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 - 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]

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.

Anaplastic lymphoma kinase (ALK) inhibitor-related pneumonitis (ALK-IIP) is relatively rare but sometimes fatal, so the timely diagnosis of ALK-IIP is important for enabling prompt management. However, the detailed radiologic characteristics and clinical course of ALK-IIP are still unclear. This study was performed to investigate the clinical and radiologic characteristics and risk factors of ALK-IIP in patients with non-small cell lung cancer (NSCLC).A total of 250 NSCLC patients who had been treated with ALK inhibitors were retrospectively enrolled. Chest computed tomography (CT) was classified into 4 CT patterns using the 2013 guideline for idiopathic interstitial pneumonia: cryptogenic organizing pneumonia (COP), hypersensitivity pneumonitis (HP), acute interstitial pneumonia (AIP), and nonspecific interstitial pneumonia. Clinical characteristics including toxicity grading and treatment course were analyzed in regarding to CT patterns. Clinical characteristics were compared between patients with ALK-IIP and without ALK-IIP.ALK-IIP was identified in 11 patients (4.4%). The most common CT pattern was the COP pattern (n = 7, 63.6%) and followed by HP and AIP patterns (both, n = 2, 18.2%). ALK-IIP showed pneumonitis toxicity grade ranged from 1 to 4, and AIP pattern had the highest toxicity grade, followed by HP and COP patterns (median grade: 3.5, 2.5, 1). All of the patients with the COP pattern were successfully treated, while half of patients with the AIP pattern died during treatment. The smoking history and extrathoracic metastasis were more frequent in patients with ALK-IIP (P < .005). The smoking history was associated with a higher incidence of ALK-IIP (odds ratio: 3.586, 95% confidence interval: 1.058-13.432, P = .049).ALK-IIP showed a spectrum of chest CT patterns, which reflected the toxicity grades. The COP pattern was the most common CT pattern of ALK-IIP, and patients with ALK-IIP of the COP pattern were successfully treated. ALK inhibitors should be used with caution in NSCLC patients with smoking history.

Acute interstitial pneumonia (AIP) is a rare and severe form of diffuse lung injury that affects previously healthy individuals. It is a subset of idiopathic lung disease with a rapidly progressive course. The prognosis is poor with over 50% of patients dying during hospital admission from progressive respiratory failure. Presented herein is a case of a previously healthy 64-year-old woman without a prior history of tobacco use who presented with progressive hypoxia, dyspnea, and nonspecific constitutional symptoms.

A 53-year-old man with ulcerative colitis (UC) suffered fatal acute interstitial pneumonitis (AIP) post completing an accelerated infliximab induction course. This is the first case reported in this setting. A literature review found four similar cases of infliximab-induced interstitial lung disease in the setting of treating patients with UC using standard infliximab regimens had successful treatment of the subjects post infliximab discontinuation. Unfortunately, the patient we are presenting, who had an accelerated infliximab induction course, did not survive. Although a prior small trial along more recent new small studies continue to show a benefit in reducing the need for early colectomy with the accelerated infliximab induction regimen as salvage therapy, it should be used cautiously until more safety data are available. Further larger trials are required to investigate rare side effects that may be associated with this regimen such as rapidly progressive lung toxicity as seen in this patient.

A previously well, 45-year-old Pakistani lady was admitted to the medical unit on-call of Khyber Teaching Hospital (KTH) Peshawar with a 5-day history of fever, productive cough with copious mucoid sputum, dyspnea, and pleuritic chest pain. She also complained of dry eyes, mouth, and vagina. Her chest X-ray showed diffuse alveolar shadowing and arterial gas analysis confirmed type 1 respiratory failure. Over the next few days, she deteriorated rapidly making an urgent transfer to the medical intensive care unit (MICU) necessary, where she was mechanically ventilated. An HRCT followed by bronchoscopic biopsies made a diagnosis of acute interstitial pneumonitis (AIP), formerly known as Hamman-Rich syndrome. She also turned out to be positive for both anti-SS-A/Ro and anti-SS-B/La antibodies along with a positive Schirmer's test and lower lip biopsy. She received intravenous steroids and supportive care. The patient had a complete recovery after approximately three weeks' stay in the hospital with lung function returning back to normal. This is most probably the first ever case of primary Sjogren syndrome (pSjS) presenting as AIP, recovering completely in less than a month time.

