Pulmonary hemosiderosis is a rare and severe respiratory condition in children corresponding to chronic alveolar haemorrhage. Combined immune deficiencies are considered rare diseases, characterised by a quantitative or qualitative defect of T lymphocytes, associated or not with a complete or partial deficiency of immunoglobulin synthesis. We report a rare association of pulmonary hemosiderosis and class II HLA deficiency. Infant T, aged 9 months, was admitted for acute respiratory distress and pallor. The clinical examination found a marked mucocutaneous pallor, arterial oxygen saturation at 87%, a respiratory rate at 65 cycles/min, with diffuse crackling rales at both pulmonary hemifields. The blood count objectified with regenerative normocytic normochrome anemia and neutropenia. In addition, there was a CRP at 59 mg/l, a positive direct Coombs test, and a ferritin level elevated to 1095 ng/ml. Chest CT showed an aspect in favor of severe bilateral interstitial lung disease. The cytological study of bronchoalveolar lavage objectified a hemorrhagic fluid, with the cytological study siderophage at 46%, a positive Perls staining and a Gold score of 187. The immune assessment made it possible to make the diagnosis of combined immune deficiencies by HLA class II deficiency. T was put on antibiotic therapy, two blood cell transfusions, general corticosteroid therapy, nebulizations of salbutamol, Pulmicort, and an infusion of versatile immunoglobulins. The evolution was favorable. Treatment with allogeneic hematopoietic stem cell transplantation is ongoing. This observation recalls the importance of questioning the diagnosis of acute bronchiolitis, especially when the evolution seems atypical and unusual.

The increasing use of electronic cigarettes (e-cigarettes) among young adults has led to the emergence of electronic cigarette or vaping-associated lung injury (EVALI), which includes a wide spectrum of pulmonary complications. Diffuse alveolar hemorrhage (DAH) is a rare but life-threatening manifestation of EVALI. We aim to present a fatal case of DAH in a previously healthy young adult following recent e-cigarette use. A 23-year-old Turkish male with no prior medical history presented with dyspnea, cough, and hemoptysis 2 days after initiating frequent e-cigarette use. He had no history of chronic illness, substance use, or allergies. On admission, he was hypoxic with bilateral rales and diffuse ground-glass opacities on chest computed tomography (CT). Laboratory tests revealed severe anemia, leukocytosis, and elevated inflammatory markers. Despite treatment with high-dose corticosteroids, tranexamic acid, antibiotics, and supportive therapy, the patient's condition deteriorated, and he died on the 7[th] day of hospitalization. E-cigarette use has been increasingly associated with severe lung injuries, including DAH. The exact pathophysiology remains unclear but may involve direct alveolar epithelial damage and inflammatory responses. Our case is consistent with previously reported cases of vaping-induced DAH and highlights the potential severity of this condition. E-cigarettes are not a safe alternative to traditional tobacco. Clinicians should maintain a high index of suspicion for DAH in patients presenting with hemoptysis and respiratory failure following vaping. Early recognition and aggressive management are critical to improve outcomes.

Sevoflurane is a widely used agent for the rapid induction and maintenance of anesthesia. Diffuse alveolar hemorrhage (DAH) is characterized by acute onset of alveolar infiltrates and hypoxemia, resulting in progressive alveolar bleeding that requires urgent treatment. This report highlights the potential role of inhaled tranexamic acid (TXA) as an adjunctive therapy in DAH.

ANCA (anti-neutrophil cytoplasmic antibody)-associated vasculitis (AAV) is known to cause rapidly progressive renal dysfunction, as well as high mortality, especially in older patients. In Japan, a high prevalence of microscopic polyangiitis (MPA) with myeloperoxidase (MPO)-ANCA among older patients has been reported; however, standard immunosuppressive therapy does not always lead to improved outcomes in this population. Here we report the case of a 93-year-old woman who developed rapidly progressive glomerulonephritis (RPGN) due to MPA and successfully returned home after multidisciplinary treatment. She was transferred from another hospital because of antibiotic-refractory fever. Serological testing revealed MPO-ANCA positivity and a renal biopsy demonstrated crescentic glomerulonephritis. She was diagnosed with RPGN due to MPA and was initiated on standard glucocorticoid therapy, despite her advanced age. Because of severe disease activity complicated by diffuse alveolar hemorrhage, noninvasive positive pressure ventilation, rituximab, avacopan, and plasma exchange combined with hemodialysis were introduced. This multidisciplinary approach successfully induced remission of her AAV with partial recovery of renal function. After rehabilitation for mobilization, the patient was discharged home. She currently attends outpatient follow-up independently without assistance. Although very elderly patients are often excluded from clinical trials, resulting in limited evidence regarding the efficacy and safety of therapeutic agents, appropriately dose-adjusted multidisciplinary treatment based on overall clinical conditions may improve outcomes, even in this population.

