The update of the American Thoracic Society/European Respiratory Society (ATS/ERS) classification of interstitial pneumonias published in 2025 extends the oprior classification system beyond merely idiopathic entities, now also encompassing entities with identifiable triggers [1]. The core component of this update is the terminological reorientation of the classification towards a descriptive, primarily morphologically oriented concept with the aim of a clear differentiation of radiological and histological patterns from clinically defined diseases. Acute interstitial pneumonia (AIP) is now designated as idiopathic diffuse alveolar damage (DAD), and desquamative interstitial pneumonia (DIP) as alveolar macrophage pneumonia (AMP). The pattern of bronchiolocentric interstitial pneumonia (BIP) has been introduced as an independent morphological pattern, reserving the term hypersensitivity pneumonitis (HP) exclusively for multidisciplinary diagnosis in the future. Furthermore, the updated classification provides a biologically founded and clinically applicable categorization system of interstitial and alveolar filling patterns and the prognostically relevant separation into fibrotic and nonfibrotic phenotypes. Also, there is a stronger emphasis on the transparent reporting of the diagnostic confidence by interstitial lung disease (ILD) boards, including the use of "provisional" diagnoses or of the term "unclassifiable ILD" in cases of low and very low diagnostic certainty. The current classification can help to standardize the diagnostic course and to make the decision-making process in the ILD board more transparent. It is to be expected that this update will be the foundation for future research and for new knowledge in the field of ILD. In addition, it should however not be ignored that the new classification has been critisized by some experts with respect to the introduction of the pattern of BIP and the provisional entity of "idiopathic BIP". It is feared that this change in terminology emphasizing the morphological pattern rather than causative factors could lead to reduced attention concerning potential trigger exposures in the diagnostic process.

INTRODUCTION: Checkpoint inhibitor-associated pneumonitis (CIP) is typically characterized by various radiographic patterns, including organizing pneumonia (OP), nonspecific interstitial pneumonia (NSIP), acute interstitial pneumonia (AIP), usual interstitial pneumonia (UIP), hypersensitivity pneumonitis (HP), and diffuse alveolar damage (DAD). However, cavitary lung lesions on chest CT images have rarely been described in the literature. CASE PRESENTATION: This article reports two lung cancer patients treated with immune checkpoint inhibitors (ICIs) who developed cavitary lung lesions on chest CT. Histopathology of OP with lymphocytic infiltration was supported by multiplex immunofluorescence. After excluding infection and tumour progression, CIP was diagnosed on the basis of the patient’s history of ICI use, clinical presentation, imaging characteristics, laboratory findings, and pathological results. Both patients responded well to glucocorticoids, showing complete or near-complete resolution of cavitary lesions. After steroid discontinuation, the first patient underwent right upper lobectomy followed by adjuvant chemotherapy. After lung cancer recurrence, the patient received combined chemotherapy, immunotherapy, and radiotherapy, with no observed recurrence of CIP during follow-up. The second patient has been receiving traditional chinese medicine treatment since 2025 at another hospital. CONCLUSION: CIP rarely presents with cavitary lung lesions on CT, and careful differentiation of CIP from infectious aetiologies is essential. Empirical management may lead to treatment failure; therefore, imaging and biopsy are crucial for precise patient care.

Acute interstitial pneumonia (AIP - also known as Hamman-Rich syndrome) is an acute, rapidly progressive idiopathic pulmonary disease that often leads to fulminant respiratory failure and acute respiratory distress syndrome (ARDS).[1] It can be distinguished clinically from other types of interstitial pneumonia by the rapid onset of respiratory failure in a patient without preexisting lung disease.[2] Louis Hamman and Arnold Rich first described it in 1935 as a fulminating diffuse interstitial fibrosis of the lungs.[3] In 1986, Katzenstein introduced the term AIP differentiating it from the group of chronic interstitial pneumonia.[4][5] The American Thoracic Society (ATS) and European Respiratory Society (ERS) classify AIP under major idiopathic interstitial pneumonia, compared to other rare or unclassified idiopathic interstitial pneumonia.[1]

Hemophagocytic lymphohistiocytosis (HLH) is an uncommon but potentially life-threatening condition where the body's immune system becomes overactive, causing widespread inflammation and organ damage. In this report, we present the case of a 21-year-old woman with a history of rheumatoid arthritis who developed secondary HLH, triggered by acute interstitial pneumonitis (AIP). This case sheds light on the importance of early recognition and intervention in managing this rare condition. It emphasizes the need to consider HLH in patients presenting with unexplained systemic inflammation similar to this case, particularly when triggered by AIP, as evidenced by the respiratory involvement in this case.

Acute interstitial pneumonia (AIP) is a rare idiopathic interstitial pneumonia with histology finding of diffuse alveolar damage (DAD). It is characterized by progressive hypoxic respiratory failure, high mortality rate, and absence of guidelines for its treatment. Here we present a case of a 64-year-old woman with progressive dyspnea, acute respiratory failure, diffuse bilateral reticulonodular opacities on standard chest radiograph, diffuse ground-glass opacities on computed tomography, and biopsy proven DAD. Diagnosis of AIP was established after extensive work-up that excluded the known risk factors for acute respiratory distress syndrome. Oxygen therapy and high-dose parenteral corticosteroids led to gradual improvement and resulted in complete respiratory recovery. Since there are no existing guidelines for treating AIP, more case reports and case series if not randomized control trials are warranted in order to define the most effective therapeutic modality.

