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ABSTRACT: Gastric intestinal metaplasia can display cytoarchitectural atypia that falls short of qualifying for dysplasia but can be classified as indefinite for dysplasia. Yet few studies have evaluated the prevalence, the morphologic, and biologic characteristics of this variant. Out of a cohort of 554 biopsies with chronic atrophic gastritis and/or dysplasia, we categorized the cases as either (1) simple intestinal metaplasia; (2) intestinal metaplasia with hyperplasia; (3) intestinal metaplasia with basal gland atypia; and (4) gastric dysplasia. The relationship between the subtypes and various clinicopathologic features, mucin immunophenotypes, and biologic characteristics was evaluated. The final cohort consisted of 424 cases of simple intestinal metaplasia, 93 intestinal metaplasia with hyperplasia, 16 intestinal metaplasia with basal gland atypia, and 21 gastric dysplasia. Intestinal metaplasia with basal gland atypia had a prevalence of 2.8% and similar to gastric dysplasia, 3.7%. Both of these lesions were similar in body/fundus distribution (12.5%) and paucity of goblet cells (68.8%). Intestinal metaplasia with basal gland atypia and gastric dysplasia seem to share some biologic similarities but with a lower frequency of alpha-methylacyl-CoA racemase expression (25% versus 62%), p53 expression (6.3% versus 47.6%), and increased Ki-67 index on surface/pit and isthmus in intestinal metaplasia with basal gland atypia. Alternatively, simple intestinal metaplasia and intestinal metaplasia with hyperplasia did not differ statistically with regard to the various characteristics evaluated. We concluded that gastric intestinal metaplasia can be divided into 2 broad categories that are readily defined by cytoarchitectural and biologic characteristics. Based on the characteristics of intestinal metaplasia with basal gland atypia and in keeping with others, we confirm that this subtype could represent a preneoplastic lesion that needs further evaluation.
Human pathology 10/2012; · 3.03 Impact Factor
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ABSTRACT: Nodular regenerative hyperplasia (NRH) of liver may be one of the leading causes of non-cirrhotic intrahepatic portal hypertension (NCIPH), although the exact relationship is currently unknown. Diagnosis of NRH is relatively difficult and involves surgical pathology, and thus it is necessary to improve the preoperative recognition of NRH. Here, we analyze 15 cases of NRH to better understand this disease. All the liver specimens were microscopically examined by hematoxylin-eosin staining and reticulin and Masson trichrome staining. Diagnoses of NRH were confirmed by pathological examination. Clinically, NRH presents as diffused liver lesions with mildly increased liver enzymes. Portal hypertension is the most common clinical manifestation presenting prominently as splenomegaly, hypersplenism, and esophageal varices bleeding. NRH is often associated with autoimmune or collagen vascular diseases, and such patients often present with a variety of positive autoantibodies and increased erythrocyte sedimentation rate (ESR), Ig and γ %. Pathological examination of the liver showed diffuse small regenerative nodules without fibrous septa and obstructive portal venopathy. For those patients with portal hypertension of unknown cause and preserved liver function, especially, those combined with autoimmune diseases, NRH should be considered.
Cell biochemistry and biophysics 06/2012; 64(2):115-21. · 3.34 Impact Factor
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ABSTRACT: Interdigitating dendritic cell sarcoma (IDCS) is an exceedingly rare tumor. The characteristics of IDCS and its optimal therapeutic approach have not been fully clarified.
We report the case of a 53-year-old Chinese male patient presenting with a subcutaneous nodule in the right chest wall. The histological and immunohistochemical features of the nodule confirmed the diagnosis of IDCS. Complementary examination excluded other involvement of the tumor. The patient was alive without evidence of disease 1 year after tumor resection followed by radiotherapy.
With regard to the literature, IDCS presents with a wide spectrum of clinical manifestations, and its correct diagnosis requires awareness of this rare disease and the use of appropriate markers. Surgery with curative potential might remain the first treatment option, and current data do not support adjuvant therapy. Systemic chemotherapy is mainly suggested for extensive disease while the long-term efficacy is unsatisfactory. The prognosis of IDCS seems to be associated with the initial stage of disease.
