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Hypersensitivity to acetylsalicylic acid (ASA) is characterized by the co-occurrence of symptoms so-called aspirin triad, which include bronchial asthma, chronic rhinitis and sinusitis and the nasal mucosa polyps. The disease affects about 1% of the general population and in patients with bronchial asthma incidence may be as high as 10%. Hypersensitivity to aspirin is a difficult diagnostic problem, so the increased knowledge on this subject is a very important for the physicians of many specialties.

The article below shows different forms, patomechanisms and diagnostics criteria of hypersensitivity to NSAIDs based on available literature as well as up to date outlook on implementing low salicylate diet as a treatment.

Drug-induced hypersensitivity syndrome (DIHS) is characterized by fever, rash and internal organ involvement, mostly in form of hepatitis, myocarditis, nephritis or pneumonitis, which may occur 1-8 weeks after medicine exposure. Fever is an early feature, usually preceding a widespread erythematous skin eruption, but the severity of the skin-related changes does not correlate with the extent of internal organ involvement. It is considered that anticonvulsants (particularly carbamazepine), antibiotics, allopurinol are the most frequent causative agents of DIHS. The underlying mechanisms causing DIHS are poorly understood--defective detoxification of the reactive drug's metabolites or genetic predisposition have been implicated. Diagnosis of DIHS is based on clinical presentation connected with drug intake, supported by a finding of eosinophilia, increased concentration of inflammation markers and abnormal biochemical parameters, mainly liver function tests. Treatment consists of immediate withdrawal of all suspected medicines, followed by supportive systemic corticosteroids. We describe a case of a 72-years-old female who developed symptoms of drug-induced hypersensitivity syndrome after approximately 4 weeks of taking anticonvulsant (Amizepin) due to sensual axonal polyneuropathy. Withdrawal of drug and treatment with systemic corticosteroids caused clinical improvement rapidly.

The incidence of allergic reactions during anaesthesia has been estimated to be from 1:3500 to 1:20000, with muscle relaxants being the most common allergens. Symptoms may involve all organs and systems with various intensities--from mild skin reactions to bronchospasm and cardiovascular collapse in the most severe cases. In a case of suspected perioperative allergic reaction, the management should not be limited to resuscitation and restoration of basic life functions, but must include careful investigation of potential allergens. An appropriate diagnostic strategy is essential for confirmation of an allergic reaction, identification of the allergen, and recommendations for future prevention. In this review, the various aspects of anaphylaxis and anaphylactoid reactions to muscle relaxants are discussed, including the role of tryptase and its assay in the diagnostic regimen.

The paper presents the case report of a patient diagnosed with borderline personality disorder, treated with carbamazepine. During the treatment symptoms of the infection of upper respiratory tract appeared, which evolved to allergic symptoms and then to morbilli-like and mumps-like symptoms. The patient was hospitalized due to this disorder for two weeks, in the beginning on an isolation ward and then was diagnosed and treated on a dermatological ward. The diagnosis of the disorder was doubtful due to polymorphic symptoms and their evolution. Detailed course of the disease, diagnostic process and laboratory results were presented in the case report. The authors also attempt to classify these symptoms and to analyse the relationship between the observed symptoms and drugs used during the treatment.

Aspirin hypersensitivity syndrome includes several symptoms from the respiratory tract, skin and digestive system triggered by ingestion of aspirin or other nonsteroidal anti-inflammatory drugs. Asthmatic attacks precipitated by aspirin or other nonsteroidal anti-inflammatory drugs occur in about 10% of all asthmatic patients. In subjects with aspirin hypersensitivity disruption of synthesis of prostaglandin E2 (PGE2) and overproduction of cysteinyl leukotrienes (Cys-LT) seem to be crucial in the pathogenesis of bronchial symptoms. Double blind, placebo controlled challenges are regarded as a gold standard in the diagnosis of aspirin hypersensitivity.

Recent clinical study reported that the best choosing of antiretroviral therapy for an individual patients is one that physicians have always tried to practice, making use of whatever knowledge or tools are available to treatment decisions. Individual genetic variations provide scope for a wide range of host-drug interactions that will differentiate therapeutic outcomes within an otherwise homogenous population. Pharmacogenetics looks set to become an increasingly important field to refine the medical tools to personalize antiretroviral treatment. The integration of genetic tests into routine patient management has a great challenge for HIV-guidelines and for clinical care. Pharmacogenetics will increasingly impact all medical disciplines for the candidates to therapy. It was confirmed, that genetic screening enabled to prevent abacavir hypersensitivity reaction.

