what are the causes of nasal polyps and nasal polyps
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The main causes of nasal polyps are infection, allergy and trauma
The cause of this disease is still unclear. It is believed that chronic infection and allergy of upper respiratory tract are the main causes of nasal polyps.
1. Chronic infection Woakes (1885) first proposed that repeated infection of ethmoid sinus causes necrotizing inflammation of mucosa, which eventually leads to ethmoid sinus polyps. Up to now, many people still agree with this view. Because the bacterial toxins and inflammatory mediators released in the process of infectious inflammation can cause poor lymphatic drainage in mucosa, venous blood stasis, small blood vessel dilation, increased exudation and mucosal edema. At present, toxins also cause damage to nerve endings innervating blood vessels, which further dilates blood vessels and aggravates exudation. The mucous membrane with edema for a long time weakens the barrier function, and can produce repeated infectious inflammatory reactions. The mucous membrane edema is further aggravated, and finally promotes the formation of polyps. StieRNA (1991) recently confirmed that the ostium of the maxillary sinus in animals was blocked, and then pathogenic bacteria were caused into the sinus. As a result, polyps were found in the mucosa of the sinus. In addition, nasal polyps often occur in patients with recurrent respiratory tract infection caused by some congenital respiratory mucosal abnormalities (such as cystic fibrosis and immobile ciliary syndrome). There are many neutrophils in this kind of nasal polyps, but the clinical observation shows that the application of antibiotics in the treatment of nasal polyps has little effect. Although X-ray plain films show that patients with nasal polyps often have signs of "sinusitis" with thickening of sinus mucosa, pus cells and bacteria are rarely found in sinus lavage fluid (Dawes et al. 1989). Therefore, infection may promote the growth of polyps, but it is not a necessary condition for polyps.
2. Allergy Kern and Schenck (1933), based on the analysis of clinical statistical data, believe that nasal polyps are the result of allergy. Because they found that nasal polyps have a high incidence in respiratory allergic diseases such as asthma and hay fever (seasonal rhinitis), while they are rare in respiratory infectious diseases (lung abscess, bronchiectasis and tuberculosis). Many later studies have supported this view, mainly based on: ① Nasal polyps contain high levels of histamine (Bumsted, 1979; Dong Zhen 1983); There were a lot of eosinophil infiltration and degranulated mast cells in nasal polyps (Friedman, 1989; Drake-Lee et al., 1984, 1987); IgE-producing cells were found in nasal tissue, and the level of IgE in polyp fluid was higher than that in serum (Drakee-Lee, 1984); 4. Stimulating nasal polyps with specific allergens can release the same chemical medium as IgE-mediated allergy (Kaliner et al., 1973); Compared with nasal mucosa, arachidonic acid metabolism in nasal polyps is obviously increased, resulting in a large number of leukotrienes and inflammatory cell chemokines (Jung, 1987). The above facts suggest that, IgE-mediated allergy occurs locally in nasal mucosa, A large amount of histamine, leukocyte triene and inflammatory cell chemokine are released. These chemical mediators can make local blood vessels dilate and exudate, tissue edema, gland hyperplasia and eosinophils infiltrate. Eosinophils can release cytotoxic substances such as major basic protein (MBP), which destroys nerve endings on the wall of small blood vessels and is more conducive to dilation and exudate of small blood vessels. This local allergy is difficult to detect by routine allergen skin test or serological test, because specific IgE mainly exists in polyp sac fluid (Jones et al., 1987; Frenkiel et al., 1985).
Dong Zhen (1983) found that the level of IgG immune complex in serum of some patients with nasal polyps was positively correlated with the content of IgG in polyp fluid, but the content of IgG in polyp fluid of such patients was relatively low. Ogawa (1986) and Small (1986) found high levels of IgE immune complexes in polyp fluid. Therefore, it is speculated that type III allergy (immune complex type) may be one of the formation mechanisms of nasal polyps, but Jankowski (1989) did not find immune complex deposition around small vessels and epithelium in polyps by immunofluorescence method.
Other scholars have different meanings on the role of allergy in the formation of nasal polyps based on large samples of clinical data and laboratory analysis. Of the 3000 individuals identified by Caplin et al. (1971), the incidence of nasal polyps was 0.5%. Settipane et al. (1977) found in 6037 patients with asthma and rhinitis that the incidence of nasal polyps was 5% in those who were positive for allergen skin test, while the incidence of nasal polyps was 12% in those who were negative for skin test. Drake-lee (1984) investigated 200 patients with nasal polyps admitted to Addenbrooke Hospital in Cambridge in recent two years. The results showed that the characteristics of medical history, allergen skin test and serum IgE test were not related to allergy. In addition, children who are prone to allergic diseases rarely have nasal polyps. Jan-Kowski et al. (1989) found a large number of eosinophil infiltration in polyps by immunohistochemical method, but failed to confirm the relationship with allergy, and there were very few IgE-producing cells in polyps. Therefore, he believes that only by clearing the infiltration mechanism of eosinophils in polyp tissue can we understand the causes of nasal polyps.
Zhao Xiujie et al. (1995) found a large number of estradiol receptor positive cells in nasal polyps by immunohistochemical method, which were related to the number and distribution of mast cells, but not related to gender. It is known that estradiol can enhance the ability of mast cells to release histamine, so the existence of estradiol receptor positive cells,It is suggested that estradiol may play a certain role in the formation of polyps.
Petruson et al. (1988) found that nasal polyps contain high concentrations of insulin-like growth factor ⅰ (IGF-I). Therefore, it is speculated that in closed sinuses, due to the stimulation of infectious or allergic inflammatory reaction of sinus mucosa, macrophages in mucosa release IGF-I and accumulate in mucosa, which can stimulate mucosal proliferation for a long time. When the proliferating mucosa fills the sinus cavity, it protrudes into the nasal cavity from the sinus ostium. This long-standing growth stimulation and local inflammatory reaction are important factors leading to polyp formation.
To sum up, nasal polyps are the result of many factors. The factors that play a major role may vary according to conditions, but they all cause inflammatory reaction of local mucosa. Eosinophil infiltration, degranulated mast cells and extreme edema of tissues constitute the pathological basis of nasal polyps.
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