Rhinitis pseudoallergic J130.-; Z88.-

Non-IgE-mediated inflammatory (pseudoallergic) disease of the mucous membrane of the nose (and eyes), which is related in time to exposure to cyclooxygenase inhibitors (especially acetylsalicylic acid, also other NSAIDs).

Recently, this complex of symptoms has been summarized under NERD (NSAID exacerbated respiratory disease) (see also NSAID hypersensitivity).

Presence of a dysbalance in the arachidonic acid metabolism. Arachidonic acid is provided by phosopholipases from the phospholipids of the cell membranes of eosinophils, mast cells and leucocytes. Via lipoxygenases and cyclooxygenases (COX) two metabolic pathways are optionally taken, some of whose products have an antagonistic effect. Prostaglandins (e.g. prostaglandin E2) are produced via the leukotriene C4 (LTC4) cyclooxygenase metabolic pathway. Peptide leukotrienes (PLT) are formed via the lipoxygenase metabolic pathway. In contrast to prostaglandins, PLT have a bronchospastic and mucous-forming effect. Patients with pseudoallergic rhinitis tend to produce PLT in excess, probably due to an increased activity of LTC4 synthetase (cause: possible polymorphism of the gene sequence of LTC4 synthetase on chromosome 5q). An increased interleukin-5 synthesis is conspicuous, which correlates with eosinophilia.

20-30 years

Intolerance reactions to acetylsalicylic acid (including NSAIDs), NERD, manifest themselves predominantly in the respiratory tract as chronic rhinitis. Furthermore, chronic sinusitis and nasal polyps are found (in about 90% of patients). These symptoms are supplemented by bronchial asthma(requiring corticosteroids). Less frequent are urticaria and angioedema.

First symptoms of the NSAID intolerance reaction, NERD, are usually " vasomotor " unspecific symptoms of perennial rhinitis. The analgesic intolerance syndrome leads to a permanent nasal obstruction in the nasal region within months to a few years. Characteristic are bilateral eosinophilic nasal polyps. Later, bronchial asthma may develop.

Oral nasal or bronchial provocation under stationary conditions. Various protocols are available for oral provocation (oral protocols usually run for 2 days, increasing the acetylsalicylic acid dose to 500 mg/p.o.; nasal protocols: lysine acetylsalicylic acid in a dose of 0.5-2.0 mg (sometimes up to 16 mg) is recommended for provocation.

Acetylsalicylic acid withdrawal: Avoid further Cox-1 inhibitors. Cox-2 inhibitors may be an alternative.

Leukotriene receptor antagonists: In some patients, leukotriene receptor antagonists (e.g. montelukast) prove to be helpful.

Alternative: Adaptive, oral deactivation by a long-term, monitored, continuously increased intake of acetylsalicylic acid (up to 500mg/day p.o.).

In 20% of the patients with nasal polyps there is an analgesic intolerance syndrome. If patients suffer from bronchial asthma and nasal polyposis, 40% have an analgesic intolerance syndrome. Weak cyclooxygenase inhibitors have to be dosed appropriately high (often > 1000 mg) to trigger these clinical symptoms. The previously suspected cross-reaction to preservatives and food colourings is now doubted.

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