Increasing body of evidence indicate that besides the central nervous system, antiepileptic drugs may also affect the immunoactivity. Experimental data showed that classical antiepileptic drugs affect peripheral immunological parameters. To this end, phenytoin and carbamazepine attenuate both humoral and cellular response, and an engagement of CD8+ cells in these effects was suggested. Other authors reported that valproate and phenobarbital diminished humoral response and lymphocyte T cytotoxicity in mice, respectively. On the other hand, withdrawal of carbamazepine and phenytoin enhanced autoimmune response in experimental encephalomyelitis in mice. Few data concern effects of new antiepileptic drugs on immune system. It was found that topiramate reversed seizures-induced decrease in lymphocyte T proliferative activity in rats. Some new antiepileptic drugs, e.g., felbamate, stiripentol, loreclezole and tiagabine suppress mitogenes-stimulated proliferative activity of mouse splenocytes in vitro. Results of clinical studies indicate that phenytoin, carbamazepine, and valproate, show immunosuppressive activity, inhibit protein synthesis in lymphocytes, decrease CD4+/CD8+ ratio, decrease IgA, and induce changes in IgG and IgM plasma levels. Cytokine synthesis is also affected by antiepileptic drugs, although in a complex manner. Carbamazepine inhibits IL-2 and IL-4 but stimulates IL-10 and TGFb production in vitro. Treatment of epileptic patients with carbamazepine increases IL-2 level, whereas phenytoin elevates IL-1 blood concentration. In vitro valproate inhibits TNFa and IL-6 production, whereas in epileptic patients this drug enhances IL-1, IL-6 and IL-5 concentration. With respect to undesired effects of antiepileptic drugs, lamotrigine, carbamazepine, phenobarbital and phenytoin may induce hypersensitivity of immune system. The suggested mechanism of the hypersensitivity involves activation of drug specific CD4+ and CD8+, increase in IL-4 and IL-5 level, receptor T polymorphism or direct interaction of drug with lymphocyte T receptors. Summing up, majority of antiepileptic drugs show immunosuppressive effects, however under certain conditions they can also stimulate immune system. Further studies on chronic administration of traditional and new antiepileptic drugs on immune system activity are warranted.

Unlabelled: Nasal polyposis is still a disease of unknown etiology. Looking at its clinical course it seems to be not homogenous pathology. Inflammation of the mucosa, mainly eosinophilic is probably the most important factor, which leads to the development of nasal polyps., The Aim of Study: To analyze and compare the history data and eosinophilic inflammation parameters in patients with nasal polyps., Material and Methods: 67 patients with nasal polyposis were included into the study. They were divided into three groups: PP-primary nasal polyps (n = 33-49.2%); A-polyps and bronchial asthma without aspirin intolerance (n = 19-28.4%); ASA-polyps and aspirin-induced asthma (n = 15-22.4%). The history data were taken using patient's questionnaire. To assess the eosinophilic inflammation intensity the blood and nasal eosinophilia and serum eosinophilic cationic protein (ECP) concentration were measured., Results: The average age of all patients was 55 +/- 1.5 (range 32-76), the age distribution was comparable in all groups. The ratio males:females--1.5:1 (PP--2.7:1; A--1.1:1; ASA--0.7:1. The females with nasal polyps much more often suffer from asthma than males (p = 0.036). The age when polyps were first seen was 45.1. The duration of nasal polyps was 10 +/- 10 years (range 0.5-30 years): PP-- 10 +/- 9; A-- 14 +/- 11; ASA-- 7 +/- 7 (A/ASA-- p = 0.045). Period of 6.6 years of rhinitis had preceded the diagnosis of nasal polyposis (PP--7.3; A--7.1; ASA--4.5). Age when asthma was developed (A+ASA groups)--45.5; the duration of asthma was 11 +/- 9 years. 58% of patients had polypectomy/ethmoidectomy (PP--45%; A--60%; ASA--80%). The number of operations per one patient: 1.3 (PP--1.0; A--1.2; ASA--2.0), the most often performed in ASA group (PP/ASA-- p = 0.01 and A/ASA-- p =0.045). The mean interval between polypectomies in all patients--9.1 years (PP--10; A--12, ASA--3.5). Blood eosinophilia: 5.6 +/- 0.4% (PP-- 4.6 +/- 0.5; A-- 6.2 +/- 0.9; ASA-- 7.2 +/- 0.9% and PP/ASA-- p = 0.019; PP/A+ASA-- p = 0.03). Nasal eosinophilia: 18.5 +/- 3% (PP-- 15.0 +/- 4; A-- 15.5 +/- 6; ASA-- 30.0 +/- 8% and PP/ASA-- p = 0.01; A/ASA-- p = 0.02). Serum ECP concentration: 24 +/- 2 microg/l., Conclusions: The patient's history and the intensity of eosinophilic inflammation are not similar in all nasal polyposis patients, that support the classification into PP, A and ASA groups. The most severe clinical picture and the highest values of eosinophilic parameters are observed in ASA group. Aspirin intolerance seems to be unfavourable prognostic factor in nasal polyposis.

