对慢性鼻窦炎鼻息肉临床分型分期的几点意见

中华医学会耳鼻咽喉科学分会和中华耳鼻咽喉科杂志编辑委员会于1997年在海口制订了“慢性鼻窦炎鼻息肉临床分型分期及内窥镜鼻窦手术疗效评定标准”(简称海口标准)。通过7年的临床实践，海口标准为推动我国内镜下鼻窦手术的开展、手术疗效的评价，以及学术交流起到了巨大的促进作用。但随着研究工作的深入，海口标准中部分内容已经不能适应临床工作的需要，因此有必要对该标准进行修订。本文作者结合国内外学者对慢性鼻窦疾病的分型分期的不同认识，提出了一些很有意义的见解。发表本文的目的是希望引起广大专家、读者、作者对此问题的关注，并积极地参与到该标准的讨论中来，陈述自己相同的或不同的见解(整理成文后可寄至本刊编辑部)，为将来修订海口标准做好前期准备工作。     

Ⅲ型鼻窦炎鼻息肉临床分期探讨以及各期手术疗效分析

目的 探讨不同病变程度的Ⅲ型鼻窦炎鼻息肉内窥镜鼻窦手术的疗效和并发症。方法 将随访6-18个月的104例（208侧）Ⅲ型鼻窦炎鼻息肉依据病史、解剖结构、病变程度的临床上分为3期,并对各期手术临床疗效、并发症进行比较分析。结果 1、2、3期临床总有效率分别为93.06%、82.89%和70.00%;并发症发生率分别为5.56%、14.47%和25.00%。结论 Ⅲ型患者的解剖学改变（窦口鼻道复合体的完整性）及病变程度（肉芽增生及筛窦窦骨质增生）决定了手术的难度、风险及疗效,也应列为临床分期的客观依据。     

慢性鼻窦炎鼻息肉再次内镜鼻窦手术

目的 探讨需行再次内镜鼻窦手术的原因，评价再次内镜鼻窦手术的疗效。方法 对114例（161侧）需行再次内镜鼻窦手术的患者术前行鼻内镜和鼻窦CT扫描检查，术后随访2例以上。结果 114例（161侧）中复发性鼻窦炎98例（129侧），复发性鼻息肉16例（32侧）。额隐窝狭窄2例（3例），前组筛窦炎18例（24侧），前组筛窦炎和上颌窦自然开口堵塞31例（46侧），中鼻甲粘连6例（7侧），后组筛窦炎18例（24侧），后组筛窦和蝶窦炎36例（54侧），蝶窦炎3例（3侧）。伴有鼻中隔偏曲者15例。经2年以上随访，复发性鼻窦炎者88例（111侧）痊愈，10例（18侧）症状缓解，16例（32侧）复发性鼻息肉患者11例（22例）痊愈，5例（10例）症状缓解。结论 行再次内镜鼻窦手术的原因主要是前次手术未彻底清除病变（首先与术者经验不足有关）；其次为鼻息肉病。再次内镜鼻窦手术效果满意，无严重并发症。     

鼻窦炎鼻息肉内窥镜手术的临床分析

2002年4月至2004年4月我们开展鼻内镜下治疗慢性鼻窦炎、鼻息肉手术117例,术后随访1～1．5年,效果较好,报告如下。     

鼻内镜下治疗79例慢性鼻窦炎鼻息肉的临床观察

慢性鼻窦炎、鼻息肉是耳鼻咽喉科的常见病、多发病，传统的治疗方法是在额镜下手术，光线弱，或采用鼻外手术，损伤重，并且病变切除不彻底。鼻内镜的临床应用，使慢性鼻窦炎、鼻息肉治疗提高到了一个新的水平。我院自2001年6月～2003年6月期间，施行鼻内镜手术治疗79例慢性鼻窦炎、鼻息肉。现总结、分析如下。     

