Amiodarone hydrochloride is an antiarrhythmic drug, with proven efficacy in prevention and treatment of numerous arrhythmias, atrial fibrillation especially, or ventricular arrhythmias, with a long half-life (55–60 days). The increased risk of developing amiodarone-induced pulmonary fibrosis is directly related to the dose and the duration of the intake. Amiodarone-induced pulmonary toxicity is conditioned by dose, patient’s age, and pre-existent pulmonary pathologies. The pattern for drug-induced lung injury may vary in many forms, but the amiodarone can cause polymorphous injuries such as diffuse alveolar damage, chronical interstitial pneumonia, organizing pneumonia, pulmonary hemorrhage, lung nodules or pleural disease. The pathological mechanism of pulmonary injury induced by amiodarone consists of the accumulation of phospholipid complexes in histocytes and type II pneumocytes. Differential diagnosis of pulmonary fibrosis induced by amiodarone is made mainly with idiopathic pulmonary fibrosis, left ventricular failure or infectious disease. Before starting treatment with amiodarone, patients should be informed of potential adverse effects and any new respiratory symptoms should promptly be reported to their family physician or attending physician. The assessment carried out at the initiation of amiodarone treatment should include at least chest X-ray and respiratory function tests and extrapulmonary evaluation.

Basal cell carcinoma (BCC) and cutaneous squamous cell carcinoma (cSCC) are the most frequently occurring non-melanocytic skin cancers. The objective of our study is to present the pathophysiology of BCC and cSCC and its direct relationship with the histopathological diagnostics and the differential diagnostics of these types of cancer, based on the morphological characteristics, immunohistochemical profile, and genetic alterations. The qualitative study was based on emphasizing the morphological characteristics and immunohistochemistry profiles of BCC and cSCC and the differential diagnostics based on the tissue samples from the Clinical Pathology Department of Mures Clinical County Hospital between 2020 and 2022. We analyzed the histopathological appearances and immunohistochemical profiles of BCC and cSCC in comparison with those of Bowen disease, keratoacanthoma, hyperkeratotic squamous papilloma, metatypical carcinoma, pilomatricoma, trichoblastoma, Merkel cell carcinoma, pleomorphic dermal sarcoma (PDS), and melanoma. Our study showed the importance of the correct histopathological diagnosis, which has a direct impact on the appropriate treatment and outcome for each patient. The study highlighted the histopathological and morphological characteristics of NMSCs and the precursor lesions in HE and the immunohistochemical profile for lesions that may make the differential diagnosis difficult to establish.

Cutaneous malignant melanoma is an extraordinarily aggressive and heterogeneous cancer that contains a small subpopulation of tumor stem cells (CSCs) responsible for tumor initiation, metastasis, and recurrence. Identification and characterization of CSCs in melanoma is challenging due to tumor heterogeneity and the lack of specific markers (CD271, ABCB5, ALDH, Nanog) and the ability of cells to dynamically change their phenotype. Phenotype-maintaining signaling pathways (Wnt/β-catenin, Notch, Hedgehog, HIF-1) promote self-renewal, treatment resistance, and epithelial–mesenchymal transitions. Tumor plasticity reflects the ability of differentiated cells to acquire stem-like traits and phenotypic flexibility under stress conditions. The interaction of CSCs with the tumor microenvironment accelerates disease progression: they induce the formation of cancer-associated fibroblasts (CAFs) and neo-angiogenesis, extracellular matrix remodeling, and recruitment of immunosuppressive cells, facilitating immune evasion. Emerging therapeutic strategies include immunotherapy (immune checkpoint inhibitors), epigenetic inhibitors, and nanotechnologies (targeted nanoparticles) for delivery of chemotherapeutic agents. Understanding the role of CSCs and tumor plasticity paves the way for more effective innovative therapies against melanoma.

Foster care young people have an increased overall risk for the development of chronic health conditions.Smoking is a major risk factor for many conditions with inflammatory component. We performed a cross-sectional pilot study to assess the correlation between tobacco consumption status and inflammatory profile among adolescents living with foster parents in the central region of Romania. A number of 35 teenagers aged 10-18 were enrolled. Blood samples were collected by venipuncture for complete blood count (CBC), fibrinogen, Interleukin-6 (IL 6), C reactive protein (CRP). Exhaled CO was measured and urine samples were collected in the same session for cotinine assessment. Of the 123 teenagers initially enrolled, 35 completed the entire study protocol. Urinary cotinine accurately reflected smoker status. Smoking did not affect hemoglobin levels or other hematological parameters in foster care teenagers. The value of C-reactive protein was higher in smokers. Plasma fibrinogen correlated with the daily number of cigarettes. Interleukin-6 did not correlate with the smoker status or the daily number of cigarettes consumed. Our study highlights the existence of an inflammatory response to smoking in foster care adolescents, a social category otherwise predisposed to various addictive behaviors.

Central sleep apnea (CSA) is a heterogeneous group of sleep-related breathing disorders characterized by intermittent absence of respiratory effort during sleep. CSA results from impaired neurological signaling from the respiratory centers to the respiratory muscles, leading to airflow cessation for at least 10 s. Major causes include heart failure, opioid use, central neurological disorders, and altitude exposure. This review outlines the pathophysiology of CSA, emphasizing ventilatory instability and brainstem dysfunction as key mechanisms. It details the classification of CSA subtypes, including Cheyne–Stokes respiration, high-altitude CSA, and drug-induced CSA. Clinical manifestations range from excessive daytime sleepiness to cardiovascular complications. Diagnostic approaches encompass polygraphy, polysomnography, and various laboratory tests to evaluate comorbidities. Treatment requires a multidisciplinary approach, addressing underlying conditions while utilizing positive airway pressure (PAP) therapy, adaptive servo-ventilation (ASV), supplemental oxygen, and pharmacological interventions. Newer modalities, such as phrenic nerve stimulation, offer promising outcomes for CSA management. This review underscores the necessity of an individualized, interdisciplinary strategy to improve patient outcomes in CSA.

Background and objective: Analysis of inflammatory biomarkers, along with the neutrophil/lymphocyte ratio (NLR) or platelet/lymphocyte ratio (PLR), supports the connection between inflammation and carcinogenesis. Methods: We conducted a retrospective observational study at the Clinical County Hospital Mureș involving patients with lung cancer. The parameters analyzed included histopathological type (NSCLC: squamous cell carcinoma or adenocarcinoma; SCLC), molecular mutations (EGFR, ALK, PD-L1), parameters from the complete blood count, inflammatory parameters, and associated comorbidities. Results: A total of 380 patients were included: 115 patients in the cancer group and 265 patients in the control group. Among patients in the lung cancer group, 88 were diagnosed with NSCLC (44 adenocarcinomas, 44 squamous cell carcinomas) and 27 with SCLC. Both NLR and PLR were significantly higher in cancer patients than in the control group (5.30 versus 2.60, p < 0.001; 217 versus 136, p < 0.001, respectively). NLR and PLR differ between men and women (p = 0.005 and p = 0.056, respectively). C-reactive protein was not correlated with either NLR (p-value: 0.0669) or PLR (p-value: 0.6733) in lung cancer patients. Conclusions: The NLR and PLR values may serve as new predictive biomarkers for the diagnosis of disease in patients with lung cancer, especially those with NSCLC.