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Granulomatöse Vaskulitiden
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Coronavirus disease 2019 (COVID‐19), caused by severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) infection, is currently spreading worldwide, causing the worst pandemic experienced this century. During the present outbreak, reports have been accumulating that various types of cutaneous manifestations were observed in COVID‐19 patients. We read with interest the recent article by Amatore et al. describing a COVID‐19 case who presented with a febrile rash consisting of annular, polycyclic, and circinate erythema, presumably specific to COVID‐19.
Granulomatous lung diseases are a heterogeneous group of disorders that have a wide spectrum of pathologies with variable clinical manifestations and outcomes. Precise clinical evaluation, laboratory testing, pulmonary function testing, radiological imaging including high-resolution computed tomography and often histopathological assessment contribute to make a confident diagnosis of granulomatous lung diseases. Differential diagnosis is challenging, and includes both infectious (mycobacteria and fungi) and noninfectious lung diseases (sarcoidosis, necrotising sarcoid granulomatosis, hypersensitivity pneumonitis, hot tub lung, berylliosis, granulomatosis with polyangiitis, eosinophilic granulomatosis with polyangiitis, rheumatoid nodules, talc granulomatosis, Langerhans cell histiocytosis and bronchocentric granulomatosis). Bronchoalveolar lavage, endobronchial ultrasound-guided transbronchial needle aspiration, transbronchial cryobiopsy, positron emission tomography and genetic evaluation are potential candidates to improve the diagnostic accuracy for granulomatous lung diseases. As granuloma alone is a nonspecific histopathological finding, the multidisciplinary approach is important for a confident diagnosis.
The respiratory system may be involved in all systemic vasculitides, although with a variable frequency. Aim of our review is to describe radiographics and high-resolution computed tomography (HRCT) findings of pulmonary vasculitides and to correlate radiological findings with pathological results. Lung disease is a common feature of antineutrophil cytoplasmic autoantibody (ANCA)-associated small-vessels vasculitides, including Granulomatosis with polyangiitis (Wegener's), Eosinophilic granulomatosis with polyangiitis (Churg-Strauss) and Microscopic Polyangiitis. Pulmonary involvement is less frequent in immune complexmediated small-vessels vasculitides, such as Behçet's disease and Goodpasture's Syndrome. Pulmonary involvement associated to large-vessels (Gigantocellular arteritis and Takayasu's disease) or medium-vessels (Nodose Polyarteritis and Kawasaki's disease) vasculitides is extremely rare. The present review describes the main clinical and radiological features of pulmonary vasculitides with major purpose to correlate HRCT findings (solitary or multiple nodules, cavitary lesions, micronodules with centrolobular or peribronchial distribution, airspace consolidations, "crazy paving", tracheobronchial involvement, interstitial disease) with pathological results paying particular attention to the description of acute life-threatening manifestations. A thorough medical history, careful clinical examination and the knowledge of radiological patters are mandatory for a correct and early diagnosis.
Eosinophilic granulomatosis with polyangiitis (EGPA) is a rare chronic inflammatory systemic disease that occurs in patients with bronchial asthma and is associated with significant blood and tissue eosinophilia. Another characteristic is vasculitis of small and/or medium-sized vessels, which may be absent in prodromal stages of the disease and is therefore no longer an obligatory part of the disease definition. Antineutrophil cytoplasmic antibodies (ANCA) can be detected in approximately one third of patients. The ANCA-positive and ANCA-negative EGPA are genetically distinct diseases with common clinical manifestations, which, however, occur with different frequencies. Cardiac involvement is associated with a poor prognosis. Permanent organ damage often occurs as a result of the underlying disease or treatment, especially with glucocorticoids (GC). The standard treatment of EGPA consists of GC in combination with cyclophosphamide for severe organ involvement or medium potency immunosuppressants for more prognostically favorable manifestations. Biologics are increasingly being used in the treatment of EGPA. The interleukin (IL) 5 antagonist mepolizumab reduces the risk of relapses and decreases the demand for GC in patients with relapsing EGPA without severe organ involvement. In analogy to the approach to other ANCA-associated vasculitides, the use of rituximab in ANCA-positive EGPA patients with severe vasculitis recurrence is a possible option, even though formal evidence for such an approach is currently low and formal approval is lacking.
