Turku University Hospital

Bladder exstrophy and epispadias complex is a rare congenital anomaly with significant medical and psychosocial implications. We employed a dual approach to evaluate the prevalence and risk factors of psychiatric morbidity in bladder exstrophy and epispadias patients, by combining a systematic review with a retrospective national registry study. To evaluate the prevalence and risk factors of psychiatric morbidity in bladder exstrophy and epispadias complex. We conducted a systematic literature review following Preferred Reporting Items for Systematic Reviews and Meta-analyses guidelines, including studies on psychiatric disorders or symptoms and quality of life in bladder exstrophy and epispadias patients of all ages. Article quality was assessed using the Newcastle-Ottawa Scale. Prevalence data for psychiatric conditions and scores from psychiatric and quality-of-life questionnaires were extracted. Additionally, all bladder exstrophy and epispadias patients born in Finland 2001-2006 were identified from national registries. A matched and randomized control group without congenital malformations was selected from the same population. We evaluated the prevalence and risk factors for psychiatric diagnoses in this cohort. Of the 3850 retrieved results, 30 studies with 1179 participants were included. The overall prevalence of psychiatric morbidity was 31 %, [95 % CI 17 %-47 %]. Psychiatric morbidity was highest in adolescents, while morbidity in adults was comparable to the general population. In the Finnish cohort, 80 % (n = 16/20) of bladder exstrophy and epispadias patients had a psychiatric diagnosis compared to 26 % (n = 21/80) of the controls (OR 11.2, [95 % CI 3.37-37.4], p < 0.001). The severity of the anomaly, number of surgeries, maternal unemployment, or maternal psychiatric diagnosis were not significantly associated with increased psychiatric morbidity. Bladder exstrophy and epispadias is associated with an elevated risk of psychiatric morbidity. Our dual approach highlights the need for systematic mental health assessment and support in this population.

Neighbourhood socioeconomic disadvantage correlates with cardiovascular disease risk. However, its relationship with subclinical atherosclerosis from childhood to midlife is not well-defined. We examined whether cumulative neighbourhood disadvantage is associated with carotid artery plaques, a measure of subclinical atherosclerosis. We analysed data from 1998 participants in the Cardiovascular Risk in Young Finns Study, a cohort followed from childhood (mean age 10.7years in 1980) to adulthood (mean age 48.6years in 2018-2020). Neighbourhood disadvantage was derived from national grid-based socioeconomic data and computed cumulatively across the life course. The number of carotid artery plaques (mean plaque count) was assessed by standardized ultrasound imaging. Multivariable Poisson regression models were used to evaluate the associations. Mediation analyses were used to assessed the role of ideal cardiovascular health (CVH) metrics. Higher cumulative neighbourhood disadvantage from childhood to mid-adulthood was associated with a 1.24-fold increase in mean plaque count for every 1 standard deviation increase in cumulative disadvantage. This relationship persisted after controlling for parental carotid artery plaques, polygenic coronary artery disease risk score, and Framingham risk score. The association was partially explained by ideal CVH metrics, particularly smoking and blood pressure, which collectively accounted for almost half of the association. Long-term exposure to neighbourhood socioeconomic disadvantage beginning in childhood is associated with subclinical atherosclerosis in midlife, independently of achieved socioeconomic position. These findings highlight the importance of cumulative socioeconomic environments across the life course and suggest that behavioural risk factors may partly explain observed neighbourhood-level associations with atherosclerosis.

