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Background: Pulmonary fibrosis (PF) and post-infectious fibrotic lung disease are characterized by marked heterogeneity in radiologic patterns, physiologic impairment, and clinical presentation. Conventional analytic approaches often fail to capture non-linear and multimodal relationships between structural imaging findings and functional limitation. Integrating imaging-derived representations with clinical and functional data using artificial intelligence (AI) may provide a more comprehensive characterization of disease heterogeneity. Objectives: The objective of this study was to develop and evaluate a multimodal AI framework combining imaging-derived embeddings and structured clinical data to identify atypical clinical–radiologic profiles in patients with pulmonary fibrosis using unsupervised anomaly detection. Methods: A retrospective cohort of 41 patients with radiologically confirmed pulmonary fibrosis or post-infectious fibrotic lung disease was analyzed. Deep imaging embeddings were extracted from baseline thoracic CT examinations using a pretrained convolutional neural network and integrated with standardized clinical and functional variables. A multimodal variational autoencoder (VAE) was trained in an unsupervised manner to learn the distribution of typical patient profiles. Patient-specific anomaly scores were derived from reconstruction error plus latent regularization (β·KL divergence). Associations between anomaly scores, disease severity, and clinical markers were assessed using Spearman rank correlation. Results: Anomaly scores were right-skewed (median 26.91, IQR 22.87–32.11; range 19.75–46.18). Patients above the 85th percentile (anomaly score ≥ 33.85) comprised 7/41 (17.1%) of the cohort and occurred across all clinician-assigned severity categories (mild 3, moderate 1, severe 3). Anomaly scores overlapped substantially across severity groups, with similar medians (mild 26.47, moderate 28.55, severe 28.23). Correlations with conventional severity markers were weak and non-significant, including DLCO (% predicted; ρ = −0.25, p = 0.115) and FEV1 (% predicted; ρ = −0.22, p = 0.165), a pattern consistent with anomaly scores reflecting multimodal deviation rather than severity alone, while acknowledging the exploratory nature of the analysis. Highly anomalous patients frequently exhibited discordant clinical–radiologic profiles, including preserved functional capacity despite marked imaging-derived deviation or disproportionate physiological impairment relative to imaging patterns. Conclusions: This proof-of-concept study demonstrates that multimodal VAE-based anomaly detection integrating imaging-derived embeddings with clinical data can quantify clinical–radiologic heterogeneity in pulmonary fibrosis beyond conventional severity stratification. Unsupervised anomaly detection provides a complementary framework for identifying atypical multimodal profiles and supporting individualized phenotyping and hypothesis generation in fibrotic lung disease. Given the modest cohort size, these findings should be interpreted as illustrative and hypothesis-generating rather than generalizable.

Despite the early recognition of obesity as an epidemic with global implications, research on its pathogenesis and therapeutic approach is still on the rise. The literature of the 21st century records an excess weight found in up to 1/3 of children. Both the determining factors and its systemic effects are multiple and variable. Regarding its involvement in the potentiation of cardio-vascular, pulmonary, digestive, metabolic, neuro-psychic or even dermatological diseases, the information is already broadly outlined. The connection between the underlying disease and the associated comorbidities seems to be partially attributable to oxidative stress. In addition to these, and in the light of the recent COVID-19 pandemic, the role played by oxidative stress in the induction, maintenance and potentiation of chronic inflammation among overweight children and adolescents becomes a topic of interest again. Thus, this review’s purpose is to update general data on obesity, with an emphasis on the physiopathological mechanisms that underlie it and involve oxidative stress. At the same time, we briefly present the latest principles of pathology diagnosis and management. Among these, we will mainly emphasize the impact played by endogenous and exogenous antioxidants in the evolutionary course of pediatric obesity. In order to achieve our objectives, we will refer to the most recent studies published in the specialized literature.

Being defined as an autoimmune, chronic pathology, frequently encountered in any age group, but especially in pediatrics, celiac disease (also called gluten enteropathy), is gaining more and more ground in terms of diagnosis, but also interest in research. The data from the literature of the last decades attest the chameleonic way of its presentation, there may be both classic onset symptoms and atypical symptoms. Given the impact played by celiac disease, especially in the optimal growth and development of children, the current narrative review aims to highlight the atypical presentation methods, intended to guide the clinician towards the inclusion of the pathology in the differential diagnosis scheme. To these we add the summary presentation of the general data and therapeutic lines regarding the underlying condition and the existing comorbidities. In order to place the related information up to date, we performed a literature review of the recent articles published in international databases. We bring forward the current theories and approaches regarding both classic celiac disease and its atypical manifestations. Among these we note mainly constitutional, skin or mucous, bone, neuro-psychic, renal, reproductive injuries, but also disorders of biological constants and association with multiple autoimmunities. Knowing and correlating them with celiac disease is the key to optimal management of patients, thus reducing the subsequent burden of the disease.