Idiopathic interstitial pneumonias (IIPs) may have an acute or subacute presentation, or acute exacerbation may occur in a previously subclinical or unrecognized chronic IIP. Acute or subacute IIPs include acute interstitial pneumonia (AIP), cryptogenic organizing pneumonia (COP), nonspecific interstitial pneumonia (NSIP), acute exacerbation of idiopathic pulmonary fibrosis (AE-IPF) and AE-NSIP. Interstitial lung diseases (ILDs) including connective tissue disease (CTD) associated ILD, hypersensitivity pneumonitis, acute eosinophilic pneumonia, drug-induced lung disease and diffuse alveolar haemorrhage need to be differentiated from acute and subacute IIPs. Despite the severe lack of randomized controlled trials for the treatment of acute and subacute IIPs, the mainstream treatment remains corticosteroid therapy. Other potential therapies reported in the literature include corticosteroids and immunosuppression, antibiotics, anticoagulants, neutrophil elastase inhibitor, autoantibody-targeted treatment, antifibrotics and hemoperfusion therapy. With regard to mechanical ventilation, patients in recent studies with acute and subacute IIPs have shown better survival than those in previous studies. Therefore, a careful value-laden decision about the indications for endotracheal intubation should be made for each patient. Noninvasive ventilation may be beneficial to reduce ventilator associated pneumonia.

Azacitidine is the first-line therapeutic option for myelodysplastic syndrome (MDS). This report describes a case of MDS in a patient who developed fatal acute interstitial pneumonitis (AIP) after the first seven-day course of intravenous azacitidine (75 mg/m(2)/day) treatment. A review of previous and present studies of azacitidine-associated AIP suggests that azacitidine may cause life-threatening AIP during or after the first seven-day course of treatment, with pyrexia commonly preceding AIP. Although the non-hematologic adverse events associated with azacitidine are generally relatively mild, further accumulation of evidence may help to make an earlier diagnosis of azacitidine-associated AIP.

Acute interstitial pneumonia (AIP) is a term used for an idiopathic form of acute lung injury characterized clinically by acute respiratory failure with bilateral lung infiltrates and histologically by diffuse alveolar damage (DAD), a combination of findings previously known as the Hamman-Rich syndrome. This review aims to clarify the diagnostic criteria of AIP, its relationship with DAD and acute respiratory distress syndrome (ARDS), key etiologies that need to be excluded before making the diagnosis, and the salient clinical features. Cases that meet clinical and pathologic criteria for AIP overlap substantially with those that fulfill clinical criteria for ARDS. The main differences between AIP and ARDS are that AIP requires a histologic diagnosis of DAD and exclusion of known etiologies. AIP should also be distinguished from "acute exacerbation of IPF," a condition in which acute lung injury (usually DAD) supervenes on underlying usual interstitial pneumonia (UIP)/idiopathic pulmonary fibrosis (IPF).

Bronchoalveolar lavage is a useful diagnostic tool in diffuse or disseminated lung malignancies that do not involve the bronchial structures visible by endoscopy. The neoplastic histotype and the intraparenchymal neoplastic growth pattern are good predictors for diagnostic yield; adenocarcinoma, and tumors with lymphangitic or lepidic growth patterns are more easily diagnosed by bronchoalveolar lavage; in these cases the diagnostic yield reported is higher than 80%. In hematologic malignancies the diagnostic yield is quite good in secondary diffuse indolent B cell lymphomas and in primary B cell lymphomas of mucosa-associated lymphoid tissue (MALT) type but low in Hodgkin disease. Morphological analysis may be implemented by immunocytochemical or molecular tests to identify the cell lineage and the presence of monoclonality. Disorders in which bronchioloalveolar cell hyperplasia/dysplasia is a significant morphological component may have cytological features in bronchoalveolar lavage fluid that mimic lung neoplasms: acute respiratory distress syndrome (ARDS), acute interstitial pneumonitis (AIP), and acute exacerbation of idiopathic pulmonary fibrosis are the most important clinical entities in this group.

