Showing papers on "Hypersensitivity reaction published in 1994"

Demonstration of Delayed Hypersensitivity in Chlamydia trachomatis Salpingitis in Monkeys: A Pathogenic Mechanism of Tubal Damage

Abstract: The role of delayed hypersensitivity in the pathogenesis of Chlamydia t trachomatis salpingitis was studied in the monkey "pocket" model. Pigtailed monkeys (Macaca nemestrina) were sensitized by inoculation of live C. trachomatis organisms (E/UW-5/Cx) into subcutaneous pockets containing salpingeal autotransplants. At 21 days, affinity-purified recombinant C. trachomatis heat-shock protein (rhsp60) was injected into pockets either previously sensitized with C. trachomatis or not sensitized in the same monkey. Delayed-type hypersensitivity reaction was observed, characterized by mononuclear cell infiltration with peak reaction at 48 h. Injection of rhsp60 into the pockets of a naive animal did not induce inflammation. This study showed that C. trachomatis infection in monkeys induced delayed hypersensitivity, which is mediated by hsp60. Histologic findings of the salpinx were consistent with delayed hypersensitivity reaction observed in ocular C. trachomatis infection, further suggesting a similar pathogenesis for both salpingitis and trachoma.

Polyvalent Melanoma Cell Vaccine Induces Delayed-Type Hypersensitivity and in Vitro Cellular Immune Response

Abstract: Patients with melanoma metastatic to distant sites or at high risk for recurrent melanoma have been treated with a polyvalent melanoma cell vaccine (MCV) in phase II protocols. We assessed in vivo and in vitro cell-mediated responses to MCV in 163 patients who had undergone surgical resection of American Joint Committee on Cancer stage III melanoma. During the first 4 months of vaccine immunotherapy, 135 patients (83%) responded by developing a positive delayed-type hypersensitivity reaction ≥6 mm to MCV. In a mixed lymphocyte tumor cell reaction using peripheral blood lymphocytes, 35 of 42 patients (83%) showed a recall proliferative response to one or more of the three cell lines of MCV. There was a significant correlation between delayed-type hypersensitivity reaction and mixed lymphocyte tumor cell reaction (P = 0.013). After 4 months of MCV therapy, 8 of 11 patients had an increased mixed lymphocyte tumor cell reaction to autologous melanoma cells. During the first 4 months of vaccine therapy, 16 of 33 patients developed more than a 50% increase in cytotoxic T-cell activity against one of the cell lines of MCV. Overall survival was significantly prolonged in patients with a positive delayed-type hypersensitivity reaction (P = 0.0054) and/or increased cytotoxic T-cell activity (P = 0.02). These findings suggest that MCV induces specific T-cell responses which are correlated with clinical course; the data also suggest that some of these responses are directed against autologous melanomas and may play a major role in controlling the progression of melanoma.

Eosinophilic pustular follicular reaction: a paradigm of immune dysregulation

Abstract: Background. We encountered 10 patients whose biopsies showed an eosinophilic pustular follicular reaction, a histomorphology alleged to be pathognomonic of eosinophilic folliculitis (EF). Only seven of these patients fell within the clinical spectrum of EF. Seven patients had conditions associated with immune dysfunction, including three patients with an atopic history. Potential antigenic stimuli could be elicited in six cases. Methods. Formalin-fixed biopsy specimens from all 10 patients were available for examination. Hematoxylin and eosin-, alcian blue-periodic acid-Schiff (PAS)- and PAS-diastase-stained sections cut from paraffin-embedded tissue were examined by light microscopy. Immunoperoxidase preparations with antibody to IgE were performed on paraffin sections and the number of IgE-decorated cells quantitated in each case. Four patients also had biopsy material submitted in Michel's medium, on which direct immunofluorescent studies were conducted. Results. IgE-coated mononuclear cells were present in patients whose lesions would logically be expected to derive from dominant type I hypersensitivity mechanisms and absent or minimal in biopsies from those patients in whom the pathogenetic basis of lesions derived principally from cell-mediated immunity. Conclusions. The eosinophilic pustular follicular reaction, while characteristic of EF, is not exclusive to that entity. It represents an expression of an excessive immediate or delayed-type hypersensitivity reaction to various auto-, epicutaneous, or ingested stimuli. A background of immune dysregulation may be contributory.