Eosinophilic granulomatosis with polyangiitis (EGPA) is a rare, but severe systemic vasculitis that can affect skin and other organ systems. Diagnostic criteria have evolved, and many attempts have been made to classify the vasculitides based on clinical and/or histopathologic features, with an aim to develop standardized criteria. According to the EGPA Consensus Task Force recommendations, EGPA is a syndrome of asthma, eosinophilia, pulmonary infiltrates, and extrapulmonary vasculitis (such as cutaneous involvement with purpura). Histopathologic evidence of vasculitis in EGPA may be associated with eosinophilic infiltration and/or perivascular granulomatous inflammation. We review clinicopathologic criteria of this enigmatic vasculopathy.
Context.—Granulomas are among the most commonly encountered abnormalities in pulmonary pathology and often pose a diagnostic challenge. Although most pathologists are aware of the need to exclude an infection in this setting, there is less familiarity with the specific histologic features that aid in the differential diagnosis.
Objective.—To review the differential diagnosis, suggest a practical diagnostic approach, and emphasize major diagnostically useful histologic features. This review is aimed at surgical pathologists who encounter granulomas in lung specimens.
Data sources.—Pertinent recent and classic peer-reviewed literature retrieved from PubMed (US National Library of Medicine) and primary material from the institutions of both authors.
Conclusions.—Most granulomas in the lung are caused by mycobacterial or fungal infection. The diagnosis requires familiarity with the tissue reaction as well as with the morphologic features of the organisms, including appropriate interpretation of special stains. The major noninfectious causes of granulomatous lung disease are sarcoidosis, Wegener granulomatosis, hypersensitivity pneumonitis, hot tub lung, aspiration pneumonia, and talc granulomatosis.
The spectrum of pulmonary granulomatoses is wide and includes infectious and noninfectious entities, each with very different therapeutic consequences. The first step of histological examination discriminates between necrotizing and non-necrotizing granulomatosis. After this, an infectious cause of the granulomatosis has to be excluded by special histological stains and molecular-pathologic methods, if necessary. Diagnosis also includes clinical, radiological, and microbiological findings. The process of pathological examination should be standardized as described.
Granulomatosis with polyangiitis (GPA) is a systemic necrotizing vasculitis involving small and medium-sized blood vessels and granulomatous inflammation of upper and lower respiratory systems and/or renal system. In the limited form of GPA, there is no systemic involvement of disease with sparing of kidneys. The respiratory system is the commonly involved organ in limited GPA. Herein, we report the case of a 40-year-old male who was initially diagnosed as sarcoidosis clinically. Lung biopsy revealed necrotizing granulomatous angiitis. Diagnosis of GPA was made which was substantiated by antineutrophil cytoplasmic antibody (ANCA) positivity. This was a case of limited GPA with isolated lung involvement. The early diagnosis and initiation of treatment are critical for improved survival of patients with GPA. Tissue biopsy is necessary for the diagnosis of GPA.
Granulomatous or granulomatous-like diseases of the lung are comparatively rare. This is all the more astonishing as there is a wide number of potential triggers that cause the characteristic pathologic findings. Besides being associated with infections, e.g. by mycobacteria, or with inhalation of noxes, the finding of granulomatosis is often idiopathic with the reason so far unknown. Common feature of all these diseases is the existence of granulomas: microscopically small structures, usually, mainly composed of epitheloid cells developed from macrophages. These come along with multinucleated giant cells, lymphocytes, fibroblasts etc. In particular, necrotic granulomas can be large and hence macroscopically or radio-logically easily detectable.