Onkologie 01/2011; 34(11):634-7. · 0.87 Impact Factor
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ABSTRACT: Metabolites of arachidonic acid such as prostacyclin (PGI2) have been shown to participate in the pathogenesis of pulmonary fibrosis by inhibiting the expression of pro-inflammatory and pro-fibrotic mediators. In this investigation, we examined whether iloprost, a stable PGI2 analogue, could prevent bleomycin-induced pulmonary inflammation and fibrosis in a mouse model.
Mice received a single intratracheal injection of bleomycin with or without intraperitoneal iloprost. Pulmonary inflammation and fibrosis were analysed by histological evaluation, cellular composition of bronchoalveolar lavage (BAL) fluid, and hydroxyproline content. Lung mechanics were measured. We also analysed the expression of inflammatory mediators in BAL fluid and lung tissue.
Administration of iloprost significantly improved survival rate and reduced weight loss in the mice induced by bleomycin. The severe inflammatory response and fibrotic changes were significantly attenuated in the mice treated with iloprost as shown by reduction in infiltration of inflammatory cells into the airways and pulmonary parenchyma, diminution in interstitial collagen deposition, and lung hydroxyproline content. Iloprost significantly improved lung static compliance and tissue elastance. It increased the expression of IFNgamma and CXCL10 in lung tissue measured by RT-PCR and their levels in BAL fluid as measured by ELISA. Levels of TNFalpha, IL-6 and TGFbeta1 were lowered by iloprost.
Iloprost prevents bleomycin-induced pulmonary fibrosis, possibly by upregulating antifibrotic mediators (IFNgamma and CXCL10) and downregulating pro-inflammatory and pro-fibrotic cytokines (TNFalpha, IL-6, and TGFbeta1). Prostacyclin may represent a novel pharmacological agent for treating pulmonary fibrotic diseases.
Respiratory research 03/2010; 11:34. · 3.36 Impact Factor
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ABSTRACT: The clinical behavior of gastrointestinal stromal tumors (GISTs) ranges from benign to malignant. Recent studies suggest that loss of 13q could be correlated with GIST progression. Our objectives were: (1) to detect chromosome 13q aberrations and determine the corresponding gene status in GISTs; and (2) to assess potential roles of 13q aberrations in GIST by correlating various 13q aberrations with various histologic parameters and disease-free survival in a group of GIST patients. Ninety-one cases of primary GISTs in Chinese patients were studied by dual color fluorescence in situ hybridization (FISH), through use of a panel of bacterial artificial chromosome clones RP11-685I15, RP11-352N7, and RP11-505F3 covering the Rb, RFP2, KCNRG, and KLF5 genes, respectively. Loss of RP11-685I15 was detected in 17/91 (18.7%) cases, loss of RP11-352N7 in 11/91 (12.1%) cases, and loss of RP11-505F3 in 5/91 (5.5%) cases. Chromosome 13 polysomy was observed in 22/91 (24.2%) cases. The frequency of RP11-685I15 deletion was positively correlated with tumor risk (P=0.0460). The frequency of RP11-352N7 deletion, RP11-505F3 deletion, and chromosome 13 polysomy tended to be higher in the high-risk GISTs. Shorter disease-free survival was significantly associated with RP11-352N7 deletion (P=0.0361) and high-risk grade (P=0.0003). Chromosome 13 instability of GISTs may play a role in tumor progression. Loss of 13q, especially loss of Rb, RFP2, KCNRG, and KLF5 genes are frequent events in high-risk GISTs. Loss of 13q may be associated with tumor progression.