Acute interstitial pneumonitis (AIP), also known as Hamman-Rich syndrome, is a distinct type of idiopathic interstitial pneumonia affecting patients of both genders without pre-existing lung diseases. We describe the case of a fulminant form of AIP and discuss the pathophysiological mechanisms of AIP with reference to the histological pattern. A 15-year-previously-healthy male boy presented to the Hospital with a 6-day history of malaise, fever and cough. The clinical prodromes were followed by the acute onset of increasing shortness of breath rapidly progressing in acute respiratory failure. Chest X-ray demonstrated bilateral diffuse airspace opacification; the high resolution CT confirmed the presence of bilateral, symmetric diffuse ground-glass attenuation. The patient was admitted to the intensive care unit, but died after few hours. An autopsy was performed within 24h. The histological examination of lung specimens showed a pattern of diffuse alveolar damage. immunohistochemical, microbiological and toxicological tests were also carried out. The clinical presentation, the histological findings and the exclusion of infective, traumatic, toxic and metabolic causes of acute respiratory distress syndrome (ARDS) allowed us to conclude that the boy was affected by AIP. In conclusion, AIP is a diagnosis of exclusion. It has a mortality rate ranging about 50%, despite mechanical ventilation. In fatal cases of AIP diagnosis can be based on clinical presentation, radiological, histological and microbiological findings and can be further confirmed by immunohistochemical analysis.

Interstitial pneumonia is a rare disease, posing a diagnostic challenge to pneumologists, pediatricians, radiologists and pathologists. Only by the combined efforts of the European Respiratory Society (ERS) and the American Thoracic Society (ATS) has has been possible to standardize the formerly different European and Northern American nomenclature of interstitial lung diseases (alveolitis versus interstitial pneumonia) in adults and to clearly and unambiguously define the diagnostic criteria. The ATS/ERS classification of 2002 comprises seven entities: usual interstitial pneumonia (UIP), non-specific interstitial pneumonia (NSIP), desquamative interstitial pneumonia (DIP), respiratory bronchiolitis-associated interstitial lung disease (RB-ILD), cryptogenic organizing pneumonia (COP), lymphocyte interstitial pneumonia (LIP), and acute interstitial pneumonia (AIP). Using the ATS/ERS classification of interstitial pulmonary diseases in premature infants, infants and children is problematic, since UIP, RB-ILD and AIP do not occur at this age. Although infants with severe respiratory insufficiency may sometimes show morphological features similar to DIP or NSIP, this entity should rather be classified as chronic pneumonitis of infancy (CPI) because of differences in etiology, pathogenesis and prognostic outcome.

Acute interstitial pneumonitis (AIP) is a fulminant disease culminating in acute respiratory failure and often death. Originally described in 1935 by the pathologists Hamman and Rich, this rare syndrome is characterized by rapidly progressive pulmonary fibrosis, leading to frequent confusion with idiopathic pulmonary fibrosis. In fact, the eponym Hamman-Rich syndrome became synonymous with idiopathic pulmonary fibrosis despite clear differences in clinical presentation, radiography, pathology, and survival. In 1986, Katzenstein described eight patients with acute respiratory failure of unknown etiology. On biopsy, organizing diffuse alveolar damage was present in all specimens. Given the idiopathic nature of the disease, Katzenstein coined the phrase acute interstitial pneumonitis to distinguish it from the fibroproliferative stage of the acute respiratory distress syndrome (ARDS), which has an identical pathology. Olson et al retrospectively examined Hamman and Rich's original cases, compared them to contemporary cases of AIP, and found the two identical. Since then, little progress into understanding this disease has been made. Many questions still linger regarding the epidemiology, pathogenesis, and outcome. We recently published our experience with AIP providing new information regarding natural history. This review summarizes the current literature on AIP emphasizing diagnostic criteria, pathogenesis, and natural history.