Zusammenfassung
Ein 62-jähriger Patient mit Asthma bronchiale und chronischer Rhinosinusitis unterzog sich einer Leistenhernien-OP. Nach der Operation kam es plötzlich zu einem reanimationspflichtigen Kreislaufstillstand. Koronarangiografisch zeigte sich eine 99 %ige proximale RCA-Stenose bei ansonsten unauffälligen und glattwandigen Koronarien. Im Verlauf kam es wiederholt zu ähnlichen Ereignissen, jetzt jedoch ohne Korrelat in der Koronarangiografie. Echokardiografisch zeigte sich initial eine LVEF von 45 %. Es bestanden bipulmonale Infiltrate im Röntgen-Thorax und eine schwere periphere Eosinophilie (37 %). Die serologische Diagnostik inkl. ANA, ENA und c-/p-ANCA blieb ohne Nachweis von Antikörpern. Eine Knochenmarkspunktion zeigte keine Hinweise auf eine myeloproliferative Erkrankung. Der Patient klagte über zunehmende Schwäche, Gewichtsverlust und Belastungsdyspnoe. Ein Methylprednisolon-Puls (250 mg/Tag über 3 Tage) zeigte keinen wesentlichen Effekt, sodass der Patient schließlich bei zunehmender klinischer Verschlechterung in unsere Universitätsklinik verlegt wurde. Bei Übernahme sahen wir einen abgeschlagenen Patienten mit progredienter Muskelatrophie und Belastungsdyspnoe. Klinisch zeigte sich eine rechtsseitige Peroneusparese. In der BAL zeigte sich eine schwere eosinophile Alveolitis (37 %). Laborchemisch zeigten sich Herzenzyme und NT-proBNP stark erhöht (Troponin-T > 700 ng/l, NT-proBNP > 10,000 ng/l). In der Echokardiografie fand sich eine dramatische Verschlechterung der Pumpfunktion (LVEF 16 %). Eine interdisziplinäre Falldiskussion zwischen Kardiologen und Pneumologen war schließlich der Schlüssel zur Diagnose einer ANCA-negativen eosinophilen Granulomatose mit Polyangiitis (EGPA) mit pulmonaler und kardialer Beteiligung. Nach Einleitung einer immunsuppressiven Therapie mit erneutem Methylprednisolon-Puls (1000 mg/Tag über 3 Tage) und anschließender Cyclophosphamid-Therapie (6 Pulse im 4-wöchigen Intervall) gestaltete sich der Verlauf erfreulich mit klinischer Beschwerdefreiheit, vollständiger Regredienz der pulmonalen Infiltrationen und deutlicher Erholung der kardialen Pumpfunktion (LVEF 47 %).
Fazit ANCA-Positivität ist zur Diagnosestellung einer EGPA nicht erforderlich. Diese weisen nur 30 – 70 % der EGPA-Patienten auf, v. a. bei neurologischer und/oder renaler, seltener bei pulmonaler und/oder kardialer Beteiligung, was einen Fallstrick bei der Diagnosestellung darstellen kann. Die Induktionstherapie mit Cyclophosphamid stellt bei steroidrefraktärem Verlauf mit vital bedrohlicher Organbeteiligung die Therapie der Wahl dar.
Lung involvement is one of the most common clinical features in ANCA-associated vasculitides (AAV), including granulomatosis with polyangiitis (GPA), microscopic polyangiitis (MPA), and eosinophilic granulomatosis with polyangiitis (EGPA). In this review, we detail the five main presentations of pulmonary involvement in AAV: necrotizing granulomatous inflammation, tracheobronchial inflammation, pulmonary capillaritis, interstitial lung disease (ILD) and asthma with their clinical, radiological and therapeutic characteristics. The prevalence of these manifestations is variable according to the subtype of AAV, necrotizing granulomatous inflammation and tracheobronchial inflammation being defining features of GPA whereas ILD is primarily seen in patients with MPA, especially in association with ANCA directed against myeloperoxydase (MPO-ANCA), and asthma is characteristic of EGPA. Despite recent progresses in the diagnosis and management of these conditions, several questions remain and are discussed here, including local treatments for subglottic stenosis, the uncertain efficacy of plasma exchanges for alveolar hemorrhage, the potential role of antifibrotic agents in ILD associated with MPA, and the use of novel anti-IL-5 strategies in EGPA.
