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Ann Thorac Surg 1996;61:1477-1482
© 1996 The Society of Thoracic Surgeons

Original Articles: General Thoracic

Plasma Cell Granuloma of the Lung: Difficulties in Diagnosis and Prognosis

Marie-Christine Copin, MD, Bernard H. Gosselin, MD, Michel E. Ribet, MD

Laboratory of Pathology and Unit of Thoracic Surgery, Hôpital Calmette, University of Lille, Lille, France

Accepted for publication January 4, 1996.


   Abstract
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 Footnotes
 Abstract
Introduction
 Material and Methods
 Results
 Comment
 References
 
Background. The nature of plasma cell granuloma of the lung is still not well defined. Its diagnosis can be difficult, and its long-term prognosis is uncertain.

Methods. Four patients, aged 41/2 to 45 years, had resection of a circumscribed plasma cell granuloma. In 1 of them, it was associated with a carcinoma. The fifth patient was treated by irradiation for an invasive form of plasma cell granuloma, which was diagnosed as malignant lymphoma 1 year later. The plasma cell granulomas had a similar polymorphic pattern and were polyclonal at immunohistochemistry.

Results. The 3 patients treated by lobectomy, including the patient with an associated carcinoma, were alive and well at 12, 12, and 11 years postoperatively. The patient treated by pneumonectomy had recurrence 9 years later and died 11 years after operation: irradiation was not effective. The patient with lymphoma was treated by chemotherapy and was alive and in remission 5 years later.

Conclusions. An accurate preoperative diagnosis is difficult. The results of biopsy can be inconclusive, and an associated malignancy can be missed. Complete resection remains the best treatment. The long-term prognosis is unpredictable, and late and fatal recurrences are possible.


   Introduction
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 Abstract
 Introduction
Material and Methods
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 Comment
 References
 
In 1939, Brunn [1] described ``two interesting benign lung tumors of contradictory histopathology.'' This was the initial description of plasma cell granuloma (PCG), as it was later called by Lane and associates [2] in 1955. However, this lesion has had many different definitions. It is considered an inflammatory pseudotumor [3]. The objective of this retrospective review of five cases of PCG is to illustrate the difficulties in its diagnosis and prognosis.


   Material and Methods
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 Abstract
 Introduction
 Material and Methods
Results
 Comment
 References
 
Table 1Go summarizes the clinical presentation in the 5 patients, the preoperative workup, the tentative diagnosis, and the treatment. The histopathologic records were reviewed and confirmed. The patients were followed for 5 to 12 years. In addition to yearly standard roentgenography, computed tomography and fiberoptic bronchoscopy were used in the follow-up of the last 2 patients.


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  		Table 1. . Summary of Patient Data
 

   Results
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 Introduction
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Comment
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The mean age of the patients was 28 years. All had a history of pulmonary infections or bronchitis. The 3 adult men were cigarette smokers.

In all but the last patient, where the mass obviously invaded the upper mediastinum, the radiologic opacities were circumscribed. Patients 1, 2, and 4 had bronchial obstruction. Biopsy was not done in patient 1 because the tumor appeared to be hypervascularized (Fig 1Go). In patient 2, the biopsy results led to a diagnosis of undifferentiated carcinoma (Fig 2Go), and they missed the specific nature of the lesion in patient 4 (Fig 3Go). The results of blood tests showed signs of nonspecific inflammation in 2 patients.



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  		Fig 1. . (Patient 1.) Left main bronchial obstruction in 16-year-old girl. Endobronchial budding from plasma cell granuloma developed within left upper lobe. Biopsy was not done because of hypervascularization. Resection by sleeve left upper lobectomy.

 


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  		Fig 2. . (Patient 2.) Left lower lobe mass in 45-year-old man who was a cigarette smoker. A carcinoma was contained within the plasma cell granuloma. Resection by lobectomy.

 


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  		Fig 3. . (Patient 4.) Left hilar mass and lower lobe atelectasis in 30-year-old man who was a cigarette smoker. Endobronchial biopsy was not diagnostic. At thoracotomy, the lesion had the appearance of carcinoma. Resection by pneumonectomy showed the left atrium and esophageal muscular wall to be involved.

 
The four resected tumors ranged between 3 and 6 cm in diameter and were yellowish white. One looked encapsulated (Fig 4Go), and the others had irregular margins. Their consistency was homogeneous. One was calcified. The histologic structure consisted of a stroma of collagen and fibroblasts containing an inflammatory infiltrate comprising a majority of plasma cells or a mixture of plasma cells, lymphocytes, histiocytes, and spindle cells (Fig 5Go). Bony metaplasia was present in 1 patient. The encapsulated tumor was surrounded by a thin shell of collagen and sclerosis. Electron microscopy confirmed normal morphology of the cells and observed rare mast cells in 1 patient. Immunohistochemistry showed that the cell population was polyclonal (Table 2Go).