A male castrated Shih Tzu was evaluated for recurrent nocturnal episodes of acute respiratory distress accompanied by hemoptysis and transient erythrocytosis. The dog was clinically normal between episodes, but each nighttime event was severe and prompted repeated emergency visits. During each emergency presentation, thoracic radiographs revealed severe diffuse interstitial-to-alveolar pulmonary infiltrates, and packed cell volume showed marked but reversible increases. A stepwise diagnostic evaluation, including serial indirect blood pressure measurement, coagulation assessment, echocardiography, and bronchoscopy with bronchoalveolar lavage, progressively excluded typical infectious, cardiac, structural, and coagulopathic causes of hemoptysis and acute respiratory distress. Given the stereotyped pattern of near-acute crises with diffuse pulmonary infiltrates and hemoptysis, mechanisms analogous to noncardiogenic pulmonary edema or exercise-induced pulmonary hemorrhage were considered. Therapeutic trials with sildenafil and furosemide failed to prevent further nocturnal recurrences. Considering concurrent transient PCV surges and the proposed role of catecholamine-driven splenic contraction as a rapidly mobilizable erythrocyte reservoir, a sympathetically mediated process was suspected, and α1-adrenergic blockade with prazosin was initiated. Following prazosin therapy, sustained clinical remission was achieved, with no further emergency episodes over a 17.5-month follow-up period. The response may have reflected multiple pharmacological effects of prazosin, including attenuation of sympathetically mediated splenic α1-adrenergic activity, systemic vasodilation, and reduction in venous return. This unique case suggests that dysregulation of the sympathetic nervous system may have contributed to the recurrent hemoptysis and acute respiratory distress and highlights adrenergic modulation as a potential therapeutic consideration in similar cases.

Severe pulmonary leptospirosis (SPFL), characterized by diffuse alveolar haemorrhage (DAH) and acute respiratory distress syndrome (ARDS), carries a high mortality, often due to diagnostic delays and complex management. We report a case of a 42-year-old male with outdoor occupational exposure who presented with fever and hemoptysis, rapidly progressing to severe respiratory failure and thrombocytopenia. Chest imaging confirmed DAH/ARDS. For refractory hypoxemia, veno-venous extracorporeal membrane oxygenation (VV-ECMO) was initiated without systemic anticoagulation due to active pulmonary haemorrhage. Metagenomic next-generation sequencing (mNGS) of bronchoalveolar lavage fluid rapidly identified Leptospira interrogans, enabling targeted antimicrobial therapy alongside multidisciplinary support. The patient gradually improved, was successfully weaned from ECMO and ventilator support, and was discharged without residual organ dysfunction. This case demonstrates that early application of anticoagulation-free VV-ECMO combined with mNGS-based rapid diagnosis and multidisciplinary care can improve outcomes in SPFL, highlighting the importance of considering this diagnosis in febrile patients with DAH and environmental exposure.

Background: Influenza is a common cause of hospitalization in young children, particularly infants. While most infections are self-limited, severe and life-threatening complications may occur. Diffuse alveolar hemorrhage (DAH) is a rare pulmonary manifestation of influenza, predominantly reported in adults, and is exceedingly uncommon in immunocompetent infants. Case Presentation: We report the case of an 8-month-old previously healthy female infant who presented with influenza A infection and rapidly progressed to acute respiratory failure and shock despite antiviral therapy. Bleeding was noted from the nasal cavity prior to clinical deterioration, and during emergent endotracheal intubation, blood was observed flooding the bronchial tree, consistent with massive pulmonary hemorrhage. Flexible bronchoscopy showed diffusely erythematous and friable airway mucosa without an identifiable focal bleeding source, and early bronchoalveolar lavage was nondiagnostic. Nasopharyngeal testing confirmed influenza A (H3). Laboratory findings revealed severe systemic inflammation, leukopenia with neutropenia, and anemia with normal coagulation parameters. Chest imaging demonstrated bilateral pulmonary infiltrates. After exclusion of autoimmune, coagulation, immunodeficiency, and alternative infectious causes, a diagnosis of diffuse alveolar hemorrhage secondary to influenza A infection was established. The patient was successfully managed with supportive care, antiviral therapy, tranexamic acid, and empiric antibiotics, without corticosteroid treatment, and made a full recovery. Conclusions: This case emphasizes that influenza-associated DAH in infants may occur without overt hemoptysis and may not demonstrate classical BAL findings early in the disease course. Clinicians should maintain a high index of suspicion in rapidly deteriorating infants with influenza and diffuse pulmonary infiltrates. The optimal role of corticosteroids remains uncertain and should be individualized.

Diffuse alveolar haemorrhage (DAH) is a rare but potentially life-threatening syndrome with diverse etiologies. Human metapneumovirus (hMPV) infection has rarely been reported as a cause of DAH. We report two cases of DAH associated with hMPV infection in immunocompetent adults. In both patients, bronchoalveolar lavage fluid (BALF) showed progressively haemorrhagic returns and hemosiderin-laden macrophages, consistent with DAH. Multiplex polymerase chain reaction (PCR) using BALF detected hMPV, while extensive investigations excluded autoimmune, bacterial, and other viral causes. These cases suggest that lower respiratory tract infection with hMPV can be associated with DAH, even in immunocompetent adults. Screening for hMPV should be considered in cases of DAH of unknown aetiology, and multiplex PCR using BALF is a useful diagnostic tool.

