Purpose: The outcome of performing a tracheostomy in patients with coronavirus disease (COVID-19) seems promising based on the reported 30-day survival rate. However, long-term outcomes are still lacking. Therefore, our aim in this study was to evaluate the long-term outcomes of tracheostomy performed in critically ill COVID-19 patients. Methods: This was a retrospective analysis of 27 COVID-19 patients on whom tracheostomy was performed between February 28, 2020, and April 7, 2020, at Tongji Hospital (Wuhan, China). Patients' clinical characteristics, complications, and outcomes were analyzed. Results: All patients underwent successful bedside tracheostomy. Thirteen patients (48.1%) were successfully weaned off ventilation within 1 month. The survival rate at one, three, and nine months after tracheostomy were 63.0%, 37.0%, and 29.6%, respectively. At nine months after tracheostomy, 8/27 patients had survived, with five (62.5%) being discharged home while the remaining were dependent on nursing care. Conclusion: The survival rate of COVID-19 patients who underwent tracheotomy decreased markedly from 1 to 3 months after tracheotomy, remaining stable between 3 and 9 months. Medical support is much needed for COVID-19 patients over the first 90 days after tracheotomy.

This study examined the potential roles of CC10 (Clara cell 10-kD protein) and ILC2s (type 2 innate lymphoid cells) in allergic rhinitis (AR). After ovalbumin was used to construct the AR model, microarray analysis was performed to reveal the key differentially expressed genes. The phenotypic changes of nasal mucosa were examined by H&E staining. Western blot analysis, qRT-PCR, ELISA and immunohistochemistry were performed to identify the levels of cytokines. The lineage markers (CD127 and CD117) of ILC2s were detected using immunofluorescence. The microarray analysis and qRT-PCR results showed that CC10 overexpression inhibited the expression of A20, BAFF, and IL-4 R in vivo. Also, CC10 overexpression was found to ameliorate the damage of nasal mucosa in AR mice. Investigations revealed that the ILC2s were activated in AR mice and AR patients with high levels of IgE, IgG1, IL-4, IL-5, IL-13, IL-25, and IL-33. Moreover, CD127+ was found to activate ILC2s. However, CC10 overexpression suppressed the activation of ILC2s. In conclusion, this research suggested that CC10 could suppress the activation of ILC2s to attenuate the damage of nasal mucosa and that CD127+ may be a biomarker of the activation of ILC2s in AR mice and AR patients.

Background Tracheostomy, as an aerosol-generating procedure, is considered as a high-risk surgery for health care workers (HCWs) during the coronavirus disease (COVID-19) pandemic. Current recommendations are to perform tracheostomy after a period of intubation of > 14 days, with two consecutive negative throat swab tests, to lower the risk of contamination to HCWs. However, specific data for this recommendation are lacking. Therefore, this study aimed to evaluate viral shedding into the environment, including HCWs, associated with bedside tracheostomy in the intensive care unit. Methods Samples obtained from the medical environment immediately after tracheostomy, including those from 19 surfaces, two air samples at 10 and 50 cm from the surgical site, and from the personal protective equipment (PPE) of the surgeon and assistant, were tested for the presence of severe acute respiratory syndrome coronavirus 2 in eight cases of bedside tracheostomy. We evaluated the rate of positive tests from the different samples obtained. Results Positive samples were identified in only one of the eight cases. These were obtained for the air sample at 10 cm and from the bed handrail and urine bag. There were no positive test results from the PPE samples. The patient with positive samples had undergone early tracheostomy, at 9 days after intubation, due to a comorbidity. Conclusions Our preliminary results indicate that delayed tracheostomy, after an extended period of endotracheal intubation, might be a considerably less contagious procedure than early tracheostomy (defined as < 14 days after intubation).

