Atypical trigeminal neuralgia (ATN) is a chronic pain condition characterized by persistent facial pain that does not respond well to conventional medical treatments, often leading to significant impairment in quality of life. This study examined the clinical characteristics and surgical outcomes of microvascular decompression combined with nerve combing in patients with ATN.

We conducted a retrospective analysis of surgical techniques, clinical data, and treatment outcomes in 40 patients from January 2009 to January 2018. Pain levels and patient prognoses were assessed using the Visual Analog Scale and the Barrow Neurological Institute (BNI) pain score. Dynamic monitoring of arterial blood pressure was performed, and levels of total adrenaline, norepinephrine, and dopamine were measured before and during the nerve combing procedure.

During surgery, veins combined with arachnoid adhesions and arachnoid adhesions alone were observed compressing the trigeminal nerve in seven patients (17.50%) and 33 patients (82.50%), respectively. Immediate postoperative BNI scores indicated excellent outcomes (P = 2) in 30 patients (75.00%) and good outcomes (P = 3) in four patients (10.00%). Long-term postoperative BNI scores showed excellent outcomes (P = 2) in 25 patients (62.50%) and good outcomes (P = 3) in seven patients (17.50%). All patients experienced an increase in arterial blood pressure during nerve combing, and the mean levels of adrenaline and norepinephrine before combing showed significant improvement (P < 0.05).

Microvascular decompression combined with nerve combing achieves favorable results in treating ATN. Long-term trigeminal nerve compression and central sensitization may contribute to the etiology in these patients.

Glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) receptor agonists are increasingly used in the management of type 2 diabetes mellitus and obesity due to their ability to stimulate insulin secretion, delay gastric emptying, and suppress appetite. The combination of GLP-1 and GIP agonists improves glycemic control and promotes weight loss. However, the introduction of these novel therapies has raised safety concerns, including the risk of cholestatic hepatitis. We report a case of a patient with obesity who was prescribed a GLP-1/GIP dual-receptor agonist as part of his treatment regimen. Importantly, both before the initiation of this therapy and during the course of treatment, the patient was not taking any other medications. Shortly after receiving four doses of the therapy, the patient developed symptoms of severe cholestatic hepatitis, including jaundice and elevated liver enzyme levels. During hospitalization, no alternative causes for the condition were identified, and a liver biopsy confirmed the diagnosis of drug-induced cholestatic hepatitis. This is the first recorded case of cholestatic hepatitis induced by a GLP-1/GIP dual agonist, and it aimed to raise global awareness of this potential side effect.

Castleman disease (CD) is a lymphoproliferative condition with a broad range of morphological and clinical presentations. It is categorized into distinct pathological and clinical subtypes, including localized unicentric CD, idiopathic multicentric CD, and human herpesvirus 8-associated or human herpesvirus 8-negative variants. Diagnosing CD requires adherence to internationally recognized guidelines that integrate clinical, laboratory, and histological findings. However, distinguishing CD from other diseases can be complex, as numerous benign and malignant conditions can mimic its features. Additionally, individuals diagnosed with CD are at an elevated risk of developing various malignancies. In this article, we reviewed benign and malignant conditions that can mimic CD.

Literature search is conducted and reviewed.

Mimickers of CD include follicular hyperplasia, indolent B-cell lymphoproliferative disorders, peripheral T-cell malignancies, classic Hodgkin lymphoma, follicular dendritic cell tumors, plasma cell disorders, immunoglobulin G4 -related lymphadenopathy, autoimmune-associated lymphadenopathy, infectious causes of lymphadenopathy, and systemic syndromes like POEMS and TAFRO. Various malignancies are associated with CD, including plasma cell proliferations, lymphomas, follicular dendritic cell neoplasms, and Kaposi sarcoma.

This review explores the differential diagnoses and neoplasms linked to CD, emphasizing their role in accurate classification, treatment decisions, and patient management. A comprehensive understanding of CD and its mimickers is crucial for ensuring accurate diagnosis and appropriate patient management in clinical practice.