慢性鼻-鼻窦炎鼻息肉内镜鼻窦术后上颌窦口黏膜恢复过程观察

目的 试图通过对内镜鼻窦手术(endoscopic sinus surgery，ESS)后患者鼻腔鼻窦黏膜的内镜、光镜、透射电镜和扫描电镜下连续动态观察，揭示病变黏膜转归的过程。方法 选取2001年1～12月行ESS的慢性鼻一鼻窦炎伴鼻息肉患者31例(53侧)作为研究对象，其中Ⅱ型2期11例(20侧)、3期12例(20侧)，Ⅲ型8例(13侧)。分别于ESS术前、术后2～3周、8～11周、13～16周钳取上颌窦口后囟相同部位的黏膜组织进行观察。结果 术前均可见上皮剥蚀、鳞状上皮化生、腺体及纤维组织增生(53侧)；微管结构异常、线粒体减少(53侧)。术后2～3周，形态学观察与术前比较没有明显的改变。术后8～11周，纤毛柱状细胞增多，并可见许多带有微绒毛的柱状细胞和大量短纤毛，所有病例均可见病理性腺体及纤维组织增生。术后13～16周，Ⅱ型2、3期和Ⅲ型患者术腔光滑干净，上皮化较好(50侧)，窦口通畅(53侧)。纤毛覆盖面积增加，方向一致(50侧)。微管结构清晰，线粒体狭长致密(49侧)。3侧无纤毛柱状细胞排列整齐，形成病理性修复。结论 ESS术后，黏膜形态的基本恢复一般需要3个月左右；有些病理改变是不可逆的；病变程度与黏膜修复情况有关；术中尽可能多地保留黏膜组织、术后局部及时清理换药，有利于黏膜纤毛的形态和功能的恢复。     

鼻内镜手术治疗Ⅲ型慢性鼻窦炎鼻息肉150例临床分析

Ⅲ型慢性鼻窦炎鼻息肉常有前期手术史,正常解剖标志多在以前的手术中遭到破坏,所以手术难度大,术后疗效欠佳,容易出现各种并发症。这一直是困扰鼻科医生的一大难题。近年来国内外广泛开展的鼻内镜手术,把Ⅲ型慢性鼻窦炎和鼻息肉的手术疗效提高到了一个新的水平。现将我科1999年1月～2002年2月经鼻内镜治疗,并完成随访6个月～1年150例患者的临床资料进行分析,借以提高本病内镜手术治疗的效果,减少并发症。报告如下。     

Treatment of recurrent chronic hyperplastic sinusitis with nasal polyposis

OBJECTIVE: To demonstrate the long-term efficacy of intranasal furosemide, an inhibitor of the sodium chloride cotransporter channel at the basolateral surface of the respiratory epithelial cell, vs no therapeutic intervention vs intranasal mometasone furoate, a corticosteroid, in preventing relapses of chronic hyperplastic sinusitis with nasal polyposis. DESIGN: Randomized prospective controlled study. Patients were examined every 6 months during follow-up (range, 1-9 years). PATIENTS: One hundred seventy patients with bilateral obstructive or minimally obstructive chronic hyperplastic sinusitis with nasal polyposis. INTERVENTION: All patients were surgically treated in the ENT Department, University of Siena Medical School. One month after surgery, group 1 patients (n = 97) started treatment with intranasal furosemide, group 2 (n = 40) received no therapeutic treatment, and group 3 (n = 33) were treated with mometasone. MAIN OUTCOME MEASURES: Clinical and instrumental evaluation of postoperative outcomes. RESULTS: Seventeen (17.5%) of 97 patients in group 1, 12 (30.0%) of 40 patients in group 2, and 8 (24.2%) of 33 patients in group 3 experienced nasal polyposis relapses. We noted a prevalence of early-stage relapse in patients treated with furosemide or mometasone, whereas patients who did not receive any treatment experienced more severe grades of chronic hyperplastic sinusitis with nasal polyposis (P<.005). CONCLUSION: Use of intranasal furosemide represents a valid therapeutic treatment in the prevention of chronic hyperplastic sinusitis with nasal polyposis.     

