results: The search strategy identified 53 articles with 40,958 patients for final review. Overall incidence of postoperative neurological complications was 7% (95% CI, 5.0%–9.0%; p < 0.001; I2 = 98.34%) in which incidence estimates for patients with adult spinal deformity and underwent 3-column spinal osteotomies were 12% (95% CI, 9%–16%; p < 0.001; I2 = 93.17%) and 18% (95% CI, 8%–31%; p < 0.001; I2 = 94.68%) respectively. Preoperative neurological deficit was the risk factor with highest overall odds ratio (OR, 2.86; 95% CI, 1.85–4.41; p = 0.01; I2 = 76.20%), followed by the presence of kyphosis (OR, 1.13; 95% CI, 0.75–1.70; p = 0.02; I2 = 81.80%) and age at surgery (OR, 1.04; 95% CI, 1.01–1.08; p = 0.04; I2 = 68.80%). Conclusion Preoperative neurological deficit, the presence of kyphosis and age at surgery were significant risk factors for postoperative neurological complications. Therefore, comprehensive preoperative assessment and surgical planning are crucial to minimize the risk of developing postoperative neurological complications or the deterioration of pre-existing neurologic deficits.

Purpose: This study evaluated the postoperative quality of life (QoL) after various types of gastrectomy for gastric cancer. Materials and Methods: A multicenter prospective observational study was conducted in Korea using the Korean Quality of Life in Stomach Cancer Patients Study (KOQUSS)-40, a new QoL assessment tool focusing on postgastrectomy syndrome. Overall, 496 patients with gastric cancer were enrolled, and QoL was assessed at 5 time points: preoperatively and at 1, 3, 6, and 12 months after surgery. Results: Distal gastrectomy (DG) and pylorus-preserving gastrectomy (PPG) showed significantly better outcomes than total gastrectomy (TG) and proximal gastrectomy (PG) with regard to total score, indigestion, and dysphagia. DG, PPG, and TG also showed significantly better outcomes than PG in terms of dumping syndrome and worry about cancer. Postoperative QoL did not differ significantly according to anastomosis type in DG, except for Billroth I anastomosis, which achieved better bowel habit change scores than the others. No domains differed significantly when comparing double tract reconstruction and esophagogastrostomy after PG. The total QoL score correlated significantly with postoperative body weight loss (more than 10%) and extent of resection (P<0.05 for both).Reflux as assessed by KOQUSS-40 did not correlate significantly with reflux observed on gastroscopy 1 year postoperatively (P=0.064). Conclusions Our prospective observation using KOQUSS-40 revealed that DG and PPG lead to better QoL than TG and PG. Further study is needed to compare postoperative QoL according to anastomosis type in DG and PG.

Background: s/Aims: Plasma pregenomic hepatitis B virus RNA (pgRNA) is a novel biomarker in chronic hepatitis B infection (CHB). We aimed to describe the longitudinal profile of pgRNA and factors influencing its levels in CHB patients on nucleoside analogue (NUC). Methods: Serial plasma samples from 1,354 CHB patients started on first-line NUC were evaluated. Time of NUC initiation was taken as baseline (year 0), followed by 1-year, 3-year and 5-year of NUC therapy. pgRNA was measured by Research Use Only RealTime HBV RNA v2.0 (0.2 mL) (Abbott Diagnostics) with lower limit of detection of 0.8 log U/mL (~20 copies/mL). Results: Among 1,354 subjects (median age at baseline 49.8 [interquartile range, IQR 40.2–57.3]) years, 65.2% male, 16.1% hepatitis B e antigen (HBeAg)-positive, 28.6% cirrhotic), baseline median HBV RNA was 3.68 (IQR 2.42–5.19) log U/mL. Upon NUC therapy, median pgRNA levels were 2.45 (IQR 1.82–3.62), 2.23 (IQR 1.67–3.05) and 2.14 (IQR 1.48–2.86) log U/mL at 1, 3 and 5 years, respectively, with the corresponding log U/mL reductions of 0.82, 1.20 and 1.54. Undetectable/ unquantifiable pgRNA was achieved in 13.5%, 15.9% and 20.1% of patients at 1, 3 and 5 years, respectively. Older age, male sex, HBeAg-negativity and high PAGE-B score were associated with lower pgRNA. Conclusions Plasma pgRNA declines are modest under NUC therapy, with only 16.3% achieving RNA undetectability after 5 years of first-line NUC indicating cccDNA silencing has not been achieved in the majority of patients. Clinical characteristics should be taken into consideration when interpreting the plasma pgRNA level.

Functional cure, defined as sustained hepatitis B surface antigen (HBsAg) seroclearance with unquantifiable hepatitis B virus (HBV) DNA at 24 weeks off treatment, is a favorable treatment endpoint in chronic hepatitis B (CHB). Nonetheless, functional cure is rarely attained with the current treatment modalities of nucleos(t)ide analogues (NUCs) and pegylated interferon alpha. Multiple novel virus-targeting agents and immunomodulators are under development for HBV with functional cure as the treatment goal. Among virus-targeting agents, antisense oligonucleotides and small-interfering RNAs are the most advanced in the developmental pipeline, and can induce potent and sustainable HBsAg suppression. The other virus-targeting agents have varying effects on HBsAg and HBV DNA, depending on the drug mechanism. In contrast, immunomodulators have modest effects on HBsAg and have limited roles in monotherapy. Multiple combination regimens incorporating RNA interference agents with immunomodulators have been studied through many ongoing clinical trials. These combination strategies demonstrate synergistic effects in inducing functional cure, and will likely be the future direction of development. Despite the promising results, research is warranted to optimize treatment protocols and to establish criteria for NUC withdrawal after novel therapies. Functional cure is now an attainable target in CHB, and the emerging novel therapeutics will revolutionize CHB management.

Chronic hepatitis B (CHB) poses a major global public health challenge and is a leading cause of cirrhosis and liver cancer. Hepatic steatosis is common in individuals with CHB compared to the non-CHB population and is particularly prevalent in hepatitis B virus (HBV)-endemic regions, affecting about one-third of CHB patients. The interaction between hepatic steatosis and CHB-related disease progression is complex and still under debate. Evidence demonstrates that co-existing steatosis may worsen liver fibrosis while paradoxically increasing the likelihood of achieving better HBV control. In particular, despite the association of steatotic liver disease (SLD) with lower HBV viral loads and higher rates of HBsAg seroclearance, the coexistence of CHB and SLD can potentially accelerate liver disease progression. Factors such as fat deposition, lipotoxicity, oxidative stress, and chronic inflammation in SLD may foster a pro-fibrotic and pro-carcinogenic environment, accelerating the disease progression. Additionally, loss of global DNA methylation, changes in the immune microenvironment, and genetic susceptibility further contribute to the development of CHB-related cirrhosis and hepatocellular carcinoma (HCC). This review examines the mechanisms driving liver disease progression and the heightened risk of cirrhosis and HCC in patients with concurrent CHB and steatotic liver disease, underscoring the importance of prioritizing antiviral therapy for CHB in addition to addressing SLD.