Background: Post-COVID-19 syndrome (PCS) is defined as the persistence or development of new symptoms 3 months after the initial infection with the SARS-CoV-2 virus, these clinical aspects being most often associated with functional respiratory changes, as well as imagistic modifications. This study aimed to evaluate longitudinal changes in pulmonary function among patients with PCS, in relation to the severity of the acute COVID-19 episode and the time elapsed since infection. Methods: A retrospective, observational study was conducted at the Clinical Hospital of Pulmonary Diseases Iași, Romania, between January 2021 and December 2022, including 97 adult patients with confirmed PCS. Demographic, clinical, and functional data were collected from medical records. Pulmonary function tests (PFTs) were performed according to ATS/ERS standards, assessing Forced Vital Capacity (FVC), Forced Expiratory Volume in the First Second (FEV1), FEV1/FVC ratio (Tiffeneau Index), Maximal Expiratory Flow at 50% and 25% of FVC (MEF50, MEF25), Diffusing Capacity of the Lung for Carbon Monoxide (adjusted for haemoglobin) (DLCO), Carbon Monoxide Transfer Coefficient (KCO), Alveolar Volume (AV), Total Lung Capacity (TLC) and Residual Volume (RV). Patients were grouped by time elapsed since infection (1-3, 4-7, 9-12, and up to 22 months). Statistical analyses included the Mann-Whitney U test, Spearman's correlation, ROC curve analysis, and Principal Component Analysis (PCA). Results: A progressive improvement in FVC was observed up to 9-18 months post-infection (p < 0.05), while FEV1 remained stable, suggesting a predominantly restrictive ventilatory pattern. Patients with moderate acute COVID-19 presented significantly lower FVC%, FEV1%, DLCO%, and KCO% values compared with those with mild disease (p < 0.05). Diffusion abnormalities (DLCO and KCO) persisted beyond 12 months, indicating lasting alveolar-capillary impairment. ROC analysis identified TLC (AUC = 0.857), AV (AUC = 0.855), and KCO (AUC = 0.805) as the most discriminative parameters for residual dysfunction. PCA revealed three major functional domains-airflow limitation, diffusion capacity, and lung volume-explaining up to 70% of total variance. Conclusions: We are facing the emergence of a new phenomenon, namely a secondary post-COVID-19 pandemic of patients confronting with persistent post-COVID-19 symptoms who present with functional respiratory changes and who require careful monitoring in dynamics, personalized treatments and a multidisciplinary approach.

Impulse oscillometry system (IOS) is an effort-independent pulmonary function testing technique that assesses respiratory system mechanics during tidal breathing and has gained increasing interest as a complementary modality to traditional pulmonary function tests (PFTs), while its physiological relevance and clinical role alongside conventional tests remain incompletely defined. This narrative literature review synthesises evidence on the correlations between IOS parameters and traditional PFT indices, summarises clinical applications across major chronic respiratory diseases, and discusses emerging developments including artificial intelligence-based approaches; the review is based on studies published since 2010 that compare IOS with spirometry, body plethysmography, and diffusing capacity of the lung for carbon monoxide (DLCO) in chronic obstructive pulmonary disease (COPD), asthma, and interstitial lung disease (ILD). Correlation studies indicate that IOS resistance-related parameters are more closely associated with obstructive ventilatory impairment, particularly in COPD and asthma, whereas reactance-related parameters show stronger associations with restrictive ventilatory abnormalities, lung volumes, and diffusion impairment, especially in ILD. Across disease entities, R5-20 and resonant frequency consistently demonstrate higher sensitivity for detecting small airway dysfunction. Clinically, IOS provides value in assessing bronchodilator responsiveness, evaluating asthma control, detecting small airway involvement when spirometry is preserved, and monitoring exposure-related airway effects. Artificial intelligence-based models integrating multidimensional IOS data further highlight its potential in disease screening and classification. Overall, IOS provides complementary physiological and clinical information beyond traditional PFTs, and further large-scale, multicentre studies and methodological standardisation are needed to support its broader clinical implementation.