Paranasal sinus melanoma masquerading as chronic sinusitis and nasal polyposis

Malignant melanoma of the nose and paranasal sinuses can be a devastating disease, typically presenting at an advanced stage, with a 5-year survival rate ranging between 20 and 30%. It is an uncommon process, often misdiagnosed both clinically and pathologically. We present the case of an 80-year-old man who had a 2-month history of progressively worsening left-sided epistaxis and nasal obstruction. Radiographic evidence indicated the presence of soft tissue in the left maxillary sinus and nasal cavity resembling massive nasal polyposis and chronic fungal sinusitis. Magnetic resonance imaging was not performed because the patient had a pacemaker. After endoscopic debridement of the soft-tissue mass, frozen-section analysis detected no evidence of tumor. The final pathologic diagnosis was malignant melanoma. Otolaryngologists should be familiar with the difficulties inherent in the diagnosis and management of sinonasal melanomas.     

Superantigen hypothesis for the early development of chronic hyperplastic sinusitis with massive nasal polyposis

PURPOSE OF REVIEW: The pathogenesis, pathophysiology, and immunobiology of chronic hyperplastic sinusitis with massive nasal polyposis are starting to become unraveled. Allergy, viral infection, bacterial infection, fungal infection, and environmental pollution have all been suggested as possible initial triggers that may upregulate inflammation of the lateral wall of the nose to develop nasal polyposis. The purpose of this review is to present data from our laboratory that suggest that one of the possible early events in the development of inflammation of the lateral wall of the nose in chronic hyperplastic sinusitis with massive nasal polyposis is the production of exotoxins from Staphylococcus aureus. The exotoxins may act as superantigens and cause activation and clonal expansion of lymphocytes with specific Vbeta regions, resulting in massive cytokine production. RECENT FINDINGS: Recent published studies suggest that S. aureus is the most common organism isolated from the mucus adjacent to massive nasal polyposis. Staphylococci produce exotoxins. These exotoxins, sometimes known as enterotoxins, include SEA, SEB, and TSST-1. These exotoxins are capable of acting as superantigens and therefore, reacting with T lymphocytes with specific Vbetas in the lateral wall of the nose. Thereafter, it is possible that these lymphocytes are stimulated to produce both TH1 and TH2 cytokines, which have also been demonstrated in the nasal polyp. The consequence of these findings may be the upregulation and increased survival of eosinophils in the nasal polyp. SUMMARY: Staphylococcus aureus is present in the mucin adjacent to nasal polyps in about 60 to 70% of cases of massive nasal polyposis. These organism, as studied up to the present, always produce exotoxins, which may act as superantigens, causing activation and clonal expansion of lymphocytes with specific Vbeta region in the lateral wall of the nose. The present review suggests that activation of these lymphocytes produce both TH1 and TH2 cytokines. The potential damage to the nasal mucosa from eosinophils is briefly discussed. Theoretically, topical antibiotics to suppress the colonization of S. aureus may be a logical approach to downregulate the production of superantigen in the lateral wall of the nose after appropriate endoscopic sinus surgery.     

A superantigen hypothesis for the pathogenesis of chronic hyperplastic sinusitis with massive nasal polyposis

BACKGROUND: The pathogenesis of chronic hyperplastic sinusitis with massive nasal polyposis is still an enigma; however, the molecular biology of this disease is beginning to become unraveled and the proinflammatory cytokines and the message and the product of these cytokines have all been identified in nasal polyps. However, the initial trigger that causes inflammation of the lateral wall of the nose to up-regulate lymphocytes and eosinophils is still unknown. METHODS: Thirteen patients with massive polyposis were studied. The mucus of the nasal cavities surrounding the nasal polyps was studied for both bacterial and fungal species. The lymphocytes of the nasal polyps were extracted and evaluated for the T-cell receptor, particularly, the variable beta region of this receptor. Enterotoxins (superantigens) of the bacteria were studied. Finally, the histopathology of nasal polyps was studied. RESULTS: Fifty-five percent of the patients had toxin-producing Staphylococcus aureus in the nasal mucus adjacent to the polyps. Three different enterotoxins were isolated, including Staphylococcus enterotoxin A, Staphylococcus enterotoxin B, and toxic shock syndrome toxin 1. The variable B specificity for these superantigens was identified also in the polyp lymphocyte T-cell receptor. CONCLUSION: A superantigen hypothesis for massive polyposis is suggested because the most common bacterial species found in the nasal mucus is Staphylococcus aureus. These bacteria produce enterotoxins in all of the cases studied and the corresponding variable beta region of the T-cell receptor also was up-regulated in the polyp lymphocytes in cases studied thus far. These data taken together suggest that the initial injury to the lateral wall of the nose may be the result of toxin-producing Staphylococci. Superantigens (enterotoxins) may up-regulate lymphocytes to produce cytokines that are responsible for the massive up-regulation of lymphocytes, eosinophils, and macrophages, the three most common inflammatory cells found in massive nasal polyposis.     