Eosinophilic granulomatosis with polyangiitis is characterized by asthma, blood and tissue eosinophilia and small-vessel vasculitis. The clinical presentation is variable, but two main clinic-pathologic subsets can be distinguished: one hallmarked by positive ANCA and predominant 'vasculitic' manifestations (e.g. glomerulonephritis, purpura and mononeuritis multiplex) and the other by negative ANCA and prominent 'eosinophilic' manifestations (e.g. lung infiltrates and cardiomyopathy). The pathogenesis is not fully understood but probably results from the interplay between T and B cells and eosinophils. Eosinophilic granulomatosis with polyangiitis must be differentiated from several conditions, including hypereosinophilic syndromes and other small-vessel vasculitides. The overall survival is good; however, patients frequently relapse and have persistent symptoms. The recently developed monoclonal antibodies targeting B cells and eosinophilopoietic cytokines such as IL-5 are emerging as valid alternatives to conventional immunosuppressive therapies. In this review, we discuss the essential features of eosinophilic granulomatosis with polyangiitis, with particular respect to the most relevant issues concerning clinical presentation and management.
With its award-winning, innovative approach, the new edition of Practical Pulmonary Pathology, by Kevin O. Leslie, MD and Mark R. Wick, MD, provides comprehensive, practical guidance in the accurate identification and interpretation of neoplastic and non-neoplastic diseases of the lungs. Lavishly illustrated in full color throughout, this "one-stop" resource captures key morphologic patterns for a full range of common and rare conditions and assists in the interpretation of complex diagnostic puzzles. An easily accessible format with a unique "visual index" places in-depth diagnostic guidance quickly at your fingertips-in print or online at www.expertconsult.com.
Eosinophilic granulomatosis with polyangiitis (EGPA) (formerly Churg-Strauss syndrome) is a small vessel vasculitis associated with asthma and eosinophilia. Despite its rarity, continuous gains are being made in understanding the disease with knowledge advancements regarding its epidemiology, heterogeneous clinical manifestations, management, and outcomes. Large knowledge gaps remain, however, particularly surrounding pathophysiologic and diagnostic uncertainties. There is still an incomplete understanding of the interplay between the eosinophilic and vasculitic processes that are features of disease pathogenesis. EGPA is also a conceptually difficult disorder given its dual categorization with hypereosinophilic syndromes and systemic vasculitides and the absence of a biomarker that can reliably distinguish between the two. In addition, recent evidence points to distinct, but partly overlapping, disease phenotypes, yet there is insufficient understanding to inform phenotype-tailored therapies. EGPA also remains a diagnostic challenge in part because asthma may be the primary or predominant manifestation for years, and the chronic corticosteroid requirement may mask other disease features. Efforts are ongoing to better elucidate pathophysiologic mechanisms, resolve classification issues, better characterize disease manifestations, and further clarify disease subcategorization, all of which will translate into better diagnosis and treatment with the possibility of specifically adapted therapies.
To develop disease-specific recommendations for the diagnosis and management of eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome) (EGPA).
The EGPA Consensus Task Force experts comprised 8 pulmonologists, 6 internists, 4 rheumatologists, 3 nephrologists, 1 pathologist and 1 allergist from 5 European countries and the USA. Using a modified Delphi process, a list of 40 questions was elaborated by 2 members and sent to all participants prior to the meeting. Concurrently, an extensive literature search was undertaken with publications assigned with a level of evidence according to accepted criteria. Drafts of the recommendations were circulated for review to all members until final consensus was reached.
Twenty-two recommendations concerning the diagnosis, initial evaluation, treatment and monitoring of EGPA patients were established. The relevant published information on EGPA, antineutrophil-cytoplasm antibody-associated vasculitides, hypereosinophilic syndromes and eosinophilic asthma supporting these recommendations was also reviewed.
These recommendations aim to give physicians tools for effective and individual management of EGPA patients, and to provide guidance for further targeted research.
Copyright © 2015. Published by Elsevier B.V.
