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J Thorac Cardiovasc Surg 1994;108:395-396
© 1994 Mosby, Inc.
LETTERS TO THE EDITOR |
First Department of Surgerya
Department of Pathologyb
Teikyo University of Medicine
Tokyo, 173, Japan
To the Editor:
Reports indicate the onset of malignant fibrous histiocytoma (MFH) in the chest wall after old pleuritis or pyothorax, 
1radiotherapy, 2 or burns, 3 but they rarely indicate that MFH develops after operations 4 We treated a patient who had contracted tuberculous pleuritis and tuberculous pyothorax and in whom MFH developed in the chest wall 16 years after pleuropneumonectomy carried out for tuberculous pyothorax.
The patient was a 69-year-old man with cough and pyrexia. When he was 19 years old, complete rest had been prescribed for the treatment of left-sided tuberculous pleuritis. At the age of 53 years, he had undergone pleuropneumonectomy for left-sided tuberculous pyothorax at our hospital. In March 1992, cough and fever (38° C) appeared. He was admitted to the department of internal medicine of our hospital and received combination drug therapy with isoniazid (INH), rifampicin (RFP), etambutol (EB), and various antibiotics for about 2 months. Despite these medications, remittent fever persisted.
Repeated thoracentesis at the department of internal medicine yielded no materials sufficient for bacteriological examination. Inasmuch as no definitive diagnosis was established, he was referred to our department for open chest biopsy on May 15, 1992. After he was transferred to our department, laboratory examination revealed an erythrocyte count of 348 x 10 4/mm 3, a hematocrit value of 27.1%, and a hemoglobin level of 8.9 gm/dl, indicating anemia. Anemia had progressed during the 2 months after the initial examination at the department of internal medicine. In addition, marked inflammation was apparent: the leukocyte count was 9800/mm 3, erythrocyte sedimentation rate 143 mm/hr, and C-reactive protein 22.6 mg/dl. The purified protein derivative test was 0/22 x 20 mm. Roentgenogram of the chest showed that the left lung was absent because of past pleuropneumonectomy. The left sixth rib was absent, and the seventh rib was deformed. Comparison with the previous chest x-ray films indicated that the defect and deformity were due to the operation carried out 16 years previously. A computed tomographic scan of the chest visualized marked deformity of the thorax and ribs. A wall with a uniform thickness on both the pleural and mediastinal sides surrounded the thoracic cavity, which contained no obvious protruding tumor. By gallium 67 scintigraphy, an image of abnormal accumulation was observed in the area corresponding to the left thoracic cavity. In summary, no abscess could be aspirated by thoracentesis, fever did not subside after antibiotic administration, and the chest roentgenogram showed no air fluid level. These findings did not suggest bacterial infection, and the reaction to the purified protein derivative test was too weak to suggest active tuberculosis. Because the patient became anemic in a short period of time, a malignant tumor of the chest wall was suspected, and open chest biopsy was performed on June 5, 1992.
A left posterolateral incision revealed the intercostal spaces to be narrowed and to show yellowish white thickening. A portion of the parietal pleura was resected through the narrowed fifth intercostal space. Prompt pathologic examination revealed sarcomatoid malignant cells. Thoracotomy was done in the fifth intercostal space to collect tissue from the thoracic cavity. Malignant cells were also present in this area. The yellowish white intercostal thickening involved the other intercostal spaces and ribs. The tumor in the thoracic wall was thought to have invaded the mediastinal side. Because a curative operation was judged to be impossible because of the extensive lesion, part of the third, fourth, and fifth ribs, the neighboring parietal pleura, and the tissue in the thoracic cavity were collected to end the surgical procedure. Specimens of the parietal pleural tissue were stained with hematoxylin and eosin. Low-power magnification of the specimens visualized a tumor in which spindle cells grew while forming a storiform pattern. The tumor appeared to be a polymorphic sarcoma marked by atypical giant cells. High-power magnification of the image revealed tumor cells consisting of fusiform fibroblastic cells and slightly oval histiocytic cells. These cells were positive in
1-antichymotrypsin staining but were negative in all of cytokeratin (KL-1), epithelial membrane antigen (EMA) and S-100 protein staining. These findings led to a histologic diagnosis of MFH. Histologic findings of the resected bone also showed invasion of the bone marrow by the MFH.
Postoperatively, three courses of CYVADICT therapy (cyclophosphamide, vincristine, doxorubicin, and dactinomycin) were given. Subsequently, the chemotherapy could not be continued because of debilitation. The patient died of general debilitation caused by tumoral fever 5 months after the operation. Consent for autopsy was not obtained.
The common sites of occurrence of MFH include the proximal regions of the extremities, such as the thigh, buttock, upper arm and shoulder, and the posterior peritoneum. The chest wall is a rare site of origin. 5 Reports indicate that MFH develops 8 to 14 years after radiotherapy, 2 16 to 25 years after burns, 3,6 and in the cicatricial wound 6 to 8 years after the operation. 4 It also has occurred 10 months after the onset of bone marrow infarction 7 and in the area having a vascular prosthesis 1 year later. 8 Malignant tumors frequently occur in the chest wall and thoracic cavity after chronic pleuritis and pyothorax. Epithelial tumors include squamous cell carcinoma, and nonepithelial tumors include malignant lymphoma, liposarcoma, angiosarcome, rhabdomyosarcoma, malignant mesothelioma, and MFH. Myoui and associates 1 found soft tissue sarcoma originating in the chest wall or thoracic cavity in two of 134 patients with tuberculous pyothorax and reported that the prevalence was about 1000 times that among normal individuals. They also reported that 65% of patients with MFH originating in the thoracic cavity had histories of chronic pleuritis or pyothorax, drawing attention to the relationships between histories of these disorders and the onset of MFH. The reported interval between chronic pleuritis or pyothorax and the outbreak of soft tissue sarcoma is 15 to 50 years. 1
Our patient had had tuberculous pleuritis 50 years previously and had undergone pleuropneumonectomy for tuberculous pyothorax at our department 16 years earlier. This operation involved en bloc resection of parts of both lungs and the parietal, mediastinal, and diaphragmatic pleurae. Since then, tuberculous pleuritis or pyothorax had not recurred. A surgically resected pleura regenerates, during which histiocytes and fibroblastic cells play an important role. We think that in rare cases these two types of cells and undifferentiated mesenchymal cells become malignant, causing MFH. Chronic inflammation has been found to develop in a surgical wound, 3 and Tanz 9 reported the occurrence of fibrosarcoma in a laparotomy wound. In our patient, postoperative chronic inflammation caused by surgery and slight residual tuberculosis may have led to pleural formation, inducing the onset of MFH. The mechanism of onset of malignant tumors as a result of malignant cellular changes remains to be clarified.
References
1-antitrypsin–like material in neoplastic cells. Am J Clin Pathol 1980;74:820-6.[Medline]
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