Aspirin is among drugs most commonly used all over the world, therefore considerable prevalence of acetylsalicylic acid (ASA) intolerance has lately been reported. There is no in vitro test for the identification of ASA intolerance and even clear-cut clinical symptoms are not sufficient for diagnosis of ASA intolerance. Provocation tests therefore, remain to be the only relevant method used for the diagnosis of both AIAR (aspirin-intolerant asthma and rhinitis) and ASA intolerance of organs other than respiratory tract. There are 5 types of provocation tests, depending on the route of ASA administration: oral, bronchial (inhaled), nasal and seldom used intravenous and intrabronchial challenges. The protocols used in different centers, vary not only in the ways of ASA administration, but also in doses used, duration of observation period and in criteria for evaluation of the results. We present here current principles regarding indications and contraindications for detailed challenge procedures and methodology of different ASA provocation tests. We summarized both advantages and the defects of all enumerated challenge procedures, which may be helpful for correct patient qualification, test performance and interpretation of the results.

Background: Leukotrienes (LTC4, LTD4, LTE4) belong to eicosanoids and they play important role in allergic inflammation. Leukotrienes are 5-lipooxygenaze products of arachinoid acid. It is known that concentration of LTE4 increases in patients with bronchial asthma, after some allergy provocation and in patients with bronchial asthma and intolerance of on steroids anti-inflammatory drugs. The aim of the study was estimated the urinary concentration of LTE4 in patients with bronchial asthma and intolerance of no steroids anti-inflammatory drugs., Material and Methods: The study group consisted of 21 patients with asthma and intolerance of non steroids antiinflammatory drugs (F 19, M 2) in age from 21 to 72 years old (mean = 49 +/- 14), with middle time of asthma duration mean = 13.4 +/- 12.9 years In study group 11 person had positive skin test, 7 nasal polyps, and 8 person positive family history of bronchial asthma. After oral provocation aspirin challenge in 5 subjects' aspirin induced asthma was confirmed, 3 persons were not qualified to test. Urinary concentration of LTE4 before and 24 h after aspirin provocation was analyzed in all the patients. Leukotriene were detected by enzymatic Leukotriene E4, EIA Kit, Cayman Chemical test., Results: In group of patients with aspirin asthma basic concentration of LTE4 was 416.6 +/- 374.4 pg/mL, and after provocation 496.6 +/- 485.3 pg/mL, in the group without sensitivity to aspirin appropriate 262.9 +/- 404.0 vs 261.2 +/- 259.66 pg/mL, and in the group disqualified to test 181.6 +/- 55.75 pg/mL., Conclusion: 1 Patients with aspirin asthma have higher concentration of LTE4. 2. Excretion of LTE4 in patients with aspirin induced asthma raised after oral aspirin provocation and higher level was detected is til 24 hours after challenge. 3. This results confirmed the role of cysteinic leukotrienes in pathogenesis of aspirin induced asthma.

The paper includes a survey of issues concerning evolution of allergy to antibiotics. Particular attention is paid to penicillin allergy as this antibiotic has been the drug most frequently causing sensitization since 1960s until today, although the frequency of the allergy is continuously decreasing. In addition, the paper deals with the importance of replacing benzyl penicillin with semi-synthetic penicillins and the impact of these process on the nature of immune response (a decrease in the immediate allergy incidence, an increase in the delayed allergy incidence), cross reactions, the significance of the hidden allergen sources. Apart from that, the paper discusses the most important issues concerning the evolution of allergy to other antibiotics, especially the aminoglycoside antibiotics and cephalosporins.

In this paper current data on the pathogenesis of benzylpenicillin allergy is presented. Individual allergic reaction and susceptibility for the drug perhaps is not related to chemical properties of benzylpenicillin. An association between bacterial infection and allergy to benzylpenicillin is reviewed.

