Background—Children with genetic disorders have multiple anatomical and physiological conditions that predispose them to obstructive sleep apnea syndrome (OSAS). They should have priority access to polysomnography (PSG) before establishing their therapeutic protocol. We analyzed the prevalence and the severity of OSAS in a particular group of children with genetic disorders and strengthened their need for a multidisciplinary diagnosis and adapted management. Methods—The retrospective analysis included children with genetic impairments and sleep disturbances that were referred for polysomnography. We collected respiratory parameters from sleep studies: apnea–hypopnea index (AHI), SatO₂ nadir, end-tidal CO₂, and transcutaneous CO₂. Subsequent management included non-invasive ventilation (NIV) or otorhinolaryngological (ENT) surgery of the upper airway. Results—We identified 108 patients with neuromuscular disorders or multiple congenital anomalies. OSAS was present in 87 patients (80.5%), 3 of whom received CPAP, 32 needed another form of NIV during sleep, and 15 patients were referred for ENT surgery. The post-therapeutic follow-up PSG parameters confirmed the success of the treatment. Conclusions—The upper airway obstruction diagnostics and management for children with complex genetic diseases need a multidisciplinary approach. Early detection and treatment of sleep-disordered breathing in children with genetic disorders is a priority for improving their quality of life.

Although cisplatin plays a vital role in chemotherapy protocols, its impact on hearing should not be overlooked. The ototoxic effects of cisplatin can lead to hearing loss. Childhood hearing loss can significantly impact various aspects of development. Understanding the mechanism of cisplatin-induced ototoxicity is crucial due to its high level of complexity. The process involves multiple interconnected steps, ranging from cisplatin absorption to its interaction with the cellular antioxidant defense system, nuclear DNA, mitochondria, and the cytokine cascade. Each of these interactions contributes to the overall pathophysiology of ototoxicity and is closely interrelated. Based on these, various hypotheses and conclusions were outlined, and we tried to analyze them as broadly as possible. Knowledge of these mechanisms has given rise to promising avenues and otoprotection strategies to combat ototoxicity. Although there is only one drug approved by the FDA (Food and Drug Administration), there are numerous drugs that target the mechanisms presented, but that need more evidence to be able to be used safely. In addition to these, the role of the multidisciplinary team should not be neglected and protocols should be established for periodic follow-up of patients treated with cisplatin to prevent hearing loss. This narrative review aims to point out all the aspects presented, based on the analysis of the literature and the conclusions drawn over time. We have selected the articles of interest and analyzed the studies that have obtained promising results to bring an overview of how cisplatin acts at the cochlear level, what can be done to combat these mechanisms, what solutions exist now and how we can prevent hearing loss.

Background/Objectives: The association between chronic obstructive pulmonary disease (COPD) and metabolic syndrome (MetS) is a common one, with long-term therapeutic and prognostic impact. In view of the high pulmonary and cardiovascular morbidity and mortality, self-management contributes to decreasing the risk of an acute cardiac event or pulmonary decompensation. Methods: We conducted a prospective cohort study on 100 patients admitted to Iasi Clinical Rehabilitation Hospital who were divided into two groups according to the presence (67 patients) or absence (33 patients) of MetS. All patients benefited from multidisciplinary counseling sessions on their active role in improving modifiable cardiovascular risk factors and thus increasing quality of life. The aim of this study was to examine the impact of metabolic syndrome on lung function and the role of self-management in a 6-month follow-up period. The demographic, anthropometric, cardiovascular risk factors, and respiratory function were analyzed at baseline and at 6 months. Results: The presence of MetS was associated with higher fasting blood glucose (p = 0.004) and triglycerides (p = 0.003) but not with higher levels of interleukins or TNF-alpha. At the 6-month follow-up, abdominal circumference, forced expiratory volume in one second (FEV1), dyspnea severity, and blood pressure values improved in male patients with COPD. Systolic and diastolic blood pressure decreased in the COPD group as a whole, but especially in male patients with and without associated MetS. BMI was positively correlated with FEV1 (r = 0.389, p = 0.001) and the FEV1/forced vital capacity (FVC) ratio (r = 0.508, p < 0.001) in all COPD patients and in the MetS subgroup. In the COPD group as a whole. the six-minute walk test (6MWT) results (m) were positively correlated with FEV1 and FVC. The correlation remained significant for FVC in COPD patients with and without MetS. An increase in BMI by one unit led to an increase in TG values by 3.358 mg/dL, and the presence of metabolic syndrome led to an increase in TG values by 17.433 mg/dL. Conclusions: In our study, MetS is a common comorbidity in patients with COPD and is associated with higher BMI, fasting glucose, and triglycerides but not with the inflammatory parameters. A mixed pulmonary–cardiovascular rehabilitation intervention leads to improvement in various parameters in both female and male COPD patients.

