Overlap syndrome of systemic sclerosis and idiopathic inflammatory myopathies is an increasingly frequent entity, but the association with immune-mediated necrotizing myositis has rarely been described. While myositis or myopathy may be features of scleroderma, it is imperative to correctly diagnose an overlap syndrome of these two, since it can be considered a different entity with specific management and a worse prognosis. Anti-signal recognition particle (anti-SRP) antibodies target the striated muscle fiber and inhibit myoblast regeneration, resulting in myofiber atrophy and necrosis. Anti-SRP antibodies are specific in immune-mediated necrotizing myopathy characterized by myonecrosis and minimal inflammatory reaction, with proximal muscle weakness and typical extra-muscular manifestation. There are controversial data on the association of cardiac manifestations and the presence of these antibodies, and recent studies cannot prove a significant correlation between the two. Myocarditis is a complication with an unpredictable, potentially severe outcome from heart failure and dilated cardiomyopathy to fatality. It can be difficult to diagnose, and a myocardial biopsy can be problematic in daily practice; thus, most practitioners rely on cardiac magnetic resonance with suggestive images for the correct diagnosis. This paper seeks to address the challenges associated with the diagnosis and treatment of collagen diseases by evaluating the role of anti-SRP antibodies in the pathogenesis of cardiac involvement.

Background: Immunotherapy and targeted therapy have gained ground over conven-tional chemotherapy in treating various cancers. While pulmonary toxicity associated with these agents is rare, it represents a significant factor in both mortality and morbidity and may influence the overall success of cancer treatment. This case series report adds to the emerging evidence of cancer therapy-induced pneumonitis features and cortico-therapy outcomes. Patients and methods: This case series report consists of a retrospective analysis of 12 cases of patients undergoing immunotherapy (4 Nivolumab, 4 Pembrolizumab) or targeted therapy (3 Obinutuzumab, 1 Abemaciclib) for cancer (7 lung, 3 non-Hodgkin lymphoma, 1 breast, 1 renal) that developed pneumonitis during their follow-up. Results: The onset of pneumonitis ranged from 6 to 48 months (median = 18.5), and in 4 cases it occurred after discontinuation of oncologic treatment. The diagnosis was estab-lished with a high probability based only on clinical picture, radiologic features, and concomitant oncologic therapy. The cases with onset after discontinuation of oncologic treatment required a more thorough investigation (including bronchoscopy with BAL analysis). The main symptom was dyspnea (10/12 cases), and 3 of 12 patients had res-piratory failure (SpO2≤88%). The CTCAE severity grades were: 1 mild, 7 moderate, 3 severe, and 1 life-threatening. The CT scan showed different patterns (7 OP, 4 NSIP, and 1 HP). 11 patients received oral methylprednisolone (0.40 to 0.82 mg/kg) for 5 to 16 weeks. 2 patients continued oncologic treatment, and 6 discontinued. All patients showed fa-vorable outcomes. Conclusions: Immunotherapy and targeted therapy-induced pneumonitis can express various features and severities, and prompt recognition and diagnosis based on clinical, radiologic and contextual elements is mandatory. Corticotherapy regimens used, based on severity and treatment response, had a favorable outcome. The follow-up can consist only of clinical assessment and chest X-ray, and extensive tests are reserved for non-responsive cases.

