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Omalizumab-induced reductions in mast cell Fce psilon RI expression and function.

BACKGROUND: By design, omalizumab binds free IgE in the circulation and prevents its attachment to the surface of mast cells and basophils, thereby preventing them from responding to allergens. Previously, omalizumab rapidly reduced free IgE levels, as well as basophil high-affinity IgE receptors, leading to significant reductions in basophil mediator response to allergen. It is assumed that tissue mast cells are similarly altered in their Fc epsilon RI density and function. OBJECTIVE: We examined the phenotypic shift of skin mast cells in parallel to that of blood basophils in 3 subjects infused with omalizumab. METHODS: Three subjects with allergic rhinitis underwent intradermal skin test titration with house dust mite antigen at days 0, 7, 70, and 196 of omalizumab treatment. As control subjects, 5 untreated subjects with allergic rhinitis were evaluated at similar time points. All subjects underwent skin biopsy 18 to 24 hours later at the site of allergen injection. Biopsy specimens were characterized by means of immunohistochemisty for tryptase and Fc epsilon RI alpha immunoreactivity, as well other markers (CD3, CD45RO, CD68, cutaneous lymphocyte antigen, and major basic protein). RESULTS: Omalizumab recipients, but not control subjects, demonstrated reductions in Fc epsilon RI alpha immunoreactivity at days 70 and 196 in parallel with reductions in the acute wheal response to allergen. However, no reductions in tryptase-positive cells were noted at these time points. CONCLUSION: Reductions in free IgE levels by omalizumab leads to a rapid reduction in basophil Fc epsilon RI receptor expression. In contrast, the time course for the decrease of Fc epsilon RI expression in skin mast cells is slower and associated with decreased acute allergen wheal size.

Allergens↗

Mast cells and eosinophils in feline allergic dermatitis: a qualitative and quantitative analysis.

Mast cells (MCs) and eosinophils are prominent in the perivascular infiltrate of cats with allergic dermatitis. In the skin of allergic cats MCs were mainly observed diffusely in the superficial dermis, while eosinophils were found mainly in the deep dermis in a perivascular pattern. MC counts were significantly higher in cats with allergic dermatitis (P < 0.05) than in healthy control cats, but the number varied widely. Moreover, the numbers of eosinophils in the skin of allergic and control cats differed significantly (P < 0.05) none being found in the latter. There was no significant correlation between numbers of mast cells and eosinophils in the same biopsy sample. In the allergic cats, a significantly lower number of MCs was detected by staining for tryptase than by staining for chymase or by Astra blue staining. Additionally, the chymase: tryptase ratio in healthy cats was reversed in cats with allergic dermatitis. These changes were observed in lesional and nonlesional skin of cats with allergic dermatitis. The findings indicate a generalized effect on MCs in allergic dermatitis. In addition, eosinophils are an important indicator of allergic dermatitis.

Animals↗

Inhibition of trypsin-induced mast cell activation by acanthoic acid.

Acanthoic acid (AA) is a pimaradiene diterpene isolated from the Korean medicinal plant, Acanthopanax koreanum (Araliaceae). In the present study, we examined whether AA has the inhibitory effect on the production of inflammatory mediators and activating signals induced in trypsin-treated human leukemic mast cell-1 (HMC-1). HMC-1 cells were stimulated with trypsin (100 nM) in the presence or absence of AA (1, 10, and 100 microg/ml). We assessed the production of TNF-alpha and tryptase by enzyme-linked immunosorbent assay (ELISA) or reverse transcription-PCR, ERK activation by Western blot, and NF-kappaB activation by gel shift assay. AA (10 and 100 microg/ml) significantly inhibited production of both TNF-alpha and tryptase in a dose-dependent manner in trypsin-stimulated HMC-1. Furthermore, AA inhibited ERK phosphorylation and NF-kappaB activation induced by trypsin treatment without blocking of trypsin activity even with 100 microg/ml. These results suggest that AA may inhibit the production of inflammatory mediators through inhibition of ERK phosphorylation and NF-kappaB activation pathway in human mast cells. It supports the evidence that AA may be used to blocks the development of inflammation caused from mast cells.

Cells, Cultured↗

The expression pattern of three mast cell specific proteases during mouse development.

