Background: Post-psychotic depression (PPD) is an underestimated but clinically significant affective syndrome that occurs during remission from psychosis, particularly in schizophrenia. Material and Methods: This comprehensive review traces the evolution of this concept over five decades of research, starting from its initial differentiation from primary depression and schizoaffective disorders in the 1970s. Relying on more than thirty studies, we analyze historical definitions, biological and psychosocial mechanisms, diagnostic controversies, and therapeutic implications. Results: Research indicates that PPD develops from multiple contributing factors, including psychological insight, autobiographical disturbances, pharmacological influences, and social losses, rather than simply as a byproduct of psychosis or pharmacological treatment. We discuss the persistence of depressive symptoms after acute remission, their role in suicidal tendencies, and the diagnostic challenges arising from the overlap of negative symptoms and demoralization. Despite its exclusion from current diagnostic standards, PPD continues to affect a significant fraction of patients, particularly those with high insight and early onset. Conclusions: Effective treatment requires a multidimensional, phase-specific approach combining antidepressants, atypical antipsychotics such as lurasidone, and psychological interventions targeting identity, self-esteem, and narrative processing. We argue that PPD should be reintroduced as a distinct clinical unit and incorporated into psychiatric guidelines to reduce diagnostic oversights and improve patient outcomes.

Background/Objectives: Ustekinumab has been approved for the treatment of moderate to severe ulcerative colitis. Real-world data regarding its efficacy and the discovery of predictive factors of response need to be studied further. We aimed to evaluate the efficacy and identify predictors of response to induction treatment with ustekinumab in patients with ulcerative colitis. Methods: This is a multicenter, prospective cohort study. Clinical response (CR) at week 16 was the primary endpoint, and steroid-free clinical remission (SFCRem) and endoscopic response were the secondary endpoints. Baseline histology, mucosal gene expression, and pharmacokinetics were studied for their effect on response to treatment. Results: We included 123 patients (mean age = 50.3 years). CR was recorded in 70.8% (75/106), SFCRem in 48% (59/123), endoscopic improvement in 71.4% (40/56), and mucosal healing in 28.6% (16/56). Higher PRO-stool frequency (OR = 0.49, p = 0.027), concomitant use of 5-ASA (OR = 3.69, p = 0.021), platelet number of ≥284 × 109/L (OR = 6.52, p = 0.001) at baseline, and a drop in the total count of platelets by 108/L (OR = 1.23, p = 0.022) at week 8 were independently associated with CR. Elevated trough levels of ustekinumab at week 16 were associated with a higher probability of endoscopic improvement (median difference = 3784 ng/mL, p = 0.013), with an optimal cut-off value of 3500 ng/mL (AUC = 0.82, 95% CI: 0.66–0.96). Increased mucosal mRNA expression for IL-23 (p = 0.007) and IL-23R (p = 0.031) at baseline was associated with increased probability of CR. Higher continuous Geboes scores at baseline were associated with a lower probability of CR (OR = 0.80, p = 0.045), with an optimal cut-off value of 14 (AUC = 0.75, 95% CI: 0.57–0.93). Conclusions: Clinical, laboratory, and molecular markers may identify patients with ulcerative colitis who are more likely to respond to ustekinumab.

Background/Objectives: Despite substantial progress in understanding its pathophysiology and risk factors, gastric cancer remains a significant global health burden. Advances in endoscopic technology have improved the potential for early detection, yet variability in clinical practice persists. In this comprehensive narrative review, we summarize the most recent epidemiological trends in gastric pre-neoplastic and neoplastic lesions and critically appraise current evidence on optimizing endoscopic techniques and strategies for the detection of early gastric neoplasia, with an emphasis on emerging innovations. Methods: The relevant literature on epidemiology, risk factors, pathophysiology, and endoscopic management of GC was selectively reviewed based on the authors’ expertise and appraisal of contemporary evidence. Results: Marked global disparities persist in GC incidence, mortality, and stage at diagnosis. Interval GC—including missed lesions and so-called “true” interval cancers—remains a clinically relevant challenge and is frequently identified at advanced stages. These gaps are partly attributable to inconsistent quality in diagnostic esophagogastroduodenoscopy (EGD). High-quality EGD relies on adequate mucosal inspection time, systematic photodocumentation, optimal gastric preparation, and the use of standardized terminology, including mucosal visibility scores. Routine integration of chromoendoscopy and magnification techniques further enhances detection rates. Looking ahead, artificial intelligence holds promise as a transformative adjunct to standardize and augment real-time lesion recognition and quality assurance. Conclusions: High-quality endoscopic evaluation, coupled with tailored surveillance strategies, enables earlier detection of pre-neoplastic lesions and early gastric cancer, improving clinical outcomes. Future priorities include broadening access to high-quality endoscopy, harmonizing performance standards, and promoting continuous training alongside technological integration.