Libman-Sacks endocarditis (LSE), characterized by sterile valvular vegetations, is a recognized complication of systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS). However, its occurrence as the initial manifestation of previously undiagnosed autoimmune disease is uncommon and may create significant diagnostic uncertainty. A 27-year-old female presented to the emergency department with acute-onset exertional dyspnea, cough, and severe anemia, with a history of three consecutive first-trimester miscarriages. Initial evaluation revealed severe mitral regurgitation with valvular masses, raising suspicion for infective endocarditis. Further workup demonstrated elevated inflammatory markers, autoimmune hemolytic anemia, nephrotic-range proteinuria, and positive autoimmune serology, including antinuclear antibodies, anti-double-stranded DNA, anticardiolipin IgG, anti-β2-glycoprotein I IgG, and lupus anticoagulant. Transthoracic echocardiography showed severe mitral regurgitation with valvular masses and reduced left ventricular ejection fraction, while transesophageal echocardiography confirmed Libman-Sacks vegetations. Computed tomography of the chest revealed diffuse alveolar hemorrhage. The patient was diagnosed with new-onset SLE and APS, presenting with LSE and multisystem involvement. Management included pulse methylprednisolone therapy, hydroxychloroquine, cyclophosphamide, therapeutic anticoagulation, and plasma exchange for alveolar hemorrhage, resulting in clinical improvement with resolution of hemoptysis and improvement in cardiac function. This case is particularly notable because severe valvular disease led to the initial recognition of previously undiagnosed SLE and APS in the setting of simultaneous pulmonary, hematologic, renal, and obstetric manifestations. It highlights the importance of considering autoimmune etiologies in young patients with unexplained valvular heart disease, particularly in the presence of suggestive systemic features.

The lungs are the primary target of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), with the infection resulting in lung inflammation, pulmonary vascular leakage and diffuse alveolar damage. Polymerase delta-interacting protein-2 (Poldip2) mediates lung inflammation and vascular permeability after lipopolysaccharide-induced acute respiratory distress syndrome; however, whether it also affects the pathological consequences of SARS-CoV-2 infection is completely unknown. Here, we assessed the role of Poldip2 in inflammation, immune cell infiltration and lung tissue damage in response to SARS-CoV-2. Our data show that Poldip2 expression was elevated in human lung vascular endothelium after infection. In a Poldip2-deficient heterozygous mouse model, acute clinical symptoms were not affected. However, seven days after infection, Poldip2 knockdown reduced viral load, decreased infiltration of myeloperoxidase (MPO)-positive neutrophils into inflamed lungs, and reduced tissue damage. Poldip2 also modulated the inflammatory response to viral infection in a heterogeneous manner, reflecting its diverse regulatory roles. These data support the concept that targeting Poldip2 could potentially attenuate severe lung injury following SARS-CoV-2 infection.

Microscopic polyangiitis (MPA) and drug-induced vasculitis represent significant diagnostic challenges. Carbimazole-induced antineutrophil cytoplasmic antibodies (ANCA)-associated vasculitis is a rare, life-threatening complication of thionamide therapy. We describe a 29-year-old female patient on long-term carbimazole therapy for 15 years who presented with acute type-1 respiratory failure due to diffuse alveolar hemorrhage. Investigations confirmed myeloperoxidase (MPO)-ANCA-positive microscopic polyangiitis with co-existent definitive antiphospholipid syndrome and atypical "immune-complex-mediated" renal deposits. This case highlights the "triple-hit" of drug-induced vasculitis, thrombosis, and immune-complex deposition. The patient's rapid clinical stabilization following the initiation of plasmapheresis emphasizes the role of this intervention as a life-saving therapeutic bridge in complex vasculitis presentations.

This study presents a detailed histopathological analysis of lung tissue from 44 deceased COVID19 patients, aiming to elucidate the mechanisms driving severe disease progression. Postmortem biopsies were systematically examined, revealing diffuse alveolar damage in 95.5% of cases, predominantly in the acute/exudative phase. Characteristic features included extensive hyaline membrane formation, alveolar septal thickening, fibrin deposition, and red blood cell extravasation. Notably, advanced fibrosis, indicative of ongoing tissue remodeling, was observed in 86.4% of cases, highlighting the chronic pathological impact of the disease. Patient demographics showed a predominance of older males with comorbidities such as hypertension and diabetes, aligning with known high-risk profiles. The methodology involved meticulous autopsy procedures and standardized histopathological assessments to ensure the reliability of findings. This study provides key insight into histological changes in the lungs of COVID-19 patients, helping to clarify the disease's progression. It provides valuable insights that may contribute to a better understanding of long COVID and the potential long-term pulmonary complications in these patients. These findings may ultimately support improved management approaches and therapeutic strategies for COVID-19 care.