This narrative review aims to analyze and compare the current literature on multisystem inflammatory syndrome in children (MIS-C) and Kawasaki disease (KD), with a focus on case definitions, clinical features, diagnostic approaches, treatment strategies, and outcomes. Through a comprehensive review of relevant studies, including screening titles, abstracts, and full-text articles, key similarities and differences were identified. Both MIS-C and KD involve immune system dysregulation and share clinical manifestations such as rash, gastrointestinal symptoms, and cardiovascular involvement, with treatments often centered around immunomodulatory therapies. However, significant differences were observed, particularly in terms of age distribution, demographic prevalence, clinical presentation, and diagnostic criteria, with KD primarily affecting younger children and being associated more prominently with coronary artery abnormalities. While both diseases raise concerns about severe cardiac involvement and the need for intensive care, their pathogenic mechanisms have not been fully understood. Ongoing research is critical to elucidating these mechanisms, refining diagnostic criteria, and optimizing therapeutic approaches to improve outcomes for affected children. This comparative analysis is essential for advancing the understanding of both conditions, as accurately distinguishing between MIS-C and KD has significant implications for clinical decision-making and patient management. Given their overlapping yet distinct clinical features, precise differentiation is critical for ensuring timely diagnosis, optimizing therapeutic strategies, and improving patient outcomes. The concern among pediatric patients stems from the potential for severe complications, particularly cardiac involvement, which underscores the need for heightened awareness, early recognition, and evidence-based treatment strategies to minimize long-term morbidity and mortality.

Diabetes is a complex condition with a rising global incidence, and its impact is equally evident in pediatric practice. Regardless of whether we are dealing with type 1 or type 2 diabetes, the development of complications following the onset of the disease is inevitable. Consequently, contemporary medicine must concentrate on understanding the pathophysiological mechanisms driving systemic decline and on finding ways to address them. We are particularly interested in the effects of oxidative stress on target cells and organs, such as pancreatic islets, the retina, kidneys, and the neurological or cardiovascular systems. Our goal is to explore, using the latest data from international scientific databases, the relationship between oxidative stress and the development or persistence of systemic damage associated with diabetes in children. Additionally, we highlight the beneficial roles of antioxidants such as vitamins, minerals, polyphenols, and other bioactive molecules; in mitigating the pathogenic cascade, detailing how they intervene and their bioactive properties. As a result, our study provides a comprehensive exploration of the key aspects of the oxidative stress-antioxidants-pediatric diabetes triad, expanding understanding of their significance in various systemic diseases.

Background and Objectives: The ponticulus posticus (PP) is a bony bridge that emerges from the posterior aspect of the superior articular process, to connect the posterior arch of the atlas. It is often associated with neurological symptoms. The aim of this study was to obtain an insight into this malformation, and prevalence in the North East region of the Romanian population. Materials and methods: This anatomical variant was analyzed through an observational and retrospective study which was carried out in St. Spiridon Hospital Iasi. The duration of the study was 10 months and, a number of 487 patients who presented neurological symptoms without cranio-cerebral traumatisms were enrolled and a computed tomography (CT) scan was performed. We proposed a new classification of PP in five types. The prevalence of PP was calculated and Skewness test, ANOVA test with Bonferroni correction, and Student’s t-test were used for statistical analysis. Results: Among the sample of 487 patients, PP was found in 170 cases (34.90%) in an age group of 8–90 years (mean age = 59.52 years, SD ± 19.94 years). Type I was found in 11.29%, followed by Type II—8.21%, Type III—5.13%, Type IV—5.54%, and Type V—4.72% (p = 0.347). It was 19.5%, mirroring the incomplete type, whereas the complete type was reported in 15.40% of cases (p = 0.347), the highest prevalence, namely 41.17% was found in the “41 to 60 years” age group, followed by 36.95% in the “21 to 40 years” group (p = 0.00148). The mean age was higher in patients with PP Type III (61.16 years, SD ± 19.98), while patients with PP Type V recorded the lowest mean age (56.48 years, SD ± 22.13). The differences between the comparative average ages on types were not statistically significant (p = 0.411). The gender and age were not good predictors of PP Type V (AUC < 0.600). Conclusion: according to our study, incomplete types of PP were found to be more prevalent as compared to complete types. No difference between males and females was detected. PP is more frequent in adults and young adults than in the elderly population. It is confirmed that gender and age were not good predictors of the bilateral complete type of PP.

