Expression of glucose transporter protein 1 and desmin in reactive mesothelial hyperplasia and epithelioid malignant mesothelioma / 中华病理学杂志

<p><b>OBJECTIVE</b>To investigate the expression of glucose transporter protein 1 (GLUT-1) and desmin in benign and malignant mesothelial lesions, including reactive mesothelial hyperplasia (RMH), epithelioid malignant mesothelioma (EMM) and metastatic adenocarcinoma (MAC).</p><p><b>METHODS</b>One hundred and forty two pleural biopsy specimens were collected in this study, including 58 cases of RMH, 53 cases of EMM and 31 cases of MAC. Immunohistochemical EliVision method was performed to detect GLUT-1 and desmin expression.</p><p><b>RESULTS</b>The positive rates for GLUT-1 in RMH, EMM and MAC were 13.8% (8/58) , 81.1% (43/53) and 77.4% (24/31) , respectively, with statistically significant differences between RMH and others (both P < 0.01). The positive rates for desmin in RMH, EMM and MAC were 77.6% (45/58) , 9.4% (5/53) and 0 (0/31) , respectively, with statistically significant difference between RMH and others (both P < 0.01). The combined expression pattern of positive GLUT-1 and negative desmin was found in 1 (1.7%, 1/58) RMH cases, 41 (77.4%, 41/53) EMM cases and 24 (77.4%, 24/31) MAC cases, with statistically significant difference between RMH and others (both P < 0.01).</p><p><b>CONCLUSIONS</b>GLUT-1 and desmin may be used as immunohistochemical markers in separating RMH from EMM. Combined application of two antibodies may improve the specificity.</p>

Pulmonary capillary hemangiomatosis: a clinicopathologic analysis of 2 cases with review of literature / 中华病理学杂志

<p><b>OBJECTIVE</b>To investigate the clinicopathologic features of pulmonary capillary hemangiomatosis (PCH).</p><p><b>METHODS</b>The clinical and pathologic profiles of 2 PCH cases were evaluated. Immunohistochemical study (EnVision method) was performed on fixed tissues. The biologic behavior was analyzed with follow-up data.</p><p><b>RESULTS</b>The main presenting symptom was dyspnea. Chest radiography of the two cases depicted diffuse, ground-glass nodules, accompanied by enlarged central pulmonary arteries. Microscopically, the most distinctive feature was proliferation of capillary channels within pulmonary interstitium and alveolar walls, accompanied by muscularization of arterioles. Immunohistochemical study showed an abundance of mast cells in the lesion, and staining for platelet-derived growth factor receptor-beta (PDGFR-β) localized to vascular smooth muscles surrounding the proliferating capillaries and the mast cells. The index of Ki-67 was less than 1 percent and the p53 was negative.</p><p><b>CONCLUSIONS</b>PCH is a rare vascular proliferative disease of yang patients. Increased number of mast cell and the up-regulation of PDGFR-β may suggest mechanism for PCH. The clinical and radiologic diagnosis of PCH can be very difficult, and the histological examination is regarded as the most reliable means to establish the diagnosis. Pathologists should improve their knowledge on PCH.</p>

Pathologic diagnosis and clinical analysis of chronic extrinsic allergic alveolitis / 中华病理学杂志

<p><b>OBJECTIVE</b>To study the clinicopathologic features and diagnostic approach of chronic extrinsic allergic alveolitis (EAA).</p><p><b>METHODS</b>Seven cases of chronic EAA diagnosed by open lung biopsy or lung transplant were enrolled into the study. The clinical and pathologic features were analyzed and the literature was reviewed.</p><p><b>RESULTS</b>There were altogether 4 men and 3 women. The age of the patients ranged from 30 to 65 years (mean = 48 years). All cases represented chronic form and five cases diagnosed by open lung biopsy also showed features of recent aggravation, leading to hospitalization. Four cases had known history of exposure to inciting gases, pollens and pets, and only 2 cases were positive for allergens. High-resolution CT scan showed ground-glass attenuation and reticular pattern that often had a patchy distribution and central predominance. Bronchoalveolar lavage analysis showed marked lymphocytosis, with CD4(+)/CD8(+) ratio less than 1. Lung function test demonstrated a restrictive ventilatory defect, with decreased compliance, reduced diffusion capacity and high airway obstruction. Five cases had open lung biopsy performed and two cases had undergone lung transplantation. Pathologic examination showed bronchiolocentric cellular interstitial pneumonia, interstitial fibrosis, non-caseating epithelioid granulomas, epithelioid histiocytic infiltrate in the respiratory bronchioles and intraluminal budding fibrosis. The five cases with open lung biopsy performed also showed neutrophilic infiltrate in the alveoli. The two lung transplant cases were complicated by severe fibrotic changes.</p><p><b>CONCLUSIONS</b>Chronic EAA demonstrates characteristic pathologic features. Definitive diagnosis requires correlation with clinical and radiologic findings due to possible morphologic mimicry of other diffuse parenchymal lung diseases.</p>

X-chromosome inactivation patterns of different tumor nodules in multiple leiomyomas of uterus / 中华病理学杂志

<p><b>OBJECTIVE</b>To describe the relationship among different tumor nodules in multiple leiomyomas of uterus.</p><p><b>METHODS</b>Genomic DNA was extracted from fresh tissue samples, digested through incubation with methylation-sensitive Hha I or Hpa II, and amplified via PCR for androgen receptor (AR) and phosphoglycerate kinase (PGK) genes. The length polymorphism on AR gene was demonstrated by denaturing polyacrylamide gel electrophoresis and silver staining, the PGK gene products were treated with Bst XI and resolved on agarose gels.</p><p><b>RESULTS</b>112 cases of leiomyomas and one case of leiomyosarcoma were examined, 89% showing the length polymorphism for AR gene and 30% carrying the polymorphic Bst XI site at PGK locus. Loss of X-chromosome inactivation mosaicism was observed in all the 321 tumor nodules examined from 77 cases, reflecting their clonal cellular composition. The relationship between different nodules was evaluated by their X-chromosome inactivation patterns in the 295 tumor nodules taken from 57 multiple leiomyomas. Similar inactivated alleles were found in all nodules in 30, in most nodules in 7 cases, similar to a multi-nodular leiomyosarcoma, while 20 cases showed near-random distribution of the inactivated alleles in different nodules, indicating their multicentric origins. No relevance was found between this difference and any histopathological parameters including number of mitotic figures and occurrence of bizarre nuclei and degeneration. In addition, an identical mutation and loss of heterozygosity were found at the AR locus in two apparently discrete tumor nodules in one case, providing further evidence for the unicellular origin of these lesions.</p><p><b>CONCLUSIONS</b>The multi-nodular leiomyomas may be classified into multicentric, unicentric types, as well as a mixed type. It remains to be clarified whether different nodules in the unicentric cases originate from a parent tumor by migration or by spreading.</p>