Woringer-Kolopp disease. A lymphomatoid hypersensitivity reaction.

Abstract: We report two cases of unilesional pagetoid reticulosis (Woringer-Kolopp disease). Histopathological, immunohistological, ultrastructural, and genotypic studies showed both lesions to be lymphomatoid hypersensitivity reactions, as characterized by polyclonal proliferations of T-lymphocytes; CD8+ T cytotoxic-suppressor (Tc/s) lymphocytes were predominant in one case, whereas CD4+ T helper (Th) lymphocytes were predominant in the other. The nosology of Woringer-Kolopp disease is discussed.

Systemic reactions to immunotherapy: the American Academy of Otolaryngic Allergy morbidity and mortality survey.

Abstract: Anaphylaxis may be defined as a systemic, immunoglobulin E-mediated (Gell-Coombs type I) hypersensitivity reaction triggered by exposure to an antigen in a previously sensitized patient. Anaphylaxis may occur in a variety of circumstances; however, when it occurs as the result of immunotherapy, it is of great concern to the practicing allergist. When describing or reporting anaphylaxis relating to immunotherapy, most allergists speak in terms of the types of reactions, local vs. systemic. Germane to this discussion is the use of the term systemic reaction, which can mean anything from mild allergy symptoms resulting from an allergy injection to bradycardia and hypotension (shock). In this article we report serious or significant systemic reactions, which are characterized by any of the following symptoms: urticaria, sneezing or nasal obstruction, throat tightness or congestion, wheezing, and shock (bradycardia or hypotension). There were no fatalities reported from the survey group. The overall reaction rate was 0.3%.

Immediate hypersensitivity reaction to cyclophosphamide

Abstract: We report a case of an acute anaphylactic reaction to intravenous cyclophosphamide in a patient with systemic lupus erythematosus. Skin testing for reactivity to cyclophosphamide and one of its metabolites, 4-hydroperoxycyclophosphamide, was performed on the patient and on 6 controls. The patient exhibited positive skin test responses; all controls had negative responses. The results suggest an acute hypersensitivity reaction related to sensitivity to cyclophosphamide and to 4-hydroperoxycyclophosphamide, through a shared antigenic determinant or dual sensitization.

Systemic hypersensitivity reaction to intravesical BCG.

Abstract: BCGosis is a recognised complication of intravesical BCG immunotherapy for superficial bladder carcinoma. We present here a case of granulomatous hepatitis, pneumonitis and probable pericarditis resulting from an hypersensitivity reaction to intravesical BCG.

Hypersensitivity to ketoconazole.

Abstract: We report a patient who experienced generalized urticaria and facial angioedema following oral administration of ketoconazole. Skin prick tests with ketoconazole and oral challenge were positive. Conjugates of ketoconazole with human serum albumin were used for the in vitro study, obtaining a positive result in the histamine release test. No significant levels of IgE antibodies to ketoconazole were found by RAST. Controls did not react to any of these tests. These results suggest that the patient developed a type I hypersensitivity reaction to ketoconazole. In this case, skin prick tests with ketoconazole and histamine release test with a conjugate of ketoconazole with human serum albumin were useful in ketoconazole hypersensitivity diagnosis. Finally, skin tests with other imidazole agents were carried out, including metronidazole, ornidazole, and fluconazole that were negative.

Dermal cellulitis--a hypersensitivity reaction from dobutamine hydrochloride.