Background/Objective: The parotid gland is the largest salivary gland, and tumors arising from it exhibit wide histopathological diversity. Management approaches vary according to tumor characteristics and carry a risk of postoperative complications, particularly facial nerve injury. However, local data remain limited. This study aimed to describe the clinicopathological characteristics, surgical approaches, and postoperative outcomes of patients undergoing parotidectomy. Method: A retrospective cohort study was conducted at a high-volume tertiary center in Saudi Arabia. All consecutive patients who underwent parotidectomy between June 2015 and January 2025 were included. Demographic data, histopathological diagnoses, surgical procedures and postoperative complications were extracted from electronic medical records. Statistical analyses were performed using SPSS version 26, with A p-value of <0.05 considered statistically significant. Results: A total of 154 patients were included, with a mean age of 45.2 ± 12.6 years; 61% were male. Benign lesions constituted 87% of cases, with pleomorphic adenoma being the most common histopathological diagnosis. Malignancies accounted for 13% of cases, most frequently mucoepidermoid carcinoma. The most common postoperative complications were facial nerve palsy, followed by sensory numbness. Conclusions: The majority of parotid gland tumors in this cohort were benign, with pleomorphic adenoma as the most common histological subtype. Facial nerve palsy and sensory disturbances were the most common postoperative complications. These findings provide valuable local data on parotid gland lesions in Saudi Arabia and support current surgical management practices.

Background/Objectives: Chemically induced hepatotoxicity is widely used in experimental research to model liver disease pathophysiology and to support preclinical studies. Thioacetamide (TAA) is a well-established hepatotoxic agent in conventional laboratory rodents; however, its effects in synanthropic rats—characterized by genetic heterogeneity and chronic environmental exposure—remain poorly defined. This study aimed to establish and characterize a preclinical model of TAA-induced hepatotoxicity in synanthropic rats and to assess its relevance for experimental liver disease research. Methods: Female synanthropic rats representing four phenotypic variants (albino, mottled, black, and brown; total n = 132) were housed under controlled conditions and assigned to control or TAA-treated groups. TAA was administered intraperitoneally at doses ranging from 200 to 300 mg/kg. Clinical parameters, including body weight and vital signs, were periodically monitored. Hematological profiles and serum biochemical markers of liver function were analyzed. Hepatic injury was evaluated by histopathological examination using hematoxylin–eosin staining. Statistical analyses were performed using R software, with p ≤ 0.05 considered statistically significant. Results: TAA-treated rats developed consistent clinical manifestations of hepatotoxicity, including progressive weight loss and reduced activity. Biochemical analyses revealed significant increases in serum transaminases, gamma-glutamyl transferase, and alkaline phosphatase, accompanied by alterations in hematological parameters. Histological evaluation demonstrated dose-dependent liver injury characterized by centrilobular necrosis, inflammatory infiltration, hepatocellular degeneration, and architectural disruption across all synanthropic rat variants. Conclusions: Synanthropic rats exhibit reproducible biochemical, hematological, and histopathological features of TAA-induced liver injury comparable to those reported in conventional laboratory strains. This model represents a robust preclinical approach for studying chemically induced hepatotoxicity and may provide enhanced translational relevance due to its genetic and environmental heterogeneity.

