| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Original Report |
1
Department of Radiology, Samsung Medical Center, Sungkyunkwan University
School of Medicine, 50, Ilwon-Dong, Kangnam-Ku, Seoul 135-710, Korea.
2
Department of Diagnostic Pathology, Samsung Medical Center, Sungkyunkwan
University School of Medicine, Seoul 135-710, Korea.
3
Department of Thoracic Surgery, Samsung Medical Center, Sungkyunkwan
University School of Medicine, Seoul 135-710, Korea.
4
Department of Diagnostic Radiology, Yongdong Severance Hospital, Yonsei
University Medical College, 6-17, Dogok-Dong, Kangnam-Ku, Seoul 135-612,
Korea.
Received May 24, 1999;
accepted after revision August 11, 1999.
Address correspondence to K. S. Lee.
Abstract
 Top Abstract IntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
CONCLUSION. Semiinvasive pulmonary aspergillosis should be considered in the mildly immunocompromised patient with CT findings that reveal persistent parenchymal abnormalities. Patterns include consolidation and mass.
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
Radiographic findings of semiinvasive pulmonary aspergillosis include areas of focal consolidation or indolent masslike lesions with upper lobe predilection and, in some cases, pleural thickening [3, 11,12,13,14,15]. Case reports have described the CT findings of semiinvasive aspergillosis [11,12,13,14, 16]; however, to our knowledge the CT-pathologic correlation has not been examined. We describe the chest CT and pathologic findings of semiinvasive pulmonary aspergillosis in six patients.
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
Five patients had underlying diseases, including diabetes in three patients (insulin dependent, one; noninsulin dependent, two), cerebral palsy and pulmonary tuberculosis in one, and chronic alcoholism in one. Patients complained of cough (n = 4), sputum (n = 4), hemoptysis (n = 2), or fever (n = 1) (symptom duration, 3 months to 4 years; mean, 14 months). One patient (for whom radiographic abnormalities were detected on routine chest radiography) had no symptoms.
For all patients, chest radiographs and CT scans were obtained within 25 days of each other (range, 1-25 days; median, 12 days). The mean intervals between pathologic diagnosis and chest radiography or CT were 29 days and 20 days, respectively. Chest radiographs were obtained with an FCR 9501 computed radiography system (Fuji, Tokyo, Japan) (120 kVp; nominal focus, 0.6 or 1.2 mm; film-focus distance, 183 cm; oscillating grid, 12:1; exposure, phototimed). In four patients, CT included helical scans and high-resolution scans using a HiSpeed Advantage scanner (General Electric Medical Systems, Milwaukee, WI). For two patients (for whom scans were obtained at an outside hospital) CT included conventional CT scans (10-mm collimation) with IV contrast medium. Helical CT scans were obtained through the thorax with 7-mm collimation and a pitch of 1 after IV injection of 100 ml of iopamidol (Iopamiron 300; Bracco, Milan, Italy). High-resolution CT scans were obtained through the main lesion with 1.0-mm collimation at 5-mm intervals.
Chest radiographs and CT scans were retrospectively assessed by two chest radiologists. Decisions on the findings were reached by consensus. Radiologists assessed the patterns and distribution of parenchymal abnormalities.
An experienced lung pathologist reviewed all pathology specimens. Special stainings with methenamine silver stain and periodic acid-Schiff stain were performed in addition to routine H and E staining. Special stains were used to identify specific microorganisms.
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
|
|
|
|
|
|
|
Gross pathologic examination (n = 4) showed a mass or consolidation of destroyed lung with fibrous scarring, several foci of bronchiectasis and abscess cavity (n = 3) (Figs. 1A,1B and 2A,2B), and cavity with thick fibrous wall and rim of organizing consolidation (n = 1). Two of the three patients with mass or consolidation had aspergilloma in the central cavity (Fig. 1A,1B) and dilated bronchus (Fig. 2A,2B). Histologic examination (n = 6) showed areas of mixed active inflammation and fibrous scarring with microscopic abscess cavity (n = 5) (Fig. 4A,4B) and central bronchiectasis with dense peribronchial inflammation, fibrosis, and fungal colonization (n = 1). In all pathology specimens, special staining showed septate hyphae with a right-angle branch suggestive of Aspergillus species.
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
Yousem [10] describes the necrotizing granulomatous pneumonia pattern as an extensive alveolar consolidation with a central region of infarctlike parenchymal necrosis containing Aspergillus hyphae and peripheral granulomatous reaction with occasional giant cells.
