Anorexia nervosa (AN) represents a disorder with the highest mortality rate among all psychiatric diseases, yet our understanding of its pathophysiological components continues to be fragmentary. This article reviews the current concepts regarding AN pathomechanisms that focus on the main biological aspects involving central and peripheral neurohormonal pathways, endocrine function, as well as the microbiome–gut–brain axis. It emerged from the unique complexity of constantly accumulating new discoveries, which hamper the ability to look at the disease in a more comprehensive way. The emphasis is placed on the mechanisms underlying the main symptoms and potential new directions that require further investigation in clinical settings.

Anorexia nervosa (AN) causes the highest number of deaths among all psychiatric disorders. Reduction in food intake and hyperactivity/increased anxiety observed in AN are also the core features of the activity-based anorexia animal model (ABA). Our aim was to assess how the acute ABA protocol mimics common AN complications, including gonadal and cardiovascular dysfunctions, depending on gender, age, and initial body weight, to form a comprehensive description of ABA as a reliable research tool. Wheel running, body weight, and food intake of adolescent female and male rats were monitored. Electrocardiography, heart rate variability, systolic blood pressure, and magnetic resonance imaging (MRI) measurements were performed. Immediately after euthanasia, tissue fragments and blood were collected for further analysis. Uterine weight was 2 times lower in ABA female rats, and ovarian tissue exhibited a reduced number of antral follicles and decreased expression of estrogen and progesterone receptors. Cardiovascular measurements revealed autonomic decompensation with prolongation of QRS complex and QT interval. The ABA model is a reliable research tool for presenting the breakdown of adaptation mechanisms observed in severe AN. Cardiac and hormonal features of ABA with underlying altered neuroendocrine pathways create a valid phenotype of a human disease.

BACKGROUND Echogenic masses in the mitral annulus are often incidental findings during routine echocardiography examinations. Most represent the wide spectrum of underlying mitral annular calcifications and usually do not require further diagnostic workup. However, a rare variant called "caseous calcification of the mitral annulus" (CCMA) can be challenging to diagnose and often requires an extensive workup with the use of multiple imaging studies in order to accurately confirm the pathology. CASE REPORT The aim of this case series was to illustrate the range of challenges associated with CCMA in various clinical scenarios to highlight the importance of multi-modality imaging in the differential diagnosis. Patient 1 was a 78-year-old asymptomatic woman with a round echo-dense structure incidentally found during a routine echocardiographic examination. Patient 2 was a 79-year-old woman with a suspected mitral abscess. Patient 3 was a 73-year-old woman with an incidentaloma (lung mass), with a concomitant lesion of the mitral annulus. All 3 patients required a unique combination of confirmatory imaging studies to ultimately confirm their diagnosis. CONCLUSIONS The incidental detection of CCMA-like changes requires multi-modality imaging to differentiate from abscesses and proliferative changes in the mitral annulus. Transthoracic echocardiography, transesophageal echocardiography, computed tomography, and cardiac magnetic resonance imaging play a key role in this diagnostic workup. Using a combination of these imaging modalities can enhance diagnostic accuracy and strongly influence the subsequent treatment and management strategies.

Background/Objectives: ST-segment deviation (STD) on electrocardiography (ECG) may reflect myocardial injury in critically ill patients. However, its prognostic significance in non-cardiac intensive care unit (ICU) populations remains unclear. We aimed to assess the association between STD on ICU admission and 30-day mortality and to evaluate its incremental prognostic value beyond the SOFA score. Methods: In this retrospective single-center study, we included 307 consecutive ICU patients (median age: 64.0 years; 65.5% men). Patients with acute cardiac conditions were excluded. STD was defined as ≥1 mm ST elevation or depression in any lead on standard 12-lead ECG performed on admission. The primary outcome was 30-day all-cause mortality. Prognostic associations were assessed using multivariable Cox regression adjusted for SOFA score. Discriminative performance was evaluated by comparing ROC curves for models with and without STD, with bootstrap-based testing (1000 iterations) to assess significance. Results: STD was present in 126 patients (41.0%) and occurred more frequently in non-survivors (47.6% vs. 36.5%, p = 0.033. In Cox regression, STD was independently associated with 30-day mortality (HR = 1.534; 95% CI: 1.081–2.177; p = 0.017), even after adjustment for SOFA score. This association remained statistically robust in bootstrap validation. The addition of STD amplitude to the SOFA score modestly improved model discrimination with a borderline significant difference between the areas under the curve (ΔAUC = 0.005, p = 0.0581). Conclusions: ST-segment deviation on the admission ECG is an independent predictor of 30-day mortality in non-cardiac critically ill patients and may enhance risk stratification beyond the SOFA score.