Glomus tumors (GTs) are mesenchymal neoplasms that are typically benign. Gastric GTs are uncommon and occur mainly in the upper gastrointestinal tract. Malignant gastric GTs are extremely rare, constituting less than 1% of gastric tumors. Because their features are similar to those of other tumors found in the same gastrointestinal region, such as stromal tumors, leiomyomas, lymphomas, and lipomas, the diagnosis is challenging. A 52-year-old male patient presented with fatigue and melena. The initial endoscopic examination did not locate any source of bleeding. Six months later, pan-gastroscopy, performed due to progressive microcytic anemia, revealed a 40 × 30 mm polypoid lesion with deep ulcerations; histopathological analysis confirmed that it was a gastric GT with expression of alpha-actin and cadherin 17 and a Ki-67 index of 20%. The patient delayed surgical therapy until his symptoms worsened. Laparoscopic sleeve resection revealed a 65 × 45 × 25 mm tumor, and secondary immunohistochemical analysis revealed extensive spread into the mucosa and subserosa. Focally, the tumor bulged into some large veins. Genetic examination with RNA isolation further supported the histopathological diagnosis of gastric GT with uncertain malignant potential. This case underscores the diagnostic challenges posed by gastric GTs because they are rare and their clinical features are similar to those of other gastric tumors. Thorough histopathological and molecular analysis is essential for an accurate diagnosis. Surgical intervention remains the primary therapeutic approach. This case also emphasizes the need for long-term follow-up due to the potential for recurrence and malignancy.

Background: Type 2 diabetes mellitus (T2DM) is often associated with hyperuricemia, both conditions worsening kidney function. Sodium–glucose cotransporter 2 (SGLT2) inhibitors improve glycemic control and kidney function; however, data on their long-term antihyperuricemic effects in real-world clinical settings remain limited. Therefore, we aimed to compare the effects of SGLT2 inhibitors versus allopurinol on serum uric acid (sUA), kidney function, and clinical outcomes. Methods: This retrospective cohort study evaluated patients with T2DM and hyperuricemia initiated on 10 mg empagliflozin (n = 70), 10 mg dapagliflozin (n = 78), or 100 mg allopurinol (n = 66) between 1 January 2017, and 1 January 2020. Drug dosages were kept constant throughout the study. Baseline and follow-up data (3, 6, 12, 24, and 36 months) were collected. Results: Over 36 months, empagliflozin and dapagliflozin significantly reduced sUA (from 452 (95) to 399 (69) µmol/L and from 450 (81) to 364 (71) µmol/L, respectively) and stabilized eGFR without a significant decline. Allopurinol also reduced sUA (from 430 (89) to 345 (69) µmol/L) but was associated with a progressive eGFR decline (from 70 (35) to 57 (32) mL/min/1.73 m²). Mortality was the highest in the allopurinol group; however, therapy discontinuation was the lowest with this treatment. Conclusions: SGLT2 inhibitors achieved comparable sUA reduction to allopurinol by 36 months while preserving eGFR. Allopurinol was associated with higher mortality and hospitalization rates; SGLT2 inhibitor therapy was associated with favorable multidomain outcomes, but strategies to address adverse effects are needed to enhance adherence.

