Ezeani, Chukwunonso

Inflammatory myofibroblastic tumors (IMTs), originating from mesenchymal cells, are rare neoplasms with intermediate biological potential. Despite being predominantly benign, they can progress to locally aggressive disease and may recur over time. IMTs are predominantly seen in the pediatric population, making our case of IMT in an older adult even rarer. A 67-year-old female with a 42-pack-year smoking history presented with cough, fever, and progressively worsening exertional dyspnea. Imaging studies, including chest X-ray followed by chest computed tomography, identified a right lower lobe lung nodule without evidence of metastasis. Subsequent evaluation with robotic bronchoscopy and endobronchial ultrasound revealed densely cellular reactive lung tissue on lymph node biopsy. Ultimately, the patient underwent a robotic-assisted right lower lobectomy. Final pathology confirmed the diagnosis of an IMT. IMTs are characterized by the presence of spindle cells associated with dense monomorphic inflammatory cells. It has been found that IMT arises from chromosomal rearrangements that aberrantly activate various kinase signaling pathways. This understanding of the molecular mechanisms underlying IMT development has elucidated the neoplastic nature of the disease and has also been pivotal in distinguishing IMT from other inflammatory pseudotumors. Surgical resection remains the cornerstone of treatment, with targeted therapies offering promising results for unresectable or advanced cases. IMTs pose a multifaceted challenge in clinical practice due to their diverse clinical manifestations, histopathological variability, and unclear etiopathogenesis, underscoring the need for continued research and a multidisciplinary approach to optimize patient outcomes.

Objectives: Diabetes mellitus and chronic pancreatitis are established risk factors for pancreatic ductal adenocarcinoma (PDAC). The co-occurrence of exocrine and endocrine pancreatic dysfunction may increase the risk of progression to PDAC and could play a role in early detection. We sought to explore this hypothesis by comparing PDAC risk among patients with diabetes mellitus (DM) and low fecal elastase (FE) in a real-world cohort of patients. Materials and Methods: A retrospective cohort study was conducted using the TriNetX research network including adults with continuous follow-up from 2016 to 2023. The cohort was stratified into 4 groups based on the presence or absence of DM, and normal FE (>200 µg/g) or low FE (<200 µg/g). The 4 groups included: (1) low FE and DM, (2) low FE without DM, (3) normal FE and DM, (4) normal FE without DM. Propensity score matching was performed to balance covariates including age, sex, race, comorbidities to allow for a 6-way comparison of PDAC risk between groups. Time-to-event analyses were conducted with Kaplan-Meier curves and Cox proportional hazards models to estimate hazard ratios (HR) and 95% CIs for the primary outcome of PDAC incidence. Results: Of the study cohort, 29,207 had fecal elastase levels. Low FE (<200 µg/g) was observed in 33% (n = 9585) of these patients. After 6-way comparisons, we observed a higher PDAC risk among individuals with both DM and low FE compared with other groups. The highest PDAC risk was observed in patients with both a low FE (<200 µg/g) and DM compared with those with a normal FE and without a history of DM (HR: 3.68; 95% CI, 2.07–6.53; P < 0.001). Sensitivity analysis using a stricter fecal elastase cutoff of <100 µg/g showed a similar finding, with the highest hazard ratio for PDAC among patients with both DM and very low FE levels (HR: 3.07, 95% CI, 1.37–6.91; P = 0.004). Conclusions: The coexistence of low fecal elastase and DM amplifies the risk of pancreatic ductal adenocarcinoma in our cohort of patients. These results suggest that fecal elastase values may be used to enrich the diabetic population for future PDAC risk stratification, though more studies are needed to validate these findings.