Background: Although patients with malignant melanoma in situ (MIS) have a high survival rate, a risk of recurrence or upstaging remains. Thus, a comprehensive understanding of its prognosis is essential for optimal patient management. Objective: To investigate the clinical characteristics and survival outcomes of Korean patients with MIS. Methods: We retrospectively analyzed the medical records and photographs of patients with MIS treated at a single tertiary center between 2008 and 2021. Clinical features, including diagnosis, treatment, recurrence, and mortality, were examined. Results: A total of 156 patients with MIS were included, with a mean age of 59.3 years. The most common subtype was acral lentiginous melanoma (80.8%). Delayed diagnosis was associated with subungual MIS (SUMis; p ＜0.05). Among the subtypes other than SUMis, 77.3% met three or more of the ABCD criteria for melanoma.Hutchinson’s sign was observed in 67.3% of cases of SUMis. Ulceration was present in only two cases (1.3%).Recurrence occurred in nine patients (5.8%), with four (2.6%) experiencing relapse after 5 years. Upstaging was observed in two patients (1.3%) due to intralymphatic or regional nodal metastasis occurring at 19 and 10 months post-treatment. The 5-year and 10-year melanoma-specific/overall survival rates were 100.0/96.9% and 100.0/89.0%, respectively. Conclusion Although the survival rates of patients with MIS are high, long-term and close follow-up after treatment is essential because of the possibility of late recurrence and rare instances of intralymphatic or regional nodal metastasis. Additionally, the presence of clinical ulceration is highly suggestive of invasive melanoma.

Intracranial hypotension typically presents with orthostatic headache caused by cerebrospinal fluid (CSF) hypovolemia, most commonly resulting from spontaneous or iatrogenic CSF leaks. Traumatic rupture of an occult congenital sacral meningocele following a minor injury is exceptionally rare and may be diagnostically challenging. We report the case of a 40-year-old woman in Korea who developed sudden severe orthostatic headache immediately after a minor coccygeal contusion. Magnetic resonance myelography demonstrated a 5.8-cm dural ectasia/meningocele at the S3 level with a focal CSF fistula extending into the presacral space, accompanied by a tethered cord and an intradural lipoma. Given the anticipated risks associated with definitive surgical repair, a targeted trans-sacrococcygeal epidural blood patch was administered, resulting in substantial symptomatic improvement. This case highlights that while most post-traumatic CSF leaks occur at the cervical or thoracic level, occult spinal dysraphism should be considered a rare predisposing factor in post-traumatic orthostatic headache, particularly when trauma involves the sacrococcygeal region or when standard imaging findings are unrevealing. This finding also suggests that targeted caudal epidural blood patches may serve as a reasonable and less invasive treatment option when surgical intervention carries a high risk.

Purpose: This study investigated the results of antinuclear antibody (ANA) testing in Korean patients with uveitis, examining its relationship with the clinical course of uveitis and systemic diseases. Methods: We conducted a retrospective analysis of the medical records of 64 patients with noninfectious uveitis who underwent ANA testing and were followed for at least 6 months at the Department of Ophthalmology at Seoul St. Mary's Hospital from January 2006 to December 2021. Patients were divided into ANA-positive and ANA-negative groups and correlations between uveitis-related factors and ANA status were assessed. Results: Among the 516 patients tested for ANA, 6.58% (34/516) were positive. The initial visual acuity (logMAR) before treatment was significantly better in the ANA-positive group (0.21 ± 0.20) than in the ANA-negative group (0.59 ± 0.68) (p = 0.002). However, the final visual acuity after treatment showed no statistically significant difference between the two groups. Additionally, no statistically significant differences were observed in terms of immune deficiency status, types of associated rheumatic disease, rheumatoid factor positivity, erythrocyte sedimentation rate, C-reactive protein (define) levels, or treatment modalities. No significant correlation was found between ANA titers and the severity of uveitis. Conclusions Relationships between ANA positivity and the etiology, treatment outcomes, and systemic diseases associated with uveitis are unclear. Routine ANA testing is not recommended for the diagnosis of uveitis.

