Waldenström macroglobulinemia (WM) is a rare indolent B-cell lymphoproliferative disorder characterized by bone marrow infiltration and monoclonal immunoglobulin M (IgM) secretion, which poses diagnostic challenges in the early stage. The present study reported on a 63-year-old male with WM presenting with cough, hyperviscosity syndrome (dizziness, weakness, fatigue, blurred vision), severe anemia and cold agglutination in August 2023. After 37˚C incubation to eliminate cold agglutination interference, laboratory tests confirmed severe anemia (hemoglobin, 54 g/l), hyperglobulinemia (globulin, 92 g/l) and markedly elevated serum IgM (83.6 g/l). Peripheral blood smear showed erythrocyte rouleaux formation and plasmacytoid lymphocytes. Bone marrow biopsy revealed 80% infiltration of B-lymphomatous cells, 10% abnormal plasma cells and only 10% residual normal hematopoietic cells. Serum/urine immunoelectrophoresis identified IgM-λ paraprotein and free λ light chains. Bone marrow flow cytometry detected a prominent abnormally mature B-lymphocyte population (72.2% of lymphocytes) positive for CD19, CD20 and cytoplasmic λ (cλ); partially positive for CD23, CD25 and CD27; and negative for CD5, CD10 and CD103. Abnormal plasma cells (0.3% of nucleated cells) showed cλ restriction; strong expression of CD38, CD138 and CD19; partial expression of CD20 and CD27; and absence of CD5, CD10 and CD56. Genetic testing confirmed the MYD88 innate immune signal transduction adaptor (MYD88) L265P mutation positivity via allele-specific PCR and 14q32/11q13 translocation negativity using fluorescence in vitro hybridization, confirming the diagnosis of WM. The patient received therapeutic plasma exchange (TPE) followed by bortezomib-dexamethasone chemotherapy, resulting in resolved cold agglutination, alleviated hyperviscosity syndrome and improved laboratory indicators. Follow-up was performed immediately after discharge; however, it was terminated after 1 month (November 2023) due to re-admission for pulmonary infection. In conclusion, cold agglutination is a pivotal diagnostic clue for WM; combined immunophenotyping and MYD88 L265P detection enables definitive diagnosis, and early TPE plus chemotherapy effectively ameliorates clinical manifestations.

The present case report evaluated the application and outcomes of endocardial radiofrequency ablation (ERFA) in children with hypertrophic cardiomyopathy (HCM). The clinical data, procedural details and short-term follow-up of two pediatric patients with HCM admitted to the department of cardiology from 2023 to 2024. In addition, literature published between 2012 and 2025 was reviewed using the key words 'endocardial radiofrequency ablation', 'children' and 'hypertrophic cardiomyopathy' to summarize the current status and efficacy of ERFA in pediatric HCM. The first reported case was that of a 9-year-old boy who presented with reduced exercise tolerance for 6 months. An echocardiography revealed asymmetric hypertrophy of the interventricular septum and left ventricular wall, positive systolic anterior motion (SAM) sign and left ventricular outflow tract (LVOT) obstruction. Genetic testing indicated variants in LZTR1, suggestive of Noonan syndrome type 10. Despite medication (metoprolol and captopril), LVOT obstruction progressed (gradient >50 mmHg). ERFA was performed, and follow-up at 2 months showed reduced septal thickness and alleviated LVOT obstruction. The second case was that of an 11-year- and -11-month-old girl who presented with 3 years of dizziness and fatigue. An echocardiography confirmed asymmetric left ventricular hypertrophy, LVOT obstruction and SAM sign. Post-ERFA, LVOT obstruction significantly improved. Literature reports on ERFA for pediatric HCM are limited. Combined with adult series, ERFA appears safer than surgical myectomy or alcohol septal ablation, although long-term efficacy requires further validation. On the whole, the present case report demonstrates that ERFA is a safe and effective intervention for pediatric HCM when pharmacological therapy fails, providing a viable minimally alternative.

