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PubMed1994

Elevated serum tryptase levels in a patient with protracted anaphylaxis.

BACKGROUND: Anaphylactic reactions usually occur seconds to minutes after exposure to the relevant antigen. Late onset, biphasic, and protracted anaphylaxis also occur. The incidence of prolonged responses is unknown, but may be common. In all nonfood-related cases, levels of tryptase were not measured during protracted episodes. Tryptase has been shown to be a useful specific indicator of mast cell involvement in anaphylaxis. OBJECTIVE: To determine whether mast cell activation, as demonstrated by elevated serum tryptase concentrations, can occur in protracted anaphylaxis. METHODS: Case report; serum tryptase concentrations were measured by radioimmunoassay. RESULTS: A 33-year-old white man developed hives three days prior to admission. The next day, vomiting, abdominal cramps and bloating, lower lip swelling, wheezing, and a feeling of tightness over his throat and chest were experienced. The gastrointestinal symptoms continued until his hospital admission. One day prior to admission, he developed transient lightheadedness. On admission he had generalized urticaria and abdominal tenderness. Blood pressure of 115/58 mm/Hg rose to 180/60 and heart rate fell from 107/min to 90/min following 2.2 L of intravenous fluids. Serum tryptase levels were elevated at 7.2 ng/mL and 5.1 ng/mL on the first and second hospital days (fourth and fifth days of symptoms). Serum tryptase was < 1.0 ng/mL 5 months later. CONCLUSIONS: The elevated serum tryptase levels at 96 and 120 hours following the onset of symptoms strongly suggest that continued mast cell degranulation can occur during protracted anaphylaxis. This strengthens the argument that mast cell activation is important in the pathophysiology of protracted anaphylaxis.

Adult↗

PubMed1997

Life-threatening, recurrent anaphylaxis caused by allergy to gliadin and exercise.

BACKGROUND: Exercise-induced urticaria or anaphylaxis is regarded as a distinct form of physical allergy. In some patients the symptoms occur only after ingestion of various food products in connection with exercise. We have come across patients with cereal dependent exercise-induced anaphylaxis. OBJECTIVES: The purpose of the present study was to analyse the allergens in cereals responsible for the severe anaphylactic symptoms and to verify the test methods suitable for screening the patients with cereal dependent exercise-induced anaphylaxis. METHODS: The patients underwent skin-prick tests (SPT) with common inhalant and food allergens as well as with various cereal extracts. IgE-immunoblotting was used to identify the allergenic fractions. RESULTS: Five patients found positive in SPT with NaCl wheat suspension had IgE antibodies to wheat, rye, barley and oats, especially directed against the ethanolsoluble protein fractions in immunoblotting. No IgE antibodies were detected against other cereals. The patients had been unaware of any cereal allergy since anaphylaxis occurred only in association with exercise postprandially. The patients were directed to follow a gluten-free diet and have been free from symptoms, being able to continue their outdoor physical activities. CONCLUSION: Wheat gliadin and the corresponding ethanol-soluble proteins of taxonomically closely related cereals were found to be the allergens in cereal-dependent exercise-induced anaphylaxis. Skin-prick testing with NaCl wheat suspension was a simple and practical test to screen patients with this kind of occult, possibly life-threatening, allergy to cereals.

Adult↗

PubMed1998

Drug-attributed anaphylaxis.

