Massive honey bee envenomation-induced rhabdomyolysis in an adolescent. (65/345)

Massive envenomations by honey bees are capable of causing multiorgan dysfunction as a result of the direct toxic effects of the large venom load received. Although all varieties of honey bee have the potential for these attacks, the Africanized honey bee (Apis mellifera scutellata) is the most commonly implicated subspecies. In the United States, the Africanized strain is found primarily in the southwestern states and is known for its highly defensive behavior if disturbed. Mechanisms behind the multiorgan dysfunction produced by these mass envenomations are not clearly understood. We present a case of a 13-year-old male who was stung by approximately 700 honey bees and developed progressive upper-body swelling and systemic manifestations of mass envenomation including rhabdomyolysis, renal insufficiency, and a transient transaminase elevation.  (+info)

Ultrarush immunotherapy in a patient with occupational allergy to bumblebee venom (Bombus terrestris). (66/345)

Bumblebee venom allergies, though uncommon among the broad public, pose a significant risk in plant industry and scientific occupation. Since a significant IgE cross-reactivity between bumblebee and honeybee venom has been described in several cases and bumblebee venom for immunotherapy has been available only from a few suppliers, SIT with honeybee venom was frequently used for bumblebee venom allergic patients in the past. We present the case of occupational bumblebee allergy in a biologist who developed anaphylactic reactions with subsequent stings. He was lacking cross-reactivity to honeybee venom, therefore we initiated immunotherapy with bumblebee venom extract. Two months after reaching the maintenance dose of 80 microg, the efficacy of the treatment was demonstrated by sting challenge.  (+info)

PLA2 inhibitory activity of marine sesterterpenoids cladocorans, their diastereomers and analogues. (67/345)

Inhibition of secretory phospholipase A(2) (sPLA(2)) by cladocorans A and B and their diastereomers almost equaled that of manoalide.  (+info)

In vitro basophil activation using CD63 expression in patients with bee and wasp venom allergy. (68/345)

The diagnosis of insect venom allergy and the indication for specific immunotherapy is based on history, skin tests and demonstration of hymenoptera venom-specific IgE-antibodies. Cellular tests can add useful information but the role of basophil activation tests for the different venoms has to be elucidated further. We evaluated positive reactions in a basophil activation test using CD63 expression as marker independently for bee or wasp venom in patients with hymenoptera allergy. Fifty-seven patients with a history of insect venom anaphylaxis were examined (12 x bee venom, 39 x wasp venom, 6 x bee plus wasp venom). Skin tests and determination of specific IgE-antibodies were performed. Basophil activation test (BAT) using CD63 expression was performed after stimulation with different concentrations of bee and wasp venom. The BAT is based on double staining with anti-IgE antibodies and anti-CD63 and subsequent determination of the percentage of activated basophils by flow cytometry. In patients with bee venom allergy, BAT was positive in 100% to bee venom and 75% to wasp venom. In patients with bee and wasp venom allergy, positive reactions for both venoms were found in 100%. In patients with wasp venom allergy, 97% reacted positive to wasp venom and only 56% to bee venom. These results show the reliability of the basophil activation test as a cellular test in the in vitro diagnosis in patients with bee and wasp venom allergy. They also show that positive reactions in the basophil activation test reflect both sensitization status and cross-reactivity between venom species.  (+info)

Interplay between lipoproteins and bee venom phospholipase A2 in relation to their anti-Plasmodium toxicity. (69/345)

We previously showed that the in vitro intraerythrocytic development of the malarial agent Plasmodium falciparum is strongly inhibited by secreted phospholipases A(2) (sPLA(2)s) from animal venoms. Inhibition is dependent on enzymatic activity and requires the presence of serum lipoproteins in the parasite culture medium. To evaluate the potential involvement of host lipoproteins and sPLA(2)s in malaria, we investigated the interactions between bee venom phospholipase A(2) (bvPLA(2)), human triglyceride-rich lipoproteins, and infected erythrocytes. Even at high enzyme concentration (100x IC(50)), bvPLA(2) binding to Plasmodium-infected or normal erythrocytes was not detected. On the contrary, tight association with lipoproteins was observed through the formation of buoyant bvPLA(2)/lipoprotein complexes. Direct involvement of the hydrolysis lipid products in toxicity was demonstrated. Arachidonic acid (C20:4), linoleic acid (C18:2), and, to a lesser extent, docosahexaenoic acid (C22:6) appeared as the main actors in toxicity. Minimal oxidation of lipoproteins enhanced toxicity of the lipolyzed particles and induced their interaction with infected or normal erythrocytes. Fresh or oxidized lipolyzed lipoproteins induced the parasite degeneration without host cell membrane disruption, ruling out a possible membranolytic action of fatty acids or peroxidation products in the death process. In conclusion, our data enlighten on the capability of secreted PLA(2)s to exert cytotoxicity via the extracellular generation of toxic lipids, and raise the question of whether such mechanisms could be at play in pathophysiological situations such as malaria.  (+info)

Safety of specific immunotherapy using a four-hour ultra-rush induction scheme in bee and wasp allergy. (70/345)