The past decade has witnessed a change in landscape of cancer management with the advent of precision oncology. Immune checkpoint inhibitors (ICIs) have revolutionized cancer treatment and have played an important role in improving patient survival. While the patients are living longer, treatment with ICIs are sometimes associated with adverse effects, some of which could be fatal. Radiologists can play a crucial role by early identification of some of these adverse effects during restaging scans. Our paper focuses on the imaging features of commonly occurring ICI toxicities based on organ system.

Acute interstitial pneumonia (AIP) of cattle has been recognized for many decades. While the pathogenesis and risk factors for this condition in pastured cattle are relatively well characterized, there remains a poor understanding of the disease as it occurs in intensively fed cattle such as in beef feedlots. Specifically, in pastured cattle, AIP results from excessive ruminal production of the pneumotoxicant 3-methylindole (3-MI). In feedlot cattle, the evidence to substantiate the role of 3-MI is comparatively deficient and further investigations into the cause, pathogenesis, and control are sorely needed. This review highlights our current understanding of AIP with a focus on the disease as it occurs in feedlot cattle. Additionally, it illustrates the need for further work in understanding the specific animal factors (e.g. the ruminal microbiome, and the role of concurrent diseases), management factors (e.g. animal stocking and vaccination protocols), and dietary factors (e.g. dietary supplements) that may impact the development of AIP and which are relatively unique to the feedlot setting. All stakeholders in the beef industry stand to benefit from a greater understanding of what remains a pressing yet poorly understood issue in beef production.

The purpose of the present study was to investigate the expression of α-SMA and SM22α in airway smooth muscle (ASM) of bronchioles from children younger than 14 years who died of acute interstitial pneumonia (AIP). This is based upon the hypothesis that as contractile marker proteins α-SMA and SM22α can serve as an index of the overcontractile phenotype of ASM that is seen in AIP. Lung tissue samples of children were obtained from autopsies and divided into the AIP group (55.9% male and 44.1% female, between 0.4 and 132 months old, n = 34) and the control group (60% male and 40% female, between 2 and 156 months old, n = 10). We recorded the post-mortem interval (PMI), height, clinical symptoms and abdominal fat thickness (AFT) of each case. Haematoxylin-and-eosin-stained sections were used to examine the luminal area and observe the morphological changes in the bronchioles. Immunohistochemistry and Masson's trichrome staining were used to detect the expression of contractile marker proteins and the degree of pulmonary fibrosis respectively. Compared with the control group, the luminal areas of bronchioles in the AIP group were smaller (p < .001). The expression differences in α-SMA and SM22α between the two groups were statistically significant (p = .01 and p = .02 respectively). Also, there was no significant correlation of the contractile marker proteins expression with PMI, height, clinical symptoms and AFT. The collagen deposition difference in lung between the two groups was not statistically significant (p = .224). These findings suggest that enhancement of ASM contractile function appears to be involved in the death mechanism of children with AIP, which affords more insights into the understanding of AIP.

Acute interstitial pneumonia (AIP) is a significant disease of cattle and many aetiologies have been implicated on the basis of the characteristic pathological lesions. Bovine respiratory syncytial virus (BRSV) is one of the key aetiological factors in bovine respiratory disease complex and several studies have suggested, controversially, that BRSV may be an underlying cause of bovine AIP. BRSV infection is known to cause several distinctive histopathological changes, including epithelial syncytia formation and intracytoplasmic viral inclusions. However, distinguishing bovine AIP from BRSV-related pneumonia by clinical presentation, gross pathology or histopathology can sometimes be challenging. In order to identify the potential distinguishing features, we compared the histopathological findings of AIP that were, and were not, associated with BRSV infection in naturally occurring cases. We found that multinucleated giant cells were more frequently identified in cattle with AIP while bronchiolitis was more common in BRSV-infected cattle. However, this was not considered a sole indicator of either disease group. Statistically, we identified that a combination of several histopathological features, including alveolar septal necrosis, presence of multinucleated giant cells and bronchiolitis, can serve as an excellent indicator for distinguishing between idiopathic AIP and BRSV-related pneumonia, with a strong statistical significance (P = 0.0004). Based on the results of this retrospective study, we present a histopathological scoring system for predicting BRSV-associated AIP.

Acute interstitial pneumonia (AIP) in foals is a rare but challenging syndrome. Diagnostic imaging is crucial for its diagnosis. While there are some reports on radiographic findings, ultrasound is sparsely described. Variability in the evaluation of radiographs in AIP has been well described in human literature. Part one of this study is a prospective, observational, observer agreement study investigating inter- and intraobserver agreement in the assessment of thoracic radiographs. Part two is a prospective, controlled, descriptive study on thoracic ultrasonography in foals with AIP. Eighteen foals with AIP were examined daily by thoracic ultrasound. Thoracic radiographs were taken on three successive occasions. Blinded radiographs were assessed by three observers based on two semi-quantitative scores (pattern recognition, subjective evaluation). Foals that died underwent postmortem examination (n = 9); postmortem findings were compared to ultrasound findings on the day of death. Ultrasonographic findings were consistent with postmortem findings. Comet tail scores in foals with AIP were significantly higher (p < 0.0001) than in control foals. Interrater agreement for the assessment of radiographs was none to moderate (κ = 0.07-0.65) for pattern recognition and weak to moderate (κ = 0.58-0.62) for subjective scoring. Intrarater agreement varied from minimal to strong (κ = 0.30-0.80) for pattern recognition but was strong (κ = 0.83) for subjective scoring. In conclusion, the diagnostic value of thoracic ultrasound in foals with AIP is high due to good conformity with postmortem findings. The evaluation of thoracic radiographs showed high variability in inter- and intra-agreement.