Immunoglobulin E to staphylococcal and streptococcal toxins in patients with chronic sinusitis/nasal polyposis

BACKGROUND: The role of infectious agents and their contribution to the inflammation in chronic sinusitis/nasal polyposis (CS/NP) is not clear. Staphylococcal and streptococcal toxins have superantigen activity and have been implicated in inflammatory conditions such as atopic dermatitis, psoriasis, and asthma. OBJECTIVE: We investigated the presence of immunoglobulin (Ig)E antibodies to staphylococcal and streptococcal toxins in the serum of individuals with CS/NP. METHOD: IgE antibodies to staphylococcal exotoxins, A, B, and toxic shock syndrome toxin-1 and streptococcal pyrogenic exotoxin A, B, and C were measured in 23 individuals with CS/NP before functional endoscopic sinus surgery and in controls (7 atopic and 6 nonatopic) individuals without chronic sinusitis. Presence of IgE to the toxins was also correlated with disease severity on sinus computed tomography (CT) scans. RESULTS: Staphylococcal and streptococcal toxin specific IgE antibodies were detected in 18 of 23 (78%) and 7 of 21 (33.3%) patients, respectively. None of the controls had IgE to the staphylococcal or streptococcal toxins (P <.0001). There was no association between radiographic severity of sinus disease and the presence of IgE antibody to the toxins. CONCLUSION: A significantly greater proportion of CS/NP patients had IgE to staphylococcal or streptococcal toxins. Evidence of IgE antibodies directed against staphylococcal and streptococcal toxins in the sera of patients with CS/NP suggests a potential role of these toxins with established superantigen effects in the pathogenesis of CS/NP.     

An update on the impact of Staphylococcus aureus enterotoxins in chronic sinusitis with nasal polyposis

Nasal polyps in adults, characterized by abundant eosinophils, local overproduction of immunoglobulin E, and often associated with asthma, have been appreciated as an eosinophilic inflammation, potentially of allergic origin, but unrelated to a bacterial impact. Evidence accumulates, however, that Staphylococcus aureus colonizes chronic rhinosinusitis with, but not without polyps, with significantly increased prevalence. The germs release enterotoxins, which act as superantigens and induce a topical multiclonal IgE-formation as well as a severe, possibly steroid-insensitive eosinophilic inflammation. Recently, S. aureus could be demonstrated to reside intraepithelially, and potentially to release superantigens into the tissue from within the epithelial cells. An immune defect, either in the innate or adaptive immunity, might be responsible for this phenomenon. Follicle-like structures and lymphocyte accumulations, specifically binding enterotoxins, can be found within the polyp tissues, giving rise to local IgE formation. The superantigen-induced immune response also leads to a modulation of the severity of the eosinophilic inflammation, and may be linked to lower airway co-morbidity in polyp patients. Interestingly, IgE antibodies to enterotoxins can be found in the majority of aspirin-sensitive polyp tissues, associated with a substantial increase in ECP and IL-5. The possible role of S. aureus enterotoxins in polyp disease in Europe, the US and Asia has meanwhile been supported by several studies, demonstrating the presence of IgE antibodies to enterotoxins and inflammatory consequences in nasal polyp tissue. First studies also point to an involvement of S. aureus derived enterotoxins in lower airway disease, such as severe asthma and exacerbated COPD, clearly suggesting a clinical need for diagnosis and treatment of the germ and its related effects. Therapeutic approaches are so far empirical, and need further study, also serving to proof the clinical relevance of the concept.