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  		Fig 4. . (Patient 3.) This well-circumscribed calcified mass was diagnosed as a congenital lesion in a 41/2-year-old girl. Resection by lobectomy. The plasma cell granuloma was surrounded by a thin shell of sclerosis and contained zones of bony metaplasia.

 


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  		Fig 5. . Clusters of plasma cells (center) are interspersed among spindle cells. (Hematoxylin and eosin; x400 before 33% reduction.)

 

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  		Table 2. . Immunohistochemistry
 
In patient 2, in whom the diagnosis was cancer, there was a poorly differentiated squamous carcinoma developing within a PCG, which was itself contained in an area of chronic pneumonia infiltrating the whole lobe. The tumor was staged T2 N0.

The margins of resection and dissected lymph nodes were healthy in all patients. The 3 patients treated by lobectomy, which includes the patient with carcinoma, were alive and well with no sign of recurrence 12, 12, and 11 years after operation. Patient 4 underwent pneumonectomy and returned to work. His course was unremarkable for 9 years. Then he was seen because of dysphagia. Computed tomograms showed a mediastinal recurrence (Fig 6Go). The esophageal compression was first dilated and then bypassed with a substernal gastric tube, and the mediastinum was irradiated (50 Gy). However, the compression progressed to the trachea, which was stented 1 year later, and the patient died of pulmonary infection 11 years after pneumonectomy.



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  		Fig 6. . (Patient 4.) Computed tomogram showed compressive mediastinal recurrence 9 years after pneumonectomy.

 
Patient 5 had the only tumor that was not resected. It had invaded the mediastinum (Fig 7Go), and a diagnosis was finally reached after three biopsies. The first two had resulted in a diagnosis of a nonspecific inflammatory infiltration of lymphocytes, histiocytes, and fibrosis. An axillary thoracotomy allowed large samples, and this led to the diagnosis of PCG. The upper mediastinum was irradiated (50 Gy), and the caval syndrome subsided.



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  		Fig 7. . (Patient 5.) Right paratracheal mass invading mediastinum and causing superior vena cava syndrome. The diagnosis of plasma cell granuloma was made after three biopsies, and the patient received irradiation.

 
One year later, after a cervical node biopsy, histiocytosis was diagnosed, and 3 months later, a radiologic shadow appeared at the junction of the apical and posterior basal segments of the right lower lobe (Fig 8Go). A transthoracic fine-needle aspiration biopsy led to a diagnosis of a chronic nonspecific infiltrate. Four months later, the patient complained of sternal pains, and a small defect in the anterior surface of the bone was observed at radiology. A lung segmentectomy and a sternal biopsy were performed. In both locations, histopathology showed a proliferation of large undifferentiated cells within a polymorphic infiltration of lymphocytes, plasma cells, and histiocytes. At immunohistochemistry, the large cells were marked with anti-MB2 and anti-L26 antibodies. The diagnosis was multifocal large B-cell non-Hodgkin's malignant lymphoma. Three courses of chemotherapy, combining doxorubicin, cyclophosphamide, vinblastine, bleomycin sulfate, and prednisone were administered. Five years later, the patient was in complete remission apart from an abnormal scintigraphic finding on the sternum, where biopsy results showed granulomatous and fibrous tissue.



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  		Fig 8. . (Patient 5.) The response to treatment was good, and the caval syndrome subsided. Fifteen months later, a shadow appeared in the right lower lobe along with a small sternal defect. The diagnosis was malignant lymphoma.

 
In summary, no accurate and definitive diagnosis was made preoperatively. Two PCGs were associated with malignancy or had been malignant from the start. One led to a late and ultimately fatal recurrence 9 years after resection.


   Comment
Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
References
 
Clinical Presentation
Plasma cell granulomas constitute less than 1% of all tumors of the lung [4]. There is no sex preponderance. More than half the patients are less than 40 years of age, and 15% are 1 year to 10 years old [3, 5]. Plasma cell granuloma represents the most frequent pseudotumoral lung opacity seen in patients not yet 16 years of age [6]. A history of prior lung infection is noted in one third of the patients [3, 7], and a history of previous pulmonary malignancy has been mentioned [6]. The lesion provokes thoracic symptoms in 70% of patients: cough, chest pain, dyspnea, and hemoptysis. Clubbing has been observed, particularly in young patients. Fever may be present. Plasma cell granuloma is sometimes discovered on routine radiographs, and it can be an incidental finding during thoracotomy for another cause [8].