In patients with obstructive coronary artery disease, early revascularization does not improve outcomes but may reduce angina symptoms. The objective of this study was to examine whether changes in health status outcomes following revascularization are explained by the extent of myocardial perfusion defects and improvement in myocardial perfusion. Two trials enrolling stable patients with new-onset chest pain suggestive of obstructive coronary artery disease, the ISCHEMIA (International Study of Comparative Health Effectiveness With Medical and Invasive Approaches) and the Dan-NICAD (Danish Study of Noninvasive Testing in Coronary Artery Disease) trials, were analyzed. Patients with single-vessel coronary artery disease who underwent nuclear myocardial perfusion imaging (nMPI) were included. In the ISCHEMIA trial, patients with moderate/severe ischemia were randomized to either optimal medical therapy alone or optimal medical therapy and invasive angiography. The Dan-NICAD trial enrolled patients with suspected stenosis on coronary computed tomographic angiography undergoing nMPI. Test-guided revascularization blinded to nMPI was performed, and patients with initially abnormal nMPI were reassessed after 12 months. The primary outcome was the change in the Seattle Angina Questionnaire angina frequency score. In total, 584 patients were eligible. In patients with a summed difference score of 5≤10 (n=149 [25%]) and ≥10 (n=152 [26%]), revascularization was associated with an improved angina frequency score (mean change ±SD: 16.4±20.9 and 19.0±24.1). No improvement was demonstrated in patients with a summed difference score <5. In multivariable logistic regression analysis (n=91), an increase in hyperemic myocardial blood flow at follow-up was associated with freedom from angina (odds ratio, 2.89 [95% CI, 1.04-8.70]). In patients with single-vessel coronary artery disease, nMPI may identify patients more likely to experience improved symptoms from revascularization, potentially reflecting enhanced myocardial perfusion.

The worldwide acceleration of digital transformation in healthcare underscores the need for professionals to continuously adapt and sustain robust digital health competence, shaped not only by individual characteristics and institutional environments but also by broader social, cultural, and geopolitical factors. This study aimed to identify distinct clusters of digital health competence among healthcare professionals across 19 diverse countries and regions, and to examine the factors influencing the development and distribution of these competence clusters. A cross-sectional international survey study was conducted between 2023 and 2024, using a validated survey instrument measuring digital health competence and its influencing factors. Data were collected from healthcare professionals in 19 countries and regions (n=6440; n=5945 used for this study), following a harmonised protocol with shared demographic templates and instruments. K-means cluster analysis was employed to derive digital competence profiles, with comparative analyses conducted to investigate associations between the identified clusters and individual characteristics (e.g., age, education, professional experience). Five distinct clusters of digital health competence were identified: (1) Beginners, (2) Developing Professionals, (3) Emerging Users, (4) Proficient Practitioners, and (5) Pioneers. Higher competence clusters (4 and 5) were associated with younger age, higher education, hospital-based work, and stronger perceived support from management, organisational structures, and colleagues. In contrast, lower-performing clusters reported limited digital engagement and minimal support. Perceived leadership influence, particularly managerial commitment to digital change, was a key differentiator across clusters. The findings demonstrate substantial variation in digital health competence across healthcare professionals internationally. Cluster-specific strategies, such as targeted upskilling, peer mentoring, and leadership engagement, are needed to address competence gaps. The results provide a foundation for policy development and workforce training frameworks aimed at strengthening digital readiness in global healthcare systems. Future research should explore longitudinal competence development and evaluate targeted interventions.

Cardiac organ damage (OD) is associated with increased risk of cardiovascular disease. However, limited knowledge exists on cardiac OD in young patients with cryptogenic ischaemic stroke (CIS). To explore prevalence and covariates of cardiac OD in patients with CIS compared to controls participating in the SECRETO study. We analysed data from 427 patients with CIS aged <50 years and 361 age- and sex-matched controls. OD was defined as presence of abnormal left ventricular (LV) geometry (LV hypertrophy or concentric remodelling) or left atrial enlargement (LAE) assessed by echocardiography, using sex-specific threshold values. Compared to controls, patients had higher prevalences of obesity and tobacco smoking, patent foramen ovale (PFO) (52% vs. 25%) and abnormal LV geometry (12% vs. 7%, all p < 0.01), while presence of LAE did not differ. In multivariable analyses, CIS was associated with presence of abnormal LV geometry (odds ratio 1.86 [95% confidence interval 1.09-3.20], p=0.024). In separate multivariable analyses in patients only, obesity was associated with both abnormal LV geometry and LAE (both p < 0.01), and higher systolic blood pressure only with presence of abnormal LV geometry (p < 0.001). No significant association with PFO was found. In young patients with CIS participating in the SECRETO study, abnormal LV geometry was more prevalent compared to age- and sex-matched controls and associated with presence of higher blood pressure and obesity. The results point to the importance of blood pressure and weight control in CIS to prevent progression of cardiac OD and recurrent cardiovascular events.

