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Tryptase is a protein released by mast cells, which is involved in the enhancement of inflammatory sequences in immune-mediated reactions. According with our experience, some patients having a reaction clinically classified as anaphylaxis, showed high levels of tryptase (> 20 ng/l) but also of serum specific IgE, showing the immune-mediated nature of the reactions. On the other hand workers without specific IgE and with low levels of tryptase probably had developed pseudoallergic (anaphylactoid) reactions. So, tryptase can be used as biomarker of occupational anaphylaxis and appear to be able to make out immune and nonimmune mediated reactions.

Specific vasomotorial rhinopathy, or allergic rhinitis is to be seen as a systemic pathology characterized by a condition of hyperactivity, the target organ of which is the nose. Particular attention, among the diagnostic tests, should be reserved to the specific nasal provocative test (sNPT), which has been part of the clinical routine for years but has nonetheless failed to achieve a suitable level of standardization. With this intent, we have devoted the present work to the assay of several phlogosis mediators (tryptase, specific IgE and ECP) before and after performing the sNPT. We have studied 20 patients affected by allergic rhinitis, aged between 13 and 61, with single or multiple allergen sensitivities, but in any case with a predominant sensitization, who underwent sNPT between October 2000 and July 2001. In every patients we performed ECP, tryptase and specific IgE assay via direct incubation in the nasal mucosa, before and after specific nasal provocation. The results of the sNPT (rhinomanometry and symptoms score) were compared with the variations in the phlogosis mediators assayed at nasal level. On the basis of the variations in the rhinomanometric resistance and symptoms score, the sNPT was positive in 10 patients (50%). Tryptase and specific IgE increased to a statistically significant degree (respectively, p = 0.01 and p < 0.05) in all of the patients; the ECP variations, instead, were not significant (p > 0.05). Overall, the simultaneous assay of ECP, tryptase and specific IgE, increasing the sensibility of the sNPT, enabled a positive result to be ascertained in 60% of the subjects examined. The method is furthermore based on the principle of local reactivity in that it assays the phlogosis mediators not at systemic level, but directly in the target organ, showing itself to be more specific than level I and II tests.

During general anesthesia adverse reactions are not uncommon, and the hypothesis of an anaphylactic response cannot be excluded. In these situations, a differential diagnosis from other events which often present identical clinical manifestations is necessary. For this purpose measurement of serum tryptase, as a biochemical marker of the release of mast-cell granules, is considered a valuable and specific method, especially if it is carried out on several hematic samples, obtained in successive times, for pointing out the progressive reduction of the values. If an anapyhlactic pathogenesis is confirmed, the identification of the responsible drug is necessary for a safer approach of the patient in view of a further anesthesia. A severe and protracted reaction has been observed after a standard induction of anesthesia, in which measurement of serum tryptase has shown high values of this protease 2 hours after the reaction which a subsequent decrease in the samples repeated after 5, 8, 11 e 20 hours, suggesting an anaphylactic etiology of the reaction. The specific RAST for the substances employed has excluded a role for muscle relaxant, plasma expander and latex, while it was positive for tiopenthal, suggesting in this case a true anaphylactic reaction caused by the hypnotic drug.

Activated mast cells are present in human coronary atheromas, as well as in the adventitia of patients with variant angina, and may play an important role in plaque rupture and coronary vasomotion. To assess whether or not activation of mast cells is a primary event, we measured serum levels of tryptase, a specific marker of mast cell activation, in 8 patients with unstable angina during a spontaneous ischemic episode (Group 1) and in 5 patients with variant angina (Group 2) during ergonovine-induced coronary spasm. Blood samples were collected as soon as possible after the onset of pain and ECG changes (0 min), and after 5, 15 and 60 min. Tryptase levels in Group 1 were 0.13 U/l (range 0.017-0.44) at the onset of pain and significantly raised to 0.75 U/l (range 0.05-2.49) at 5 min, decreasing to 0.076 U/l (range 0.018-0.16) at 15 min and to 0.085 U/l (range 0.01-0.25) at 60 min (p = 0.035). Conversely, tryptase levels in Group 2 were 0.09 U/l (range 0.07-0.13) at 0 min, 0.11 U/l (range 0.07-0.22) at 5 min, 0.10 U/l (range 0.07-0.18) at 15 min, 0.11 U/l (range 0.07-0.17) at 60 min (NS). In conclusion, tryptase levels raise during spontaneous ischemic episodes in unstable angina, but not after ergonovine-provoked ischemia in variant angina, suggesting that a primary, yet unknown stimulus, may activate mast cells during some ischemic episodes in unstable angina.