Mast cell chymases and tryptases are major constituents of mast cell granules exhibiting an intriguing but potentially confusing variety of forms and functions. Thanks to recent genetic and biochemical advances, a clearer picture of phylogenetic and functional relationships in this large group of mammalian enzymes is emerging. While different in vivo and in vitro studies characterize the function of these proteases in adult tissues, only sparse information is available about these enzymes during embryogenesis. In the present study, we followed the expression patterns of three different mast cell proteases--mcpt5 (chymase), mcpt6 and 7 (tryptases)--during the development of the mouse embryo. Using specific probe sets for Northern blot analysis, nested PCR and in situ hybridization we describe the expression patterns of the three proteases in different stages of the developing embryo. Furthermore, we try to localize the expression pattern of the three proteases to a certain region and subset of cells. Based on the spatial and temporal expression patterns of mcpt5, 6 and 7 we hypothesize that these molecules play specific and distinct roles in the prenatal and postnatal stages.

Animals↗

Mast cell numbers in airway smooth muscle and PC20AMP in asthma and COPD.

INTRODUCTION: Most patients with asthma and many patients with COPD show bronchial hyperresponsiveness to adenosine (BHR(AMP)). BHR(AMP) may be caused by release of mast cell histamine, which induces smooth muscle contraction. AIM OF THE STUDY: To evaluate whether mast cell numbers in airway smooth muscle are increased in patients with asthma and COPD compared to their age-matched controls, and whether mast cell numbers are correlated with BHR(AMP). PATIENTS: Twenty-two non-smoking subjects with asthma (age 31yr, FEV(1): 89% pred, PC(20)AMP: 2.7mg/ml), 18 ex-smoking subjects with COPD (age 62yr, FEV(1): 58% pred, PC(20)AMP: 52.4mg/ml). METHODS: Snap-frozen bronchial biopsies were immunostained with anti-mast cell tryptase and anti-desmin antibodies. Mast cell number was expressed as the number of tryptase positive cells per area of smooth muscle. RESULTS: There were no significant differences in mast cell number between patients with asthma, COPD, and their respective age-matched healthy controls. Furthermore, there was no significant correlation between mast cell number and FEV(1) or PC(20)AMP in any of the groups. Surprisingly, the mast cell number was negatively correlated with reversibility to salbutamol in COPD patients (rho -0.47, P<0.05). CONCLUSION: Mast cell numbers in central airway smooth muscle apparently do not contribute importantly to bronchial hyperresponsiveness to adenosine.

Adenosine↗

Extensive mast cell degranulation in bovine respiratory syncytial virus-associated paroxystic respiratory distress syndrome.

Bovine respiratory syncytial virus (BRSV) infection is an important cause of outbreaks of respiratory disease among calves. This virus commonly induces mild to severe respiratory signs but, in a substantial proportion of cases, is also reported to be associated with paroxystic respiratory distress syndrome (PRDS). The pathogenesis of this 'malignant' clinical form has not been fully elucidated. The present study aimed at determining whether mast cell (MC) degranulation plays a role in the physiopathologic cascade leading to the PRDS. Paired serum samples were taken in herds during outbreaks of severe respiratory diseases (acute sera) and 3 weeks after (convalescent sera). Based on seroconversion to BRSV and clinical picture, 67 pairs of sera were selected from calves with a BRSV-associated PRDS for circulating MC tryptase determination. A MC metachromatic score was measured in post-mortem lungs from animals died from a BRSV-associated PRDS (principals) and compared with reference scores obtained from healthy lungs (controls). Levels of tryptase were significantly higher in acute sera (26.6 +/- 12.4 microg/l) compared to convalescent sera (8.4 +/- 7.8 microg/l; P<0.001). Metachromatic scores yielded significantly different results between controls and principals (P<0.01), demonstrating a significant disappearance of metachromatic granules from lung MCs in principals. Taken together, these data demonstrate the presence of an extensive MC degranulation in BRSV-associated PRDS.

Animals↗

Increase in nerve fibers and loss of mast cells in polycystic and postmenopausal ovaries.