Lower abdominal surgeries in children are associated with significant postoperative pain. While caudal block (CB) is widely used, ultrasound-guided truncal blocks such as retrolaminar block (RLB) may provide more targeted and prolonged analgesia. In this double-blind, randomized controlled trial conducted at two tertiary hospitals (March 1-September 1, 2025), children aged 1-7 years (ASA I-II) scheduled for unilateral orchidopexy were randomized to RLB or CB. CB received 0.125% bupivacaine 1 mL/kg (max 20 mL); RLB received 0.25% bupivacaine 0.1 mL/kg, both under standardized general anesthesia with intraoperative IV paracetamol (10 mg/kg). FLACC scores were recorded at 30 min and 1, 2, 4, 6, 12, and 24 h. Rescue analgesia was IV paracetamol for FLACC 2-4 and IV tramadol for FLACC >4. Primary outcome was analgesic efficacy (FLACC at 12th hour). Secondary outcomes were time to first analgesic and total consumption within 24 h. Sixty-two patients were analyzed (N.=31 per group); baseline demographics did not differ. RLB yielded lower FLACC scores at 6 h (P=0.002), 12 h (P=0.007), and 24 h (P=0.018), with no difference at 30 min or 1 h (P>0.05). Time to first analgesic was longer with RLB (P<0.001), and total 24-h consumption was lower (P=0.001). Fewer patients required rescue analgesia with RLB (3/31) than CB (14/31). No major block-related complications occurred. In pediatric orchidopexy, RLB provided superior and more durable analgesia than CB, reduced 24-h analgesic requirements, and delayed first rescue dosing without major complications, supporting its role within opioid-sparing pediatric ERAS pathways.

Background and ObjectivesThe mechanisms underlying tremor generation in Parkinson disease (PD) remain unclear. Previously, we demonstrated a connection between rest tremor amplitude and higher dopamine transporter (DAT) binding in the ipsilateral striatum among the Parkinson Progression Markers Initiative cohort. Here, we investigated the association of parkinsonian motor symptoms with striatal DAT binding in a sizable and clinically representative sample of patients with parkinsonian signs to validate the previously observed ipsilateral relationship in PD.MethodsThis observational cross-sectional study included right-handed patients referred for [123I]FP-CIT SPECT because of clinically uncertain parkinsonism or tremor at Turku University Hospital and the Helsinki and Uusimaa Hospital District, Finland. Each patient underwent a comprehensive clinical evaluation and follow-up (median 3.0 years [interquartile range (IQR) 2.5]). Associations between striatal tracer binding and symptoms were investigated using voxel-wise linear models, adjusting for age, sex, motor symptom severity, and medication. The primary outcome measure was the association between rest tremor amplitude and striatal DAT binding.ResultsAt the end of the follow-up period, of the 414 patients included (median age 68 years [IQR 14], 49.4% female), 148 were evaluated to have PD and 79 other forms of parkinsonism with striatal DAT deficit. In total, 187 patients had normal binding. Among the patients with PD, left and right rest tremor amplitudes were positively associated with ipsilateral striatal DAT binding (β = +0.12 [95% CI +0.05, +0.19] and +0.10 [+0.05, +0.15] specific binding ratio [SBR] per point; pFWE + Bonf. < 0.05, respectively). Left and right bradykinesia (β = −0.16 [−0.22, −0.09] and −0.18 [−0.25, −0.10] SBR per 5 points, pFWE + Bonf. < 0.05, respectively) and rigidity (β = −0.07 [−0.08, −0.04] and −0.08 [−0.11, −0.05] SBR per point, pFWE + Bonf. < 0.05, respectively) mainly showed a negative association with contralateral striatal DAT binding. No consistent associations were observed in non-PD groups.DiscussionThese findings confirm the positive association between rest tremor amplitude and ipsilateral striatal DAT binding in a clinical sample of PD patients. However, the non-PD groups were diagnostically heterogeneous, limiting conclusions about disease specificity.