Background and Objectives: Very preterm infants are vulnerable to late-onset infection and prolonged NICU exposure, with potential downstream effects on caregiver health. We evaluated neonatal outcomes and caregiver psychosocial status across culture-confirmed infection phenotypes. Methods: We investigated a single-center prospective cohort (March 2023–December 2025) of 87 preterm infants assigned to one of three groups: no proven infection (n = 44), bacterial sepsis (n = 31), or candidemia (n = 12). Neonatal outcomes included a composite adverse endpoint (death or major morbidity) and resource utilization. Caregivers completed the SF-36, WHOQOL-BREF, HADS, PHQ-9, GAD-7, and Body Image Scale near discharge. Results: Candidemia occurred later than bacterial sepsis (day of life 17.8 ± 4.8 vs. 10.1 ± 3.9; p < 0.001) and had a longer time to effective therapy (23.3 ± 9.5 vs. 13.3 ± 5.3 h; p = 0.004). The composite adverse outcome was 27.3% in the no-infection group versus 54.8% in the bacterial group and 58.3% in the candidemia group (p = 0.025); ROP requiring treatment increased from 4.5% to 29.0% and 25.0% (p = 0.012). Length of stay rose from 39.7 ± 10.2 to 50.1 ± 11.9 and 60.9 ± 13.1 days (p < 0.001), and ventilation days from 15.7 ± 7.6 to 23.3 ± 7.5 and 34.2 ± 10.4 (p < 0.001). Caregiver SF-36 mental health (MCS) scores decreased from 44.7 ± 7.5 to 38.5 ± 6.0 and 36.7 ± 6.4 (p < 0.001), while PHQ-9 scores increased from 9.4 ± 3.9 to 11.6 ± 3.3 and 15.5 ± 4.6 (p < 0.001); NICU burden correlated with PHQ-9 scores (r = 0.52, p < 0.001). Conclusions: Culture-confirmed infection, particularly candidemia, was associated with higher neonatal morbidity, markedly greater resource use, and substantial caregiver distress at discharge.

Objectives: Strictures are a major complication of Crohn’s disease (CD) affecting up to 20% of patients at diagnosis. Endoscopic balloon dilation (EBD) is the first-line endoscopic approach; however, it entails complications and a need for reintervention. Endoscopic stricturotomy (ESt) and stricturoplasty (ESTx) are promising alternatives. This review aims to provide an up-to-date and comprehensive assessment of their efficacy and safety in CD-associated strictures. Methods: A literature search was performed until August 2025. Primary outcomes were clinical and technical success. Secondary outcomes included adverse events, additional endoscopic or surgical treatments, medication escalation, emergency department visits and hospitalization following intervention. A minimum of four studies were required for meta-analysis, and pooled estimates were calculated using random-effects meta-analysis. Study quality was assessed using CASP checklist. Results: Fifteen studies including 1050 IBD patients (470 CD) were included. Strictures were short (0.9–2.4 cm) and some had prior EBD (7.8–57.1%) or surgery (3.6–91%). Technical success of ESt ranged from 88% to 100% and clinical success from 50% to 96%. The bleeding rate was up to 11.8%, but perforation rate was mostly <2%. The need for additional intervention, endoscopic (18.2–66.6%) or surgical (0–18.2%), varied considerably. Additionally, ESTx’s technical success ranged from 91.7% to 100% whereas clinical success ranged from 71.4% to 91%, with bleeding ranging from 5.2% to 8.8% and perforation from 0% to 3.4%. Similarly, the need for additional endoscopic procedures (7.1–57.1%) and surgery (9.5–25%) varied considerably. Conclusions: ESt and ESTx are safe and effective for managing CD-related strictures, particularly when short, straight, accessible, fibrotic, anastomotic, or refractory to EBD.

Background: Resuscitative endovascular balloon occlusion of the aorta (REBOA) is increasingly employed in patients with hemorrhagic shock and cardiovascular collapse; however, its impact on mortality remains controversial. Differences in geographic regions and patient populations may influence clinical outcomes. Methods: We conducted a systematic review and meta-analysis of observational studies comparing mortality between patients receiving REBOA and those managed without REBOA. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using random-effects models. Subgroup analyses were performed according to propensity score (PS) matching, trauma versus non-trauma populations, and geographic regions. Results: A total of 10 studies involving 18,611 patients were included. Overall, REBOA was not associated with a significant reduction in mortality compared with non-REBOA (pooled OR = 0.52, 95% CI: 0.19–1.39, p = 0.19). In PS-matched studies, the pooled OR was 0.82 (95% CI: 0.34–1.98, p = 0.66), whereas in non-PS-matched studies it was 0.40 (95% CI: 0.12–1.26, p = 0.12). Geographic analyses revealed no significant mortality benefit in either Western studies (OR = 0.47, 95% CI: 0.12–1.89; p = 0.29) or non-Western studies (OR = 0.60, 95% CI: 0.11–3.38; p = 0.56). No survival benefit was observed among trauma patients (OR = 0.57, 95% CI: 0.20–1.61; p = 0.29), whereas a significant reduction in mortality was observed in non-trauma patients (OR = 0.21, 95% CI: 0.05–0.88; p = 0.03). Conclusions: In this systematic review and meta-analysis, REBOA was not associated with a significant reduction in mortality in the overall population or in trauma patients. However, in a single small non-trauma study (n = 53), REBOA was associated with significantly reduced mortality; this finding is exploratory and requires confirmation in larger prospective studies. These findings suggest that the clinical benefit of REBOA may depend on patient population and underlying etiology of hemorrhage.