OBJECTIVE: To quantify nerve fibers and mast cells in human ovaries at different functional stages. DESIGN: Retrospective study. SETTING: Research laboratory of the university. SPECIMEN(S): 8 human ovaries in the follicular (cyclic) phase, 7 polycystic ovaries, and postmenopausal ovaries with (n=5) or without (n=7) hyperthecosis. MAIN OUTCOME MEASURE(S): Single- and double immunohistology for the S100 antigen in glial cells of autonomic nerve fibers, for chymase and tryptase in mast cells, and for the common leukocyte antigen on leukocytes. Histometric evaluation was also performed. INTERVENTION(S): None. RESULT(S): Polycystic ovaries contained significantly more S100-positive nerve fibers in the corticomedullary region than did cyclic ovaries (mean +/- SD per 2-mm(2) area, 476 +/- 136 and 224 +/- 133; P<.01). Postmenopausal ovaries with or without hyperthecosis had the highest density of nerve fibers. In cyclic and polycystic ovaries, more tryptase-positive mast cells than chymase-positive mast cells were found in the interstitial cortex and the medulla. In cyclic ovaries, areas with a moderate density of nerve fibers contained many mast cells. Hence, with increasing nerve fiber density in polycystic ovaries, the number of mast cells decreased strikingly compared with cyclic ovaries (p<.001). Almost no mast cells were seen in postmenopausal ovaries with and without hyperthecosis. The number of leukocyte antigen-positive leukocytes was similar in all groups. CONCLUSION(S): The high density of nerve fibers in polycystic and postmenopausal ovaries, together with a conspicuous decrease in mast cells, indicates altered neuroimmune communication.

Aged↗

Release of mast cell mediators into the jejunum by cold pain stress in humans.

BACKGROUND & AIMS: The central nervous system regulates gut functions via complex interactions between the enteric nervous and immune systems. The aim of this study was to investigate whether mast cell mediators are released into the human jejunal lumen during stress. METHODS: A closed-segment perfusion technique was used to investigate jejunal release of tryptase, histamine, prostaglandin D2, and water flux in response to the cold pressor test in 8 healthy subjects and 9 patients with food allergy. In 6 food-allergic patients, jejunal biochemical responses to cold pain stress were compared with those induced by food intraluminal challenge. RESULTS: Cold pain stress elevated heart rate and blood pressure and increased luminal release of mast cell mediators and jejunal water secretion in both groups. Stress-induced release of tryptase and histamine, but not of prostaglandin D2 and water flux, was greater in food-allergic patients than in healthy volunteers. In food-allergic patients, jejunal biochemical responses induced by cold pain stress were similar to those induced by antigen challenge. CONCLUSIONS: These results show the ability of the central nervous system to modulate intestinal mast cell activity and suggest that mast cells have a role in stress-related gut dysfunction.

Adult↗

Segmental allergen challenge induces plasma protein leakage into the airways of asthmatic subjects at 4 hours but not at 5 minutes after challenge.

We have investigated whether increased plasma protein leakage is present early after segmental allergen challenge in allergic asthma. Seven asthmatic subjects with mild allergy (AA group) and 5 non-asthmatic subjects with allergy (ANA group) were challenged with allergen doses based on similar early skin reactions; 5 healthy control subjects without allergy (C group) were challenged with the highest dose applied in the subjects with allergy. Bronchoalveolar lavage (BAL) fluid was obtained before, at 5 minutes after, and at 4 hours after challenge from different segments. Levels of albumin (Alb) and alpha2-macroglobulin (A2M) were measured in BAL fluid and serum. In addition, we calculated the relative coefficient of excretion as follows: RCE = ((A2M in BAL fluid)/(A2M in serum))/((Alb in BAL fluid)/(Alb in serum)). Also, levels of tryptase as a marker of mast cell activation and tumor necrosis factor-alpha (TNF-alpha), a possible inducer of plasma protein leakage, were determined. At 5 minutes after challenge, in none of the groups was a significant change found in the parameters for protein leakage. Levels of tryptase were increased in the subjects with allergy at 5 minutes after challenge only (P = .004). At 4 hours after challenge, levels of Alb (P = .03) and A2M (P = .04) and the RCE (P = .04) were increased in the AA group only. At 4 hours, levels of TNF-alpha were increased, with no significant differences among the three groups. In the asthmatic subjects with allergy, levels of TNF-alpha correlated with levels of Alb (r = 0.85, P = .02). In conclusion, at 4 hours after segmental allergen challenge, plasma protein leakage was increased in the asthmatic subjects only. The increase in levels of TNF-alpha in all groups indicates that the presence of TNF-alpha alone was not sufficient to cause plasma protein leakage within 4 hours after allergen challenge. Our results confirm the concept that plasma exudation after allergen exposure is a pathophysiologic event associated with asthma.

Allergens↗

Immunologic studies in presumed amniotic fluid embolism.

