Abu-Zeinah, Khalid

Abstract Background Lyme arthritis is the most common late manifestation of disseminated Lyme disease in the United States. While most patients respond to antibiotic therapy, a subset develops postantibiotic Lyme arthritis (PALA), characterized by persistent noninfectious inflammatory arthritis. Data describing predictors of PALA and treatment patterns remain limited. Methods We conducted a retrospective observational cohort study of patients with polymerase chain reaction (PCR)−confirmed native joint Lyme arthritis treated at our institution from 2004 to 2025. Clinical, laboratory, imaging, treatment, and outcome data were abstracted from electronic health records. Continuous variables were compared using the Mann–Whitney U test, and categorical variables using Fisher's exact test. Results Seventy-seven patients with PCR-confirmed native joint Lyme arthritis were identified: 64 adults and 13 children. Children more frequently presented with fever and had significantly higher synovial fluid white blood cell counts compared with adults. Knee monoarthritis was the predominant presentation in both groups. Among adults, 41 (64%) achieved complete symptomatic resolution following antibiotic therapy, while 19 (29.7%) developed PALA. Adults who developed PALA had significantly lower synovial fluid white blood cell counts and more extensive joint involvement. The use of intravenous antibiotics and longer total antibiotic duration was more common among PALA patients without evidence of improved outcomes. Conclusions In this cohort of PCR-confirmed native joint Lyme arthritis, a substantial proportion of adults developed PALA. Failure to respond to initial antibiotic therapy and certain clinical features may identify patients at increased risk. These findings support judicious antibiotic use and early consideration of noninfectious mechanisms in persistent arthritis.

Background: Southeast Asian Americans (SEAAs) experience a disproportionately high burden of hepatocellular carcinoma (HCC), with incidence in several subgroups (i.e., Cambodian, Laotian, and Vietnamese individuals) reaching up to nine times that of non-Hispanic Whites. HCC in SEAAs is largely driven by chronic hepatitis B (HBV), hepatitis C (HCV), metabolic dysfunction–associated steatotic liver disease (MASLD), and alcohol-associated liver disease (ALD). Despite established screening guidelines, under-detection and delayed diagnosis remain common. Objective: To summarize epidemiologic patterns, risk factors, screening challenges, and potential interventions aimed at reducing HCC disparities among SEAAs. Design and Methods: This narrative review synthesized evidence from population based epidemiologic studies, community-based interventions, health services research, and policy analyses. Attention was given to studies reporting disaggregated SEAA subgroup data. Findings derived from SEAA specific studies were distinguished from evidence drawn from broader Asian American or general cirrhosis populations, with inferential steps explicitly noted where subgroup specific data were limited. Key Findings: HCC incidence varies widely across SEAA subgroups, with elevated HBV- and HCV-related HCC in Vietnamese, Cambodian, and Laotian communities, and increasing MASLD-related HCC including among lean individuals who fall outside many surveillance frameworks. Screening and surveillance remain suboptimal, with fewer than 30% of patients with cirrhosis receiving recommended semiannual HCC surveillance and even lower uptake among SEAAs. Barriers include low HBV/HCV screening rates, limited disease awareness, language barriers, underinsurance, provider knowledge gaps, and lack of automated EHR-based reminders. Structural challenges such as poverty, transportation barriers, and limited access to specialty care further delay diagnosis. Proposed Interventions: Culturally tailored outreach programs, bilingual navigators, and community-based screening initiatives have demonstrated improved HBV/HCV testing and linkage to care. AI-enabled EHR tools may enhance identification of high-risk patients, streamline follow-up, and increase surveillance adherence. Expanded use of non-invasive fibrosis assessment and recognition of MASLD-related risk in non-obese individuals may support earlier detection. Policy priorities include mandatory Asian subgroup data disaggregation, expanded insurance coverage, and strengthened community-level healthcare infrastructure. Conclusions: SEAAs face a substantial and preventable HCC burden. A coordinated approach combining culturally tailored community engagement, improved provider support systems, and policy reforms is essential to improving early detection and reducing HCC disparities in this diverse population.

Abstract The practice patterns of fluorine 18–labeled fluorodeoxyglucose positron emission tomography/computed tomography ([18F] FDG PET/CT) use in cardiac implantable electronic device infection remain undefined. Among 258 Emerging Infections Network respondents, 69% reported never or rarely using [18F] FDG PET/CT. Limited access and insurance barriers were the most common obstacles.

Abstract Patent foramen ovale (PFO) has a prevalence of approximately 25%. Its association with pyogenic brain abscess (PBA) is unclear. We reviewed adults with PBA and known PFO status from 1 January 2009 through 31 December 2021 at Mayo Clinic. High PFO prevalence (40.5%) was seen. PBA patients with PFO had distinct abscess characteristics but unchanged 1-year, all-cause mortality.