The idiopathic interstitial pneumonias have unknown etiology and are characterized by diffuse parenchymal lung involvement and the potential to develop pulmonary fibrosis. Most portend a reduction in life expectancy due, in part, to the absence of effective therapies. The symptoms of idiopathic interstitial pneumonia develop insidiously. In contradistinction, acute interstitial pneumonia (AIP, also known as acute interstitial pneumonitis) is unique in that it has a very rapid to fulminant onset, leading to early hospitalization and a high initial case fatality ratio but, potentially, a more favorable long-term prognosis for survivors. Despite its contemporary description nearly 20 years ago, knowledge of this disease has increased little. This review focuses on AIP and its current place among the idiopathic interstitial pneumonias.

Acute interstitial pneumonitis (AIP) is an acute, idiopathic interstitial lung disease characterized by rapidly progressive diffuse pulmonary infiltrates and hypoxemia requiring hospitalization. The case-fatality ratio is high. Previous reports suggested that survivors of the acute event have a favorable outcome. We undertook this study to examine the natural history of survivors. We had observed several patients who experienced recurrent episodes of AIP and chronic progressive interstitial lung disease. We sought to determine longitudinal survival in these patients and to compare our experience with that in the medical literature. Overall, we identified 13 biopsy-proven cases of AIP. The mean patient age was 54 years in our review, which is identical to previous reports. Twelve patients were hospitalized and all 12 required mechanical ventilation. Overall hospital survival was 67%. All patients demonstrated abnormalities in gas exchange at presentation. Radiographs typically demonstrated bilateral patchy densities that progressed to a diffuse alveolar filling pattern in nearly all cases. All biopsy specimens showed organizing diffuse alveolar damage. Longitudinal data were available for 7 patients. Two died of AIP recurrences. A third died of complications of heart failure shortly after hospital discharge. One patient progressed to end-stage lung disease and required lung transplantation. Two patients experienced persistent pulmonary symptoms, accompanied in 1 by progressive lung fibrosis. One patient had nearly complete recovery of lung function 2 years following AIP. (Follow-up information was unavailable for 2 survivors.) In our literature review, 5 of 7 patients reported experienced some recovery of lung function. One case of progressive interstitial lung disease requiring lung transplantation was reported. The reported mortality was much higher than in our experience (74% versus 33%). The mean time from symptom onset to death was 26 days, compared with 34 days in our experience. The use of corticosteroids did not appear to influence survival, although this has not been tested in a rigorous manner. The better survival in our series may be related in part to a survivor selection bias. In contrast to previous reports, we found that survivors of AIP may experience recurrences and chronic, progressive interstitial lung disease. We did not identify any clinical or pathologic features that predict mortality in these patients. Likewise, there were no features that predicted the longitudinal course in survivors. Further study to identify causal factors is required in the hope of preventing morbidity and mortality related to this disease.

The term "acute interstitial pneumonia" (AIP) describes an idiopathic clinicopathological condition, characterized clinically by an interstitial lung disease causing rapid onset of respiratory failure, which is distinguishable from the other more chronic forms of interstitial pneumonia. It is synonymous with Hamman-Rich syndrome, occurring in patients without pre-existing lung disease. The histopathological findings are those of diffuse alveolar damage. AIP radiologically and physiologically resembles acute respiratory distress syndrome (ARDS) and is considered to represent the small subset of patients with idiopathic ARDS. It is frequently confused with other clinical entities characterized by rapidly progressive interstitial pneumonia, especially secondary acute interstitial pneumonia, acute exacerbations and accelerated forms of cryptogenic fibrosing alveolitis . Furthermore, many authors use the above terms, both erroneously and interchangeably. It has a grave prognosis with >70% mortality in 3 months, despite mechanical ventilation. This review aims to clarify the relative clinical and pathological issues and terminology.