BACKGROUND:The mechanisms underlying mucosal eosinophilia in chronic rhinosinusitis with nasal polyps (CRSwNP) remain poorly clarified. The nervous system and neuropeptides play an important role in the regulation of immune response. Herein we explore the expression and function of hemokinin-1 (HK-1), a newly identified tachykinin, along with its receptor neurokinin 1 receptor (NK1R) in CRSwNP.METHODS:HK-1, NK1R, and C-C motif chemokine ligand 24 (CCL24) expression in nasal tissues (53 eosinophilic CRSwNP, 32 non-eosinophilic CRSwNP, and 33 controls) was investigated by quantitative reverse transcript polymerase chain reaction (RT-PCR) and immunofluorescence staining. THP-1, a human monocytic leukemia cell line, and eosinophilic polyp tissues were stimulated with HK-1. Cells, tissues, and culture supernatants were subsequently collected for detection of the production of various inflammatory cytokines and chemokines by quantitative RT-PCR and enzyme-linked immunoassay.RESULTS:HK-1 and NK1R mRNA and protein expression were upregulated in eosinophilic and non-eosinophilic nasal polyps compared with control tissues, with eosinophilic polyps demonstrating a higher upregulation compared with that of non-eosinophilic polyps. Eosinophils constituted the major source of HK-1, whereas macrophages were the predominant cell type exhibiting NK1R in eosinophilic polyps. HK-1 induced CCL24 production from macrophages differentiated from THP-1 cells; this was abolished by an NK1R antagonist. HK-1 also induced CCL24 production from ex vivo-cultured eosinophilic nasal polyps. CCL24 was expressed by macrophages in eosinophilic but not non-eosinophilic polyps. The expression level of HK-1 correlated with CCL24 expression and tissue eosinophilia in eosinophilic nasal polyps.CONCLUSION:Eosinophil-derived HK-1 induces CCL24 production from macrophages and therefore exaggerates eosinophilic inflammation in CRSwNP.

目的:探讨OSAHS风险与静脉麻醉手术患者术后发生认知功能障碍的关系.方法:采用NoSAS评分对55例静脉麻醉手术患者进行OSAHS风险评估,并将其分为对照组23例(NoSAS＜8分)和OSAHS组32例(NoSAS≥8分),以蒙特利尔认知评估量表(MoCA)对两组患者在术前和术后第一天进行认知功能评估,计算每位患者手术前后MoCA评分的差值△MoCA(术前MoCA-术后MoCA),比较两组患者手术前后的MoCA评分及△MoCA.结果:OSAHS组术前MoCA评分(25.83± 1.80)明显低于对照组术前MoCA评分(28.05± 1.31)(P＜0.05).OSAHS组术后MoCA评分(25.13± 1.64)较术前无明显变化(P＞0.05),对照组术后MoCA评分(26.73± 1.17)明显低于术前(P＜0.05).OSAHS组△MoCA(0.39± 1.03)明显低于对照组(1.32±1.08),主要表现为视空间与执行功能[(0.09± 0.29) vs.(0.30± 0.32)]、注意力[(0.09± 0.60) vs.(0.47± 0.70)]和延时回忆力[(0.17± 0.39) vs.(0.47±0.51)]两方面(P＜0.05).结论:OSAHS高风险患者静脉麻醉术后认知功能障碍的程度较OSAHS低风险人群显著降低.

Background: The function of follicular regulatory T (T-FR) cells, especially in regulating IgE production in patients with allergic diseases, is poorly understood. Objective: We sought to investigate the phenotype, function, and clinical relevance of T-FR cells in patients with allergic rhinitis (AR). Methods: The phenotype and frequency of tonsillar and circulating T-FR cells were characterized by using flow cytometry. T-FR cell function was examined in an assay by coculturing with follicular helper T cells and B cells. The associations between T-FR cells and the clinical features in patients with AR before and after allergen immunotherapy (AIT) were analyzed. Results: T-FR cells were detected in germinal centers of tonsils, but compared with subjects without AR, the frequencies decreased in patients with AR who were allergic to house dust mites. Circulating T-FR cells in blood were phenotypically and numerically correlated with tonsillar T-FR cells, and a reduction of circulating T-FR cells but not total or CXCR5(-) regulatory T cells was noted in patients with AR compared with healthy control subjects. Moreover, circulating T-FR cells in patients with AR showed a specific defect in suppressing IgE production but were capable of suppressing production of other immunoglobulin types. We identified negative associations of circulating T-FR cell frequencies and function with antigen-specific IgE levels or disease severity in patients with AR. After AIT, the frequencies and function of circulating T-FR cells were improved, which positively associated with disease remission. Conclusion: Impairment in T-FR cells might contribute to aberrant IgE production in patients with AR, and AIT improves defective T-FR cell function. T-FR cells might serve as a potential biomarker to monitor clinical response to AIT.