Objectives: The purpose of our study was to analyze the rate of hypersensitivity reactions (HSRs) to paclitaxel in patients with advanced ovarian carcinoma. We also analyzed the possibility of re-administration paclitaxel with adequate treatment after hypersensitivity reactions., Materials and Methods: The incidence of HSRs was analyzed retrospectively in 112 patients who received 24-hr infusions of paclitaxel (135 mg/m2) for advanced ovarian cancer at the Department of Gynecology Medical University of Gdańsk between the January 2000 and the February 2002. Before each course of the paclitaxel administration patients received orally dexamethasone (20 mg p.o., 12 and 6 hours prior to the chemotherapy) and thirty minutes prior to the infusion of paclitaxel all patients received, diphenhydramine (50 mg), and cimetidine (300 mg) intravenously (i.v.). When HSR was observed administration of paclitaxel was temporally stopped and before the re-challenge additional intravenous dosage of hydrocortisone (200-500 mg) and diphenhydramine (25 mg) was given., Results: Severe hypersensitivity reactions occurred in 9 patients (8%) and the administration of paclitaxel was withdrawn. Mild hypersensitivity reactions were observed in 8 patients (7%) and all of these patients were successfully retreated with paclitaxel without HSRs., Conclusion: We conclude that this premedication and treatment strategy provides lower hypersensitivity reactions rate and allows for continuing administration of paclitaxel in patients with advanced ovarian carcinoma.

Asacard is a microcapsulated, controlled-release form of acetylsalicylic acid, which delivers very low but constant amount of the drug directly into the intestine. The dose 162.5 mg Asacard, used in prevention of cardiovascular diseases, is thus sufficient to block platelets in the portal vein from synthesizing thromboxane but not high enough to enter the systemic circulation and block the formulation of prostacyclin and other prostaglandins. It is generally accepted that in aspirin-induced asthma (AIA) the bronchospasm is provoked by inhibition of prostaglandin synthesis with overproduction of cysteinyl leukotrienes. The aim of our study was to verify the hypothesis if Asacard, as a form of aspirin, which theoretically does not block prostacycline synthesis in systematic circulation, would be well tolerated by patients with AIA. We thus studied in an open study the tolerability of three single, increasing doses of Asacard in 10 patients with confirmed by oral challenge test aspirin intolerance (4 males, 6 females, mean age 40 years). Initially, the patients received 40 mg of Asacard and FEV1 and clinical symptoms were assessed every 30 minutes for 8 hours. A positive reaction was defined as a > or = 20% decline in FEV1 from baseline. Patients with negative reaction received 75 mg Asacard 7 days later. In absence of the reaction, the last dose 162.5 mg was administered a week later. In 5 out of 10 patients studied, Asacard given at single doses up to 162.5 mg was tolerated well. In the remaining 5, it provoked bronchospasm, a fall in FEV1 > or = 20% and other extrabronchial symptoms of aspirin intolerance. No correlation was found between the doses of regular aspirin, which provoked a fall in FEV1 > or = 20% during baseline oral provocation test and Asacard doses. In conclusion, any form of aspirin, even controlled-release, should not be prescribed for patients with AIA, because it may provoke symptoms of intolerance to this drug.

Aspirin intolerance is characterized by polypous rhinosinusitis, bronchial asthma and adverse reactions to aspirin. The common intolerance to all cyclo-oxygenase inhibitors allows us to focus study of the pathogenesis of AI on the metabolism of arachidonic acid. Nasal polyposis is a chronic inflammatory condition that is mostly characterized by an infiltration of eosinophils. How this eosinophilic inflammation leads to polyp formation remains largely unclear. Eosinophils are the major source of cysteinyl leukotrienes--potent pro-inflammatory mediators they can by responsible for nasal blockade, rhinorrhoea and hyperresponsiveness. A role of prostaglandins (PGs) and leukotrienes (LTs) in the pathogenesis of nasal polyps has been recently suggested and leukotriene levels have been shown to be elevated in patients with asthma as well as in those with sinonasal polyposis and sinusitis. Because leukotriene receptor antagonists inhibit activity of endogenous leukotrienes and decrease tissue eosinophilia it is speculated that these drugs may be useful also in the management of nasal polyps. Our study was designed to determine the efficacy of zafirlukast, a cysteinyl leukotriene receptor antagonist, in nasal polyposis. We conclude that antileukotrienes might play a role in controlling polyposis and their symptoms, and they might be a alternative to long-term steroid therapy and repeated surgical therapy.