Resectable locally advanced EGFR-mutant non-small cell lung cancer (NSCLC) represents a distinct therapeutic challenge. Owing to an inherently immunosuppressive tumor microenvironment-frequently characterized by absence of or low PD-L1 expression and sparse CD8+ tumor-infiltrating lymphocytes-patients with EGFR alterations have been routinely excluded from landmark perioperative immunotherapy trials or have demonstrated negligible pathological responses. Consequently, the optimal neoadjuvant strategy for this population remains undefined, and the potential efficacy of immune checkpoint inhibitors combined with chemotherapy in selected EGFR-mutant subtypes is largely unexplored. We report two patients with resectable stage IIIA lung adenocarcinoma and concurrent high PD-L1 expression (tumor proportion score 60%) who achieved pathological complete response (pCR) following neoadjuvant chemoimmunotherapy. Case 1, a 60-year-old male harboring an EGFR exon 19 deletion, received three cycles of pemetrexed, carboplatin, and pembrolizumab, followed by R0 resection; postoperative adjuvant pembrolizumab was discontinued after one cycle because of grade 2 dizziness (CTCAE v5.0). Case 2, a 52-year-old female with an EGFR exon 21 L861Q missense mutation co-occurring with TP53 and PIK3CA alterations, exhibited primary resistance to afatinib with radiographic progression after one month. She subsequently underwent three cycles of pemetrexed, carboplatin, and sintilimab, achieving R0 resection with pCR, and declined further postoperative therapy. After 16 and 22 months of follow-up, respectively, the two patients remain disease-free. These cases suggest that for a specific subset of EGFR-mutant NSCLC-particularly those with high PD-L1 expression and in whom targeted therapy has failed-neoadjuvant chemoimmunotherapy may serve as a potent individualized strategy capable of overcoming pre-existing immune tolerance and inducing profound pathological responses. Nevertheless, this evidence remains strictly anecdotal; validation through large-scale, prospective, biomarker-driven clinical trials is imperative before any modification of standard clinical practice.

ABBV-552, a positive modulator of synaptic vesicle glycoprotein 2A (SV2A), was under investigation as a treatment for cognitive impairment related to Alzheimer's disease. This Phase 1, multicenter, open-label, parallel cohort study (NCT05686980) was conducted to examine the pharmacokinetics (PK), safety, and tolerability of ABBV-552 in healthy adult Japanese and Han Chinese participants and to compare PK and safety findings with healthy adult Western participants from previous studies. Japanese participants in Cohort 1 (N = 10) received three ascending single oral doses (5, 15, and 40 mg) of ABBV-552 with a washout of 7 days between doses. Han Chinese participants in Cohort 2 (N = 7) received a single oral dose of 40 mg ABBV-552. After a single oral dose of 40 mg ABBV-552, PK was comparable between both cohorts. Additionally, the range of individual ABBV-552 concentrations and mean 24-h profiles were comparable with historical data in healthy adult Western participants. In this small study population, single doses of ABBV-552 were well tolerated at all tested doses. Common adverse events reported were dizziness (39%), somnolence (11%), and fatigue (11%). No unique safety signals following single dose ABBV-552 administration were observed in the Japanese or Han Chinese populations examined compared with the previously examined Western population.

Dizziness and vertigo are frequent leading symptoms also in the ophthalmological practice and hospitals. They require a structured clinically oriented diagnostic approach. This article provides a practical approach based on a focused history taking using four key questions as well as a systematic examination of ocular motility (four static and four dynamic tests) and four tests assessing the vestibular system. The focus is on differentiating peripheral from central causes through structured history taking and clinical examination. In addition, the functional anatomy of the brainstem and cerebellum is outlined to enable clinically relevant topographic localization of ocular motor findings.

Medication burden in older patients with chronic kidney disease (CKD) is substantial, and simple medication counts are insufficient for identifying those at elevated risk of inappropriate prescribing. This study characterized medication burden by assessing the number of medications, potentially inappropriate medications (PIMs) and anticholinergic burden in dialysis and non-dialysis patients with CKD aged ≥ 65 years. This retrospective study included patients with a CKD diagnosis who had hospital contact at the Department of Nephrology, Aalborg University Hospital, Denmark, between January and December 2022. Patients were classified as receiving dialysis or not, and polypharmacy and hyper-polypharmacy were defined as ≥ 5 and ≥ 10 medications, respectively. PIMs were identified using the EU(7)-PIM list, and anticholinergic burden was evaluated using the ACB scale with a cut-off of ≥ 3 points. In total, 140 dialysis patients and 534 non-dialysis patients were included. Polypharmacy was present in all dialysis patients and in 83% of non-dialysis patients, whereas hyper-polypharmacy affected 89% and 56%, respectively. Dialysis patients had a higher median number of PIMs (3 vs. 2) and a greater proportion with an ACB score ≥ 3 (44% vs. 27%). Proton pump inhibitors (PPIs), opioids and non-benzodiazepine hypnotics (Z-drugs) were identified as common PIMs, whereas bladder antimuscarinics (tolterodine and solifenacin), sedating antihistamines (clemastine and promethazine) and antipsychotics with anticholinergic properties (quetiapine) were the most frequently used medications with strong anticholinergic properties. In conclusion, medication burden in patients with CKD is high, and incorporating PIMs and ACB scores may identify prescribing risks not captured by medication counts alone.