OBJECTIVE: To evaluate the potential role of immunologic mechanisms that involve mast cell degranulation (anaphylaxis) or complement activation in the mechanism of amniotic fluid embolism. METHODS: This study was a case series of nine women with presumed amniotic fluid embolism and a control group of 22 women who had normal labor. Women were from community and tertiary referral hospitals in Japan and the United States. Main outcome measures were maternal peripartum complement levels (C3 and C4), serum levels of tryptase, urinary histamine concentrations, and serum levels of a fetal antigen (sialyl Tn). RESULTS: Serum tryptase and urinary histamine measurements were negative in women with amniotic fluid embolism; seven of nine had elevated levels of fetal antigen. All eight who had serum available for testing had abnormally low levels of complement. Mean C3 level of 44.0 mg/dL and C4 level of 10.7 mg/dL were significantly lower than corresponding postpartum control values of 117.3 mg/dL and 29.4 mg/dL (P =.018 for C3, P =.012 for C4). Postpartum C3 and C4 levels decreased by 8% and 5%, respectively, compared with intrapartum values (P =.003 for C3, P =.021 for C4) but were still within normal range. CONCLUSION: Serologic findings suggest a role for complement activation in the mechanism of amniotic fluid embolism. Laboratory data from this series did not implicate mast cell degranulation (anaphylaxis) in the pathophysiology of the disease.

Antigens, Tumor-Associated, Carbohydrate↗

Chemokines in seasonal allergic rhinitis.

Monocyte chemotactic and activating factor/monocyte chemoattractant protein-1 (MCAF/MCP-1), RANTES, and macrophage inflammatory protein (MIP)-1 alpha are chemokines known to activate basophils (MCAF/RANTES) and eosinophils (RANTES/MIP-1 alpha). IL-8 inhibits MCAF-induced histamine release from basophils. We questioned whether a relationship exists between the levels of these chemokines and various inflammatory mediators released from mast cells, eosinophils, and basophils as assessed in nasal secretions obtained from patients during the allergy season and out of season. Samples were assessed for MCAF/MCP-1, RANTES, MIP-1 alpha, IL-8, histamine, tryptase and eosinophil cationic protein (ECP) in three subject groups: subjects with allergic rhinitis (n = 18), atopic subjects without rhinitis (n = 9), and healthy individuals (n = 6). Statistically significant differences were apparent only in the subjects with symptoms as follows. MCAF/MCP-1 increased during the season from 336 +/- 47 pg/ml to 829 +/- 137 pg/ml (p < 0.001), whereas IL-8 decreased from a baseline of 1932 +/- 335 pg/ml to 1070 +/- 202 pg/ml (p < 0.028). The ratio of IL-8 to MCAF/MCP-1 decreased during the symptomatic season from the baseline of 6.66 +/- 1.06 seen during winter to 1.3 +/- 0.22 during ragweed season (p < 0.001). Histamine increased from 6.3 +/- 1.5 to 89 +/- 15.5 ng/ml (p < 0.001), ECP increased from 20.6 +/- 6.4 to 237.1 +/- 50.2 ng/ml (p < 0.001), and tryptase increased from 2.34 +/- 0.6 to 9.7 +/- 2.3 U/ml (p < 0.001). Most samples did not have detectable quantities of MIP-1 alpha or RANTES. We also found a correlation between the level of MCAF/MCP-1 and IL-8 and the level of histamine or IL-8 and ECP. Our results suggest that the chemokines MCAF/MCP-1 and IL-8 may participate in the pathogenesis of allergic rhinitis, contributing to the attraction of the proinflammatory cells and mediator release, which might be very important during the late phase of the allergic reaction. Furthermore, the ratio of certain chemokines, such as MCAF/MCP-1 and IL-8 may reflect the magnitude of the reaction, as does the presence of histamine and ECP.

Basophils↗

Nasal airway changes assessed by acoustic rhinometry and mediator release during immediate and late reactions to allergen challenge.