Objective:To investigate the effects of microfibrillar collagen hemostat (Avitene) in endoscopic adenoidectomy.Methods:Fifty eight patients treated with endoscopic adenoidectomy were randomly divided into group A (compression and Avitene), group B (compression and electrocautery) and group C (only compression).The operation time, hemostasis time, degree of bleeding, difficulty of hemostasis, pain, diet time and surgical complications were compared among three groups.Results:No significant difference was found in the degree of bleeding among three groups (P＞0.05).The Operation time, hemostasis time and difficulty of hemostasis in group A were significantly lower than those in group B and group C (P＜0.05).The postoprative pain and diet revovery time of group A were lower than those of group B (P＜0.05).No surgical complications, including postoperative hemorrhage, infection or aspiration occurred in either group.Conclusions:The application of microfibrillar collagen hemostat in endoscopic adenoidectomy proved to be rapid, effective, simple and safe.

BACKGROUND:M2 macrophages are characterized by high interleukin-10 (IL-10) expression and are critical for resolving inflammation. Although increased accumulation of M2 macrophages has been demonstrated in chronic rhinosinusitis with nasal polyps (CRSwNP), particularly the eosinophilic type, their functional relevance in CRSwNP remains poorly understood. METHODS:M1 and M2 macrophages and IL-10 expression in sinonasal tissues were detected by double-immunofluorescence staining. THP-1 cells, a human monocytic leukemia cell line, were stimulated with various cytokines to study macrophage polarization and IL-10 expression. Polyp size, computed tomography (CT) scans, and symptom severity were scored. RESULTS:Compared with numbers in control tissues, the numbers of total CD68+ macrophages, interferon regulatory factor 5-positive and CD68+ M1 macrophages, and CD163+ CD68+ and CD206+ CD68+ M2 macrophages were increased in both eosinophilic and non-eosinophilic polyps. However, compared with non-eosinophilic polyps, eosinophilic polyps contained fewer M1 macrophages and more M2 macrophages. Consistent with this, the M1/M2 macrophage ratio was increased in non-eosinophilic polyps, whereas it decreased in eosinophilic polyps. Strikingly, the numbers of IL-10+ CD68+ macrophages and the percentage of IL-10+ CD68+ macrophages relative to the total number of macrophages were decreased in eosinophilic polyps, despite the upregulation of M2 macrophages in this type of polyp. The number of IL-10+ CD68+ M2 macrophages correlated negatively with total symptoms scores, polyp sizes, total CT scores, and the total number of inflammatory cells in patients with eosinophilic CRSwNP. Poly I:C downregulated IL-10 expression in M2 macrophages differentiated from THP-1 cells in vitro. CONCLUSION:Impaired IL-10 production by M2 macrophages may contribute to sustained inflammation in eosinophilic CRSwNP.vv.

ObjectiveActivation of mast cells associates with eosinophilic inflammation in chronic rhinosinusitis with nasal polyps (CRSwNP). The disease‐specific mast cell‐triggering mechanisms apart from immunoglobulin E are poorly understood in CRSwNP. CD30L/CD30 are members of the tumor necrosis factor/receptor superfamily and display immune modulatory function on mast cells. The aim of this study was to explore the expression and function of CD30 and CD30L in CRSwNP.MethodsThe mRNA expression of CD30 and CD30L was analyzed by real‐time polymerase chain reaction. The cellular expression of CD30L was determined by immunofluorescence staining. The soluble CD30 levels in nasal tissues were detected by enzyme‐linked immunosorbent assay. HMC‐1 cells, a human mast cell line, were cultured and stimulated with CD30.ResultsCompared with control tissues, CD30 mRNA expression levels were increased in eosinophilic polyps, and soluble CD30 protein levels were upregulated in both eosinophilic and noneosinophilic polyps with a greater increase in eosinophilic type. CD30 was expressed by T cells and B cells in nasal polyps. The CD30L mRNA expression levels and the number of CD30L+ cells and CD30L+tryptase+ mast cells were increased in eosinophilic polyps but not in noneosinophilic polyps as compared with control tissues. Mast cells accounted for 60% of CD30L+ cells in eosinophilic polyps. CD30 induced HMC‐1 cells to produce interleukin (IL)‐4 and IL‐13 without degranulation. Mast cells expressed IL‐4 and IL‐13 in eosinophilic polyps. The number of CD30L+tryptase+ mast cells was positively correlated with the number of eosinophils and total inflammatory cells in eosinophilic polyps.ConclusionCD30/CD30L‐mediated mast cell activation may promote the eosinophilic inflammation in CRSwNP.Level of EvidenceNA Laryngoscope, 129:E110–E117, 2019