Diagnostic molecular pathology: the American journal of surgical pathology, part B 06/2009; 18(2):72-80. · 1.58 Impact Factor
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ABSTRACT: CD8+ T cells may participate in cigarette smoke (CS) induced-lung inflammation in mice. CXCL10/IP-10 (IFNgamma-inducible protein 10) and CXCL9/Mig (monokine induced by IFN-gamma) are up-regulated in CS-induced lung injury and may attract T-cell recruitment to the lung. These chemokines together with CXCL11/ITAC (IFN-inducible T-cell alpha chemoattractant) are ligands for the chemokine receptor CXCR3 which is preferentially expressed chiefly in activated CD8+ T cells. The purpose of this investigation was to study the contribution of CXCR3 to acute lung inflammation induced by CS using CXCR3 knockout (KO) mice.
Mice (n = 8 per group) were placed in a closed plastic box connected to a smoke generator and were exposed whole body to the tobacco smoke of five cigarettes four times a day for three days. Lung pathological changes, expression of inflammatory mediators in bronchoalveolar lavage (BAL) fluid and lungs at mRNA and protein levels, and lung infiltration of CD8+ T cells were compared between CXCR3-/- mice and wild type (WT) mice.
Compared with the WT littermates, CXCR3 KO mice showed less CS-induced lung inflammation as evidenced by less infiltration of inflammatory cells in airways and lung tissue, particularly fewer CD8+ T cells, lower levels of IFNgamma and CXCR3 ligands (particularly CXCL10).
Our findings show that CXCR3 is important in promoting CD8+ T cell recruitment and in initiating IFNgamma and CXCL10 release following CS exposure. CXCR3 may represent a promising therapeutic target for acute lung inflammation induced by CS.
Respiratory research 01/2009; 9:82. · 3.36 Impact Factor
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ABSTRACT: To understand the diagnosis and treatment of pulmonary cryptococcosis.
Patients diagnosed as having pulmonary cryptococcosis in the past 15 years were retrospectively studied. Their demographic data, respiratory symptoms, diagnostic methods, chest radiograph, immune state, antifungal therapy and follow-up results were analyzed.
Thirty cases of cryptococcosis were diagnosed, of which 7 were diagnosed as having pulmonary cryptococcosis, one of them presented with concomitant meningitis. Of the 7 patients, 4 were male and 3 were female, with a median age of 41.8. All were HIV negative; one case was immunocompromised with a history of colon cancer and glucocorticoid therapy for 8 months, while others were immunocompetent. Three patients complained of low fever or cough and sputum, while 4 others presented no symptoms. The X-ray and chest CT showed unilateral or bilateral patches, nodules or cavities. The diagnosis was made by pathology and bacterial culture of sputum or bronchoalveolar lavage fluid. Amphotericin B plus flucytosine were initially given to 4 patients, all of them developed liver and renal abnormalities to some degree after therapy. Three patients were given fluconazole or itraconazole initially. All the 7 patients with pulmonary cryptococcosis responded favorably to antifungal therapy and the prognosis was good.
Clinically pulmonary cryptococcosis was less common than cryptococcal meningitis. Pathology and cryptococcal culture were essential to the diagnosis. For immunocompetent patients with pulmonary cryptococcosis, the prognosis was good.
Zhonghua jie he he hu xi za zhi = Zhonghua jiehe he huxi zazhi = Chinese journal of tuberculosis and respiratory diseases 11/2002; 25(10):610-2.
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ABSTRACT: To discuss the clinicopathological characteristics and differential diagnosis of nodular regenerative hyperplasia of the liver (NRH).
9 cases of NRH were collected and their clinical and pathological features were reviewed.
NRH is an important cause of non-cirrhotic portal hypertension which is frequently associated with autoimmune disease, malignant tumors and administration of certain drugs. Clinically NRH presents portal hypertension, but with almost normal liver function. Pathological examinations found diffuse nodules of hyperplastic hepatocytes in liver without fibrous septa in between. The obliteration of portal veins are frequently seen. This suggests that ischemia caused by alteration of portal veins may play an important role in the development of nodular regenerative hyperplasia of the liver.
Histopathology of NRH is characteristic and it should be differentiated from cirrhosis, focal nodular hyperplasia and hepatocellular adenoma.
Zhonghua bing li xue za zhi Chinese journal of pathology 03/2002; 31(1):34-7.