[This corrects the article DOI: 10.3389/fimmu.2024.1394869.].

The overexpression of cyclin-dependent kinase inhibitor p16 (INK4a) is widely recognized as a surrogate marker for high-risk human papillomavirus (HPV) in anogenital malignancies, but its significance in invasive breast carcinoma is complex and remains frequently debated. While historically investigated as a viral proxy, emerging evidence suggests that elevated p16 levels in breast tissue may instead reflect intrinsic cell-cycle dysregulation and retinoblastoma (Rb) pathway disruption, though direct molecular confirmation is lacking in this area of research. This study aims to evaluate the role of p16 as an indicator of tumor aggressiveness for high-risk phenotypes. We conducted a retrospective study of 100 female patients with invasive breast carcinoma. Employing a purposive sampling strategy rather than a consecutive series, we analyzed a targeted cohort consisting predominantly of triple-negative breast cancer (TNBC) and high-grade tumors to evaluate biomarker patterns specifically in advanced disease contexts. Immunohistochemical assessment was performed using a standardized cumulative nuclear and cytoplasmic scoring system, with expression thresholds defined by receiver operating characteristic (ROC) curve analysis optimized for histological grade. p16 overexpression was a predominant characteristic of these aggressive tumors and was identified in 68% of cases. Statistical evaluation revealed a robust and significant correlation between p16 overexpression and the triple-negative molecular subtype, as well as a marked inverse relationship with estrogen receptor (ER) status. Although p16 levels were frequently associated with specific aggressive phenotypes, no statistically significant difference in overall survival was observed between expression groups, a finding attributable to the uniformly high-risk nature of the selected cohort. This study suggests an association between p16 expression levels and aggressive tumor features, although the study design limits causal inferences. A non-significant trend towards p16 overexpression was observed in ductal carcinomas compared to lobular subtypes, while high p16 expression was noted exclusively in G3 tumors within this selected cohort, a finding influenced by the purposive sampling strategy and the ROC-based cutoff definition. Tumor necrosis was more prevalent in p16-overexpressing tumors. Furthermore, p16 levels showed a strong inverse relationship with estrogen receptor (ER) status, as they were significantly elevated in ER-negative and triple-negative tumors compared to luminal phenotypes.

Pediatric nephrotic syndrome remains a complex clinical entity, with incompletely elucidated pathogenetic mechanisms, in which oxidative stress appears to have a substantial etiopathogenic role. Recent evidence supports the involvement of redox imbalance in podocyte damage, impaired glomerular function, and systemic decline. All this suggests that antioxidant interventions can favorably modulate the course of the disease. This narrative review aims to synthesize the most relevant data from the current literature on the interaction between oxidative stress and nephrotic syndrome in children, with a focus on the therapeutic potential of antioxidants. The analysis focuses on the molecular mechanisms by which oxidative stress contributes to the progression of renal dysfunction, the role of oxidative biomarkers in disease monitoring, and the ability of antioxidants to reduce the need for immunosuppressants and corticosteroids, thus contributing to the decrease in associated morbidity. The translational perspectives of antioxidant therapy are also discussed, in the context of the urgent need for effective adjuvant strategies with a safety profile superior to conventional therapies. By integrating these data, the paper supports the valorization of antioxidant interventions as an emerging direction in the management of pediatric nephrotic syndrome and substantiates the need for controlled clinical trials, with rigorous design, in this field.

Connective tissue represents the support matrix and the connection between tissues and organs. In its composition, collagen, the major structural protein, is the main component of the skin, bones, tendons and ligaments. Especially at the pediatric age, its damage in the context of pathologies such as systemic lupus erythematosus, scleroderma or dermatomyositis can have a significant negative impact on the development and optimal functioning of the body. The consequences can extend to various structures (e.g., joints, skin, eyes, lungs, heart, kidneys). Of these, we retain and reveal later in our manuscript, mainly the respiratory involvement. Manifested in various forms that can damage the chest wall, pleura, interstitium or vascularization, lung damage in pediatric systemic inflammatory diseases is underdeveloped in the literature compared to that described in adults. Under the threat of severe evolution, sometimes rapidly progressive and leading to death, it is necessary to increase the popularization of information aimed at physiopathological triggering and maintenance mechanisms, diagnostic means, and therapeutic directions among medical specialists. In addition, we emphasize the need for interdisciplinary collaboration, especially between pediatricians, rheumatologists, infectious disease specialists, pulmonologists, and immunologists. Through our narrative review we aimed to bring up to date, in a concise and easy to assimilate, general principles regarding the pulmonary impact of collagenoses using the most recent articles published in international libraries, duplicated by previous articles, of reference for the targeted pathologies.