Background/Aims: Gastric antral vascular ectasia (GAVE) is a rare but important cause of gastrointestinal (GI) bleeding. The clinical course of GAVE is not well-known, and recurrent bleeding from GAVE is a therapeutic challenge. Therefore, we investigated the clinical course of GAVE and identified the risk factors for bleeding from it. Methods: We retrospectively reviewed the records of patients diagnosed with GAVE using upper GI endoscopy at Asan Medical Center between January 2004 and December 2019 and evaluated the clinical course and risk factors for bleeding from GAVE. Results: Of the 348 patients (mean age, 62.3 ± 10.7 years; male, 62%), bleeding from GAVE occurred in 123 (35%) patients during follow-up (median, 17.3 months; interquartile range [IQR], 4.2–46.6). GI bleeding from GAVE was significantly associated with Child–Pugh class B or C liver cirrhosis (odds ratio [OR], 2.55; 95% confidence interval [CI], 1.57–4.16), chronic kidney disease (CKD) (OR, 2.77; 95% CI, 1.52–5.07), use of antithrombotic agents (OR, 2.34; 95% CI, 1.13–4.82), and involvement of the duodenal bulb (OR, 3.21; 95% CI, 1.76–5.86). Rebleeding occurred in 39 of 123 patients (32%), in whom CKD (OR, 2.55; 95% CI, 1.12–5.81) was significantly associated with rebleeding. Endoscopic hemostasis was most commonly performed using argon plasma coagulation, and the median number of endoscopic hemostasis performed was 2 (IQR, 1–3). Conclusions A careful follow-up for bleeding is needed in GAVE patients with liver cirrhosis, CKD, use of antithrombotic agents, and duodenal bulb involvement.

Background: The 2020 European Society of Cardiology (ESC) 0-hr/1-hr algorithm using high-sensitivity cardiac troponin I (hs-cTnI) for non-ST-segment elevation acute coronary syndrome (NSTE-ACS) aims at early diagnosis and shorter emergency department (ED) stays. While this algorithm has been well-established in controlled studies, real-world implementation remains challenging. We evaluated the algorithm’s clinical performance and risk stratification capability in patients with chest pain or discomfort. Methods: We measured hs-cTnI in 4,678 patients suspected of NSTE-ACS between August 2022 and July 2023, using an Atellica IM Analyzer (Siemens Healthineers, Erlangen, Germany). We categorized patients into rule-in, observe, or rule-out groups according to the algorithm and assessed its diagnostic performance for NSTE-ACS. The final diagnosis of NSTE-ACS was adjudicated by two independent physicians. Additionally, we evaluated 30-day all-cause mortality, hazard risk, and ED length of stay across the three groups. Results: The algorithm categorized 3,408 (72.9%), 573 (12.2%), and 697 (14.9%) patients into the rule-out, observe, and rule-in groups, respectively. Among 90 patients diagnosed as having NSTE-ACS, none were falsely categorized into the rule-out group. Survival analysis revealed significant differences (P < 0.001), with Cox hazard ratios of 2.38 (95% confidence interval: 1.20–4.71) and 6.39 (3.45–11.86) in the observe and rule-in groups, respectively. ED stays shortened in the order of rule-out, observe, and rule-in groups (P < 0.001). Conclusions The 2020 ESC 0-hr/1-hr algorithm demonstrates excellent diagnostic accuracy without false rule-outs and effective risk stratification, and contributes to efficient ED throughput, supporting its clinical utility in real-world emergency settings.

Background/Aims: Endoscopic anti-reflux therapy is a therapeutic option for gastroesophageal reflux disease (GERD), providing durable effects. However, clinical data from Korea remain limited. This study evaluates the clinical outcomes of endoscopic radiofrequency Stretta therapy in Korean patients. Methods: A retrospective analysis was conducted on 71 patients with GERD who underwent Stretta therapy at 2 tertiary hospitals in Korea between November 2015 and July 2021. Clinical outcomes, including patient satisfaction, medication cessation or reduction, and complications, were evaluated. Pre- and post-procedural esophageal manometry and 24-hour pH monitoring test results were also analyzed. Results: Patient satisfaction rates at 1, 6, and 12 months post-procedure were 54.7% (35/64), 70.0% (28/40), and 75.0% (21/28), respectively. Medication cessation or reduction was achieved in 31.2% (20/64) at 1 month, 70.0% (28/40) at 6 months, and 67.9% (19/28) at 12 months. Esophageal manometry (n = 21) showed no significant changes in mean lower esophageal sphincter pressure (18.7 mmHg [2.5-52.9] vs 17.4 mmHg [0.0-43.0], P = 0.702) or mean integrated relaxation pressure (8.2 mmHg [0.0-28.0] vs 10.1 mmHg [0.0-31.0], P = 0.840). The 24-hour pH monitoring (n = 18) demonstrated a nonsignificant decrease in acid exposure time (pH < 4) from 2.3% (0.0-8.4) to 1.6% (0.0-7.3) (P = 0.182). Similarly, the DeMeester score decreased non-significantly from 8.4 (0.8-27.7) to 6.6 (0.8-21.8) (P = 0.352). No procedure-related complications occurred. Conclusion Endoscopic radiofrequency Stretta therapy appears to be a safe treatment option for GERD and may provide favorable patient satisfaction and medication reduction.

