Arachidonic Acid Metabolites in Human Nasal Polyps

Ogino, Satoshi; Irifune, Morihiro; Hashizume, Tamotsu; Kikumori, Hiroshi; Matsunaga, Toru

doi:10.3109/00016489309126222

Cited by 17 publications

(8 citation statements)

References 3 publications

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“…LT were shown to play a role in the development and manifestation of bronchoconstriction, mucous hypersecretion, and recruitment of additional eosinophils in the lower airway 35 . It has also been found that LT may influence the pathophysiology of nasal polyposis and CRS in general 36,37 . We found that mucosal LTC 4 levels were higher in asthmatics than nonasthmatics, but the difference was not statistically significant.…”

Section: Discussioncontrasting

confidence: 49%

“…Asthmatics had higher symptom scores at 1 year after surgery than nonasthmatics (13.6 ± 2.9 vs. 9.1 ± 2.2, respectively, P = .226) and a lower symptom improvement rate (61% vs. 72%, P = .267). The differences were not statistically significant, perhaps because of the relatively low number of patients with asthma 16 compared with the number of patients without asthma 36 …”

Section: Resultsmentioning

confidence: 88%

“…The differences were not statistically significant, perhaps because of the relatively low number of patients with asthma 16 compared with the number of patients without asthma. 36…”

Section: Clinical Conventional Objective and Subjective Parametersmentioning

confidence: 99%

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Molecular and Cellular Staging for the Severity of Chronic Rhinosinusitis

Arango²,

et al. 2004

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We suggest the following severity classification system for CRS: 1) eosinophilic chronic hyperplastic rhinosinusitis (ECHRS): patients with polyps and sinus tissue eosinophilia; 2) noneosinophilic chronic hyperplastic rhinosinusitis (NECHRS): patients with polyps but without sinus tissue eosinophilia; 3) eosinophilic chronic rhinosinusitis (ECRS): patients without polyps but with sinus tissue eosinophilia; 4) noneosinophilic chronic rhinosinusitis (NECRS): patients without polyps and without sinus tissue eosinophilia.

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Section: Discussioncontrasting

confidence: 49%

Section: Resultsmentioning

confidence: 88%

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Molecular and Cellular Staging for the Severity of Chronic Rhinosinusitis

Arango²,

et al. 2004

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“…According to these studies, several AAMs, such as 15-hydroxyeicosatetraenoic acids (HETE), leukotriene (LT)B4, LTC4 and prostaglandins (PGs) are suggested to play some role (7)(8)(9)(10)(11)(12)(13)(14). However, no study paid particular attention to the contribution of AAMs in the pathogenesis of ACP.…”

Section: Introductionmentioning

confidence: 99%

Arachidonic Acid Metabolites in Antrochoanal Polyp and Nasal Polyp Associated with Chronic Paranasal Sinusitis

Jang

Rhee²,

Oh³

et al. 2000

Acta Oto-Laryngologica

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The aim of this study was to investigate the role of arachidonic acid metabolites (AAMs) in the pathogenesis of antrochoanal polyp (ACP). Using high-performance liquid chromatography (HPLC), we assayed the tissue concentrations of 6-keto-PGF1alpha, leukotrienes (LTs) and hydroxyeicosatetraenoic acids (HETE). Concentrations of AAMs in ACP were compared with the level in the control turbinate tissues and nasal polyps associated with chronic paranasal sinusitis (NPS). The concentrations of 6-keto-PGF1alpha were not significantly different in the control turbinate, ACP and NPS groups. In ACP, concentrations of LTC4, 15-HETE and 12-HETE were significantly lower than in the control turbinate. The striking differences in the profile of AAMs between ACP and NPS included a lack of production of LTD4 and LTE4 in ACP, also detectable in NPS, and markedly lower concentrations of 15-HETE and 12-HETE in ACP. The results of this study indicate that decreased lipoxygenase pathway products in arachidonic acid metabolism may be involved in the pathogenesis of ACP. However, in the pathogenesis of NPS, increased production of LTD4 and LTE4 may have an important role. Taken together, our results demonstrate a difference in pathogenesis between ACP and NPS, particularly in terms of arachidonic acid metabolism.

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“…inflammation, especially mast cells, basophils, eosinophils and macrophages and monocytes [4]. There is evidence that these cells are involved in nasal airway inflammation [5] and especially in nasal polyp pathogenesis [6]. The pathogenesis of asthma [7] is tightly linked with leukotriene effects.…”

Section: Discussionmentioning

confidence: 98%

Is there a role for leukotriene antagonists in the prevention of recurrent nasal polyps?

Rasp

2010

Current Opinion in Allergy &Amp; Clinical Immunology

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In the surgery of nasal polyps, recurrence is the main problem. Steroids are the current standard therapy, but the limitations are obvious. The role of leukotrienes in the disorder of nasal polyps is well established now, and with the antagonists available, interest rose in treating nasal polyps. A total of 356 patients took part in several studies involving leukotriene antagonists in the nasal polyp population. Some studies have minor levels of evidence; the data show positive effects for patients in preoperative and postoperative studies and medical treatments. There were benefits as an add-on to steroids and data from allergic rhinitis studies also show possible synergism with antihistamines. There are hints for a positive effect on eosinophil inflammation, clinical symptom scores, nasal airflow, sneezing and postnasal drip. Although some effects are shown, more controlled studies are necessary for reliable data.

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Arachidonic Acid Metabolites in Human Nasal Polyps

Cited by 17 publications

References 3 publications

Molecular and Cellular Staging for the Severity of Chronic Rhinosinusitis

Molecular and Cellular Staging for the Severity of Chronic Rhinosinusitis

Arachidonic Acid Metabolites in Antrochoanal Polyp and Nasal Polyp Associated with Chronic Paranasal Sinusitis

Is there a role for leukotriene antagonists in the prevention of recurrent nasal polyps?

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