Triptase is an enzymatic protein found in the mastocytes. Although the biological role of this substance is not fully understood, significant amounts of it are found in the nasal secretions of allergic subject both when naturally exposed to the allergen and when subject to specific nasal provocation tests. The present study uses a radioimmunological method (Pharmacia, Uppsala, Sweden) to assay the amount of triptase in two groups: one composed of 10 subjects suffering from allergic rhinitis and the other of 10 non allergic controls. All subjects were submitted to nasal wash with a saline solution prior to endonasal administration of an allergen extract (Poa Pratensis or Dermatophagoides Farinae). Fifteen minutes after nasal provocation the nose was once more washed out with a saline solution. All the wash liquids, both before and after stimulation, were assayed to determine the triptase content and the results for the two groups were compared. The results did not follow a normal distribution and were compared. The results did not follow a normal distribution and were processed with non parametric statistical methods. The allergic subjects showed base values, of 1.4 U/l (mean) while after allergic stimulation this jumped to 14.5 U/l (mean) (p < 0.005). On the other hand, the pre- and post-stimulation values were comparable for the non allergic group. In addition, there was no statistically significant difference between the basic pre-trial triptase levels in the allergic and non allergic subjects. The results indicate that assaying the triptase content in nasal wash liquid can provide a useful support in the diagnosis of allergic rhinitis.

Mediator release from activated mast cells is also likely to take place in the asthmatic airways in vivo during adenosine-induced bronchoconstriction. To test this hypothesis, we evaluated mast cell mediator release directly into the airways of 9 asthmatic subjects after endobronchial challenge with adenosine by bronchoalveolar lavage (BAL). The mediators measured were histamine, tryptase, and PGD2. When compared to the saline-challenged segment, the response to AMP instillation was characterized by a prompt reduction in airway calibre paralleled by a significant 4.2-fold increase in PGD2 levels in the BAL fluid (p = 0.004). There were also increases in median histamine (from 200.1 to 433.6 pg/mL) and tryptase levels (from 0.31 to 0.46 ng/mL) recovered after AMP challenge, although they were not significant. These findings support the view that acute bronchospastic response to AMP in asthmatic airways is paralleled by the local release of mast cells derived products, particularly PGD2.

Numerous studies have shown that alcohol causes both acute and chronic damage to gastroduodenal mucosa. The methods of damage differ however, and experimental studies in animals have shown that the degranulation of mast cells in gastric mucosa causes acute hemorrhagic lesions after the consumption of alcohol. It is not known whether this mechanism also operates in man. The aim of the present study was therefore to evaluate whether there is a correlation between mast-cell activation, determined by assaying tryptase levels in gastric mucosa, and the consumption of alcohol in patients with ulcerative diseases. Thirty-one patients with cicatrized ulcerative lesions (13 gastric ulcers, 18 duodenal ulcers) were included in the study. Biopsies at the level of the gastric fundus and antrum and the duodenal bulb were performed in all patients to determine tryptase levels. Biopsy material was frozen and subsequently homogenized; the enzyme was assayed in the supernatant using a radioimmunometric method. The mean daily alcohol consumption was calculated in clinical terms for each patient over the past 5 years and patients were subdivided into non-drinkers and moderate (< 60 g alcohol/day) and excessive (> 60 g alcohol/day) drinkers. It was found that tryptase concentrations were higher in the fundus compared to the gastric antrum and duodenal bulb, irrespective of alcohol consumption both in patients with gastric ulcer and duodenal ulcer. The importance of mast cells in provoking alcohol-dependent damage was studied at a gastric level. Alcohol leads to their degranulation and therefore contributes to the formation of gastric lesions.(ABSTRACT TRUNCATED AT 250 WORDS)