To investigate the role of Let-7a in mouse allergic rhinitis,a total of 24 8-week old mature femaleC57BL/6 mice were randomly divided into four groups:Let-7a group,Let-7a control group,OVA group and PBSgroup,with 8 mice in each group.Mice in Let-7a group,Let-7a control group and OVA group were sensitized withovalbumin(OVA)to construct allergic rhinitis model.Mice in Let-7a group were administrated with Let-7a andliposome2000 mixture half an hour before the first,second and third challenge,and mice in Let-7a control groupreceived Let-7a control and liposome2000.PBS group was given PBS instead of OVA.Nasal rubs,eosinophilic cellinfiltration and goblet cell hyperplasia was estimated and local IL-4,IL-13 and IFN-γ cytokines in the localmucosa were measured.We found that compared with Let-7a control group,Let-7a group had more nasal rubs,eosinophilic infiltration and goblet cell hyperplasia,and increased levels of IL-4 and IL-13 in nasal mucosa(P<0.05),while no significant difference was observed for IFN-γ.So we concluded that Let-7a promotes the occurrenceand development of allergic rhinitis.

The concept of united airway diseases (UAD) has received increasing attention in recent years. Sustained and increased inflammation is a common feature of UAD, which is inevitably accompanied with marked gene modification and tight gene regulation. However, gene regulation in the common inflammatory processes in UAD remains unclear. MicroRNA (miRNA), a novel regulator of gene expression, has been considered to be involved in many inflammatory diseases. Although there are an increasing number of studies of miRNAs in inflammatory upper and lower airway diseases, few miRNAs have been identified that directly link the upper and lower airways. In this article, therefore, we reviewed the relevant studies available in order to improve the understanding of the roles of miRNAs in the interaction and pathogenesis of UAD.

BACKGROUND:The role of atopy to aeroallergens in chronic rhinosinusitis without nasal polyps (CRSsNP) remains unclear. This study aimed to investigate the mucosal immunopathologic characteristics of CRSsNP with and without atopy to inhalant allergens.METHODS:Thirteen nonatopic CRSsNP patients, 9 atopic CRSsNP patients, and 11 nonatopic control subjects were enrolled in this study. The expression of type 1, 2, and 17 cytokines, growth factors, and chemokines for T cell subsets and granulocytes in sinonasal mucosa was detected using Bio-Plex suspension chip technology or enzyme-linked immunosorbent assay (ELISA). Subjective symptoms were scored on a visual analogue scale (VAS), while disease severity on computed tomography (CT) was graded by the Lund-Mackay CT scoring system.RESULTS:There was no significant difference in VAS and CT scores between atopic and nonatopic CRSsNP. Compared with control, both atopic and nonatopic CRSsNP demonstrated increased interferon γ (IFN-γ) levels in sinonasal mucosa. In contrast, although no difference in interleukin 5 (IL-5), IL-13 and eotaxin-1 expression, or mucosal eosinophil infiltration, was found between the control and whole CRSsNP group, atopic CRSsNP manifested an increased expression of IL-5, IL-13 and eotaxin-1, as well as an enhanced infiltration of mucosal eosinophils in comparison with control and nonatopic CRSsNP. Mucosal eosinophil infiltration correlated with IL-5 and eotaxin-1 expression. No difference in IL-12, IL-4, IL-6, IL-17A, IL-8, myeloperoxidase, "regulated upon activation normal T cell expressed and presumably secreted" (RANTES), or chemokine (C-X-C motif) ligand 10 (CXCL10) protein expression was found among control, atopic CRSsNP, and nonatopic CRSsNP.CONCLUSION:Atopic and nonatopic CRSsNP have distinct mucosal immunopathologic profiles. CRSsNP is a heterogeneous disorder consisting of multiple groups of biological subtypes, or "endotypes," which may argue for different therapeutic strategies.

