Background and Objectives: Postoperative alignment after medial open-wedge high tibial osteotomy (MOWHTO) reflects both osseous correction and load-dependent joint response. We evaluated the internal radiographic performance of a prespecified threshold-based latent medial laxity (LML) adjustment and explored alternative deduction models. Materials and Methods: Seventy-two consecutive eligible knees were retrospectively analyzed. LML, defined operationally as the difference between joint-line convergence angles on supine valgus-stress and standing radiographs, was treated as a composite load-and-stress response. One-third of LML was deducted from the target correction angle when LML was ≤5°, and one-half when LML was >5°. The primary outcome was 1-year hip–knee–ankle (HKA) error within ±1.0°. Change in mechanical medial proximal tibial angle (ΔmMPTA) served as a radiographic proxy for executed osseous correction. Alternative deduction rules were compared by internal counterfactual analysis with leave-one-out cross-validation for fitted models. Results: Fifty-two knees (72.2%; 95% CI, 60.4–82.1%) were within ±1.0° of target. Mean signed error was −0.38 ± 0.95° (p = 0.001), with Bland–Altman limits of agreement from −2.25° to 1.49°. Mean ΔmMPTA was 6.03 ± 2.59°, versus a planned osseous correction of 6.81 ± 1.41°; the execution proxy averaged −0.78 ± 2.13° (p = 0.003). The residual planning component averaged +0.40 ± 2.04° (p = 0.098). In the internal comparison, the threshold rule yielded an MAE of 0.76° and 72.2% within ±1.0°, versus 1.79° and 41.7% with no adjustment. An exploratory continuous model (deduction = −1.77 + 0.736 × LML) yielded an MAE of 0.66° and 79.2% within ±1.0° (leave-one-out MAE, 0.68°). Conclusions: Threshold-based LML adjustment reproduced the individualized 1-year HKA target within ±1.0° in 72.2% of knees. This simple method appears feasible for preoperative planning; however, the small target-relative undercorrection bias warrants further refinement and prospective comparative validation.
Background and Objectives: Donor acute kidney injury (AKI) is increasingly recognized in deceased-donor kidney transplantation, but its association with long-term graft outcomes remains controversial. We examined the association between donor AKI and death-censored graft failure (DCGF) while accounting for confounding and competing risks. Materials and Methods: We conducted a retrospective cohort study of 258 adult deceased-donor kidney transplant recipients (144 with AKI donors, 114 with non-AKI donors); all exposure, outcome, and follow-up data were verified against the primary registry before analysis. Propensity score matching (1:1, caliper 0.2 SD of the logit) created 100 matched pairs, with robust variance estimation clustered on pairs. DCGF was analyzed with Fine–Gray competing-risk regression, treating death with a functioning graft as a competing event: a primary donor-level model in the matched cohort and an exploratory post-transplant event model in the full cohort, with biopsy-proven acute rejection as a time-dependent covariate. Results: DGF occurred in 49.0% of recipients of kidneys from donors with AKI and in 33.0% of matched controls (p = 0.031), and lasted longer after donor AKI (median 10 vs. 7.5 days, p = 0.039); DGF frequency rose steeply with AKI Stages 2–3 (63.0% and 80.8%), whereas Stage 1 was comparable to the non-AKI group (23.4% vs. 33.0%). Donor AKI was not significantly associated with DCGF (sHR 1.91, 95% CI 0.95–3.86, p = 0.07; 5-year cumulative incidence 23.1% vs. 13.8%, Gray p = 0.064). In the exploratory post-transplant event model, DGF >14 days was associated with DCGF (sHR 3.29, 95% CI 1.53–7.07, p = 0.002), and time-dependent acute rejection was independently associated with DCGF (sHR 2.71, 95% CI 1.16–6.33, p = 0.021). Conclusions: Donor AKI was associated with a higher incidence and, in particular, a longer duration of DGF, but not significantly with long-term DCGF, and a clinically relevant association cannot be excluded. Prolonged DGF (>14 days) remained associated with DCGF after multivariable adjustment in the exploratory model. Kidneys from donors with AKI may be considered for transplantation within an appropriate clinical context, with particular attention to the early post-transplant course.
