Abstract Adult-onset Still’s disease (AOSD) is a rare systemic inflammatory disease manifesting with a persistent high-spiking fever, a typical rash, and lymphadenopathy. Endogenous factors related to interleukin-1, such as S100A8/A9 and several chemokines including CXCL10, CXCR3, and CXCL13, potentially play roles in its pathogenesis. We describe the histopathological features and chemokine expression pattern in lymph nodes (LNs) of patients with AOSD. Formalin-fixed, paraffin-embedded excisional LN tissues from 48 patients with AOSD were histologically reviewed. CXCL10, CXCR3, CXCL13, and S100A8/A9 expression was evaluated immunohistochemically. The pathology of LN was characterized by paracortical hyperplasia with proliferation of histiocyte, immunoblast, CD8-positive lymphoid cell and blood vessel. Most cases required differential diagnosis from dermatopathic lymphadenitis (n = 16, 33.3%), T cell lymphoma (n = 11, 22.9%), and histiocytic necrotizing lymphadenitis (HNL) (n = 9, 18.8%). The expression levels of CXCL10 and CXCR3 were higher in patients with AOSD than in those with T cell lymphoma, HNL, tuberculous lymphadenitis, and reactive hyperplasia. It is important to recognize the aforementioned histopathologic findings of nodal involvement of AOSD because improper diagnosis and treatment can be avoided. Immunohistochemical staining for chemokines, CXCL10 and CXCR3, may aid in differentiating AOSD from other mimickers.
Kyeong Deok Kim, Gyu-Seong Choi, Sunghae Park, Young Ju Oh, Sang Oh Yun, Manuel Lim, Eun Sung Jeong, Ji Eun Kwon, Jaehun Yang, Jinsoo Rhu, Jong Man Kim, Jae-Won Joh. Korean J Transplant 2021;35:131. https://doi.org/10.4285/ATW2021.PO-1257
Background: Non-melanoma skin cancers are caused mainly by prolonged UV exposure. However, there is no effective prevention other than avoiding sun exposure. Recently, ablative fractional laser(FL) treatment is actively being carried out for facial rejuvenation. Objectives: We elucidated whether the occurrence of skin tumors caused by exposure to UV can be decreased by multiple sessions of ablative CO2 FL. Methods: Two groups of hairless mice were treated with either ablative CO2 FL or nothing at 3-week intervals during the 20 weeks of UV exposure period. At the 30-week, representative tumors were taken to evaluate the type of tumor and check the mRNA expression levels of the MMP-13 and type-1 procollagen. In addition, we evaluated the change of skin barrier function at 12 weeks and 20 weeks. Results: At 30 weeks, the UV plus FL treated group(group I) showed a significantly lower average size of tumor and a lower occurance rate of tumors than the UV only treated group(group II). Tumors in the group II showed more malignant progression. And the groups II showed significantly greater trans-epidermal water loss than the group I. The group II showed significantly decreased collagen and elastic contents than the group I. The group I presented a higher mRNA level of type-1 procollagen, and a lower level of MMP-13 than the group II. Conclusion: Ablative CO2 FL can be effective for not only skin rejuvenation but also for prevention of skin tumors induced by UV.
Background Exposure to cigarette smoking (CS) is a major risk factor for airway inflammation. However, little is known about the effects of CS exposure on eosinophilic rhinosinusitis with nasal polyps (ERSwNPs). Histopathological and molecular studies were performed to investigate its effects using a murine model of ERSwNPs. Methods Mice were assigned to one of the following four groups (n = 8 for each group): control group, CS exposure (CS group), ERSwNP (ERS group), and ERSwNPs exposed to CS (ERS + CS group). Histopathological changes were investigated using various stains, including hematoxylin and eosin for inflammation and polyp-like lesions, Sirius red for eosinophils, toluidine blue for mast cells, Alcian blue for goblet cells, and Masson's trichrome stain for collagen fibers. mRNA expression of cytokines from nasal mucosae was measured. Serum I and systemic cytokine levels were measured by enzyme-linked immunosorbent assays. The expression of vascular endothelial growth factor (VEGF) and hypoxia-inducible factor (HIF) 1-alpha was evaluated by immunohistochemical staining. Results The ERS + CS group showed more severe symptoms, increased the number of polyp-like lesions filtration of eosinophils, goblet cell hyperplasia, and subepithelial fibrosis, compared with the ERS group. Additionally, mRNA expressions of IL-4 and IL-17A were up-regulated in ERS + CS group and higher levels of IL-4, IL-6, IL-17A, and interferon gamma from splenocytes were observed significantly in the ERS + CS group compared with the ERS group. In the ERSwNP murine model, exposure to CS enhanced the expression of VEGF and HIF-1-alpha in nasal epithelial cells. Conclusion Chronic exposure to CS aggravated eosinophilic inflammation and promoted airway remodeling and nasal polyp formation in a murine model of ERSwNPs. The underlying mechanism might involve up-regulated expression of VEGF and HIF-1-alpha.
Hepatocellular adenoma is a benign tumor of the liver occurring predominantly in young women taking oral contraceptives. The malignant transformation of hepatocellular adenoma into hepatocellular carcinoma has rarely been reported. Herein, we report the case of an elderly male patient with hepatocellular carcinoma that developed from hepatocellular adenoma. The patient's high risk for surgery and conflicting biopsy and imaging results made it difficult to determine the treatment direction. Eventually, the mass was completely removed by laparoscopic left hemi-hepatectomy without complications.
Kim JY, Bae BN, Kwon JE, Kim HJ, Park K. Prognostic significance of epidermal growth factor receptor and vascular endothelial growth factor receptor in colorectal adenocarcinoma, APMIS 2011; 119: 449–59. The purpose of this study was to evaluate the association between the expression of growth factors and the clinicopathological variables of colorectal adenocarcinoma. Immunohistochemistry and fluorescence in situ hybridization (FISH) were used to evaluate the amplification and expression of epidermal growth factor receptor (EGFR), vascular endothelial growth factor (VEGF), VEGF-D, VEGF receptor (VEGFR)-2, VEGFR-3, transforming growth factor (TGF)-β1, and insulin-like growth factor-1 receptor (IGF-1R) in a tissue microarray of 292 colorectal adenocarcinomas. The expression of EGFR, VEGF, VEGF-D, VEGFR-2 and VEGFR-3 was detected in 5.1%, 10.0%, 6.8%, 5.2%, and 57.2%. EGFR expression was associated with angioinvasion (p < 0.05) and lymph node metastasis (p < 0.005). VEGFR-3 expression was higher in the rectum than in the colon (p < 0.05). VEGF expression correlated with VEGF-D (p < 0.05) and VEGFR-3 (p < 0.005) expression, while VEGF-D expression showed no significant association with VEGFR-2 or VEGFR-3. EGFR amplification was present in 10.6% and was not associated with EGFR protein expression. VEGFR-2 and VEGFR-3 expression levels were related to poor patient survival. Stage, perineural invasion, and lymph node metastasis were independent prognostic factors based on a Cox analysis. VEGFR-2 and VEGFR-3 expression are markers of a poor prognosis in patients with surgically resected colorectal adenocarcinoma, whereas EGFR has a minor influence.
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