目的:采用TOPO TA克隆技术构建及鉴定人CC10基因表达载体,并在支气管上皮细胞系BEAS-2B细胞中获得稳定表达,初步探讨CC10在呼吸道上皮细胞炎症反应中的作用.方法:提取人下鼻甲组织的总RNA,逆转录反应生成cDNA,再用PCR方法扩增出含人CC10编码区全长的DNA片段,将PCR产物直接连接到pcDNA3.1N5-His TOPO TA载体中,转化至大肠杆菌后经筛选鉴定出CC10表达载体,用脂质体法将CC10质粒转染到BEAS-2B,细胞免疫荧光法检测CC10蛋白的表达.随后用促炎细胞因子IL-1β刺激转染空质粒和CC10质粒的BEAS-2B细胞,用实时定量RT-PCR和ELISA检测炎性趋化因子RANTESmRNA和蛋白的表达.结果:目的基因与TOPO TA载体在室温下5 min的连接反应效率91.7％,用酶切法鉴定质粒并测序,人CC10基因成功克隆到真核细胞表达载体pcDNA3.1中,CC10蛋白在BEAS-2B细胞中无表达,但在体外转染CC10质粒后CC10蛋白表达明显增高.转染CC10质粒的BEAS-2B细胞可抑制IL-1β诱导的RANTES mRNA和蛋白的表达.结论:利用TOPOTA克隆技术可高效、快速的构建人CC10基因表达载体,并能够在BEAS-2B细胞中获得稳定表达,CC10蛋白在呼吸道上皮细胞中可发挥抗炎作用.

目的:探讨可吸收性止血颗粒(Arista AH)在鼻内镜下经口腺样体吸切术创面止血上的应用效果.方法:54例腺样体肥大患者行鼻内镜下经口腺样体吸切术,随机分为四组,A组20例(压迫止血后喷洒Arista AH),B组15例(压迫止血后双极电凝止血),C组7例(压迫止血后Merocel高膨胀海绵填塞),D组12例(仅压迫止血).比较四组患者的止血时间、术后出血、咽痛持续时间、恢复正常通气时间等指标,同时采用视觉模拟评分法记录止血难度的主观评估.结果:A组手术时间、止血难度均低于B组、D组,差异具有统计学意义(P＜0.05),与C组无统计学差异(P＞0.05).而A组术后出血发生率低于D组(P＜0.05),与B组、C组无统计学差异.A组咽痛持续时间低于B组、C组,差异具有统计学意义(P＜0.05),与D组无统计学差异(P＞0.05).而A组恢复正常通气时间与B组、D组无统计学差异(P＞0.05).结论:可吸收性止血颗粒可用于鼻内镜下经口腺样体吸切术创面止血,具有快速简便、安全有效的特点.

目的:探讨伴有和不伴有过敏性鼻炎慢性鼻-鼻窦炎的临床资料的区别,发现过敏性鼻炎对慢性鼻-鼻窦炎的影响,从而提高慢性鼻-鼻窦炎的治疗效果.方法:选取我院2012年2月至2014年10月138位慢性鼻-鼻窦炎患者,分为伴有过敏性鼻炎组和不伴有过敏性鼻炎组,记录患者一般临床资料,采用Visual analog scale (VAS,视觉类比评分)记录患者主观症状评分;Lanza-Kennedy法记录鼻内镜评分,Lund-Mackay法记录CT评分;抽外周血查血常规;最后比较两组之间指标的差异.结果:138例慢性鼻-鼻窦炎患者中,有36(26.2％)名患者合并过敏性鼻炎;伴有过敏性鼻炎的慢性鼻-鼻窦炎患者组中有52.78％的患者有变应性体质,22.2％的患者有哮喘病史;而不伴有过敏性鼻炎的慢性鼻-鼻窦炎组有21.57％的患者有变应性体质,3.9％的患者有哮喘病史,差异具有统计学意义(P值均≤ 0.001);伴有过敏性鼻炎慢性鼻-鼻窦炎组总VAS评分、鼻塞和流鼻涕症状评分明显高于不伴有过敏性鼻炎慢性鼻-鼻窦炎组,两组评分差异具有统计学意义(P值均＜0.05);在血常规检查中发现,外周血白细胞、中性粒细胞、嗜酸粒细胞和单核细胞在伴有过敏性鼻炎的慢性鼻-鼻窦炎组中显著增加,其检测结果与不伴过敏性鼻炎组的差异具有统计学意义(P值均≤ 0.001).结论:过敏性鼻炎的慢性鼻-鼻窦炎患者相对于不伴有过敏性鼻炎的慢性鼻-鼻窦炎患者有更多的变应性体质和哮喘病史;鼻塞和流鼻涕的的症状更重;对于这部分病人应该给予更充分的认识和抗过敏的针对性药物以及手术治疗,使患者的生活质量得到更好的改善.血常规可帮助诊断.