Achalasia is a motility disorder of the esophagus, characterized by failure of relaxation of the lower esophageal sphincter and disordered peristalsis. Although it is a rare condition, its incidence is rising, likely due to advances in diagnostic techniques and the adoption of standardized definitions. Achalasia is associated with significant morbidity, and currently, there is no cure. Pharmacologic, endoscopic, and surgical interventions are aimed at symptom control. Laparoscopic Heller myotomy (LHM) has been the standard of care for achalasia since the 1990s. Over the past two decades, per-oral endoscopic myotomy (POEM) has emerged as a viable treatment option. Today, LHM and POEM represent the two most effective treatment modalities available for achalasia. This review aims to compare outcomes following LHM and POEM for achalasia and to explore patient characteristics and technical factors that guide optimal treatment selection. We examine the evidence regarding dysphagia relief, reflux, complications, and reintervention rates for both procedures, taking into account factors such as prior surgical history, achalasia subtype, and patient comorbidities.

Coronary artery disease (CAD) is increasingly observed in patients with liver cirrhosis. However, data on the incidence and prevalence of CAD in cirrhotic patients are heterogeneous, and the association remains uncertain. In this study, we aimed to conduct a systematic review and meta-analysis to address these issues.

PubMed, EMBASE, and Cochrane Library databases were searched. Incidence, prevalence, and factors associated with CAD were pooled using a random-effects model. Risk ratio (RR) and odds ratio (OR), with their 95% confidence interval (CI), were calculated to evaluate differences in CAD incidence and prevalence between patients with and without liver cirrhosis.

Fifty-one studies were included. The pooled incidences of CAD, acute coronary syndromes, and myocardial infarction (MI) were 2.28%, 2.02%, and 1.80%, respectively. Liver cirrhosis was not significantly associated with CAD incidence (RR = 0.77; 95% CI = 0.46–1.28) or MI (RR = 0.87; 95% CI = 0.49–1.57). The pooled prevalence of CAD, acute coronary syndromes, and MI was 18.87%, 12.54%, and 6.12%, respectively. Liver cirrhosis was not significantly associated with CAD prevalence (OR = 1.29; 95% CI = 0.83–2.01) or MI (OR = 0.58; 95% CI = 0.28–1.22). Non-alcoholic steatohepatitis, hepatitis C virus, advanced age, male sex, diabetes mellitus, hypertension, hyperlipidemia, smoking history, and family history of CAD were significantly associated with CAD in cirrhotic patients.

CAD is common in cirrhotic patients, but cirrhosis itself may not be associated with an increased CAD risk. In addition to traditional risk factors, non-alcoholic steatohepatitis and hepatitis C virus infection are also associated with CAD presence in cirrhotic patients.

Few cases of tenofovir resistance have been reported, and the appropriate treatment for such cases remains unclear. We aimed to share a case of a chronic hepatitis B mono-infected patient with potential tenofovir resistance who required combined lamivudine and tenofovir therapy to achieve adequate viral suppression. The patient’s viral load (plasma) was monitored using the cobas® hepatitis B virus Test on the cobas® 6800 system. Hepatitis B antiviral drug resistance (AVDR) mutations were assessed by amplicon-based sequencing. Plasma was extracted using the MagNa Pure 24 system, and polymerase chain reaction targeting the polymerase gene (860bp) was performed. Sequencing was conducted on GridION R10.4.1 flow cells, and the resulting FASTQ files were analyzed using DeepChek®-HBV Software. We describe a female patient in her 60s with chronic hepatitis B who was e-antigen positive. She met treatment criteria in May 2020, when her alanine transaminase levels were 1.5 times above the upper limit of normal. She was initially started on entecavir but had to switch to tenofovir alafenamide in June 2020 due to a rash. Despite three years of tenofovir therapy, her viral load remained unsuppressed. AVDR testing identified two suspected tenofovir resistance mutations (V191I and A317S). Since no mutations associated with lamivudine resistance were detected, the patient was treated with a combination of lamivudine and tenofovir, achieving viral suppression after four months. Although rare, tenofovir resistance should be considered in patients with persistent viremia despite long-term therapy. AVDR sequencing facilitated the detection of potential tenofovir resistance and guided treatment decisions, leading to successful viral suppression in this case.