Abstract Background: Disease relapse is a major cause of mortality post allogeneic hematopoietic stem cell transplantion (alloHCT) in patients with myeloid neoplasms (MN). Cytogenetic risk classification is a key prognostic factor in predicting relapse post-transplant. Next generation sequencing (NGS) offers added prognostic insight by identifying relapse-associated mutations. We assessed the impact of mutation type and burden on post-alloHCT relapse risk and relapse-free survival (RFS) in MN patients with non-adverse-risk cytogenetics. Methods: We retrospectively reviewed patients who underwent alloHCT at Mayo Clinic Rochester between 01/01/2018 - 10/01/2023. Eligible patients had MN with non-adverse-risk cytogenetics [Acute myeloid leukemia (AML) with non-adverse-risk cytogenetics per ELN 2022, myelodysplastic syndrome (MDS) with non-high/very high-risk cytogenetics per IPSS-R criteria, and myeloproliferative neoplasms (MPN) (excluding myelofibrosis), chronic myelomonocytic leukemia (CMML), or MDS/MPN overlap with non-complex and non-monosomal karyotypes]. The primary endpoint was 3-year cumulative incidence of relapse (CIR) post-alloHCT, analyzed via competing risk models. RFS was estimated via Kaplan-Meier method. Prognostic mutations were identified using univariate (UVA) and multivariate (MVA) Cox models. A decision tree was used to define mutation-based relapse risk groups. Results: Of 585 patients, 215 (37%) met inclusion criteria; 133 (62%) were male. Median age at diagnosis was 61 years (IQR 53-65.5). Diagnoses included AML (125, 58.1%), MDS (55, 25.6%), CMML (17, 7.9%), MDS/MPN (11, 5.1%), and MPN (7, 3.3%). Median follow-up post-alloHCT was 3.2 years (IQR 1.9-5.2). Donor sources were mostly matched unrelated donors (120; 55.8%), followed by matched related donors (72; 33.5%), haploidentical donors (15; 7%), mismatched unrelated donors (6; 2.8%), and cord blood transplants (2; 0.9%). Most patients reduced intensity/non-myeloablative conditioning (144, 67%), while others received myeloablative (71, 33%). Mutation frequencies were as follows: ASXL1 58 (27.0%), RUNX1 45 (20.9%), FLT3 41 (19.1%), SRSF2 41 (19.1%), DNMT3A 39 (18.1%), STAG2 22 (10.2%), SF3B1 18 (8.4%),BCOR 18 (8.4%), WT1 16 (7.4%), U2AF1 13 (6.0%), ZRSR2 10 (4.7%), TP53 6 (2.8%), EZH2 3 (1.4%). In UVA, mutations in FLT3 (HR 2.15, p=0.018), SF3B1 (SF3B1 HR 3.08, p=0.002), PTPN11(HR 2.93, p=0.032), and WT1 (HR 2.29, p=0.069) were associated with increased risk of 3-year CIR. However, only FLT3 (HR 1.98, p=0.042) and SF3B1 (HR 4.0, p<0.001) retained significance in MVA. SF3B1 correlated with inferior 3-year RFS in UVA (HR 1.99, p=0.034) but not in MVA. Mutations in ASXL1, BCOR, EZH2, RUNX1, SRSF2, STAG2, ZRSR2, U2AF1, and TP53 had no significant impact on CIR or RFS. Harboring ≥2 or ≥3 mutations did not impact CIR or RFS. A decision tree model based on SF3B1, FLT3, DNMT3A, and WT1 mutations stratified patients into 3 risk groups. The high-risk group (n=32; 15%) had 50% 3-year relapse incidence (RI) and included patients with SF3B1 mutations or SF3B1-wildtype (WT) with concurrent FLT3 and DNMT3A mutations. The intermediate-risk group (n=36; 17%) included SF3B1-WT patients with either FLT3 mutations and DNMT3A WT (21% RI), or SF3B-1-WT and FLT3-WT patients with WT1 mutations (33% RI). The low-risk group (n=147; 67%) lacked all 4 mutations and had the lowest 3-year RI of 14%. The 3-year CIR significantly differed across these 3 risk groups (51.9%, 27.3%, and 15.8% in high, intermediate, and low-risk groups respectively; p<0.001). The 3-year RFS was significantly inferior in the high-risk group (35.55%, p=0.001), but similar among intermediate and low-risk groups (67.11% and 63.4%, respectively). Conclusion: In non-adverse risk cytogenetic MN, SF3B1 and FLT3 mutations predicted relapse post-alloHCT. Notably, mutations that were traditionally associated with adverse-risk AML per ELN 2022 (e.g, ASXL1, TP53) were not associated with relapse in this cohort. The discrepancy may reflect exclusion of patients with high-risk cytogenetics, as the prognostic impact of these mutations may depend on co-cytogenetic anomalies. In non-adverse-risk cytogenetics MN, we identified 3 groups of patients based on the presence or absence of SF3B1, FLT3, DNMT3A, and WT1 mutations. Those with mutated SF3B1 or concurrent FLT3/DNMT3A mutations experienced the highest risk of relapse post-alloHCT, translating into inferior RFS. Our findings need to be verified in a larger data registry.