Background: Fixed‐ratio combinations (FRCs) provide an alternative to intensified conservative insulin treatments (ICTs); however, therapy simplification in patients with high total daily insulin dose (TDD) or high HbA _1c is a debated issue; additionally, its influence on target organ damage (TOD) is less known. Methods: Data were retrospectively collected from patients with Type 2 diabetes, including 58 patients who continued ICT and 104 patients who underwent therapy simplification between January 1, 2017, and January 1, 2023. Patient characteristics and therapy details are at baseline and 3, 6, 12, and 24 months after FRC initiation. Results: HbA _1c significantly decreased in both groups (−0.9% [−1.6%, −0.5%] with ICT vs. −1.3% [−2.1%, −0.3%] with FRC), whereas body weight significantly decreased only after simplification (−1 kg [−4, 1] vs. −5 kg [−7, −2]). Diabetes duration was not associated with therapy efficacy. Significant HbA _1c reduction and FRC dose elevation occurred earlier in patients with an initial HbA _1c > 8.0 % than in those with an initial HbA _1c < 8.0 % . FRC dose was significantly higher at 3 months in patients with a TDD of > 60 U/day than in those with lower TDD. Relative risk reduction with therapy simplification was 72.1%, 50.6%, 32.3%, and 59.7% for hypoglycemia, renal function decline, microalbuminuria, and macrovascular complications, respectively. Risk of retinopathy, neuropathy, and chronic kidney disease did not significantly change with FRCs. Discussion: FRCs are safe and as effective as ICT even in patients with high initial HbA _1c , high TDD, or long diabetes duration. A protective role of FRCs in diabetic ASCVD has been proven, but their protective role in CKD was not observed. Conclusions: The significant improvements in glycemic and weight control, as well as in TODs, suggest that therapy simplification may represent a more favorable approach compared to the continuation of previous ICT even in patients characterized by high baseline TDD and HbA _1c levels.

Background: Hyperuricemia frequently coexists with type 2 diabetes mellitus (T2DM), contributing to a heterogeneous patient population. While previous analyses compared the overall longitudinal effects of allopurinol and SGLT2 inhibitors in this cohort, it remains unclear whether baseline metabolic heterogeneity modifies treatment response. This study aimed to determine whether data-driven metabolic clustering identifies phenotypic subgroups with prognostic or predictive relevance in hyperuricemic T2DM. Methods: In a retrospective cohort of 224 patients with T2DM and hyperuricemia, model-based clustering was applied to age, diabetes duration, body mass index (BMI), serum uric acid (sUA), HbA1c, eGFR, and sex. A sensitivity analysis excluded outliers, yielding 207 patients. Longitudinal trajectories of eGFR and sUA were assessed using linear mixed-effects models and individual slopes. Effect modification by cluster was tested via three-way interactions and analysis of covariance. Results: Clustering identified two groups with weak separation: an adipose–metabolic cluster (n = 116; exclusively male, BMI 33.1 ± 5.7 kg/m², sUA 478 ± 62 µmol/L) and a lean–metabolic cluster (n = 91; exclusively female, BMI 31.3 ± 6.0 kg/m², sUA 426 ± 67 µmol/L). Treatment-agnostic analyses showed no differences in eGFR and sUA slopes or in all-cause mortality across clusters. In both clusters, SGLT2 inhibitors yielded significantly more favourable eGFR slopes than allopurinol, while sUA reductions were comparable across treatments. No significant three-way interactions were detected. Conclusions: In this cohort, although baseline metabolic characteristics differ among patients, using the selected baseline variables, no clinically actionable treatment-relevant phenotypes were identified.

Background: Colonic involvement due to endometriosis is a rare condition with a nonspecific clinical presentation. In rare instances, it may undergo malignant transformation, mimicking primary colorectal carcinoma and complicating clinical decision-making. Case presentation: We present two cases illustrating the diverse clinical manifestations of colonic endometriosis. In Case 1, a female patient underwent appendectomy for abdominal pain, but further evaluation revealed full-thickness endometriosis of the sigmoid colon, causing subtotal occlusion. In Case 2, sigmoid endometriosis was discovered during endoscopic evaluation prompted by positive occult fecal blood testing. Histopathological analysis revealed malignant transformation to endometrioid adenocarcinoma. In both cases, definitive treatment was achieved via laparoscopic sigmoid resection, highlighting the role of laparoscopic surgery in managing such conditions. Conclusions: The potential for malignant transformation of colonic endometriosis and its tendency to mimic colorectal carcinoma underscore the importance of proper tissue sampling methods and histopathological confirmation. A high index of suspicion and appropriate surgical intervention are key to effective management.