BACKGROUND: Ultra-rush induction of immunotherapy with Hymenoptera venom is a reliable and efficacious alternative to the rush induction protocol, though not widely used in European countries yet. Its safety, however, has been intensively discussed over the last few years. The aim of this retrospective case study was to examine the rate of allergic side-effects during our four-hour ultra-rush hymenoptera venom induction regimen. We evaluated risk factors for observed side-effects such as age, gender, severity of previous insect sting reactions according to the H.L. Mueller classification, concentration of venom inducing positive skin tests, level of specific IgE, serum tryptase concentration, and hymenoptera venom used for treatment. METHODS: 67 outpatients with Hymenoptera venom allergy received 80 courses of ultra-rush immunotherapy. Diagnosis and selection of patients for venom immunotherapy were carried out according to the European Academy of Allergology and Clinical Immunology. We applied a four-hour regimen, and local or systemic reactions were documented. RESULTS: In 78 courses (97.5%) the maintenance dose of 111.1 microg was reached within 4 hours and it was tolerated in 82.5% without any hypersensitivity reaction. Allergic side-effects were observed in only 17.5% (n=14): four severe local reactions (5%), eight grade I (10%) and two grade II (2.5%) systemic reactions. There was no significant difference in the number of systemic reactions comparing patients receiving wasp or honeybee venom extract. The number of systemic reactions was neither higher in patients with a severe prior insect sting reaction (grade III or IV) nor dependent on age, gender, skin test reaction, level of specific IgE or tryptase. Epinephrine as rescue medication was never needed. Interestingly, patients with a severe prior wasp sting reaction showed a significantly lower incidence of allergic side-effects during ultra-rush immunotheraphy with wasp venom extract as compared to grade III or IV honeybee venom allergic patients. CONCLUSION: Our ultra-rush immunotherapy induction regimen shows a low incidence of systemic reactions. It proved to be safe and convenient for the patient, as it could be applied in a four-hour outpatient regimen.  (+info)

The safety of allergen immunotherapy (IT) in Turkey. (71/345)

Allergen immunotherapy (IT) has encouraging therapeutic outcomes but its safety is still being questioned because of possible severe systemic reactions. The aim of this study was to determine the frequency of systemic reactions (SR), and to identify their correlation with the characteristics of therapy, such as allergen composition and IT schedule, and diagnosis. We analyzed the data of 126 patients who received IT between 2000-2003, and suffered from respiratory allergy or hymenoptera venom anaphylaxis. IT was given by rush, clustered or conventional schedules. The standardized allergen extracts used were grass pollen, house dust mite and hymenoptera venom in 88, 18 and 20 patients, respectively. None of the patients received premedication. A total 4705 injections were administered. One hundred and twenty-three adverse events (AE) (2.6% per injection) were documented in 46 patients. Sixty-one of them were SRs (1.3% SRs per injection) and they were seen in 28 patients. Asthmatics had more tendency to SRs (p=0.05). Rush (1.8%) and clustered (2.8%) IT protocols were associated with a higher rate of SRs (per injection) when compared to conventional schedule (0.9%) (rush vs conventional; p=0.013, clustered vs conventional; p=0.001). The majority of SRs corresponded to grade 3 (49%). Forty-nine (80%) of the 61 SRs were observed during the build-up phase, and mostly with pollen extracts (75.5%). Patients showed more severe SRs during the build-up phase (p<0.05). Twenty-six (42.6%) of the SRs were immediate, whereas 35 (57.4%) SRs appeared within 2 hours. Delayed SRs were significantly more frequent in polysensitized patients when compared to monosensitized subjects (p=0.018). Our data indicate that rapid IT regimens and the presence of asthma represent a greater risk for SR development. Since the late SRs occur as frequently as the early ones, we suggest a longer waiting period beyond 30 minutes, especially in polysensitized and asthmatic patients.  (+info)

Regulation of kindling epileptogenesis by hippocampal galanin type 1 and type 2 receptors: The effects of subtype-selective agonists and the role of G-protein-mediated signaling. (72/345)

The search for antiepileptic drugs that are capable of blocking the progression of epilepsy (epileptogenesis) is an important problem of translational epilepsy research. The neuropeptide galanin effectively suppresses acute seizures. We examined the ability of hippocampal galanin receptor type 1 (GalR1) and type 2 (GalR2) to inhibit kindling epileptogenesis and studied signaling cascades that mediate their effects. Wistar rats received 24-h-long intrahippocampal infusion of a GalR1/2 agonist galanin(1-29), GalR1 agonist M617 [galanin(1-13)-Gln14-bradykinin(2-9)-amide], or GalR2 agonist galanin(2-11). The peptides were administered alone or combined with an inhibitor of Gi protein pertussis toxin (PTX), Gi-protein activated K+ channels (GIRK) inhibitor tertiapin Q (TPQ), G(q/11) protein inhibitor [D-Arg1,D-Trp(5,7,9),Leu11]-substance P (dSP), or an inhibitor of intracellular Ca2+ release dantrolene. Sixteen hours into drug delivery, the animals were subjected to rapid kindling-60 electrical trains administered to ventral hippocampus every 5 min. M617 delayed epileptogenesis, whereas galanin(1-29) and galanin(2-11) completely prevented the occurrence of full kindled seizures. TPQ abolished anticonvulsant effect of M617 but not of galanin(2-11). PTX blocked anticonvulsant effects of M617 and inversed the action of galanin(1-29) and galanin(2-11) to proconvulsant. dSP and dantrolene did not modify seizure suppression through GalR1 and GalR2, but eliminated the proconvulsant effect of PTX + galanin(1-29) and PTX + galanin(2-11) combinations. We conclude that hippocampal GalR1 exert their disease-modifying effect through the Gi-GIRK pathway. GalR2 is antiepileptogenic through the Gi mechanism independent of GIRK. A secondary proconvulsant pathway coupled to GalR2 involves G(q/11) and intracellular Ca2+. The data are important for understanding endogenous mechanisms regulating epileptogenesis and for the development of novel antiepileptogenic drugs.  (+info)