Abstract: ration for colonoscopy. Gastroenterology 1982;82:435-7. 2. Ptachcinski RJ, Venkataramanan R, Burckart GJ. Clinical pharmacokinetics of cyclosporin. Clin Pharmacokinet 1986;II :I07-32. 3. Atkinson K, Biggs JC, Britton K, Short R, Mrongovius R, Concannon A, et aI. Oral administration of cyclosporin A for recipients of allogeneic marrow transplants: implications of clinical gut dysfunction. Br J Haemato/1984;56:223-31. 4. Burekart G, Starzl T, Williams L, Sanghvi A Jr, Venkataramanan R, ZiteUi B, et aI. Cyclosporin monitoring and pharmacokinetics in pediatric liver transplant patients. Transplant Proc 1985;17:1172-5. 5. Lindhola A, Henricsson S. Verapamil inhibits cyclosporin metabolism. Lancet 1987;1:1262-3.

Contact allergy reactions to Silodent impression material

Abstract: The silicon based impression materials are often used in dental practice Recently, we have observed two cases of contact allergic reaction after using Silodent (Ferrokemia) impression material Epicutaneous test has shown that the allergic reaction is provoked by the catalisator This hypersensitivity reaction is due to a previous sensibilization (eg previous impression taking or environmental hazards) No epicutaneous reaction to the other types of silicon based impression materials was found

Extrinsic Allergic Alveolitis

Abstract: The lung is the site of a variety of complex inflammatory reactions. In many instances the inflammation is a normal reaction against various infectious agents, such as bacteria and viruses, or is a response to necrotic tissue, such as infarcted lung parenchyma or degenerating tumor. In extrinsic allergic alveolitis, the inflammatory reaction characteristic of this condition is thought to represent a hypersensitivity process mediated by immunoglobulins, lymphokines, and immune effector cells. Although the four immunologic responses described by Gell and Coombs1 (Fig. 18-1) are often used in characterizing various inflammatory reactions in the lungs, the immunopathogenesis of extrinsic allergic alveolitis remains poorly understood. Extrinsic allergic alveolitis, also referred to as hypersensitivity pneumonitis or microgranulomatous hypersensitivity reaction, is a predominantly chronic inflammatory disease of the peripheral gas-exchanging portion of the lung resulting from sensitization and subsequent exposure to a variety of organic dusts. The condition was first described in 1932 in farmers exposed to moldy hay.2 Initially it was considered a mycotic process.3,4 Pepys and colleagues5,6 elucidated some of the initial immunologic mechanisms though to be operative in the disease. Williams7,8 demonstrated that the disease could be produced in sensitized farmers by the inhalation of extracts of moldy hay. Farmer’s lung disease was found to result from a hypersensitivity reaction against a species of thermophilic actinomyces, Thermoactinomyces vulgarus, that proliferated as the hay became overheated in the process of becoming moldy.9,10 Numerous organic antigens have now been recognized as causing hypersensitivity reactions in the lung, and these are usually named after the occupation in which the patient was exposed to the organic antigen. The term extrinsic allergic alveolitis was coined by Pepys11 to refer to the entire group of similar reactions to organic dusts.