Yousem [10] describes the granulomatous bronchiectatic cavity with parenchymal invasion pattern as a large cavity centered on an airway in which part of the wall is lined with pseudostratified respiratory or metaplastic squamous epithelium. This pattern is difficult to distinguish from pulmonary aspergilloma; however, a primary distinguishing feature of chronic necrotizing pulmonary aspergillosis is obvious tissue invasion and destruction. Pulmonary aspergilloma usually forms in preexisting cavities without tissue invasion. Although a study by Rafferty et al. [18] reported patients with aspergillomas seen on radiography having an invaded adjacent lung, these patients' findings probably represent variants of chronic necrotizing pulmonary aspergillosis (saprophytic aspergillosis that evolved into semiinvasive disease [3]), a disease associated with steroid therapy.
Yousem [10] describes the bronchocentric granulomatosislike pattern (the least common pattern) as morphologically resembling bronchocentric granulomatosis with bronchiolar inflammation and accompanying invasion of adjacent lung parenchyma surrounding the affected bronchioles. In our study, pathologic examination revealed five patients with necrotizing granulomatous pneumonia lesions and one with granulomatous bronchiectatic cavity with parenchymal invasion.
A study by Gefter et al. [3] described radiographic findings of semiinvasive pulmonary aspergillosis in five patients. These researchers saw consolidation or progressing cystic infiltrate subsequently forming a thick-walled cavity and aspergilloma with upper lobe predominance. In their study, pleural thickening was frequently seen.
Radiographic findings in our patients were various: lobar or segmental consolidation, a mass, or a small nodular opacity. In two patients, we noted upper lobe predilection and associated pleural thickening. In three patients for whom previous radiographic studies were available, we noted persistent and progressive parenchymal lesions.
Case reports have described the CT findings of semiinvasive pulmonary aspergillosis including chronic progressive peripheral consolidation or masslike lesion, upper lobe predilection, with or without thickening, and distortion of adjacent pleura [11,12,13,14, 16]. Additionally, extension into the chest wall and mediastinum may be seen [19]. In our study, CT findings varied and included areas of lobar or segmental consolidation and a low-attenuation mass.
In patients with semiinvasive pulmonary aspergillosis, abnormalities in the host's defense mechanism are frequently present. Typically, patients have poor nutrition caused by alcoholism, diabetes mellitus, chronic granulomatous disease, or connective tissue disorders. Additionally, patients may have undergone low-dose corticosteroid therapy [7, 15]. Pulmonary abnormalities such as a fibrotic area of Mycobacterium species, chronic obstructive lung disease, previous surgery, radiation therapy, pulmonary infarction, or pneumoconiosis may lower defense mechanisms [7]. In our study, five of six patients had underlying diseases, including three with diabetes, one with alcoholism, and one with cerebral palsy and tuberculosis. Associated pulmonary abnormalities (present in three patients) included emphysema, bronchiectasis, and prior tuberculous infection.
Chronicity of semiinvasive aspergillosis is defined as the duration of the disease process (radiologically or clinically) for more than 30 days before therapy. This time course is different from that of invasive pulmonary aspergillosis in which the rate of progression depends on the host's degree of immunosuppression (usually 2 or 3 weeks) [15]. Although one report studied semiinvasive pulmonary aspergillosis occurring in children with chronic granulomatous disease [20], most patients with semiinvasive aspergillosis are middle-aged, because underlying diseases such as alcoholism or diabetes mellitus are not frequent in young persons.
Semiinvasive aspergillosis should be considered when Aspergillus species grow from lung biopsy and bronchoscopic specimens or percutaneous lung aspirates in patients with persistent and progressive radiographic opacities [3]. There should be no evidence of disseminated aspergillosis at the time of diagnosis [7].
Differential diagnosis includes chronic pulmonary diseases such as tuberculosis, actinomycosis, histoplasmosis, and lung cancer. These diseases may appear with persistent segmental or lobar consolidation or masses with or without an internal low-attenuation area [8, 9, 21].
In conclusion, semiinvasive pulmonary aspergillosis is a rare form of pulmonary aspergillosis, originating in mildly immunocompromised patients with comorbid pulmonary conditions. CT findings are diverse, including bronchopneumonia and cavitary consolidation containing an aspergilloma. Semiinvasive aspergillosis should be considered in patients with CT findings that reveal persistent or progressive parenchymal abnormalities of various patterns. Patients with semiinvasive pulmonary aspergillosis are unresponsive to ordinary bacterial antibiotics.
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
This article has been cited by other articles:
|
|
 |
|
  O.S. Zmeili and A.O. Soubani Pulmonary aspergillosis: a clinical update QJM, June 1, 2007; 100(6): 317 - 334. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. K. Yella, P. Krishnan, and V. Gillego The Air Crescent Sign: A Clue to the Etiology of Chronic Necrotizing Pneumonia Chest, January 1, 2005; 127(1): 395 - 397. [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