Background and Objectives: Oral lichen planus (OLP) is a chronic immune-mediated disorder in which the need for systemic therapy remains difficult to predict using standardized clinical criteria. This retrospective two-center cohort study aimed to develop a multivariable clinical prediction model for systemic therapy escalation in patients with histopathologically confirmed OLP. Material and Methods: Medical records of 141 adult patients treated between 2022 and 2025 were reviewed. Baseline demographic, clinical, and laboratory variables were analyzed using univariate analyses, followed by multivariable logistic regression with backward stepwise selection and Firth penalized likelihood estimation. Discrimination was assessed by the area under the ROC curve (AUC), and internal validation was performed by bootstrap resampling (1000 samples) with repetition of the full selection procedure. Results: Four independent predictors of systemic therapy were identified: concomitant cutaneous lichen planus (penalized odds ratio (OR) 13.96, 95% CI 3.94–55.84), autoimmune thyroiditis (OR 12.67, 3.26–54.88), genital lichen planus (OR 10.21, 2.36–51.57) and oral Candida superinfection (OR 4.48, 1.10–18.82). The apparent AUC was 0.889 (95% CI 0.801–0.976); after bootstrap internal validation, the optimism-corrected AUC was 0.84 and the calibration slope 0.73, indicating moderate overfitting. Candida superinfection was the least stable predictor (selected in 43% of bootstrap samples). A prognostic risk matrix was developed to estimate the probability of systemic therapy escalation according to different combinations of predictors. Conclusions: The identified clinical factors and derived risk matrix may provide a preliminary framework for risk stratification and individualized therapeutic decision-making in patients with OLP. However, given the retrospective design and limited number of outcome events, these findings should be interpreted cautiously. Prospective external validation in larger independent cohorts is required before the model can be considered for routine clinical use.
Background and Objectives: Hepatocellular carcinoma (HCC) is a major indication for liver transplantation (LT); however, longitudinal musculoskeletal changes detectable by computed tomography (CT) during the first postoperative year remain insufficiently characterized. The aim of this study is to compare baseline CT-derived bone and muscle parameters between patients undergoing LT for HCC and controls and to evaluate longitudinal changes during the first postoperative year. Materials and Methods: This retrospective study included 64 patients who underwent LT for HCC and had technically adequate non-contrast abdominal CT examinations at baseline, postoperative day 180 (POD180), and postoperative day 365 (POD365). The control group comprised 64 patients undergoing non-contrast abdominal CT for urinary stone evaluation. CT-derived measures included L1–L4 vertebral trabecular attenuation, psoas muscle area (PMA), the psoas muscle index (PMI), and psoas muscle density (PMD). Repeated-measures analyses and adjusted linear mixed-effects models evaluated longitudinal changes within the HCC cohort. Results: At baseline, vertebral trabecular attenuation was higher in the HCC group than in controls (151 ± 36 vs. 137 ± 39, p = 0.037), whereas crude PMI, PMA, and PMD did not differ significantly. In hierarchical multivariable analysis, the between-group difference in vertebral attenuation was attenuated after adjustment, while age and baseline PMI remained independently associated with L1–L4 attenuation. In adjusted multivariate analysis, baseline PMD was higher in the HCC group than in controls (51.5 vs. 44.4, p < 0.001). Longitudinally, L1–L4 attenuation declined from baseline to POD180 and remained low at POD365 (overall p < 0.001), with no difference between POD180 and POD365. PMD also decreased over time (overall p < 0.001), whereas PMI and PMA showed no significant change. Adjusted mixed-effects analyses showed that these postoperative reductions persisted after adjustment for age, BMI, albumin, calcium, and ALP. The adjusted PMD model showed an additional decrease between POD180 and POD365 (mean difference, 1.411 HU; 95% CI, 0.065–2.757; Bonferroni-adjusted p = 0.037). Older age remained independently associated with lower vertebral attenuation and PMD. Conclusions: During the first year after LT for HCC, CT-derived vertebral trabecular attenuation and PMD showed significant longitudinal decreases, while psoas muscle quantity remained relatively stable. Muscle quality and vertebral attenuation may therefore provide earlier imaging signals of post-transplant musculoskeletal deterioration than area-based muscle-quantity measures.
Alzheimer’s disease (AD) is the leading cause of dementia worldwide and affects women more frequently than men. Although age remains the main risk factor, reproductive aging and changes in ovarian hormone exposure may also contribute to this difference. Premenopausal bilateral oophorectomy causes an abrupt loss of ovarian hormones, including estradiol, progesterone, and testosterone, and several observational studies have associated this change with a higher risk of later cognitive impairment or dementia, particularly when surgery is performed at a younger age. However, these studies have assessed different outcomes, including dementia, mild cognitive impairment, subjective cognitive changes, and AD-related imaging findings, and current evidence does not establish a direct causal relationship between oophorectomy and AD. Possible biological pathways include neuroinflammation, synaptic dysfunction, amyloid-β and tau-related changes, and cerebrovascular dysfunction, although much of the mechanistic evidence remains experimental or indirect. Genetic background, vascular health, age at surgery, and the duration of hormone deprivation may further influence individual risk. Hormone replacement therapy has an established role in the management of premature or early surgical menopause when there is no contraindication, but its effect on long-term AD prevention remains uncertain; the timing of treatment may be important, but current evidence does not confirm a preventive effect. This review summarizes current epidemiological, neuroimaging, and experimental evidence linking oophorectomy with cognitive health and AD, and discusses hormone therapy, pharmacological and non-pharmacological management, emerging research approaches, and remaining knowledge gaps. Future studies with detailed information on surgical timing, hormone exposure, genetic risk, vascular factors, longitudinal cognition, and AD-related biomarkers are needed to better define which women may be most vulnerable after premenopausal oophorectomy.