Background and Objectives: Assessment of the prothrombotic, proinflammatory, and functional status of a cohort of COVID-19 patients at least two years after the acute infection to identify parameters with potential therapeutic and prognostic value. Materials and Methods: We conducted a retrospective, descriptive study that included 117 consecutive patients admitted to Iasi Pulmonary Rehabilitation Clinic for reassessment and a rehabilitation program at least two years after a COVID-19 infection. The cohort was divided into two groups based on the presence (n = 49) or absence (n = 68) of pulmonary fibrosis, documented through high-resolution computer tomography. Results: The cohort comprises 117 patients, 69.23% females, with a mean age of 65.74 ± 10.19 years and abnormal body mass index (31.42 ± 5.71 kg/m²). Patients with pulmonary fibrosis have significantly higher levels of C-reactive protein (CRP) (p < 0.05), WBC (7.45 ± 7.86/mm³ vs. 9.18 ± 17.24/mm³, p = 0.053), neutrophils (4.68 ± 7.88/mm³ vs. 9.07 ± 17.44/mm³, p < 0.05), mean platelet volume (MPV) (7.22 ± 0.93 vs. 10.25 ± 0.86 fL, p < 0.05), lactate dehydrogenase (p < 0.05), and D-dimers (p < 0.05), but not ferritin (p = 0.470), reflecting the chronic proinflammatory and prothrombotic status. Additionally, patients with associated pulmonary fibrosis had a higher mean heart rate (p < 0.05) and corrected QT interval (p < 0.05). D-dimers were strongly and negatively correlated with diffusion capacity corrected for hemoglobin (DLCO corr), and ROC analysis showed that the persistence of high D-dimers values is a predictor for low DLCO values (ROC analysis: area under the curve of 0.772, p < 0.001). The results of pulmonary function tests (spirometry, body plethysmography) and the 6-minute walk test demonstrated no significant difference between groups, without notable impairment within either group. Conclusions: Patients with COVID-19-related pulmonary fibrosis have a persistent long-term proinflammatory, prothrombotic status, despite the functional recovery. The persistence of elevated D-dimer levels could emerge as a predictive factor associated with impaired DLCO.

This study investigates the correlation between anatomical variants of the Circle of Willis (CoW) and the presence of intracranial aneurysms (IcAs), a relationship insufficiently addressed in current literature. We conducted a 12-year retrospective observational study on 221 adult autopsied patients admitted to the “Prof. Dr. N. Oblu” Emergency Clinical Hospital in Iași, Romania. Demographic data, aneurysm morphology (location, diameter), and CoW anatomical variants were analyzed. IcAs were found in 29 cases (13.12%), most frequently located at the Anterior Communicating Artery (55.2%), with a majority measuring under 10 mm in diameter. A strong association was observed between IcAs and atypical CoW configurations (96.55%), particularly when three or four anatomical variants coexisted. No gender predisposition was identified. The mean age of patients increased with aneurysm size, yet larger aneurysms were less often associated with progression to death. Our findings suggest that the presence of multiple CoW variants significantly increases the likelihood of developing IcAs. These results may enhance prognosis and support clinical decision-making frameworks for managing cerebral aneurysms.

Background and Objective: Gliosarcoma (GS) is a rare and aggressive variant of glioblastoma (GB), accounting for 1–2% of GB cases. Our objective is to analyse the clinical, radiological, histopathological, and immunohistochemical characteristics of primary gliosarcoma in a single-center cohort and compare findings with existing literature. Material and Methods: We retrospectively reviewed ten adult patients with histologically confirmed primary gliosarcoma (GS) diagnosed between 2012–2021 at “Prof. Dr. N. Oblu” Emergency Clinical Hospital, Iași, Romania. Data extracted included demographics, clinical presentation, magnetic resonance imaging (MRI) features, surgical management, pathology, and immunohistochemistry. Results: Mean age at diagnosis was 64.1 years (range 47–79), with male predominance (male:female ratio = 6:4). Common symptoms included speech disturbances (30%), seizures (20%), and headache (20%), with a median symptom duration of 7 days. Tumours were supratentorial, primarily frontal (40%) or temporal (10%), with 50% involving multiple lobes. Histologically, all cases demonstrated biphasic glial-sarcomatous architecture; 40% showed giant-cell glioblastoma features. Immunohistochemistry revealed glial fibrillary acidic protein (GFAP) and oligodendrocyte transcription factor 2 (Olig2) positivity in glial areas, vimentin positivity in both components, isocitrate dehydrogenase 1 (IDH1) wild-type status, alpha thalassemia/mental retardation syndrome X-linked (ATRX) positivity, intermediate Ki-67 (~21%), and variable p53 expression. Conclusion: Primary gliosarcoma is an aggressive central nervous system (CNS) tumour with characteristic biphasic morphology, frequent dural contact, and meningioma-mimic imaging. Accurate diagnosis relies on histopathology, guiding maximal safe resection and adjuvant chemoradiation.