Correct diagnosis in patients with side effect during benzylpenicillin (penicillin G) treatment is highly problematic. It is accepted, that hypersensitivity to penicillin is overdiagnosed. Very little qualitative information is available on the diagnostic and differentiation of penicillin allergy. On present stage it is not techniques permitting to exclude anaphylaxis. This paper describe topical knowledge about risks administration of benzylpenicillin to patients suspected of penicillin hypersensitivity. Precious advice in diagnostic procedures and therapeutic management was given.

In 1959 Hoigne described the first cases of pseudo-anaphylactic reactions induced by intramuscular administration of procaine penicillin G. This complication, characterized by acute psychological and neurological manifestations, is still of current interest. We report cases of patient, whose Hoigne syndrome was not due to procaine penicillin G (i.e. lidocaine, edan, azlocillin, gentamycin, klaritromycin and cefuroxime). It is accepted that Hoigne syndrome can be caused by lidocaine. Further Stell i.m. and Ojo OA published similar case report of Amoxycillin-induced hallucinations. These clinical observations indicate also that using term "acute non-allergic reaction to procaine penicillin G" as synonym of Hoigne syndrome is not precise. Further classification of the reaction among psychic disturbances or adverse drug reactions is very difficult. Much of literature is devoted to the differentiation from anaphylaxis rather than other symptoms of main disease or side effects. Harmful effect of main disease is very likely. Lidocaine was taken intravenously by patient with diabetes and heart attack or locally with chronic hepatitis during topical anesthesia. Benzylpenicillin, azlocycillin, gentamycin, klaritromycin and cefuroxime was used during serious bacterial infections. These observations indicate that pathogenesis of Hoigne syndrome may be associated with main disease and organic brain disease. Then procaine kindling mechanism partly explain Hoigne syndrome. Therefore pathogenesis, definition, differentiation and classification of this complication is still unclear.

The work presents current view about toxic effects of platinum anticancer drugs. In the first part, the toxic effects of cisplatin as nephrotoxicity, ototoxicity, myelosuppression, anaphylactic-like reactions, neurotoxicity and gastrotoxicity are presented. The second part describes mechanisms of nephrotoxicity of cisplatin. In the third part, the toxicity of carboplatin and iproplatin are reviewed.

A case of anaphylactic shock which appeared in a nurse working at surgery room for many years, was described. The nurse was examined due to the anaphylactic attack at work (paroxysmal, idiopathic anaphylaxis). Among many factors the first of all occupational ones (exposure to disinfectants, latex and penicillin) were taken into consideration. Two minutes after the intradermal application of 2 units of crystalline penicillin the symptoms of anaphylaxis (including the shock) occurred. The problems of penicillin allergy in the aspect of skin tests, which make use of this antibiotic, were also described in the paper.

L-asparaginase is widely used in the treatment of acute lymphoblastic leukemia in children and adults. Use of L-aspa E. Coli as well as Erwinase is not possible in all cases because of the side effects, mainly allergic reactions and disfunction of pancreas. Recently, the new form of the enzyme PEG-L-asparaginase was introduced. Binding L-asparaginase E. coli to polyethylene glycol a decreased its toxicity, extended its plasma half-live, not significantly affecting the efficacy. The aim of the study was to examine the results of PEG-L-asparaginase administration in five children with acute lymphoblastic leukemia, and the symptoms of intolerance to L-aspa E. Coli or Erwinase. There were three children with newly diagnosed ALL and two children with first relapse of ALL, treated according to New York Protocol and BFM-90 Protocol for ALL relapses respectively. PEG-L-asparaginase (Oncaspar) was administered in the dose of 2500 IU/m2. According to the protocol four children received 11 courses of treatment with the full dose of the drug. The number of doses for individual patient varied from one to six. The short-lived nettlerash was observed in one patient during two subsequent infusions of the drug. Hydrocortisone and antihistamine drugs were administered. Treatment with PEG-asparaginase was discontinued in one child, who developed dyspnea, nausea, vomiting and face rash during the third dose of the drug. Oncaspar is the valuable drug, which enabled continuation of treatment according to protocol in four out of five children with bad tolerance to routinely used L-asparaginase preparations.

