Percutaneous endoscopic gastrostomy (PEG) tube placement is a common procedure used to provide medium- and long-term enteral nutrition to patients. Although generally considered safe, PEG tube placement can be associated with various potential complications. We report a case of gastrocolocutaneous fistula formation in a patient who presented with severe abdominal pain, new-onset diarrhea, and feculent emesis nine days after PEG tube placement. Awareness of this rare complication can facilitate the recognition of colonic perforation during gastrostomy tube placement and enable early detection of the complication post-procedurally. Additionally, we discuss various techniques that may be employed to prevent this complication during PEG tube placement.

Erdheim-Chester Disease (ECD) is a type of systemic histiocytosis mostly observed in adults, characterized by the infiltration of foamy CD68+ and CD1a- histiocytes into multiple organ systems, often associated with MAPK pathway mutations. Conventional treatment of ECD has been challenging. Currently, targeted drugs (BRAF and MEK inhibitors) are recommended. This report aimed to describe the necessity of targeted therapy for ECD. A 39-year-old Japanese man presented with complaints of weight loss, polyuria/polydipsia, bilateral leg pain, and facial xanthoma/xanthelasma palpebrarum (XP) lesions. A biopsy of the bone lesions confirmed BRAF-positive ECD. The ECD lesions initially showed a good response to the cladribine/dexamethasone regimen; however, XP lesions were exacerbated during infliximab therapy, and did not respond to other conventional regimens. Eventually, XP lesions improved with trametinib (a MEK inhibitor) and dabrafenib (a BRAF inhibitor). Targeted therapy is indispensable in the management of ECD.

FMS-like tyrosine kinase 3 (FLT3) mutations are among the most common genetic alterations in acute myeloid leukemia (AML) and play a pivotal role in leukemogenesis. The two primary mutation types, internal tandem duplications (ITDs) and tyrosine kinase domain point mutations, serve as key prognostic markers and therapeutic targets. Advances in next-generation sequencing (NGS) have revolutionized FLT3 mutation detection by providing precise insights into mutation architecture, enhancing risk stratification, and enabling personalized treatment strategies. Additionally, these advancements have facilitated molecular minimal residual disease (MRD) testing, which is instrumental in guiding post-remission management. This review summarizes the molecular characteristics, diagnostic approaches, and therapeutic implications of FLT3 mutations in hematologic malignancies.

A narrative review of the current literature on FLT3 mutations was conducted, incorporating data from original research articles, clinical trials, and recent reviews. Relevant studies were identified through a PubMed literature search and manually curated.

FLT3 mutations are detected in approximately 30% of AML cases and occur at lower frequencies in myelodysplastic syndromes, chronic myelomonocytic leukemia, acute lymphoblastic leukemia, and mixed phenotype acute leukemia. NGS enables comprehensive mutation profiling, revealing rare variants and subclonal complexity while supporting MRD detection with high analytic sensitivity. FLT3-ITD-based MRD positivity is strongly associated with relapse and poor survival in AML. Clinical trial data support FLT3 inhibitors, including midostaurin, gilteritinib, and quizartinib, in FLT3-mutated AML. Additionally, MRD-guided therapy and combination treatment strategies are promising approaches to overcoming resistance.

FLT3 mutations play a central role in the pathogenesis and treatment of AML and related malignancies. NGS-based testing and MRD monitoring transform clinical decision-making by refining risk stratification and enabling personalized therapeutic interventions. Establishing standardized testing protocols and the broader integration of FLT3-targeted therapies will be essential for optimizing patient outcomes.

Helicobacter pylori (H. pylori) infection can cause multiple secondary digestive disorders. Some studies have found that polymorphisms in Toll-like receptor (TLR) genes, including TLR10 rs10004195, may be associated with increased susceptibility to H. pylori infection. Despite conflicting reports, we conducted a meta-analysis to clarify the relationship between these factors.

We conducted an exhaustive review, encompassing all relevant literature up to February 2024, using databases such as PubMed, Embase, Web of Science, and the China National Knowledge Infrastructure. We screened studies based on specific criteria and evaluated their quality using the Newcastle-Ottawa scale. Heterogeneity testing and meta-analysis were performed using Stata 17.0 software, and SPSSAU was used for publication bias evaluation and sensitivity analysis.

Eight of the 487 identified studies met the inclusion criteria, comprising 3,004 and 2,140 individuals in the H. pylori-positive and negative control groups, respectively. Our results demonstrated that individuals carrying the AA genotype at the TLR10 rs10004195 locus had a significantly increased likelihood of H. pylori infection when analyzed using the recessive genetic model (OR: 1.64, CI: 1.04–2.58, p = 0.034). No statistically significant associations were found in the other four genetic models.

Our findings suggest that carrying the TLR10 rs10004195 AA genotype is associated with a significantly elevated risk of H. pylori infection. This information could be used to assess future risk of H. pylori infection in healthy individuals and provide personalized health guidance based on individual genetic polymorphisms.