Multisystem Hypersensitivity Reaction to Carbamazepine

Abstract: TO THE EDITOR: Transdermal nicotine (the nicotine patch) has been promoted as an aid in the treatment of tobacco addiction. It is generally safe, having minimal serious adverse effects except in patients with coronary artery disease. I This report of a postcraniotomy patient who developed a stroke shortly after applying a nicotine patch suggests that nicotine may precipitate cerebral vasospasm. A 40-year-old mansuddenly developed severe headache andsyncope. He was admined to a hospital with meningismus, butexhibited nootherneurologic abnormalities. Cranial computed tomography (CT)demonstrated blood in thesubarachnoidspace. Treatment withdexamethasone 16mg/dand nimodipine 360mg/d wasbegun. Cerebral angiography demonstrated spasm of theright middle cerebral artery andan aneurysm of the rightinternal carotid artery at itsjunction withthe posteriorcommunicating artery. Ninedays after admission thisaneurysm was clipped. Postoperatively thepatient developed leukocytosis (maximum leukocyte count46 x 1091L), but no feveror neurologic abnormalities. As thedexamethasonedosage wasdecreased, his leukocytosis resolved. Six daysafter surgery a cerebral arteriogram wasnormal exceptfor mild residual spasm of the right middlecerebral artery. Against hospital policyand the adviceof his physicians, the patient smoked cigarenes in thehospital before andaftersurgery. At the timeof discharge he requested a nicotine patch to helphimstopsmoking. Sevendaysaftersurgery and after17daysof nimodipine therapy, thepatient wasdischarged on cimetidine 800 mg/danddexamethasone 4 mg/d. Hewasgiven a prescription fornicotine patches.Nimodipine wasdiscontinued at thetimeof discharge. Theday afterdischarge the patient applied for thefirsttimea IO-mg nicotine patch. Hedenied cigarene smoking afterdischarge. About fourhours afterapplyingthepatch hedeveloped drowsiness, difficulty walking, anda leftfacial droop. He returned to the hospital. Examination showed normal bloodpressure, confusion,rightgazepreference, left homonymous hemianopia, left hemiparesis, and left-sided neglect. Leukocyte count,serumelectrolytes, and electrocardiogram werenormal. Cranial CT failed to demonstrate acutehemorrhage. Transcranial Doppler ultrasonography (TCD) demonstrated spasm of bothmiddle cerebral arteries,more prominent ontheright. These studies were consistent withtheclinical diagnosis ofa vasospastic infarct inthedistribution of theright middle cerebral artery. Largevolumes of NaCl0.9%and plasmaproteinfraction wereinfused. Nimodipine wasadministered andthedexamethasone dosage wasincreased. Thepatient'sneurologic abnormalities improved andhe wastransferred to a rehabilitation unit. Three months laterhewasableto return to parttime work with someleft arm weakness andcognitive deficits. Serious adverse effects associated with the nicotine patch have been few and limited almost entirely to patients with coronary artery disease. I This patient experienced a stroke shortly after applying a nicotine patch. TCD suggested that the stroke was caused by intracranial vasospasm. Delayed intracranial vasospasm may occur spontaneously after subarachnoid hemorrhage, typically 4-14 days after the initial event.' In this case, the close temporal relationship between the application of the patch and the onset of stroke suggests that the nicotine patch may have precipitated cerebral vasospasm. Though the vasospastic effects of nicotine are believed to be minimal.' caution is advised when prescribing transdermal nicotine in patients with vasospastic disorders such as Prinzmetal' s variant angina and Buerger's disease.' In contrast, no precaution is advised when the nicotine patch is used in patients with migraine headaches, a condition associated with intracranial vasospasm. As the underlying mechanism of cerebral vasospasm remains unknown, the possibility that nicotine may precipitate cerebral vasospasm in a susceptible individual should be considered. Diffuse cerebral vasospasm has been angiographically demonstrated in a patient with headaches who was using nicotine patches.\" In addition, nicotine also has procoagulant effects,' which could increase the risk of thrombosis. Nimodipine, a calcium-channel blocker that inhibits cerebral vasospasm,Z was administered during the patient's hospitalization and discontinued at the time of discharge. The discontinuation of nimodipine may have played a role in the patient's stroke, since he smoked throughout hospitalization (while taking nimodipine) without incident. Though he denied smoking after application of the patch, his history may not have been reliable. Smoking while wearing a patch provides higher peak concentrations of nicotine and increases the potential for adverse effects. Serious cardiac toxicity has been reported in patients who smoked while wearing the patch.I This case should alert clinicians to the fact that the detrimental health effects of smoking arecaused partly by the nicotine content, and thus, replacement of smoking with the use of the nicotine patch poses continued health risks.

Variants of secondary immune response in CBA and C57Bl/6 mice

Abstract: The manifestation of a secondary immune response to intraperitoneal and subcutaneous injection of sheep red cells in various doses was studied in CBA and C57Bl/6 mice. The parameters under study were the delayed-type hypersensitivity reaction and antibody production assessed from the levels of antibody-producing cells of classes M and G in the lymph node and spleen. The manifestation and correlations between delayed-type hypersensitivity and antibody production were found to depend on the route of antigen administration and its first immunizing dose, interval between the two immunizations, and genetic control of the immune response.