Incidence and causes of allergy to merthiolate (thimerosal) was studied in 685 patients, examined in the Nofer Institute of Occupational Medicine, during the period from 1 September 1993 to 15 October 1995. Allergy to thimerosal was diagnosed in 39 persons (5.7%) including 25 (6.3%) females and 14 (4.9%) males. Health service workers predominated among those sensitized (13.8% of all medical personnel examined during that period). In 19 persons only allergy to mercury was observed. Among them 7 showed no skin changes, 6 manifested symptoms of hand dermatitis, in 4 patients atopic dermatitis and in 2 dermatitis diseminata were diagnosed. Two patients suffered from allergic rhinitis. It was found that the general vaccination of health service workers against viral hepatitis as well as immunotherapy with pollen preparations containing thimerosal (Catalet, Biomed, Poland) were the main causes of allergy to mertiolate. Allergy to thiosalicyclic acid was not observed and two persons reacted positively to mercuric chloride.

Allergic reactions to insulin have been noted within a few years following the completion of therapy. Allergy to insulin may be manifested by discrete local skin reactions (the majority of diabetics) or generalized reaction (rarely). Allergy to insulin may be produced by: immunogenicity of the commercial animal insulin preparations, low purity of insulins, different pattern of therapy with insulin, and genetic factors. The treatment of allergy to insulin consists of a proper injection technique and optimum choice of insulin preparation. In case of generalized allergic reactions desensitization is a therapy of choice. Antihistamine agents and corticosteroids may be helpful in some cases.

In the paper clinical characteristics of patients with aspirin-induced urticaria were performed. The group of 71 patients, 49 women (69%) and 22 men (31%), mean age of sensitivity symptoms demonstration--32.5 years, underwent allergological, laryngological and histamine dihydrochloride inhalatory tests. Nasal polyps were found in 2 persons (2.8%), atopic diseases in 23 persons (32.3%) and at least one feature of atopy in 37 persons (51.9%). 49 subjects (69%) suffered from urticaria which was not associated with ingestion of aspirin. In 22 patients urticaria developed solely due to aspirin. Urticaria not associated with aspirin had been presents for 2 weeks to 30 years before the onset of sensitivity to aspirin. The authors conclude that aspirin-sensitive urticaria results from concomitance of two different phenomena in one person, i.e. sensitivity to aspirin and urticaria not associated with ingestion of the drug.

Allergic reactions of dramatic intensity were observed in 5 children treated with Teniposide (VM-26) for acute lymphoblastic leukaemia and histiocytosis X. In the further treatment this drug was replaced with epoxide, a cytostatic agent which is also a podophyllin derivative but in other chemical formulation. In none of these patients the allergic reaction returned.

The release of gentamycin sulfate from different ointment basis was studied. Contact hypersensitivity was determined in clinical studies.

The case of 52-year old patient was presented who developed urticaria and strong anginal pain after intravenous administration of uropoline. On the basis of typical clinical picture, electrocardiographical and biochemical changes acute myocardial infarction was recognised. It is thought to have developed as the consequence of anaphylactic reaction following intravenous administration of x-rays contrast substance.

Guinea pigs sensitized with DNCB, K2Cr2O7, epidian 5, hardener Z1 and dye B, in which epidermal tests confirmed sensitization, exhibited, 24 hours after the test termination, increased agglutination of neutrophils. In the blood of animals sensitized with dye B using the Polak and Türk, as well as Magnusson and Kligman techniques, percentage indices of agglutination, whether spontaneous or induced by adding 25 micrograms of the allergen, were 2,40 and 8,90 for DNCB, 6,72 and 13.30 for K2Cr2O7, 7.61 and 12.59 for epidian 5, 8.69 and 11.63 for hardener Z1, 1.38 and 2.15 and 2.17 and 3.21 for dye B. The average (from 6 control groups) number of neutrophils, both those self-agglutinated and those induced by allergen, was 2.54 and 3.24, respectively. No increase in neutrophils agglutination in guinea pigs sensitized with the Alekseeva and Sumska technique-exhibiting no allergy--was found. The results point to the usability of determinations of neutrophils agglutination in blood as an auxiliary index confirming sensitivity to a given allergen.

The aim of the present paper is to inform Polish occupational physicians about a new medical discipline called immunotoxicology which developed during last decades. The importance of immunotoxicology resides in the fact that examinations performed on its basis make it possible to understand some toxic mechanisms which could not have been explained so far studying biochemical disorders. Immunotoxicology is regarded as an extension of toxicology. According to the principles of immunology, organism's reactions to xenobiotics action depends on the mechanisms regulating immunological system, i.e. on its activity or suppression. Considering the present scientific achievements, it can be said that both these states are related to disregulation of homeostatic mechanisms. Owing to the informative nature of this paper, many examples of immunological reactions were adopted from the relatively rich world literature. Readers who are interested in more comprehensive information may refer to source literature.