Allergic type I reactions to medicines range in their clinical presentation from rhinitis and urticaria to severe bronchoconstriction and anaphylactic shock. We examined all cases of suspected drug induced reactions classified as anaphylactic reactions or shock reported in Sweden between 1972 and 1995 with regard to patient characteristics and drug(s) suspected. Some comparisons with drug sales and prescription data were also made. During the study period of a total of 1338 reports concerned anaphylactic/oid shock or reactions with at least a possible causal relation to medicine giving an overall reporting rate of seven cases per million inhabitants per year of drug-induced anaphylaxis. Of these 1338 patients 51 (3.8%) died from their reactions. Among the non-fatal cases, 460 (34.4%) were diagnosed as shock and 827 (61.8%) as anaphylactic reactions. In total 46.3% of all reports concerned men but men were over-represented among the older patients and among the fatal cases (65%). There were 201 different drugs reported as 'suspected' them most common of which were dextrans (418 reports), X-ray contrast media (161 reports) and antibiotics (153 reports). For dextrans the rate of anaphylactic reactions, shock and fatal cases reported were 128,101 and 21 per million bottles respectively. This decreased to 10.3, 9.8, and 0.4 per million bottles after the introduction of preventive treatment with dextran 1 in 1983.The reporting rate for ionic contrast media were 0.14, 0.13 and 0.02 per 1000 l for reactions, shock and fatal cases respectively whilst for non-ionic contrast media they were 0.7/1000 l for reactions, 0.02/1000 l for shock, but there was no report of a fatal case. For phenoxymethylpenicillin the reported rate of anaphylaxis was 0.14 cases per million defined daily doses and for benzylpenicillin it was 3.7 cases per million defined daily doses. During the study period several drugs have been identified as important causes of anaphylaxis and measures have been taken to decrease the risk of anaphylaxis e.g. the introduction of preventive treatment with dextran 1, the shift from ionic to non-ionic contrast media and the abolition of polyethoxylated castor oil as a solvent. Spontaneous reporting of drug-induced anaphylaxis remains an important surveillance model but needs to be complemented by better quantitative methods.

Journal Article↗

PubMed2000

Food anaphylaxis.

Food anaphylaxis is now the leading single cause of anaphylactic reactions treated in emergency departments in Westernized countries. In the US, it is estimated that there are 29,000 anaphylactic reactions to foods treated in emergency departments and 125-150 deaths each year. Peanuts, tree nuts, fish and shellfish account for the vast majority of severe food anaphylactic reactions. Immunopathogenic mechanisms responsible for food anaphylaxis may differ somewhat from other forms of anaphylaxis, since elevation of serum tryptase is rarely seen following food anaphylactic reactions. Education regarding the strict avoidance of food allergens, the early recognition of anaphylactic symptoms, and the early use of self-injectable epinephrine remain the mainstays of therapy. However, clinical trials are now underway for the treatment of patients with peanut anaphylaxis utilizing anti-IgE antibody therapy and novel immunomodulatory therapies utilizing 'engineered' recombinant proteins, overlapping peptides, and immunostimulatory deoxyoligonucleotide sequences are being tested in animal models of anaphylaxis.

Acute Disease↗

PubMed1999

Inhibition of mast cell-dependent anaphylaxis by sodium salicylate.

Sodium salicylate (NaSal) is a commonly used agent with a wide pharmacological spectrum. The objective of the present study was to investigate the effect of NaSal on anaphylaxis. NaSal (10-1 and 1 mm) significantly inhibited systemic anaphylaxis induced by compound 48/80 in rats. NaSal also significantly inhibited local anaphylaxis activated by anti-dinitrophenyl (DNP) immunoglobulin E (IgE). NaSal (10-1 and 1 mm) significantly inhibited histamine release from rat peritoneal mast cells (RPMC) activated by compound 48/80 or anti-DNP IgE. Northern-blot analysis demonstrated that a significantly reduced level of the mRNA of L-histidine decarboxylase was expressed in mast cells treated with NaSal, compared with that without NaSal. NaSal (10-2 and 10-1 mm) had a significant inhibitory effect on anti-DNP IgE-induced tumour necrosis factor-alpha secretion from RPMC. The level of cyclic AMP in RPMC, when NaSal (1 mm) was added, transiently and significantly increased about sixfold compared with that of basal cells. These results suggest a possible use of NaSal in managing mast cell-dependent anaphylaxis.

Anaphylaxis↗

PubMed1998

Inhibition of anaphylaxis by sulfasalazine in rats.

We studied the effect of sulfasalazine on anaphylaxis. Sulfasalazine dose-dependently inhibited systemic anaphylaxis induced by compound 48/80 in rats. Sulfasalazine also inhibited local anaphylaxis activated by anti-dinitrophenyl (anti-DNP) IgE. Moreover, sulfasalazine dose-dependently inhibited histamine release in the peritoneal mast cells activated by compound 48/80 or anti-DNP IgE. All of these effects were comparable to those of the disodium cromoglycate (reference drug) tested. When sulfasalazine was added, the level of cAMP in rat peritoneal mast cells transiently and significantly increased about 6-fold compared with that of basal cells. Our studies provide evidence that sulfasalazine may be beneficial in the treatment of anaphylaxis.

