Novel direct oral anticoagulants (DOACs) are prescribed worldwide in the treatment of non-valvular atrial fibrillation. Adverse reactions have been reported following the use of DOACs. One notable trend in the literature is the growing number of reported cases of esophagitis dissecans superficialis (EDS) generated by DOAC use. We hereby report the case of a 73-year-old woman who presented to the hospital with asthenia, dysphagia, and melena two days prior to admission. The patient had taken apixaban due to non-valvular paroxysmal atrial fibrillation for a few weeks. The biological panel showed moderate anemia with a hemoglobin level of 7.7 g/dL Apixaban-induced EDS was diagnosed by the characteristic endoscopic findings. The patient received treatment with a proton pump inhibitor (pantoprazole) in a double dose. Also, an iron treatment was recommended for a period of six months. The follow-up endoscopy at one month confirmed the healing of the esophageal lesions. The case was discussed with the cardiologist. The first anticoagulant treatment proposed after discharge was a vitamin K antagonist (acenocumarol) but the patient refused this medication and thus it was decided to initiate rivaroxaban. Although DOACs have demonstrated their efficacy in the prevention and treatment of stroke and thromboembolism among the aging demographic, cases of DOAC-induced EDS will continue to pose numerous challenges for physicians worldwide.

Early chronic pancreatitis (ECP) represents a potentially reversible stage in the natural history of chronic pancreatic disease. Timely diagnosis of ECP offers a possibility for intervention, yet its diagnosis remains challenging due to nonspecific symptoms, lack of standardized criteria, and the limited diagnostic sensitivity of conventional tools. This review aims to synthesize recent advancements in the understanding, detection, and management of ECP, with a focus on innovation in imaging techniques and biomarker profiling. The goal is to facilitate earlier diagnosis and more effective patient stratification. We reviewed the literature from the past five years, including original studies, meta-analyses, and expert consensus statements, to address the current evidence across genetic, inflammatory, imaging, and biochemical domains relevant to ECP. Endoscopic ultrasound and advanced magnetic resonance techniques offer high sensitivity in detecting early parenchymal changes, although inter-observer variability and lack of standardization persist. Biomarker discovery has focused on inflammatory (IL-6, sCD163), fibrotic (TGF-β1, TIMP-1), and oxidative markers, as well as novel candidates like microRNAs. Genetic predisposition (PRSS1, SPINK1, CTRC, CPA1, CLDN2) significantly influences disease onset and progression and could enable selection of high-risk individuals. Therefore, diagnosing ECP should involve a multidisciplinary precision-based approach integrating clinical, radiologic, molecular, serologic, and genetic data for individualized risk stratification.

Histoplasma capsulatum (H. capsulatum) is considered to be one of the most extensively spread dysmorphic fungi worldwide. Histoplasmosis primarily impacts patients with weakened immune systems and can result in a diverse range of clinical manifestations. In immunocompetent patients, the disease may manifest as a self-limiting or asymptomatic infection; however, in immunocompromised individuals, it can occur as a debilitating, disseminated disease. Diagnosing histoplasmosis may be challenging. A medical professional that specializes in treating endemic fungal illnesses is better able to assist with an accurate and timely diagnosis since they have a deeper grasp of these illnesses. Consequently, the process of diagnosing histoplasmosis might be difficult for less experienced physicians. The case presented is an example of the myriad faces that histoplasmosis can take on, mimicking other common infectious or malignant conditions, leading to extensive work-up and invasive procedures in establishing the diagnosis of this otherwise benign condition. We hereby report the case of disseminated histoplasmosis in a young immunocompetent female patient.

Background and Clinical significance: Plummer–Vinson (PV) syndrome is a rare medical entity diagnosed when iron-deficiency anemia, dysphagia, and esophageal webs occur in the same patient. PV syndrome has been associated with different autoimmune diseases, such as celiac disease (CD). CD is a chronic multisystemic disorder affecting the small intestine, but it is recognized as having a plethora of clinical manifestations secondary to the malabsorption syndrome that accompanies the majority of cases. However, similar to PV syndrome, a high percentage of CD patients are asymptomatic, and those who are symptomatic may present with a wide variety of gastrointestinal and extraintestinal symptoms, including iron-deficiency anemia, making the diagnosis challenging. Case presentation: We present the case of a 43-year-old Caucasian female patient with a 7-year history of iron-deficiency anemia and increased bowel movements (3–4 stools/day). Upper endoscopy demonstrated a narrowing at the proximal cervical esophagus from a tight esophageal stricture caused by a smooth mucosal diaphragm. A 36F Savary–Gilliard dilator was used to manage the stenosis. The distal esophagus and stomach were normal, but scalloping of the duodenal folds was noted, and CD was confirmed by villous atrophy and positive tissue transglutaminase antibodies. Dysphagia was immediately resolved, and a glute-free diet was implemented. Conclusions: The relationship between PV syndrome and CD is still a matter of debate. Some might argue that PV syndrome is a complication of an undiagnosed CD. In cases of PV syndrome, a CD diagnosis should be considered even in the absence of typical symptoms of malabsorption.

Introduction: Celiac disease (CD) is a prevalent autoimmune enteropathy that remains significantly underdiagnosed due to its multifaceted diagnostic pathway and diverse clinical presentations. While duodenal biopsy has historically served as the diagnostic gold standard, its clinical primacy has been challenged by the burden of invasive endoscopy and potential histological misinterpretation. Material and Methods: We conducted a prospective diagnostic accuracy study involving consecutive adult patients with suspected CD to evaluate the performance of serological markers against histological findings. Results: The study included 139 patients, with a female predominance of 105 (75.5%). Histological evaluation revealed Marsh 3a–c in 100 patients (71.9%), whereas Marsh 1–2 was observed in 39 patients (28.1%). Sixty-one patients (43.9%) presented with high-titer ≥10×ULN tTG-IgA levels, while 78 patients (56.1%) fell below this threshold. To determine the independent predictors of Marsh 3a–c, we performed a logistic regression analysis. In the univariate analysis, both tTG-IgA (OR: 1.880; 95% CI: 1.458–2.426; p < 0.001) and non-smoker status (OR: 1.865; 95% CI: 1.283–2.709; p = 0.002) were significantly associated with VA. After adjusting for confounding variables in the multivariate model, both factors remained highly significant (p < 0.001 and p = 0.014, respectively). The diagnostic performance of the ≥10×ULN tTG-IgA threshold for detecting VA was confirmed by AUROC of 0.737, CI 0.646–0.827, p < 0.001, with a sensitivity of 55.0% and a specificity of 84.6%, a PPV of 90.2% and a NPVof 42.3% (33/78), underscoring that while the ≥10×ULN tTG-IgA threshold is highly specific for atrophy, lower titers do not reliably exclude it in adults. Conclusions: In conclusion, our study demonstrates that the ≥10×ULN tTG-IgA threshold provides a reliable diagnostic surrogate for VA in adult CD. While high cut-off values minimize false positives, a diagnostic gap remains for patients with lower antibody levels or those influenced by modifiers such as smoking. The low sensitivity of the high threshold reinforces the continued necessity of duodenal biopsy for symptomatic patients with lower-range antibody elevations to avoid a significant diagnostic gap.