BACKGROUND: We have found that acoustic rhinometry is a reliable means of assessing nasal airway caliber changes during the immediate reaction to nasal allergen challenge of sensitive subjects. Comparison of such changes with symptoms and patterns of mediator release could help in the understanding of mechanisms of immediate and late-phase reactions after allergen challenge and their clinical relevance. METHODS: Nasal minimal cross-sectional area (MCA) was assessed sequentially for 6 hours after two blinded challenges in random order with pollen antigens and buffer diluent in five sensitive human subjects. Comparisons were made with: (1) symptom scores; (2) olfaction changes; and (3) nasal secretion levels of histamine, tryptase, leukotriene C4, serum albumin (a marker of vascular permeability), lactoferrin (a marker of local glandular secretion), and inflammatory cells in nasal scrapings. RESULTS: In four of five subjects there was a significantly greater decrease in MCA after antigen challenge than after diluent challenge, correlating with the degree of subjective nasal congestion. In two of these four subjects there was a prominent second late-phase decrease in MCA at 3 to 5 hours, whereas the MCA was persistently decreased in an additional subject with accompanying subjective congestion. No significant decrease in olfactory acuity occurred. Levels were significantly higher in nasal secretions obtained after antigen challenge than in those obtained after buffer challenge with histamine (9 +/- 2.7 ng/ml vs 1.2 +/- 0.5 ng/ml; p = 0.04); tryptase (95 +/- 83 ng/ml vs 3 +/- 0.9 ng/ml; p = 0.02), leukotriene C4 (5293 +/- 1385 ng/ml vs 578 +/- 183 ng/ml; p = 0.02), and albumin (123 +/- 9 ng/ml vs 19 +/- 1.6 ng/ml; p = 0.005) but not with lactoferrin (4.6 +/- 1.2 ng/ml vs 4.1 +/- 28 ng/ml; p = not significant). Granulocyte exudation was seen after antigen challenge but not after buffer diluent challenge. However, there was not a precise correlation between decreases in MCA with changes in levels of these mediators in individual subjects. CONCLUSIONS: Acoustic rhinometry can quantitatively assess congestion during immediate and late-phase reactions after nasal challenge without significant correlation to the degree of individual inflammatory events assessed.

Acoustics↗

Response to cyclosporin and low-dose methylprednisolone in aggressive systemic mastocytosis.

BACKGROUND: There is no effective treatment for aggressive systemic mastocytosis. OBJECTIVE: The purpose of this study was to investigate the effect of cyclosporin and low-dose methylprednisolone in a 64-year-old man with aggressive systemic mastocytosis. METHODS: Immunohistochemical studies were done on biopsy specimens from the skin and other organs. Mast cells, predominantly containing tryptase, were derived from human umbilical cord blood cells cultured in the presence of stem-cell factor and IL-6. IgE-sensitized cultured human mast cells were activated by anti-IgE, and the effect of cyclosporin on histamine release was investigated. In addition, blood and urine levels of various mediators were measured in the patient before and after therapy. RESULTS: Biopsy specimens of the patient's skin lesions showed an increase of mast cells; cells containing tryptase (but not chymase) comprised 20% to 50% of the skin mast cells. Histamine release from activated cultured mast cells was inhibited by cyclosporin in a concentration-dependent manner. When the patient was treated with cyclosporin and low-dose methylprednisolone, he showed a good response. CONCLUSION: Cyclosporin combined with low-dose methylprednisolone may be a reasonable therapy for aggressive systemic mastocytosis.

Bone Marrow Cells↗

Utility of flow cytometric analysis of mast cells in the diagnosis and classification of adult mastocytosis.

The diagnosis of bone marrow (BM) involvement in mastocytosis has mainly been based on conventional histology. Nevertheless, in recent years, three major methodological advances have been made: the measurement of serum tryptase levels, the immunohistochemical assessment of mast cell (MC) tryptase, and the immunophenotypical characterization of BMMC using flow cytometry (FCM). The most characteristic immunophenotypic feature in mastocytosis is the coexpression of CD2 and CD25 antigens, which are never present in normal BMMC and constitute a phenotypic hallmark of BMMC in adult mastocytosis. Such observations would support the need to include the immunophenotypic analysis of MC in the diagnosis of mastocytosis.

Biomarkers↗

New developments in the genetics and activation of mast cell proteases.

Mast cell chymases and tryptases exhibit an intriguing but potentially confusing variety of forms and functions. Thanks to recent genetic and biochemical advances, a clearer picture of phylogenetic and functional relationships in this large group of mammalian enzymes is emerging. Furthermore, there is increasing appreciation of the diversity of these enzymes among human populations. In humans, there appears to be just one mast cell chymase but multiple expressed tryptases, some of which are allelic variants and others of which are products of separate gene loci. New biological tools, including the dipeptidyl peptidase I (DPPI)-null mouse in which the entire class of mast cell chymases appears to be functionally knocked out, are helping to clarify the importance and specific roles of these most abundant of secreted mast cell proteins.

Animals↗

Increased mast cells in hepatocellular carcinoma and intrahepatic cholangiocarcinoma.