Anaphylaxis↗

PubMed1985

Immunological control of drug absorption from the gastrointestinal tract: effect of local anaphylaxis on the intestinal absorption of low molecular weight drugs in the rat.

Intestinal absorption of various drugs was examined by means of in situ recirculation technique during local anaphylaxis. The antibody was determined by passive cutaneous anaphylaxis technique in rats immunized once or three times. The optimal condition of local anaphylaxis was determined by the leakage of Evans Blue. The most significant increase in leaks of the dye was observed by the intraluminal challenge with 400 mg of ovalbumin for 10 min in ovalbumin-immunized rats, and this condition was chosen as the optimal condition of local anaphylaxis. Under this condition, intestinal absorption of caffeine, phenylbutazone, and bromthymol blue (BTB) significantly decreased in ovalbumin-immunized rats compared with the control, whereas no significant effect was noted in the intestinal absorption of salicylic acid, quinine, pralidoxime iodide (2-PAM), tetracycline, and phenol red. In normal rats, no significant decrease was obtained in the intestinal absorption of caffeine, phenylbutazone, and BTB. On the other hand, the decreased absorption of BTB was not found in ovalbumin-immunized rats by the intraluminal challenge with bovine gamma-globulin. Furthermore, there was no significant change in the decreased absorption of BTB between rats immunized once and three times. The most effective condition for decreased BTB absorption was observed by the intraluminal challenge with 200 mg of ovalbumin for 10 min in ovalbumin-immunized rats, which almost correlated with the data of Evans Blue leakage. From these observations, it appears that the mucosal immune responses affect the intestinal absorption of low molecular weight drugs.

Anaphylaxis↗

PubMed2004

A population-based study of the incidence, cause, and severity of anaphylaxis in the United Kingdom.

BACKGROUND: Anaphylaxis is an acute and potentially fatal systemic reaction usually caused by mast cell-mediated release of histamine. Symptoms can vary in onset, appearance, and severity. Some common symptoms include weakness, dizziness, flushing, angioedema, urticaria, nasal congestion, and sneezing. Severe symptoms include upper respiratory tract obstruction, hypotension, vascular collapse associated with angioedema and urticaria, gastrointestinal distress, cardiovascular arrhythmias, and/or arrest. METHODS: We conducted an observational follow-up study encompassing approximately 8 million person-years based on the UK General Practice Research Database for the period January 1, 1994, to December 31, 1999, which quantified the frequency, type, and severity of a clinical diagnosis of anaphylaxis. RESULTS: Based on 675 cases of anaphylaxis, we estimate the incidence to be 8.4 per 100 000 person-years. Approximately 10% of cases had hypotension and shock that required urgent treatment. The most common causes were insect stings and oral medicines. CONCLUSION: Anaphylaxis is an uncommon illness that has multiple causes and can be life-threatening.

Aged↗

PubMed2002

Action of Rubus coreanus extract on systemic and local anaphylaxis.

The effect was investigated of the aqueous extract of Rubus coreanus Miq. (Rosaceae) fruits (RCAE) on systemic and local anaphylaxis. RCAE (0.01-1 g/kg) dose-dependently inhibited systemic anaphylaxis induced by compound 48/80 in mice. RCAE (1 g/kg) also significantly inhibited local anaphylaxis activated by anti-DNP IgE. Pretreatment with RCAE at the same concentration before systemic anaphylaxis reduced the plasma histamine levels in a dose-dependent manner. RCAE (0.001-1 mg/mL) dose-dependently inhibited the histamine release from rat peritoneal mast cells (RPMC) activated by compound 48/80 or anti-DNP IgE. The level of cAMP in RPMC, when RCAE was added, significantly increased, compared with that of the normal control. Moreover, RCAE (0.01-1 mg/mL) had a significant inhibitory effect on anti-DNP IgE-induced tumour necrosis factor-alpha production from RPMC. These results indicate that RCAE may possess antianaphylactic action.