Thrombocytopenia is a frequent complication of patients presenting emergently across the world for a wide array of etiologies. From patients who develop thrombocytopenia due to invasive neoplastic disease affecting the bone marrow to patients who develop immune complications secondary to the formation of auto-antibody responses that drive patients’ platelet counts lower or even cause infection, these patients stress the clearest need for prompt tests to discern the more likely thrombocytopenic-inducing cause. It is in this setting that looking at other platelet variables easily obtainable from modern hematology analyzers has gained traction. One of the elements found in extended platelet profiles are immature platelets (youngest and newly released platelets), also known as reticulated platelets, which are readily measurable from a complete blood count. One of the advantages of obtaining these counts is that they represent the immediate response of the bone marrow to the thrombocytopenia and, depending on etiology inducing the thrombocytopenia, they also provide information on the marrow’s response to therapeutic approaches. It is in this context that this review will present information of how these relatively novel platelet parameters can be used in clinical practice and how they can be a rapid gauge of the body’s response to disease processes leading to platelet losses. Thrombocytopenias resulting from infection (sepsis, viremia), autoantibody formation (immune thrombocytopenia and immune-mediated thrombotic thrombocytopenic purpura), immune dysregulation (systemic lupus erythematosus), and iatrogenic (drug-induced) will be discussed and used to explain how these young platelet measurements can provide valuable clinical information.

Background: Early recognition of renal allograft dysfunction requires biochemical markers capable of detecting molecular injury before functional decline becomes apparent. Serum creatinine, a late and nonspecific indicator of renal function, has limited value for early diagnosis. Protein biomarkers implicated in tubular injury, inflammation, and immune activation—including neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), β2-microglobulin, interleukin-1β (IL-1β), and tumor necrosis factor-α (TNF-α)—have emerged as promising alternatives. This study evaluated early post-transplant serum profiles of these biomarkers and their prognostic relevance for long-term graft outcomes. Methods: Nineteen adult recipients undergoing primary kidney transplantation were prospectively enrolled. Serum creatinine and protein biomarkers were measured 24 h post-transplant using validated immunochemical assays. Biomarker concentrations were compared with values from healthy controls, and correlations with renal function at 12 months were assessed. Receiver operating characteristic (ROC) analysis was used to evaluate predictive performance. Results: Significant biochemical alterations were observed at 24 h post-transplant. KIM-1 levels were markedly elevated compared with controls (74.50 ± 98.45 vs. 10.54 ± 17.19 ng/mL; p = 0.01), consistent with early tubular injury. IL-1β and NGAL showed upward trends without reaching statistical significance. β2-microglobulin and TNF-α levels did not differ substantially from control values. Serum KIM-1 correlated with serum creatinine both at 24 h (r = 0.35) and at 12 months (r = 0.40). ROC analysis identified a KIM-1 threshold of 24.5 ng/mL (AUC = 0.68) as a potential indicator of future graft dysfunction, outperforming serum creatinine (AUC = 0.64). Six patients experienced graft dysfunction at 12 months post-transplant, five of whom had serum creatinine values > 5 mg/dL at 24 h. Based on early creatinine levels, patients were stratified into low-risk (creatinine < 5 mg/dL; n = 10) and high-risk groups (creatinine > 5 mg/dL; n = 9). Mean KIM-1 concentrations were significantly higher in the high-risk group (110.68 ± 115.29 vs. 26.67 ± 18.05 ng/mL; p = 0.05), consistent with more severe early tubular injury. Conclusions: Among the evaluated biomarkers, KIM-1 demonstrated the strongest potential as an early biochemical indicator of renal allograft dysfunction. Its rapid post-transplant elevation underscores its sensitivity to early tubular injury. Further prospective validation in larger, multicenter cohorts is warranted.