Atopic dermatitis (AD) is a chronic, relapsing inflammatory skin condition characterized by intense pruritus and a significant impact on a patient’s quality of life. Despite advancements in understanding AD pathophysiology, there remains a critical need for innovative therapeutic options to better manage this debilitating disease. This review focuses on the evolving landscape of biological therapies for AD, offering insights into their role, mechanisms of action, and potential to revolutionize patient care. In this review, we explore the underlying immunological mechanisms of AD, particularly the role of cytokines and immune pathways implicated in the disease, and how targeted biological therapies modulate these pathways. Current FDA- and EMA-approved biologics, such as Dupilumab, are also discussed in terms of their mechanisms of action, efficacy, and safety. Additionally, we compare their effectiveness, highlighting the benefits and limitations observed in clinical practice. Emerging biological therapies currently under development offer new hope, with innovative targets like IL-13, IL-31, and thymic stromal lymphopoietin (TSLP) representing promising avenues for intervention. We also delve into personalized medicine, emphasizing the importance of biomarkers for predicting treatment response and stratifying AD patients to optimize therapeutic outcomes. Moreover, the synergistic potential of combining biologics with traditional therapies is reviewed, along with a discussion of the challenges involved, including safety, long-term efficacy, and patient adherence. We address the future direction of AD treatment, including microbiome-targeting biologics and the development of next-generation immune modulators. We highlight a new era of targeted treatment possibilities for this complex condition.

Ototoxicity represents a clinically significant complication of anticancer therapy in pediatric patients. Cytotoxic agents used in oncology, particularly platinum-based chemotherapy, may induce damage to the auditory and vestibular systems, resulting in hearing loss, tinnitus, and balance disturbances. Even mild hearing impairment during childhood may negatively affect speech perception, language development, communication abilities, and subsequent educational and psychosocial functioning. This narrative review aims to synthesize current evidence on treatment-related ototoxicity in children, with particular focus on commonly implicated therapies, clinical consequences, diagnostic approaches, and potential preventive strategies. A focused literature search was conducted in PubMed for publications from 2019 to 2025 addressing ototoxicity associated with pediatric anticancer treatment and audiological monitoring methods. The analysis indicates that platinum-based compounds, especially cisplatin and carboplatin, remain the primary agents associated with ototoxicity, with reported incidence ranging from approximately 20–70% for cisplatin and 10–30% for carboplatin. Additional risk factors include young age, baseline hearing status, renal function, and exposure to other ototoxic agents such as aminoglycoside antibiotics. Early detection relies on comprehensive audiological monitoring combining behavioral and objective methods, including pure-tone audiometry, extended high-frequency audiometry, otoacoustic emissions, and auditory brainstem response testing. Standardized grading systems such as ASHA, Brock, Chang, and SIOP Boston criteria play a key role in identifying and classifying ototoxic changes. Emerging research focuses on improved monitoring protocols, biomarker identification, and the development of otoprotective strategies, including sodium thiosulfate and experimental molecular therapies. Implementing systematic hearing monitoring and preventive strategies is essential to reduce long-term auditory complications and improve quality of life in pediatric cancer survivors.

Brain tumors represent a major clinical challenge due to their complex biology, inherent resistance to conventional therapies and the limited delivery of anticancer agents across the blood–brain barrier. Natural phytochemicals such as curcumin, resveratrol and berberine have gained increasing attention for their multi-targeted anticancer properties, including induction of apoptosis, inhibition of proliferation, suppression of mitochondrial and BCL-2-family signaling and modulation of the tumor microenvironment. This comprehensive review critically examines current evidence on the use of curcumin, resveratrol and berberine in the context of brain tumor treatment, with an emphasis on gliomas’ mechanisms of action, pharmacokinetic limitations, and potential for integration into novel delivery platforms. We discuss how these compounds interact with key pathways in brain tumors—including BCL-2 inhibition, PI3K/AKT/mTOR signaling and epigenetic regulation—and the emerging strategies to overcome glioma-specific obstacles such as blood–brain barrier permeability and microenvironmental hypoxia. Furthermore, the review explores innovative formulations and carrier systems that enhance brain uptake and bioavailability of these agents, bridging the gap between preclinical promise and clinical translation. By identifying current gaps and proposing future research directions, this article aims to provide a roadmap for harnessing curcumin, resveratrol and berberine as adjuvant or combinatorial treatments in brain tumor therapy, focusing particularly on glioma treatment. The adoption of such phytochemicals may open new avenues for improved outcomes in patients with highly refractory brain malignancies.

Fever of unknown origin (FUO) remains a persistent diagnostic challenge in clinical medicine despite significant advances in laboratory testing and imaging techniques. The definition of FUO has evolved since the original criteria proposed in 1961 and currently refers to persistent fever exceeding approximately 38.2–38.3 °C without a definitive diagnosis after an adequate diagnostic evaluation. Gastrointestinal diseases represent an important but often underrecognized group of conditions associated with FUO. The aim of this review is to synthesize current evidence on the gastroenterological causes of FUO, with particular emphasis on pathophysiological mechanisms, diagnostic strategies, and therapeutic management. The analysis highlights the role of inflammatory, infectious, and neoplastic gastrointestinal disorders in the etiology of prolonged fever. Key mechanisms involve systemic inflammatory responses mediated by cytokines such as interleukin-1, interleukin-6, and tumor necrosis factor, as well as immune processes associated with the gut-associated lymphoid tissue (GALT) and interactions between intestinal microbiota and host immunity. Among the most frequently reported gastroenterological causes of FUO are inflammatory bowel diseases, intra-abdominal infections and abscesses, hepatobiliary disorders, pancreatitis, and gastrointestinal malignancies. Diagnostic evaluation requires a stepwise approach integrating laboratory testing, microbiological studies, imaging modalities, and endoscopic procedures, with advanced techniques such as computed tomography and fluorodeoxyglucose positron emission tomography improving detection of occult inflammatory or neoplastic processes. Therapeutic management is primarily guided by the identification of the underlying cause, while empirical treatment should be carefully considered to avoid masking diagnostic clues. A better understanding of the gastrointestinal mechanisms underlying FUO and the development of more efficient diagnostic algorithms may improve clinical outcomes and reduce the number of undiagnosed cases.