Background: Immunotherapy and targeted therapy have gained ground over conventional chemotherapy in treating various cancers. While pulmonary toxicity associated with these agents is rare, it represents a significant factor in both mortality and morbidity and may influence the overall success of cancer treatment. This case series report adds to the emerging evidence of cancer therapy-induced pneumonitis features and corticotherapy outcomes. Patients and methods: This single-center, retrospective case series analyzed 12 consecutive cases of patients undergoing immunotherapy (four receiving nivolumab, four receiving pembrolizumab) or targeted therapy (three receiving obinutuzumab, one receiving abemaciclib) for cancer (seven with lung cancer, three with non-Hodgkin lymphoma, one with breast cancer, one with renal cancer) who developed pneumonitis during their follow-up. Results: The interval from oncological treatment initiation to pneumonitis onset ranged from 6 to 48 months (median = 18.5), and in four patients it occurred after discontinuation of oncologic therapy. In most patients, the diagnosis was established with high probability based only on the clinical presentation, radiologic pattern, and concomitant oncologic therapy. Bronchoscopy with bronchoalveolar lavage analysis was performed in eight of the 12 patients, particularly when onset followed treatment discontinuation. The main symptom was dyspnea (10/12 cases), and three of 12 patients had respiratory failure (SpO₂ ≤ 88%). The CTCAE severity grades were: one mild, seven moderate, three severe, and one life-threatening. The CT scan showed different patterns (7 OP, 4 NSIP-like, and 1 HP). Eleven patients received oral methylprednisolone (0.40 to 0.82 mg/kg) for 5 to 16 weeks. Two patients continued oncologic treatment, and six discontinued. Pneumonitis improved or resolved in 11 of the 12 patients; one patient deteriorated after reintroduction of immunotherapy and subsequently died from cancer-related complications. Conclusions: Immunotherapy- and targeted therapy-induced pneumonitis can express various features and severities, and prompt recognition and diagnosis based on clinical, radiologic and contextual elements are mandatory. In this small, heterogeneous series the individualized corticosteroid regimens used were followed by favorable outcomes. Our observations suggest that, in selected clinically improving patients, follow-up may rely only on clinical assessment and chest X-ray, and extensive tests may be reserved for non-responsive cases.

Background/Objective: Obesity is a documented risk factor for impaired pulmonary function and abnormal oxyhaemoglobin levels during sleep. This functional impairment becomes more significant when there are additional respiratory pathologies, such as obstructive sleep apnea (OSA) and/or chronic obstructive pulmonary disease (COPD). Overnight pulse oximetry may offer an effective evaluation of nocturnal oxyhaemoglobin levels/waveform patterns. We evaluated the correlation between obesity, overnight pulse oximetry (parameters, waveform patterns) and pulmonary function in patients diagnosed with moderate–severe OSA and normal oxyhaemoglobin saturation levels during waking hours. We also compared the overnight oxyhaemoglobin saturation levels between patients with OSA alone and those with associated COPD. Methods: This was a retrospective, transversal, non-interventional study on consecutive patients with moderate–severe OSA diagnosed using overnight cardiorespiratory polygraphy over a period of 18 months. After analyzing the study population’s characteristics, the patients were divided into two subgroups: one consisting of patients with OSA alone (Group A), and the second with coexisting OSA and COPD (Group B). Results: Seventy-six patients were included in the study, and 18% were diagnosed with COPD. A higher body mass index (BMI) correlated with a higher number of ≥3% SpO₂ drops/h (ODI3) and percentage of time with oxyhaemoglobin saturation < 90% (t90) and a lower average nocturnal oxyhaemoglobin saturation (avgSpO₂). ODI3 correlated negatively with avgSpO₂ and positively with t90. After eliminating BMI as a confounding factor, lower values of forced expiratory volume in the first second (FEV1) were associated with lower avgSpO₂ and higher t90. FEV1 did not corelate with ODI3. After dividing the study population into the two subgroups, patients from Group B had a tendency towards lower average nocturnal SpO₂ levels compared to Group A. Conclusions: Different phenotypes/patterns of nocturnal hypoxemia can be identified using quantitative and qualitative analyses of overnight pulse oximetry: repetitive, consecutive obstructive respiratory events with a characteristic intermittent (saw-tooth) hypoxemia pattern and alveolar hypoventilation, resulting in a continuous (plateau) hypoxemia pattern. According to our findings, nocturnal hypoxemia is more important at lower FEV1 values (correlating with lower avgSpO₂/higher t90, but not with ODI3). The presence of a continuous hypoxemia pattern in patients with OSA may suggest that pulmonary function tests should be performed in order to differentiate patients with alveolar hypoventilation secondary to obesity (restrictive syndrome) from those with associated COPD (obstructive syndrome). This can have an impact on the management of the case and the therapeutic approach (positive pressure therapy with/without supplemental oxygen).