Hepatitis B virus (HBV) infection contributes to hepatocellular carcinoma (HCC) tumorigenesis, drug resistance, and recurrence, although the underlying molecular mechanisms remain unclear. Recent studies suggest that HBV infection may be associated with liver cancer stem cells (LCSCs), but the exact mechanisms are yet to be resolved. In this study, we aimed to analyze the role of HBV infection in regulating the stemness of HCCs, which is closely linked to drug resistance.

Sphere formation assay and real-time Polymerase Chain Reaction quantification were used to isolate and confirm liver cancer stem cells. The inhibitory concentration values of sorafenib and regorafenib were calculated and compared using the Cell Counting Kit-8 assay. HBV infection was used to assess the effect of HBV replication on LCSC markers. Co-immunoprecipitation assay was performed to detect the interaction between CD133 and SRC. Furthermore, we utilized the CRISPR-Cas9 system to knockout CD133 expression in HepG2.2.15 cells.

LCSCs derived from HCCs exhibited high expression of stem cell markers and demonstrated reduced sensitivity to sorafenib and regorafenib. HBV replication promoted both drug resistance and stemness in hepatoma cells and clinical samples. Overexpression of HBx protein in HepG2 cells upregulated the expression of CD133, EpCAM, and CD24, enhancing resistance to sorafenib and regorafenib. Knockout of CD133 expression using the CRISPR-Cas9 system significantly inhibited drug resistance to both sorafenib and regorafenib in HepG2.2.15 cells. Mechanistically, HBV replication promoted CD133 expression, which in turn interacted with the SRC/STAT3 signaling pathway.

Our data suggest that HBV replication enhances the stemness and drug resistance of HCC, providing a strong theoretical foundation for the development of targeted and efficient treatments for HBV-infected HCCs.

Esophagogastroduodenoscopy and colonoscopy play important roles in diagnosing gastrointestinal bleeding; however, they may sometimes fail to identify the source of the bleeding during the initial examination. In such cases, repeated endoscopic examination may be beneficial. Currently, no consensus exists on which patients would benefit from repeated examination. In this review, we discuss the role of repeated endoscopy and conclude that repeated esophagogastroduodenoscopy and colonoscopy can help improve detection rates. It is particularly valuable to repeat the procedure when the quality of the initial endoscopy is poor, the patient’s condition deteriorates, or other examinations suggest that lesions are within the scope of endoscopy.

This review explores the complex interplay between the microbiome and human aging, highlighting how dysbiosis impacts host physiology and health, particularly in relation to genomic stability and telomere attrition. Recent advances in cellular and molecular biology have underscored the role of both intrinsic and extrinsic factors in human aging, with the microbiome emerging as a key determinant of host physiology and health. Dysbiosis—disruptions in microbiome composition—is linked to various age-related diseases and impacts genomic stability and telomere attrition, the progressive shortening of telomeres that limits cell division and contributes to aging. This review examines how microbiome dynamics influence aging by triggering inflammation, oxidative stress, immune dysregulation, and metabolic dysfunction, all of which affect two primary hallmarks of aging: genomic instability and telomere attrition. Understanding these interactions is essential for developing targeted interventions to restore microbiome balance and promote healthy aging, offering potential treatments to extend healthspan and alleviate aging-related diseases. The convergence of microbiome and aging research promises transformative insights and new avenues for improving global population well-being.

Direct-acting antivirals (DAAs) have dramatically changed the landscape of chronic hepatitis C virus (HCV) treatment and significantly reduced the risk of HCV-related hepatocellular carcinoma (HCC) after achieving sustained virologic response. However, the risk of HCC persists, particularly in patients with pre-treatment cirrhosis or fibrosis stage 3 (F3), even after DAA-induced viral eradication. While professional guidelines agree on the need for surveillance in cirrhotic patients, there is no consensus regarding surveillance for the pre-treatment F3 population following HCV eradication. The risk of HCC in the F3 population falls below the threshold for cost-effective surveillance. However, co-existing risk factors—such as diabetes, hepatic steatosis, alcohol use, advanced age, and elevated alpha-fetoprotein levels—may warrant reconsideration of HCC surveillance in this group. This underscores the need for an individualized, risk-based approach to HCC surveillance. This review provided a simplified algorithm to assist clinicians in managing patients with HCV after DAA-induced sustained virologic response.