Wilson’s disease (WD) is a rare autosomal recessive genetic disorder that can be treated with medications. The lack of a single, specific diagnostic indicator leads to diagnostic difficulties, which may result in disease progression to cirrhosis and even liver cancer. Thus, this study aimed to analyze the clinical data, imaging, histopathological manifestations, genetic testing results, and treatment effects of patients with WD hepatic type, and to explore the factors related to WD cirrhosis.

A single-center retrospective study was performed. 48 WD patients with a Leipzig score ≥ 4 were divided into a cirrhosis group and a non-cirrhosis group based on the presence of cirrhosis. Logistic regression analysis and odds ratios were used to describe the strength of association between risk factors and cirrhosis. The predictive value of the model for cirrhosis occurrence was evaluated by calculating the area under the receiver operating characteristic curve and the cutoff value.

All 48 patients diagnosed with WD had liver damage, with males accounting for 54.17%. The median age at diagnosis was 28 years (range: 10.25–40.5 years), and 39.58% of patients had cirrhosis. The most prevalent mutation was c.2333G>T (p.Arg778Leu), found in 41.30% (19/46) of cases. Imaging revealed fatty liver in 31.25% (15/48) of patients and “honeycomb-like” cirrhosis nodules in 73.68% (14/19). Compared with the non-cirrhosis group, the cirrhosis group had a higher positive rate for the Kayser-Fleischer (K-F) ring, older age at diagnosis, and higher levels of immunoglobulin G, but lower levels of alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, white blood cells, and platelets (p < 0.05). Age at diagnosis (odds ratio = 1.072, 95% confidence interval = 1.007–1.142, p = 0.03) and the K-F ring (odds ratio = 18.657, 95% confidence interval = 1.451–239.924, p = 0.025) were independent risk factors for WD-related cirrhosis. The best values of area under the receiver operating characteristic curve for age at diagnosis combined with the K-F ring in predicting WD cirrhosis were 0.909. The average follow-up time for 33 patients was 48.6 months (range: 12–72 months). The biochemical recovery rate was over 60% after 12–72 months of treatment with zinc gluconate and/or penicillamine.

Age at diagnosis, combined with the K-F ring, is a simple and effective risk factor for WD-related cirrhosis. Zinc gluconate and penicillamine are safe and effective treatments.

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.

Among all tumors worldwide, digestive tract tumors have a higher incidence rate and a significant disease burden. Esophageal cancer, gastric cancer, liver cancer, and colorectal cancer are often diagnosed at an advanced stage, and the prognosis remains poor. Currently, tumor treatment resistance is a major global challenge, with many underlying mechanisms. Ferroptosis has been shown to reverse drug resistance. This article reviews the mechanisms and recent advancements in ferroptosis related to reversing treatment resistance in gastrointestinal tumors, aiming to provide theoretical insights and research directions for the diagnosis and treatment of digestive tract tumors.

Chiari malformation type I (CMI) is a congenital neurological disorder characterized by the herniation of the cerebellar tonsils through the foramen magnum, which impairs cerebrospinal fluid circulation at the craniocervical junction. The primary hypothesis regarding its pathogenesis involves a mismatch between the posterior cranial fossa volume and the developing nervous tissue, leading to crowding and subsequent herniation. CMI presents a wide range of clinical manifestations, including cerebrospinal fluid-related symptoms, brainstem and cranial nerve compression, and spinal cord dysfunction, typically diagnosed through magnetic resonance imaging. The surgical treatment of adult CMI remains controversial due to its heterogeneous manifestations and the lack of standardized surgical protocols. Posterior fossa decompression (PFD), with or without duraplasty (hereinafter referred to as PFDD), remains the most common intervention. In this review, we focus on the following aspects to provide an overview of the current surgical strategies: 1. Surgical indications; 2. The extent of bony decompression in PFD; 3. Choosing between PFD, PFDD, and the dura-splitting technique; 4. Atlantoaxial fixation; 5. Techniques for intradural procedures; 6. Timing and approach for syrinx shunting. Additionally, emerging surgical innovations, such as endoscopic techniques, offer promising avenues for treatment.

A colouterine fistula is an extremely rare condition that has been reported in various diseases, including diverticulitis, sigmoid colon malignancy, and complications from radiotherapy. It can also arise from iatrogenic conditions such as the insertion of intrauterine devices, endometrial curettage with urinary tract and bowel perforation, and obstetrical injury. Although colovaginal fistula caused by a foreign body has been reported, colouterine perforation by a foreign body has not been previously documented. We report the first case of foreign body colouterine perforation and its successful treatment by endoscopic removal and repair, resulting in the complete resolution of symptoms without the need for surgery. This case is highly significant due to its rare occurrence and successful treatment by endoscopic removal and repair without the usual and expected necessity for surgical intervention.