Diagnostic Procedures
Imaging techniques usually show a circumscribed, sometimes irregular mass [9]. Additional nodes can be observed in the ipsilateral or contralateral lung [10]. It is not well circumscribed in 25% of patients. Cavitation is rare, and calcifications can be present. The rate of growth is usually slow [5]. There is bronchial obstruction and atelectasis in 5% of patients [5, 10, 11]. The endobronchial aspects are not specific.

The results of bronchial cytology are not conclusive, whereas the results of biopsy are exceptionally accurate [12]. Fine-needle transthoracic aspiration can be helpful [5] but is generally considered insufficient [13, 14], as the resulting specimen can present great diagnostic difficulties for the histopathologist [15].

Abnormal laboratory test findings are few: raised white cell count, elevated erythrocyte sedimentation rate, and a rise in serum {alpha}2-globulin and immunoglobulin G levels. Thrombocytosis and hypochromic microcytic anemia have been observed in children [16].

In fact, most patients reported underwent thoracotomy with no specific diagnosis or, according to their age and habits, with the diagnosis of congenital malformation, sarcoma, or carcinoma [8, 14]. At thoracotomy, many surgeons rely on frozen sections, but these are subject to error [5]. Biopsy specimens are of greater interest when the lesion cannot be resected.

Treatment
Complete resection is the best treatment of PCG, especially when it is difficult to exclude malignancy [13, 14]. Local excision has been performed on rare occasions for endobronchial pedunculated lesions [17]. Segmentectomy or wedge excision predispose patients to recurrence [8], as peritumoral satellite islets have been described. Invasion can necessitate partial resection of neighboring structures [8, 10, 18]. Steroid therapy is not beneficial. Radiotherapy has been effective for fibrotic lesions [19], and chemotherapy has been used for multifocal and recurrent forms [10].

Pathology
On the resected specimen, PCG appears as a yellowish-white, well-circumscribed mass in the majority of patients. Its density varies because of hemorrhage, calcification, and cavitation. The tumor compresses and obstructs the alveolar spaces, the bronchioles, and the vessels. It infiltrates the lung tissue and can destroy the bronchial wall [20].

The proliferation comprises mature plasma cells, which are sometimes binuclear and often contain Russell bodies, which represent intracellular buildup of immunoglobulins. Other elements are histiocytes and macrophages, which can have a foamy aspect because of the deposit of fat contents, lymphocytes, mast cells, giant multinucleated cells, and neutrophils. Another population is made up of fibroblasts [15].

This polymorphic cellular population is supported by a stroma of granulomatous and fibrous tissue. Sclerosis sometimes surrounds the PCG. Immunohistochemistry shows a polyclonal secretion [21]. Histopathologic diagnosis should consider sclerosing hemangioma [3], malignant fibrous histiocytoma, malignant plasmacytoma, and pseudolymphoma, which can be a precursor of malignant lymphoma [22].

Nosology
There are variations in the natural history and pathology of PCG. Spontaneous resolution has been observed [3, 14]. Fast growth has been described on rare occasions [23]. Mediastinal, tracheal, or esophageal invasion can be fatal [3]. The absence of recurrence after complete resection has not always been confirmed. Recurrence can be very late [7]. Multiple extrathoracic locations have been described, sometimes associated with metastasis [10, 11, 24]. Association with carcinoma has been considered fortuitous, but this may be misleading. Malignant lymphoma and low-grade sarcoma may have areas that resemble PCG. Indeed, malignant changes in PCGs have occasionally been discussed [25].

These characteristics and the various preponderances of cell types and stromal appearances account for the many names given to PCG [3, 26]. The most frequently used is pseudoinflammatory tumor. More recently, the issue has focused on its nature: is it an overgrown inflammatory reaction to infection or a neoplasm [15, 27]? As polyclonal plasma cells are not always a major feature of its histologic pattern and as myofibroblasts, fibroblasts, and histiocytes constitute its bulk, PCG has recently been termed myofibrohistiocytic proliferation or inflammatory myofibroblastic tumor developed from primitive mesenchymal cells [24]. Some invasive cases have been shown to resemble low-grade sarcoma [28]. Positive immunostaining with P53 is potentially helpful in differentiating sarcoma from inflammatory pseudotumor [29], and a report [30] of cytogenetic clonal changes in a typical case of inflammatory tumor has recently been published.

Conclusion
Plasma cell granuloma presents difficulties in clinical and histologic diagnosis. It can be associated with or behave like a malignant lesion. Its evolution is unpredictable. Complete resection is the treatment of choice, but late recurrence is possible. A long, regular follow-up is necessary. What is currently called PCG needs more accurate pathologic definition and classification.