Anaphylaxis↗

PubMed1995

Naloxone exacerbates intestinal and systemic anaphylaxis in the rat.

Following sensitization to ovalbumin (OA), male Wistar rats were pretreated with naloxone (20 mg/kg i.p.) and subjected to antigen challenge (3 mg OA i.p.). Naloxone exacerbated both systemic and intestinal anaphylaxis when injected 10 and 90 min before the antigen challenge. This was evidenced by a more pronounced drop in rectal temperature, higher hematocrit values, and by an enhanced elevation of basal short-circuit current (an indication of the secretory tone of the small intestine studied in Ussing chambers). Pretreatment with an equipotent does of methylnaloxone (200 mg/kg i.p.), a peripherally acting opiate antagonist, exacerbated the indices of intestinal anaphylaxis but had no apparent effect on indices of systemic anaphylaxis. Thus, our data strongly suggest that in the rat, components of the systemic hypersensitivity reaction are mediated through central opioid receptors, whereas the changes in gut function characterizing intestinal anaphylaxis are mediated through peripheral opioid receptors.

Anaphylaxis↗

PubMed1979

Pulmonary anaphylaxis and the kallikrein-kinin system.

The kallikrein-kinin system has been thought to participate in the pathogenesis of anaphylaxis. Kallikrein, released from lungs, has been postulated to contribute to cardiovascular collapse. Further to test the hypothesis, we examined for the occurrence of a kallikrein-like enzyme in guinea pig lungs and examined for release of such an enzyme by isolated, perfused lungs of guinea pig sensitized to and challenged with egg albumin. In addition, we treated guinea pigs with the bradykinin potentiating agents, BPP9a and SQ 14,225. In parallel experiments, we examined for effects of non-steroidal anti-inflammatory agents on the supposition that prostaglandin-related substances may mediate or modulate actions of kinins during anaphylaxis. A plasma kallikrein-like enzyme was found in lung homogenates and occurred in concentrations greater than that of plasma itself. Similarly, a store of kininogen occurs in lungs. However, using a sensitive radioassay for kallikrein-like enzymes, we were unable to confirm that antigenic challenge of sensitized lungs causes the release of enzyme into pulmonary venous effluent. Further, we were unable to modify the acute course of anaphylaxis by pretreatment of guinea pigs with bradykinin potentiating agents. However, indomethacin and aspirin at 20-40 mg/kg were found to greatly increase the severity of pulmonary anaphylaxis in terms of increased resistance to ventilation and increased numbers of lung hemorrhages. Paradoxically, aspirin or sodium salicylate at 80-100 mg/kg prevents the characteristic rise of insufflation pressure and the formation of lung hemorrhages.

Anaphylaxis↗

PubMed1995

Association between the renin angiotensin system and anaphylaxis.

Patients with hymenoptera venom anaphylaxis before immunotherapy (n = 50) showed significantly lower renin, angiotensinogen, angiotensin I and angiotensin II as compared to healthy non-allergic controls (n = 25) (p < 0.05). A significant inverse correlation between the severity of clinical symptoms and the plasma levels of renin, angiotensinogen, angiotensin I and angiotensin II was found: the lower the levels the more severe the clinical symptoms. Hymenoptera venom allergic patients with repeated anaphylactic reactions during hyposensitizatin did not tolerate the sting of a living insect (n = 6). Sting provocation with a living insect induced clinical symptoms of anaphylaxis in all of the 6 patients. Renin, angiotensinogen, angiotensin I and II remained significantly lower in these patients as compared to healthy non-allergic controls. Likewise, no stimulation of the renin angiotensin system occurred during the anaphylactic reaction. The values of angiotensin II were similar or lower than the values before the anaphylactic reaction. In contrast, patients with successful immunotherapy (n = 27) who tolerated the sting of a living insect, renin, angiotensin I and II were significantly higher than in patients without immunotherapy. After immunotherapy, the values for renin, ANG I and ANG II were similar to the values found in healthy non-allergic controls. Patients with a history of hymenoptera venom anaphylaxis (n = 22) showed significantly lower ANG II concentrations in their leukocytes as compared to healthy non-allergic controls (n = 24). Successful immunotherapy induced a significant 9-fold increase in ANG II as compared to patients without immunotherapy. These findings suggest a possible role of the renin angiotensin system in hymenoptera venom anaphylaxis.