Objective To explore the regulatory effect of miRNA on B-cell activating factor (BAFF) in chronic eosinophilic rhinosinusitis with nasal polyp (Eso CRSwNP).Methods Ten nasal mucosal samples were collected from Eso CRSwNP patients who were admitted and treated in our hospital between January 2012 and February 2013.Normal nasal mucosal tissues (n =10) served as control.The miRNA-targeting BAFF was predicted by bioinformatics tools.Immunohistochemistry and real time polymerase chain reaction (RT-PCR) were used to assess the protein expression of BAFF and the predicted miR-NA.The correlation between the predicted miRNA and BAFF was analyzed.Results Down-regulated expression of let-a was confirmed in Eos CRSwNP,while the BAFF protein expression was increased.Let-a was positively correlated with BAFF in nasal epithelia.Conclusions Let-a might contribute to mucosal eosinophilia in eosinophilic CRSwNP via targeting BAFF.

Inflammatory upper airway diseases, particularly chronic rhinosinusitis (CRS) and allergic rhinitis (AR), have a high worldwide prevalence. CRS and AR involve sustained and exaggerated inflammation that is associated with marked changes in gene and protein expression under tight regulation. A novel group of gene expression regulators is a class of short single-stranded RNA molecules termed microRNAs (miRNAs). miRNAs can cause gene silencing through degradation of target mRNAs or inhibition of translation. Dysregulated expression of miRNAs has been shown in various human diseases, such as cancer, inflammatory skin and bowel diseases, rheumatoid arthritis, and asthma. Although studies of miRNAs in inflammatory upper airway diseases are relatively new and few, emerging evidence implicates an involvement of miRNAs in shaping the inflammation pattern in upper airways. The purpose of this review is to provide an overview on our current understanding of miRNA expression and function in CRS and AR, and to underscore the potential for clinical usage of miRNAs in CRS and AR.

RATIONALE:Eosinophilic chronic rhinosinusitis (CRS) with nasal polyps (CRSwNP) represents a hard-to-treat subtype of CRS.OBJECTIVES:To determine the pattern of expression and biologic role of microRNAs (miRNAs) in CRS, particularly in eosinophilic CRSwNP.METHODS:Global miRNA expression in sinonasal mucosa from controls, CRS without nasal polyps (CRSsNP), and patients with eosinophilic CRSwNP was compared using miRNA microarrays. MiR-125b expression was detected by means of quantitative reverse-transcriptase polymerase chain reaction. The cellular localization of miR-125b was determined by in situ hybridization. MiR-125b functional assays were performed on airway epithelial cells and mice. MiR-125b expression regulation was studied by tissue and cell culture.MEASUREMENTS AND MAIN RESULTS:CRSsNP and eosinophilic CRSwNP exhibited distinct miRNA expression profiles. MiR-125b was specifically up-regulated in eosinophilic CRSwNP. MiR-125b was mainly expressed by sinonasal and bronchial epithelial cells. EIF4E-binding protein 1 (4E-BP1) was identified as a direct target of miR-125b. MiR-125b mimic or inhibitor enhanced or decreased IFN-α/β production elicited by dsRNA in vitro or in vivo, respectively. 4E-BP1 expression was decreased, whereas IFN regulatory factor-7 and IFN-β expression was increased, in eosinophilic CRSwNP. IFN-β mRNA levels positively correlated with IL-5 mRNA levels and eosinophil infiltration in sinonasal mucosa. IFN-β stimulated B cell-activating factor of the tumor necrosis factor family production in airway epithelial cells. miR-125b could be induced by lipopolysaccharide, dsRNA, and IL-10.CONCLUSIONS:The up-regulated expression of miR-125b may enhance type I IFN expression through suppressing 4E-BP1 protein expression in airway epithelial cells, which potentially contributes to mucosal eosinophilia in eosinophilic CRSwNP.

<正>促纤维结缔组织增生性纤维瘤是一种罕见的肿瘤,虽然其形态学呈良性改变,但生物学行为表现为侵袭性生长。它主要原发于长骨的干骺端、骨盆和下颌骨,很少见于骨质的其他部位。目前有关颞骨促纤维结缔组织增生性纤维瘤的文献非常少,其中