Sarcoidosis is a systemic disease of unknown etiology, characterized by granulomatous inflammation in various organs. Elevated serum Immunoglobulin G4 (IgG4) levels are typically associated with IgG4-related disease (IgG4-RD), characterized by plasma cell infiltration and fibrosis, but their role in sarcoidosis remains unclear. Given the fibro-inflammatory nature of both conditions, this study aimed to describe a cohort of sarcoidosis patients with elevated IgG4 levels and explore the potential clinical relevance of this finding. We retrospectively analyzed biopsy-confirmed sarcoidosis cases with measured serum IgG4 levels. Clinical data were gathered, including demographics, organ involvement, pulmonary function tests (PFTs), sarcoidosis-associated pulmonary hypertension (SAPH), and markers of autoimmunity. The study cohort included ten patients with a mean age of 50 ± 15 years, comprising six males and seven Black individuals. Two patients reported a family history of sarcoidosis; the mean body mass index (BMI) was 28.5 ± 5.7. Five patients were never smokers, and four were former smokers. Eight patients had lung involvement, two with advanced Scadding stage 4, four with airflow obstruction, and two with restriction physiology on PFT. Out of seven patients with echocardiography, five had SAPH. Other organ manifestation included ocular disease in three patients, joint involvement in two, liver disease in two, and heart disease in one. Autoimmune markers were present in five patients. These findings suggest a potential overlap between IgG4-RD and sarcoidosis. Further research is needed to clarify IgG4's role in sarcoidosis and whether elevated serum IgG4 identifies a subset of patients who may benefit from B-cell depletion therapies.

Though a normal forced vital capacity (FVC) is typically thought to imply the absence of restriction, recent data suggest that restriction may in fact be common among patients with normal spirometry. However, the clinical significance of restriction with normal spirometry is unknown.

Polyarteritis nodosa (PAN) is a necrotising vasculitis that primarily affects medium-sized arteries and usually spares the lungs. Pulmonary involvement is rare and may complicate diagnosis when respiratory symptoms mimic infection or interstitial lung disease. We describe a 44-year-old woman with long-standing PAN who presented with several months of persistent dry cough and progressive shortness of breath. High-resolution computed tomography (HRCT) of the chest demonstrated a nonspecific interstitial pneumonia (NSIP) pattern. Given her long-term corticosteroid use, an atypical infection was initially suspected; however, bronchoscopy, sputum cultures, and blood studies were all negative. Despite high-dose corticosteroids, improvement was minimal, and a four-week course of co-trimoxazole led to gradual clinical improvement. Pulmonary function tests (PFTs) showed a markedly reduced diffusing capacity for carbon monoxide (DLCO) of 35% predicted, which improved by approximately 10% after five months. Other pulmonary function parameters were assessed and showed no significant interval change, with the overall pattern remaining restrictive. She had experienced a similar episode two years ago that also improved with combined antibiotic and corticosteroid therapy. Considering the recurrence, negative infectious work-up, and vasculitic background, the pulmonary abnormalities were attributed to PAN. This case highlights that, although rare, pulmonary manifestations of PAN can mimic atypical infection or interstitial lung disease. Clinicians should consider PAN-related lung disease in patients with unexplained respiratory symptoms and interstitial changes, particularly in the context of long-term immunosuppression. Multidisciplinary evaluation and careful exclusion of alternative causes are essential.

Pulmonary complications are a major cause of morbidity following pediatric allogeneic hematopoietic stem cell transplantation (allo-HSCT). However, longitudinal pulmonary function test (PFT) trajectories and early predictors of dysfunction, particularly the interplay between underlying disease, PFTs, and graft-versus-host disease (GVHD), remain poorly understood. In this retrospective single-center study, we analyzed 233 children undergoing their first allo-HSCT with ≥ 100-day survival. Patients were categorized into benign (acquired aplastic anemia, n = 142) and malignant (leukemia/lymphoma, n = 91) groups. We assessed longitudinal PFTs over 24 months and used Kaplan-Meier and multivariate logistic regression analyses to identify early predictors (including 3-month PFT values and GVHD) for subsequent Obstructive (OVD) and Restrictive Ventilatory Disorders (RVD). Over a median follow-up of 33.1 months, the malignant group exhibited significantly slower FEV1 recovery, greater severity of RVD (P = 0.006) and diffusion impairment (P = 0.040), and higher cumulative incidences of OVD (HR = 3.34, P = 0.013) and RVD (HR = 2.16, P = 0.013). The malignant group also had significantly higher rates of acute (P < 0.001) and chronic GVHD (P < 0.001). In multivariate analysis, the strongest independent predictors for RVD were lower 3-month FVC%pred (OR = 0.85, P < 0.001) and the presence of chronic GVHD (OR = 5.97, P = 0.027). For OVD, predictors were lower 3-month MEF50%pred (OR = 0.95, P = 0.030), acute GVHD (OR = 4.24, P = 0.014), and chronic GVHD (OR = 4.20, P = 0.018). Children with malignant diseases face a higher burden of post-HSCT pulmonary dysfunction, driven by both the underlying disease/treatment intensity and a higher incidence of GVHD. Early post-transplant PFTs (FVC%pred, MEF50%pred) and the development of GVHD are powerful, independent predictors of long-term ventilatory disorders. These findings underscore the need for routine, stratified longitudinal monitoring to facilitate early risk stratification and intervention.