   Footnotes
Top
 Footnotes
Abstract
 Introduction
 Material and Methods
 Results
 Comment
 References
 
Address reprint requests to Dr Ribet, Service de Chirurgie, Hôpital Calmette, F 59037 Lille, France.


   References
Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 References
 

  1. Brunn H. Two interesting benign tumors of contradictory histopathology. Remarks on the necessity for maintaining the Chest Tumor Registry. J Thorac Surg 1939;9:119–31.
  2. Lane JD, Krohn S, Kolozzi W, Whitehead RE. Plasma cell granuloma of the lung. Dis Chest 1955;27:216–21.
  3. Bahadori H, Liebow AA. Plasma cell granuloma of the lung. Cancer 1973;31:191–208.[Medline]
  4. Ishida T, Oka T, Nishino T, Tateishi M, Mitsudomi T, Sugimachi K. Inflammatory pseudotumor of the lung in adults: radiographic and clinicopathological analysis. Ann Thorac Surg 1989;48:90–5.[Abstract/Free Full Text]
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  6. Pettinato G, Manivel JC, De Rosa N, Behner LP. Inflammatory myofibroblastic tumor (plasma cell granuloma). Clinicopathologic study of 20 cases with immunohistochemical and ultrastructural observations. Am J Clin Pathol 1990;94:538–46.[Medline]
  7. Matsubara O, Tan-Liu NS, Kenney RM, Mark EJ. Inflammatory pseudotumors of the lung: progression from organizing pneumonia to fibrous histiocytoma or to plasma cell granuloma in 32 cases. Hum Pathol 1988;19:807–14.[Medline]
  8. Urschel JD, Horan TA, Unruh HW. Plasma cell granuloma of the lung. J Thorac Cardiovasc Surg 1992;104:870–5.[Abstract]
  9. McCall IW, Woo-Ming M. The radiological appearances of plasma cell granuloma of the lung. Clin Radiol 1978;29: 145–50.[Medline]
  10. Boman F, Champigneulle J, Boccon-Gibod L, et al. Tumeur fibromyoblastique inflammatoire pulmonaire à forme endobronchique, infiltrante, multifocale et récidivante. Ann Pathol 1995;15:207–10.[Medline]
  11. Rigault JY, Prevost JM, Brun J, Galateau F. Hémoptysies révélant un granulome plasmocytaire avec bourgeon endo-bronchique. Rev Mal Resp 1991;8:253–5.
  12. Maples MD, Adkins RB, Graham BS, Dao AH, Scott HW. Pseudotumor of the lung. Am Surg 1985;51:84–8.[Medline]
  13. Lal RB, Thompson JR. Postinflammatory tumor (xanthogranuloma) of the lung: an enigma. Ann Thorac Surg 1974;17:174–80.[Abstract/Free Full Text]
  14. Mandelbaum I, Brashear RE, Hull MT. Surgical treatment and course of pulmonary pseudotumor (plasma cell granuloma). J Thorac Cardiovasc Surg 1981;82:77–82.[Abstract]
  15. Anthony PP. Inflammatory pseudotumour (plasma cell granuloma) of lung, liver and other organs. Histopathology 1993;23:501–3.[Medline]
  16. Monzon CM, Gilchrist GS, Burgert EO Jr, et al. Plasma cell granuloma of the lung in children. Pediatrics 1982;70:268–74.[Abstract/Free Full Text]
  17. Schilling JA, Cunningham J, Phillips LG Jr. Fibrous histiocytoma of the bronchus. Treatment by segmental resection [Letter]. J Thorac Cardiovasc Surg 1988;96:183–4.
  18. Spyker MA, Kay S. Plasma cell granuloma of a mediastinal lymph node with extension to right lung. J Thorac Surg 1956;31:211–5.
  19. Kirkpatrick JA Jr, Harris BCG, Kushner DC. Thoracic complications of plasma cell granuloma of the lung. Ann Radiol 1984;27:145–9.
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  21. Toccanier MF, Exquis B, Groebly Y. Granulome plasmocytaire du poumon: 9 observations avec étude immuno-histochimique. Ann Pathol 1982;2:21–8.[Medline]
  22. Fisher C, Grubb C, Kenning B, Lincoln JCR, Peters JC. Pseudolymphoma of the lung. A rare cause of a solitary nodule. J Thorac Cardiovasc Surg 1980;80:11–6.[Abstract]
  23. Sweetman WR, Hartley HJ, Bauer AJ, Salyer JM. Post inflammatory ``tumor'' of the lung. Report of a case simulating malignant thymoma. J Thorac Surg 1958;35:802–6.
  24. Tang TT, Segura AD, Oechler HW, et al. Inflammatory myofibrohistiocytic proliferation simulating sarcoma in children. Cancer 1990;65:1626–34.[Medline]
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