We report the pulmonary pathologic features in 87 open lung biopsies from 67 patients with Wegener's granulo-matosis (WG) who were treated at a single institution from 1968 to 1990. At the time of open lung biopsy, 48 patients (72%) had classical WG with renal involvement; 19 (28%) had limited WG without renal involvement. The pathologic features were divided into major and minor manifestations. In the 82 specimens demonstrating no infectious organism, the three major pathologic manifestations of classical WG observed were also useful diagnostic criteria and included: (a) parenchymal necrosis, (b) vasculitis, and (c) granulomatous inflammation accompanied by an inflammatory infiltrate composed of a mixture of neutrophils, lymphocytes, plasma cells, histiocytes, and eosinophils. Parenchymal necrosis was found in 84% of biopsy specimens either as neutrophilic microabscesses (65% of specimens) or as large (67%) or small (69%) areas of geographic necrosis. Areas of geographic necrosis were usually surrounded by palisading histiocytes and giant cells. Additional granulomatous lesions consisted of microabscesses surrounded by giant cells (69%), poorly formed granulomas (59%), and scattered giant cells (79%). Sarcoid-like granulomas were uncommon (4%), and in only one specimen (1%) appeared within an inflammatory lesion of WG. Vascular changes were identified in 94% of biopsy specimens. Vascular inflammation was classified as chronic (37% arterial, 64% venous), acute (37% arterial, 29% venous), nonnecrotizing granulomatous (22% arterial, 9% venous), and necrotizing granulomatous (22% arterial, 10% venous). Fibrinoid necrosis was relatively uncommon (11% arterial, 6% venous). Cicatricial changes were found in arteries in 41% of biopsy specimens and in veins in 16%. Capillaritis was present in 31% of specimens. Minor pathologic lesions were commonly observed in biopsy specimens associated with classical WG lesions, but they were usually inconspicuous and not useful diagnostic criteria. These included interstitial fibrosis (26%), alveolar hemorrhage (49%), tissue eosinophils (100%), organizing intraluminal fibrosis (70%), endogenous lipoid pneumonia (59%), lymphoid aggregates (37%), and a variety of bronchial/bronchiolar lesions including acute and chronic bronchiolitis (51% and 64%), follicular bronchiolitis (28%), and bronchiolitis obliterans (31%). These minor lesions were often found at the periphery of typical nodules of WG. However, in 15 specimens (18%) a minor pathologic feature represented the dominant or major finding: pulmonary fibrosis (six specimens, 7%), diffuse pulmonary hemorrhage (six specimens, 7%), lipoid pneumonia (one specimen, 1%), acute bronchopneumonia (one specimen, 1%), and chronic bronchiolitis, bronchiolitic obliterans with organizing pneumonia (BOOP), and bronchocentric granulomatosis (one specimen, 1%). Bronchial stenosis was found in three specimens (4%). In 10 specimens (12%) active vasculitis affecting veins or arteries could not be identified. Diffuse pulmonary hemorrhage associated with capillaritis was the primary finding in three of these specimens. Nodular interstitial fibrosis was the primary finding in six cases, and in three of these specimens cicatricial vascular changes were also present. In the 10th specimen, geographic necrosis, microabscesses, and scattered giant cells were present. This review illustrates the wide variation and broad spectrum of pathologic features that can occur in pulmonary WG and addresses the complicated differential diagnosis that can be encountered in the lung.
Recently, a group of experts in the field suggested to rename Churg–Strauss syndrome as eosinophilic granulomatosis with polyangiitis (EGPA). This condition, first described in 1951, is a rare small- and medium-sized–vessel vasculitis characterized by an almost constant association with asthma and eosinophilia, and, by the presence of anti-myeloperoxidase (MPO) antineutrophil cytoplasm antibodies (ANCA) in 30–38% of the patients. Vasculitis typically develops in a previously asthmatic and eosinophilic middle-aged patient. Asthma is severe, associated with eosinophilia and extrapulmonary symptoms. Most frequently EGPA involves the peripheral nerves and skin. Other organs, however, may be affected and must be screened for vasculitis, especially those associated with a poorer prognosis, such as the heart, kidney and gastrointestinal tract, as assessed by the recently revised Five-Factor Score (FFS). Recent insights, particularly concerning clinical differences associated with ANCA status, showed that EGPA patients might constitute a heterogeneous group. Thus, EGPA patients with anti-MPO ANCA suffered more, albeit not exclusively, from vasculitis symptoms, such as glomerulonephritis, mononeuritis multiplex and alveolar hemorrhage, whereas ANCA-negative patients more frequently develop heart involvement. This observation led to the hypothesis that EGPA might be divided into different clinical and pathophysiological subtypes, which could be managed better with more specifically adapted therapies.