Abstract Not required.

Hepatitis C virus (HCV)–associated kidney injury can affect both the glomeruli and the renal interstitium. The aim of this single-center, prospective real-world study involving HCV patients was to assess longitudinal changes in liver and kidney parameters during HCV treatment and to examine how renal function and urine findings evolved in those with kidney manifestations prior to therapy. In total, 217 patients treated for HCV-infection were enrolled for the study. Renal abnormalities were defined as either s-creatinine above the normal limit (male > 100 µmol/l, female > 90 µmol/l), or estimated glomerular filtration rate (eGFR) below < 60 ml/min/ 1.73 m2, or number of urine red blood cells above the normal (U–erythrocytes ≥ 20 × 10(E6)/l), or tubular proteinuria above the normal (U–α 1-microglobulin, UA1M, ≥ 12 mg/l), or glomerular proteinuria above the normal (U–albumin/creatinine ratio, UACR, in men ≥ 2.5 mg/mmol, in women ≥ 3.5 mg/mmol) levels in a spot urine test. Forty patients (20%) had pretreatment kidney manifestations. Sustained virological response at 12 weeks (SVR12) was achieved in 93%, with no difference observed between patients with or without pretreatment kidney manifestations. All liver function tests improved significantly at 12 weeks. Across the study period, serum cystatin C showed a marked improvement (p = 0.0128), while the other filtration markers did not change significantly from pretreatment levels to one year. The tubular proteinuria marker UA1M decreased significantly from pretreatment to SVR12 and further to the one-year follow-up (p < 0.0001 and 0.0046, respectively). Hematuria also declined markedly from pretreatment to SVR12 (p < 0.0001). In contrast, no significant change was observed in the glomerular proteinuria marker, UACR. Successful hepatitis C eradication therapy improves kidney function assessed by serum cystatin C and reduces tubular proteinuria as well as hematuria even in patients with low grade pretreatment kidney manifestations.

Abstract Background Parkinson’s disease (PD) is a neurodegenerative disorder for which there is currently no cure or reliable biomarker for early detection or for evaluating the effectiveness of potential treatments. PD pathology is driven by misfolding and subsequent accumulation of alpha-synuclein (αSyn) protein into pathological aggregates within neurons and glial cells. Seed amplification assay (SAA) is a highly sensitive and specific diagnostic tool developed to detect pathological αSyn species in the cerebrospinal fluid (CSF) of PD patients. However, αSyn aggregates are present in multiple tissues and biosamples, including stools. In this study, we aimed to investigate the potential diagnostic value of SAA using stool samples from PD patients and healthy controls (HC). Methods Stool samples from PD patients (n=45) and healthy controls (n=35) were analysed for the presence of αSyn species using slot blot assays with a panel of six αSyn antibodies, and ELISA assays. Samples were subjected to SAA, and the end-point products (SAA EP) were characterised using transmission electron microscopy (TEM). Extracellular vesicles (EVs) were isolated from the subset of samples (n=5 per group) using size exclusion chromatography and characterized by TEM. The seeding activity of isolated EVs was evaluated using SAA, followed by TEM analysis of SAA EP. Results Protein extracts from both PD and HC stool samples revealed pathological αSyn species in the slot blot assay using the phosphorylated αSyn antibody, pS129 and conformation-specific antibodies, MJFR-14 and 5G4. ELISA showed significantly elevated total αSyn levels in PD samples compared to HC, although no differences in aggregated αSyn levels were detected. In stool protein extracts, SAA demonstrated 55.6% sensitivity and 60% specificity. When applied to stool-derived EVs from PD patients and controls, sensitivity increased to 100%, while specificity remained at 60%. Notably, SAA applied to stool-derived EVs pre-incubated with recombinant monomeric αSyn achieved 100% sensitivity and 100% specificity. Conclusion These findings suggest that SAA applied to EVs isolated from stool samples, particularly after pre-incubation with recombinant monomeric αSyn, may serve as a valuable, non-invasive screening tool for the diagnosis of PD.