BACKGROUND/AIMS: Human mast cells are categorized into those positive only for tryptase (MC(T)) and those positive for both tryptase and chymase (MC(TC)). METHODS: We investigated mast cells in "normal" livers (n=13), hepatocellular carcinoma (HCC) (n= 49) and intrahepatic cholangiocarcinoma (ICC) (n= 44) by double immunostaining and quantitative morphometry. RESULTS: In "normal" livers, mast cells were located in portal tracts, and to a lesser extent in the sinusoids. In HCC, mast cells were noted in tumoral sinusoids and fibrous septa. In ICC, many mast cells were present in tumoral stroma. Morphometry showed that densities of mast cells in HCC and ICC were significantly higher than those in "normal" livers. The density of mast cells in ICC (57.6+/-62.4/mm2) was significantly higher than that in HCC (9.32+/-12.9/mm2). The density of sinusoidal mast cells was significantly higher in HCC (1.79+/-2.35/mm2) than in "normal" livers (0.13+/-0.07/mm2). The density of stromal mast cells was significantly higher in ICC (57.6+/-62.4/mm2) than that of portal tracts in "normal" livers (28.4+/-7.0/mm2). MC(T) and MC(TC) were approximately 20% and 80%, respectively, being consistent in any anatomical compartments. CONCLUSIONS: Mast cells increase during carcinogenesis in HCC and ICC, and they may play a role in fibrosis or tumor immunology in HCC and ICC.

Adult↗

Modification of mediators of immune reaction after general anaesthesia.

UNLABELLED: The adverse reactions that may occur during a surgical intervention are of concern to anesthesiologists and allergists due to the civil responsibility they entail and the increased demand for healthcare in allergology units. The aim of the present study was to determine the prevalence of adverse reactions in our setting (Island of Lanzarote) and modifications to immune response mediators using three types of representative myorelaxants (succinylcholine, cisatracurium and vecuronium) in order to predict and prevent adverse reactions. MATERIAL AND METHODS: We performed a prospective, cross sectional, observational study in a population of 201 patients scheduled to undergo surgery in the Surgery Department of the Lanzarote General Hospital from October 1998. Three groups were retrospectively selected: vecuronium (73 patients), cisatracurium (80 patients), and succinylcholine (48 patients). Blood was extracted from all patients before and after the intervention and the following in vitro variables were evaluated: histaminemia, eosinophil cationic protein, tryptase, IgE to latex, CD4/CD8 fractions, total lymphocytes, total IgE, C3 and C4, and also the histaminuria. CONCLUSIONS: The mean age of the patients was 41 years with a predominance of women. Sixty percent had not previously undergone surgery. The mean operating time was 2 hours. Digestive surgery accounted for the greatest number of interventions (38.8 %) and most of the patients had no personal history of atopy (91.5 %). The greatest number of perioperative reactions was produced by cisatracurium (38.8 %), followed by succinylcholine (27.4 %) and vecuronium (20 %). The reactions observed were immediate type 1 and 2 reactions. All reactions were reversible without sequelae. Histaminuria levels were significantly decreased in the cisatracurium group. Histaminemia and eosinophil cationic protein showed no significant changes in any of the three groups. Tryptase concentrations in blood did not increase in the postoperative period in any of the three groups. On the contrary, concentrations were significantly lower than basal values. In the vecuronium and succinylcholine groups, CD4/CD8 fractions decreased in the postoperative period. Total lymphocytes decreased in all three groups. Total IgE tended to decrease in the cisatracurium and succinylcholine groups. IgE to latex was negative in the three groups. Specific IgE to succinylcholine was unmodified. C3 complement fraction was unmodified in all three groups and C4 fraction was reduced in the vecuronium group. In our setting and in our patients, the three myorelaxants produced immunosuppression of immune response mediators. The present study confirms that tests for allergy to myorelaxants are not indicated in the preoperative period.

Adolescent↗

Fatal anaphylactic shock during a fluorescein angiography.

The Authors describe an extremely rare fatal case (sixth case in the literature) of anaphylactic shock following a fluorescein angiography. This is the first report in which the diagnosis of anaphylactic reaction to the dye was made through laboratory analyses. The diagnosis of fatal shock due to sodium fluorescein was made based on clinical, laboratory and immunohistochemical data. Mast-cell tryptase was dosed in serum and a pulmonary immunohistochemical evaluation was performed. Tryptase, a neutral protease of human mast-cells is a potentially important indicator of mast-cell involvement in anaphylactic events.

Aged↗