For now, EGPA treatment still relies mainly on corticosteroids and, when necessary for patients with poorer prognoses, combined immunosuppressant drugs, especially cyclophosphamide. Overall survival of EGPA patients is good, despite not uncommon relapses.
Vasculitis is a destructive inflammatory process affecting blood vessels. Pulmonary vasculitis may develop secondary to other conditions or constitute a primary idiopathic disorder. Thoracic involvement is most common in primary idiopathic large-vessel vasculitides (Takayasu arteritis, giant cell arteritis, Behçet disease) and primary antineutrophil cytoplasmic autoantibody-associated small-vessel vasculitides (Wegener granulomatosis, microscopic polyangiitis, Churg-Strauss syndrome). Primary pulmonary vasculitides are rare, and their signs and symptoms are nonspecific, overlapping with those of infections, connective tissue diseases, and malignancies. The radiologic findings in primary pulmonary vasculitis vary widely and can include vessel wall thickening, nodular or cavitary lesions, ground-glass opacities, and consolidations, among others. Diffuse alveolar hemorrhage usually results from primary small-vessel vasculitis in the lungs. To diagnose vasculitis, medical teams must recognize characteristic combinations of clinical, radiologic, laboratory, and histopathologic features.
We describe 25 cases of Wegener's granulomatosis presenting with solitary lung lesions to compare the clinical and pathologic findings in these cases with those of the more common multifocal disease and also to evaluate the clinical significance of solitary lung lesions occurring in the absence of extrapulmonary disease. The clinical findings in our patients with solitary Wegener's were similar to those in generalized disease. Men were affected slightly more often than women, and the average age of onset was 53 years. Likewise, no major pathologic differences were found between solitary and multifocal disease. Classic necrotizing granulomatous inflammation and necrotizing vasculitis were the most common findings, although other variants were occasionally encountered, including the eosinophilic variant (two cases), the bronchocentric variant (one case), and small-vessel vasculitis and capillaritis (one case). Three cases had prominent areas of bronchiolitis obliterans-organizing pneumonia. Progressive disease occurred in all seven patients who manifested solitary lung lesions without extrapulmonary involvement and were not treated because the diagnosis was initially unrecognized. Pathologists need to be alert to the possibility of Wegener's granulomatosis causing solitary lung lesions because treatment should be promptly instituted.
Antineutrophil cytoplasmic antibodies (ANCA) are useful serologic markers for the diagnosis and management of patients with Wegener's granulomatosis (WG) and microscopic polyangiitis (MPA). However, problems in diagnosis and classification may occur when patients with other disorders develop ANCA. A 7-year review (1993-1999) disclosed 247 patients whose sera tested positively for ANCA by an indirect immunofluorescence method: 166 patients for cytoplasmic-ANCA (C-ANCA) and 81 patients for perinuclear-ANCA (P-ANCA) Twenty-seven patients had active pulmonary disease and underwent open-lung biopsy or transbronchial biopsy. Eight patients (30%) had a disease other than WG or MPA, and their clinical, pathological, and serological findings were reviewed. The patients, all women, ranged in age from 28 to 77 years (median, 37 y). Dyspnea (n = 6), cough (n = 6), chest pain (n = 2), and/or hemoptysis (n = 2) were present. The duration of symptoms lasted from 3 weeks to 6 years (median, 6 mo). ANCA titers were C-ANCA (n = 4; range, 1:40-1280) or P-ANCA (n = 4; range, 1:40-640). The lung biopsies disclosed nonspecific interstitial pneumonia (n = 4), bronchiolitis obliterans organizing pneumonia (n = 1), diffuse alveolar damage (n = 1), organizing diffuse alveolar hemorrhage without capillaritis (n = 1), and necrotic granuloma (n = 1). No cases showed characteristic histology for WG or MPA. The final diagnoses were various connective tissue disorders (n = 5), chronic hypersensitivity pneumonia (n = 1), postinfectious bronchitis/bronchiectasis (n = 1), and ulcerative colitis-related lung disease (n = 1). Surgical pathologists should be aware that significantly elevated ANCA titers may be associated with diverse forms of pulmonary disease. ANCA positivity alone, in the absence of appropriate clinical or pathologic findings, should not be used to substantiate a diagnosis of WG or MPA.
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