Background/Aims: Spinal cord injury (SCI) frequently impairs defecation, severely affecting the quality of life. This study examines compensatory neural remodeling after SCI, focusing on basal colonic contractility, neural responses to electrical field stimulation, and alterations in excitatory cholinergic and inhibitory nitrergic pathways. Methods: Female Sprague–Dawley rats underwent either sham surgery or T10 spinal cord transection and were categorized into 3 groups: sham, 1-week post-SCI (acute), and 4-week post-SCI (chronic). Colonic contractility was assessed in an organ bath using electrical field stimulation in the presence of a nitric oxide synthase inhibitor. Neural protein expression was analyzed by immunofluorescence and Western blotting. Results: SCI produced region- and time-dependent impairments in colonic contractility, with distinct alterations in the proximal circular and longitudinal muscles across acute and chronic phases. Neural excitability shifted dynamically, showing enhanced excitatory activity in the proximal longitudinal muscle at 1-week and the distal circular muscle at 4-week post-SCI. Protein analysis revealed increased neuronal nitric oxide synthase in the proximal colon, decreasedsoluble guanylyl cyclase in the distal colon, upregulated muscarinic M3 receptor in the proximal colon, and reduced vaso-active intestinal peptide receptor 1 in both proximal and distal regions. Conclusion SCI induces spatiotemporal remodeling of excitatory and inhibitory neural pathways, contributing to colonic dysmotility and revealing potential targets for therapeutic intervention.

Fatal hemorrhage from vascular access is a rare but life-threatening complication in patients undergoing hemodialysis. Determining the cause and manner of unwitnessed death is challenging, highlighting the importance of forensic evaluation. A 62-year-old woman undergoing long-term hemodialysis was found dead in her bathroom. Scene investigation revealed extensive bright-red blood loss and multiple bloodstain patterns. External examination revealed a 5 cm oval-shaped bulging lesion at the arteriovenous fistula site on the left upper arm, consistent with a pseudoaneurysm. The overlying skin was thinned with whitish discoloration, and two focal dark reddish lesions at the center, one with a ruptured defect. No other significant injuries were found. Death was attributed to massive hemorrhage from arteriovenous fistula rupture. Based on scene findings and external examination, homicide and suicide were excluded; necrotic changes indicated progressive deterioration, confirming spontaneous rupture. This case demonstrates that pseudoaneurysm formation and skin changes in arteriovenous fistulas may lead to fatal hemorrhage. Careful evaluation of morphological features and scene findings is essential for determining the cause and manner of death in unwitnessed cases.

Microglia are the resident immune cells of the brain; they respond rapidly to inflammatory stimuli and contribute to the progression of neurodegenerative diseases. Receptor-interacting protein kinase 3 (RIPK3) is known to mediate pro-inflammatory signaling and necroptosis, a form of regulated necrotic cell death. However, the role of RIPK3 in microglial activation remains unclear. This study aimed to investigate the role of RIPK3 in both in vitro and in vivo models of neuroinflammation and necroptosis using a selective RIPK3 inhibitor, GSK872. In lipopolysaccharide (LPS)-injected mice, GSK872 attenuated microglial activation, decreased the expression of pro-inflammatory mediators, and reduced the phosphorylation of RIPK3 and mixed lineage kinase domain-like protein (MLKL). In BV2 microglial cells, GSK872 suppressed the production of inflammatory mediators under both inflammatory and necroptotic conditions induced by LPS or LPS/Z-VAD. In particular, GSK872 reduced necroptosis-associated cell death and the release of HMGB1 and IL-1 in LPS/Z-VAD-treated cells. Detailed mechanistic studies revealed that GSK872 inhibits the c-Jun N-terminal kinase (JNK) pathway, while pharmacological inhibition of JNK using SP600125 recapitulates the effects of GSK872 on inflammatory and necroptotic markers. These results indicate that JNK plays a critical role in mediating the effects of GSK872. Notably, IL-1 released during necroptosis appears to contribute modestly to the phosphorylation of JNK and MLKL, indicating a potential feedback mechanism that reinforces necroptotic signaling. Our findings provide compelling evidence that the inhibition of RIPK3 by GSK872 alleviates neuroinflammatory responses and necroptotic cell death by modulating JNK signaling in activated microglia, offering a promising therapeutic strategy for neurodegenerative diseases.