Adolescent↗

PubMed1983

Effects of leukotrienes C4 and D4 on guinea-pig heart and the participation of SRS-A in the manifestations of guinea-pig cardiac anaphylaxis.

Synthetic leukotrienes C4 and D4 (LTC and LTD) were found to possess potent coronary vasoconstrictor and cardiac depressant actions on isolated guinea-pig hearts. We therefore went further to investigate the possibility that endogenously released slow-reacting substance of anaphylaxis (SRS-A) might be responsible for the coronary vasoconstriction and negative inotropism in guinea-pig cardiac anaphylaxis. Results using time-course analysis as well as the specific SRS antagonist FPL 55712 have shown that SRS-A released during cardiac anaphylaxis was unlikely to be responsible for the early and most dramatic phase of coronary vasoconstriction that usually occurred at the 2nd min after antigen challenge, but could possibly be responsible for the latter and more prolonged phase occurring between the 6th and 14th min. This is because SRS-A release was found to peak at the 4th min after antigen challenge, 2 min after vasoconstriction had already peaked. Moreover, this early component of coronary vasoconstriction could not be blocked by FPL 55712, whereas the latter component was significantly reduced by the antagonist. The negative inotropism following cardiac anaphylaxis was also found to be significantly reduced by FPL 55712, thus suggesting SRS-A involvement. However, our experiments did not show whether the two actions were direct effects of SRS-A or whether contractility failure was a consequence of coronary vasoconstriction.

Anaphylaxis↗

PubMed1986

The effect of lipoxygenase inhibitors and leukotriene antagonists on anaphylaxis.

The experiments whose results are reported here were carried out with the aim of showing a possible role for lipoxygenase products in the modulation of the Schultz-Dale reaction. For this purpose, the actions of nordihydroguaieretic acid (NDGA) and of FPL 55712 were tested during anaphylaxis in guinea-pig ileum and trachea in vitro. Isolated preparations from guinea-pigs, which had been subcutaneously sensitized with ovalbumin and incomplete Freund adjuvant, were challenged with increasing concentrations of antigen; in preparations isolated from the same animal an antigen-concentration anaphylactic-reaction curve was performed in the presence of the drugs. NDGA 3.3 X 10(-6) M was capable of inhibiting anaphylaxis in the trachea to a maximum extent of 40% but it did not affect anaphylactic reaction in the intestinal smooth muscle. FPL 55712 2 X 10(-6) M did not exert any activity on anaphylaxis in either preparations. The difference between SRS-A and histamine as mediators of anaphylaxis in the tissue preparations used could explain the fact that NDGA acted on the trachea alone.

Anaphylaxis↗

PubMed1999

Latex anaphylaxis causing heart block: role of ranitidine.

PURPOSE: Treatment with H2 receptor antagonists may cause the heart to be more susceptible to atrioventricular conduction delay when exposed to an overwhelming insult by histamine released during an anaphylactic reaction. We present the case of a woman, pretreated with ranitidine, who developed 3:1 heart block secondary to latex anaphylaxis. We propose that H2 antagonist premedication alone in patients susceptible to anaphylaxis increases their risk of heart block. CLINICAL FEATURES: A 38 yr old obese woman with cervical cancer presented for a radical hysterectomy. Systems review yielded a history of sleep apnea, orthopnea, gastroesophageal reflux, and sciatica. Medications included preoperative ranitidine, 150 mg. There was no history of atopy or allergy. Following general anesthesia induction, at the onset of the surgical procedure the patient developed a severe anaphylactic reaction which was heralded by the onset of 3:1 heart block, with decreases in SpO2, P(ET)CO2 and a decrease in systolic blood pressure to 45 mmHg. This was diagnosed as a possible latex reaction and treated using epinephrine boluses and infusion, fluids, 50 mg diphenhydramine, 50 mg ranitidine and 100 mg hydrocortisone. Following a 48 hr stay in the ICU the patient made an uneventful recovery. Allergy testing with intradermal latex injection and increased plasma tryptase levels confirmed a latex anaphylaxis. CONCLUSION: The use of H2 antagonists alone as a prophylaxis for gastroesophageal reflux may increase the risk of heart block in patients who develop anaphylaxis.