Elevated levels of serum surfactant protein-D (SP-D) have been previously reported in patients with idiopathic pulmonary fibrosis (IPF) and pulmonary alveolar proteinosis. To determine whether the same change is seen in other pulmonary diseases, especially pulmonary tuberculosis (TB), we measured the serum SP-D levels in active pulmonary TB (smear and/or culture: positive), acute interstitial pneumonia (AIP), IPF, acute exacerbation of IPF, hypersensitivity pneumonitis (HP), pneumoconiosis, bronchiectasis, and bacterial pneumonia by an enzyme-linked immunosorbent assay using monoclonal antibodies to human lung SP-D, and compared them with those of healthy elderly subjects over 50 years of age. The SP-D level in the healthy elderly subjects was 57.6 +/- 38.4 ng/ml (mean +/- SD, n = 287). The levels in patients with active pulmonary TB (140.6 +/- 18.2 ng/ml, n = 49), AIP (1,021 ng/ml, n = 1), IPF (307.0 +/- 180.7 ng/ml, n = 42), acute exacerbation of IPF (817.7 +/- 283.6 ng/ml, n = 3), and HP (716.6 +/- 548.8 ng/ml, n = 4) were significantly higher than those in the healthy elderly controls (p < 0.05), whereas those of pneumoconiosis, bronchiectasis, and bacterial pneumonia, 121.9 +/- 92.8 ng/ml (n = 8), 93.9 +/- 72.9 ng/ml (n = 11), and 72.7 +/- 3.4 ng/ml (n = 4), respectively, showed no significant difference with the controls. In active pulmonary TB, the percentage of patients whose serum SP-D levels were over 134.6 ng/ml (mean + 2SD of healthy elderly controls) was 34.7%, and therefore we considered the serum SP-D level was not useful for the diagnosis of pulmonary TB. However, it was significantly higher in the patients with cavity formation than in those without (p < 0.05), and there was a significant positive correlation between the serum SP-D level and the number of tubercle bacilli in the sputum (r = 0.416, p = 0.00165), erythrocyte sedimentation rate at 1 hr (r = 0.489, p < 0.01), and CRP level (r = 0.383, p = 0.003). These findings suggest that the serum SP-D level is a useful indicator of the disease activity in pulmonary TB.

Diffuse alveolar damage (DAD) and acute interstitial pneumonitis (AIP) often present clinically as the adult respiratory distress syndrome. To evaluate the usefulness of histochemical techniques and to better understand the histopathologic changes of these diffuse lung injuries, postmortem lung sections of 14 and 33 patients who had been diagnosed as having DAD in organizing stage and AIP, respectively, were studied with the use of lectins and monoclonal antibodies against surfactant apoprotein (PE-10) and collagen type IV. On hematoxylin-eosin stained sections, type II pneumocyte hyperplasia and hyaline membrane formation were the major histopathologic findings in both DAD and AIP. The binding rates of type II pneumocytes to Ulex europaeus agglutinin I (UEA-I) in both DAD (64%) and AIP (45%) cases were significantly higher than those of type I pneumocytes or alveolar macrophages (both P < 0.001). Reactions of type II pneumocytes to PE-10 varied from 40 to 44% in DAD and 0 to 100% in AIP cases depending on the use of respirator and steroid medication. Therefore, it may be said that UEA-I and PE-10 are useful methods for outlining hyperplastic type II pneumocytes in both DAD and AIP. Hyaline membrane coating alveolar septal surfaces and exudate in alveolar air spaces were also stainable with PE-10. Surfactant apoprotein remained demonstrable histochemically within type II pneumocytes and hyaline membrane despite severe inflammatory injuries of the lungs. The immunohistochemical stain using anti-collagen type IV antibody revealed discontinuous alveolar basement membrane in 50% of DAD patients with respirator use and 80% of AIP patients with steroid medication.

Increased use of open lung biopsy in the search for a treatable etiology of acute interstitial pneumonitis (AIP) in immunocompromised patients is based on the assumption that examination and cultures from biopsy specimens will yield significant information leading to beneficial treatment of the condition. To assess the true impact of the results of open lung biopsy on the subsequent treatment and outcome in such patients, a retrospective study was done of 64 consecutive patients undergoing the procedure in a recent five-year period. When open lung biopsy was performed for the diagnosis of AIP in immunocompromised patients after empiric broad spectrum treatment failed, it rarely missed a specific, treatable etiology, if present. However, the results from open lung biopsy infrequently lead to a change in the treatment that improves the patient's clinical course.