Snake (Vipera berus) bite: The cause of severe anaphylactic shock and hepatocellular injury.

Vipera berus bites lead to a variety of clinical manifestations. Local swelling, coagulopathy, nephrotoxicity, cardiac effects and myotoxicity are known to be associated with envenoming by a viper bite. Although a variety of clinical manifestations have been reported in viper bite cases, anaphylactic reactions and liver injury events have not been described. We report a unique case of an anaphylaxis and transitional liver cell injury due to a Vipera berus bite in the case of a 58-year-old man with no past history suggestive of allergy and liver disease. These observations need to be further explored with laboratory studies to identify the venom components which could have pre-disposed the patient to the development of these complications.

Treatment with a combination of omalizumab and specific immunotherapy for severe anaphylaxis after a wasp sting.

Hymenoptera venom anaphylaxis after bee or wasp sting is a common problem that affects about 1.2 percent to 3.5 percent of the general population. Venom-specific immunotherapy (VIT) is an established mode of treatment for immunoglobulin (Ig) E-mediated Hymenoptera venom allergy. However, VIT may often be associated with immediate anaphylaxis which can lead to treatment withdrawal. Several cases published in recent years suggest that omalizumab, used as add-on therapy may be able to prevent anaphylaxis during VIT. We report the case of a 30-year-old woman, suffering from mild persistent asthma, who had a history of severe anaphylactic reactions after yellow jacket sting, and after eating peanuts, contact with guinea pig hair, and i.v. administration of dexamethasone natrium phosphate. Initial specific immunotherapy had to be stopped due to severe anaphylaxis (hypotension, dyspnea, and angioedema). The immunotherapy was reintroduced accompanied by the anti-immunoglobulin (Ig) E monoclonal antibody omalizumab. Subcutaneous omalizumab 150 mg was initiated 4 weeks after the anaphylaxis incident and 1 day before the resumption of VIT. Rush treatment was uneventful, and the usual cumulative dose of 111.1 microg was successfully reached. The combination of omalizumab and VIT is a valid option of therapy for these patients and could reduce asthma and food allergy symptoms.

[Eosinophilic activation based on measurements of eosinophil cationic protein in patients with acute myocardial infarction and patients with angina pectoris]. / Aktywnosc eozynofilów oceniana na podstawie oznaczania wartosci eozynofilowego bialka kationowego (ECP) u chorych ze swiezym zawalem miesnia sercowego i pacjentów z dusznica bolesna.

Increased activation of polymorphonuclear neutrophils in the wideness of irreversible myocardial injury was described by many authors. Released proteolytic enzymes may cause deliquescence of necrotic muscle tissue and attenuate collagenic structure of myocardium, lead to endothelium damage and generate free oxygen radicals. Eosinophilic leucocytes reveal also enhanced proinflammatory activation. They take participation in inflammatory and immunologic reactions, among others, by producing and releasing many biologic mediators. One of the most important and powerful mediators is eosinophil cationic protein (ECP), the specific marker of eosinophil activation in vivo. We studied 17 patients (pts) with acute myocardial infarction (MI) and 21 pts with angina pectoris (AP). The plasma concentrations of ECP and the number of eosinophils in peripheral blood were measured 3 times-near before beginning of the treatment, and on the 4-th and 8-th day of MI. During the first 4 days measurements of CK-MB every 6 hours were made. We observed the significant increase of eosinophils and ECP correspondingly on the 8-th and 4-th day, when compared to the first day of MI (p < 0.05) and the patients with AP (p < 0.01). Despite tendency, the significant correlation of eosinophils and ECP values was not obtained (r = 0.36). In the group of patients with AP the eosinophil and ECP values were significantly higher at the pts with unstable angina, when compared to pts with stable angina (p < 0.001).

[Early post myocardial infarction syndrome--a trial of assessment based on clinical course and immunologic tests]. / Wczesny zespól pozawalowy--próba oceny w oparciu o przebieg kliniczny i badania immunologiczne.

The study analysed clinical and immunological course of 22 patients (aged 56.3 +/- 9.5) with fever (38.5 degrees C) and greatly increased erythrocyte sedimentation rate (ESR) in the first week after myocardial infarction. The control group consisted of 25 patients (aged 50.7 +/- 11.2) without inflammatory and infectious diseases. Clinical courses of the disease, chest x-ray, echocardiography, leucocytosis and serial CK-MB levels were analysed. The immunological investigations involved quantitative estimation of IgG, C3 complement, C4 complement and the identification of T and B lymphocytes on the basis of the rosette tests A, E and EAC. Post myocardial infarction syndrome (PMIS) manifested by fever and greatly increased ESR we observed in 64% of examined patients, but fully manifested PMIS in 14% with tendency to recurrences. We found the differences in immunological examinations compared to the control group. Pericardial effusion occurred in 64% of the patients. The treatment with corticosteroids brought dramatic relief of the symptoms with objective improvement of clinical condition. Patients with high temperature with accompanying greatly raised ESR in the first week after MI may demonstrate abortive form of the post myocardial infarction syndrome.

The immunologic response to tobacco antigens in smokers. III. Type III hypersensitivity skin reactions and specific serum precipitins to four different tobacco extracts in patients suffering from coronary artery disease.

In a population of 70 patients suffering from coronary heart disease (49 smokers and 21 non-smokers) intradermal tests and specific precipitation tests with four different extracts of tobacco were performed. Skin tests with tobacco extracts were positive in 41 smokers and 7 nonsmokers. In both groups the immediate and delayed type reactions were weak and of rather doubtful specificity, while the late type reaction was usually more frequent and stronger in smokers (in 14 patients it was positive with all preparations). Specific precipitins against tobacco antigens were found in the sera of 13 smokers but never in nonsmokers. The positive precipitation test correlated well with the positive late skin reactions to tobacco extracts. Such correlation with Ag 1 was observed in 9 out of 13 patients, with Ag II in four cases, with Ag IV and Ag V in 2 and 2 patients respectively. The coincidence of strongly positive late skin reactions and positive precipitation tests with tobacco extracts seems to indicate that tobacco allergy really exists and resembles, in a number of patients with coronary artery disease, type III hypersensitivity reactions to tobacco antigens. It is postulated that immune complexes of precipitins and tobacco antigens may be formed in some patients and initiate pathological processes in coronary arteries leading to their occlusion.