Adult↗

PubMed2003

Epidemiology of anaphylaxis in the United States.

Anaphylaxis is a potentially life-threatening allergic reaction characterized by a syndrome of dermatologic and systemic signs and symptoms, at times including cardiovascular collapse from distributive shock. Although it is recognized that the incidence of anaphylaxis is increasing, the extent of its prevalence, both from individual causes and in toto, remains unclear. Common causes include pharmacologic agents, such as antibiotics and radiocontrast media, as well as foods, insect stings, and latex exposure. The available literature suffers from methodologic shortcomings, limiting the accuracy of estimated prevalence. However, current data suggest that there are approximately 1500 annual deaths from anaphylaxis, and between 2.8 million and 42.7 million Americans are at risk of experiencing an episode of anaphylaxis during their lives.

Anaphylaxis↗

PubMed1991

Inhibition of active anaphylaxis in mice and guinea pigs by the new hetrazepinoic PAF antagonist bepafant (WEB 2170).

The aim of this study was to examine the ability of the novel PAF (platelet-activating factor) antagonist WEB 2170 to inhibit active anaphylaxis in mice and guinea pigs. Previous studies with other PAF antagonists have given equivocal results. This study was designed to define conditions under which a clear and significant effect of the PAF antagonist would be shown. WEB 2170 could be shown active, at concentrations of between 1 and 10 mg/kg p.o. in a model of murine anaphylaxis, in which the mice were actively sensitized and also treated with the beta-adrenoceptor antagonist propranolol to potentiate the anaphylactic response. WEB 2170 was also active in guinea pig models of anaphylaxis (tested dose range: 5 mg/kg i.v. and 0.04-3 mg/kg p.o.), in which the guinea pigs were sensitized according to one of three specified immunization schedules and pretreated with low doses of mepyramine before antigen challenge. These results suggest that PAF has a role in active anaphylaxis in mice and guinea pigs. However, to demonstrate this effect in guinea pigs, models must be used in which the effects of histamine release are minimized.

Anaphylaxis↗

PubMed1992

Relationship between mast cell degranulation and jejunal myoelectric alterations in intestinal anaphylaxis in rats.

The effects of two degranulators of mast cells and intestinal anaphylaxis on jejunal myoelectric activity were compared in rats fasted for 15 hours. Attempts to antagonize the motility changes were performed using antagonists of histamine and serotonin and a cyclooxygenase and lipoxygenase inhibitor. Hooded Lister rats were chronically fitted with electrodes implanted in the jejunal wall. A group of rats was sensitized to egg albumin and challenged 14 days later by intraduodenal infusion of antigen. Sensitized animals had serum titers greater than or equal to 1:64. The other group was administered with mast cells degranulators. Both 48/80 (1 mg/kg), a degranulator of connective mast cells, and bromolasalocid (2 mg/kg), acting on connective and mucosal mast cells, induced a phase of total spiking inhibition followed by a progressive irregular spiking activity until the recovery of migrating myoelectric complex pattern (about 3 hours after injection). In contrast, antigen challenge disrupted the migrating myoelectric complex pattern, which was replaced by a peculiar pattern characterized by propagated spike burst, lasting 98 +/- 11.3 minutes. Chlorpheniramine (1 mg/kg) antagonized only the inhibitory phase induced by degranulators and was ineffective on the intestinal anaphylaxis-induced motor changes. Methysergide (1 mg/kg) and indomethacin (5 mg/kg) significantly reduced the degranulator effects as well as the anaphylaxis-induced alterations of intestinal motility. It is concluded that anaphylaxis-induced motor disturbances are relevant to mucosal mast cell degranulation involving 5-hydroxytryptamine and arachidonic acid derivative products, whereas histamine release appears to be a minor component.

Anaphylaxis↗