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Summary: A 52-year-old man received a left pneumonectomy for pulmonary squamous cell carcinoma without signs of recurrence after surgery. At age 68 years, a capsulated huge mass developed in the left pleural cavity, which was diagnosed as chronic expanding hematoma. Two years and 8 months after detection, the lesion began to invade the chest wall, and 10 months later, the patient died of active bleeding and direct compression of the heart by the lesion. At autopsy, the left thoracic cavity was occupied by a cystic and hemorrhagic mass infiltrating into the surrounding structures. In addition, scattered tumorous nodules were observed in the right lung. Histologically, angiosarcoma with irregularly anastomosing vessels lined with atypical endothelial cells was noted in the chronic expanding hematoma. The final diagnosis was pleural cavity angiosarcoma arising in chronic expanding hematoma and its metastases to the right lung. [ABSTRACT FROM AUTHOR]

Abstract: The incidence of lung cancer (LC) is markedly increased among patients with usual interstitial pneumonia (UIP), and tobacco smoking is its superimposed risk factor. AKR1B10 (aldo-keto reductase 1B10) is frequently overexpressed in pulmonary squamous cell carcinoma and adenocarcinoma in smokers. To investigate the role of AKR1B10 in the pulmonary carcinogenesis in UIP with correlation to tobacco smoking, we examined 13 UIP cases with LC, 13 UIP cases without LC, and 30 cases of non-UIP LC using AKR1B10 immunohistochemistry. AKR1B10 immunoreactivity was confined to squamous metaplasia in honeycomb lesions of UIP and neoplastic cells of LC. Squamous metaplastic foci showed AKR1B10 immunoreactivity more frequently in UIP with LC (24/36 foci, 67%) than in UIP without LC (16/44 foci, 37%) (P<0.01). AKR1B10 expression in UIP was also more frequent in squamous metaplastic foci in smokers (38/67 foci, 57%) than in non-smokers (2/13 foci, 15%) (P<0.01). AKR1B10 expression was frequently observed in both UIP-associated LC (10/13 foci, 77%) and non-UIP LC (18/30 foci, 60%). Ki-67 labeling index was significantly higher in AKR1B10-positive squamous metaplasia of UIP than in AKR1B10-negative squamous metaplasia of UIP. Our results demonstrate that AKR1B10 is involved in the development of LC in UIP in association with smoking. AKR1B10 might be useful as a new marker for identification of high LC risk patients in UIP. [Copyright &y& Elsevier]

Abstract: Hepatic hemangiomatosis is a rare condition characterized by diffuse replacement of liver parenchyma with tissue similar to that of cavernous hemangioma. The purpose of this report is to illustrate two adult cases of hepatic hemangiomatosis and to review the pathological, radiological and clinical issues of this condition. The first case is that of a 47-year-old woman with extensive involvement of the entire liver. The right lobe was almost totally replaced, and only a limited amount of residual hepatic parenchyma was present in the left lobe. The second case is that of a 31-year-old woman with less extensive involvement. The right lobe was almost totally involved, and was accompanied with a large hematoma. The left lobe was relatively unaffected. Both cases were complicated by consumption coagulopathy (Kasabach–Merritt syndrome). The patients were successfully managed surgically, with living donor liver transplantation in the first case and extensive right lobectomy in the second case. The condition described by the term hepatic hemangiomatosis includes a wide clinical spectrum, with some cases asymptomatic, some accompanied with shunting, and some resulting in rupture or life-threatening hepatic failure. The disease has a good overall prognosis, with surgery and arterial embolization as effective treatment options. [Copyright &y& Elsevier]

Objective Tumor-associated macrophages (TAMs) are believed to influence tumor progression and the prognosis of patients. The purpose of this study was to clarify the correlation between the TAM density or location and the clinicopathological features of non-small-cell lung cancer (NSCLC) as well as to explore the prognostic impact of TAMs in NSCLC. Materials and methods CD68- and CD204-positive macrophages were detected in tumor islets, tumor stroma and alveolar space in 297 patients with NSCLC using immunochemistry. The clinicopathological and genetic factors surveyed were the disease-free survival, age, gender, smoking status, histological type, disease stage, histological grade, pleural invasion, lymph node metastasis, EGFR gene mutations and ALK rearrangements. Results There were significantly more CD68-positive macrophages than CD204-positive macrophages in each location of the tumor islets, tumor stroma and alveolar spaces, and they were strongly correlated ( P  < 0.0001 each). Factors such as male gender, being a smoker, an advanced disease stage and histological grade, positive pleural invasion and node status and wild-type EGFR gene status were significantly correlated with a higher density of CD68- and CD204-positive TAMs in tumor stroma ( P  < 0.05 each). In contrast, the age of patients was not correlated with CD68- and CD204-positive TAMs ( P  > 0.05 each). Furthermore, survival analysis revealed that a high number of CD68- and CD204-positive TAMs in tumor stroma, but not in tumor islets or alveolar space, was a significant prognostic factor for the disease-free survival time of NSCLC ( P  < 0.05, respectively). Moreover, both univariate and multivariate analyses confirmed that higher numbers of CD204-positive TAMs in tumor stroma were an independent worse prognostic predictor for adenocarcinoma. Conclusion The tumor stroma is the most suitable intratumoral area for the evaluation of TAMs in the setting of the prognostic prediction of NSCLC patients. CD204-positive TAMs are the preferable marker for prognostic prediction in NSCLC, especially in lung adenocarcinoma. [ABSTRACT FROM AUTHOR]

Eosinophilic granulomatosis with polyangiitis (EGPA), formerly called Churg-Strauss syndrome, is an uncommon disease with pathological features consisting of systemic necrotizing vasculitis, eosinophilic infiltration, and granulomatous or nongranulomatous extravascular eosinophilic inflammation. EGPA preferentially affects certain organ systems, including the airways, peripheral nerves, heart, kidney, and gastrointestinal tract. Although gastrointestinal involvement, such as ulcerations, is common in EGPA, gastrointestinal perforation is relatively uncommon and is associated with a poor prognosis. Ulceration, perforation, and stenosis of the gastrointestinal tract are assumed to be the result of ischemia caused by vasculitis. The histological finding in the biopsy specimens of EGPA is generally only eosinophil infiltration, and vasculitis is not often seen. Therefore, in biopsy specimens, it is difficult to distinguish eosinophilic gastroenteritis from the gastrointestinal involvement of EGPA. In addition, in general, steroid therapy is the first-choice treatment for EGPA, but some reports have described the frequent occurrence of acute ulcer or perforation of the gastrointestinal tract in association with steroid treatment. We herein report an EGPA patient who was treated with steroid therapy and subsequently developed perforation of the small intestine. • Eosinophilic granulomatosis with polyangiitis (EGPA), formerly called Churg-Strauss syndrome, is an uncommon disease. • We herein report an EGPA patient with intestinal perforation after steroid therapy. • Our case shows the difficulty to distinguish between eosinophilic gastroenteritis and gastrointestinal lesion of EGPA by an endoscopic biopsy. [ABSTRACT FROM AUTHOR]