Showing papers on "Hypersensitivity reaction published in 1988"

Anticonvulsant hypersensitivity syndrome. In vitro assessment of risk.

Abstract: Arene oxide metabolites of aromatic anticonvulsants (phenytoin, phenobarbital, and carbamazepine) may be involved in the pathogenesis of hypersensitivity reactions. We investigated 53 patients with clinical sensitivity to anticonvulsants by exposing their lymphocytes in vitro to drug metabolites generated by a murine hepatic microsomal system. The diagnosis of a hypersensitivity reaction was corroborated by in vitro rechallenge for each drug (phenytoin, n = 34; phenobarbital, n = 22; carbamazepine, n = 25) when cytotoxicity (% dead cells) exceeded 3 SD above the mean result for controls. Cross-reactivity among the drugs was noted. 7 out of 10 patients who had received all three anticonvulsants had adverse reactions to each. 40 out of 50 patients tested to all three drugs in vitro were positive to each. Adverse reactions were indistinguishable among anti-convulsants. Skin rash (87%), fever (94%), hepatitis (51%), and hematologic abnormalities (51%) were common clinical features of each drug. 62% of reactions involved more than two organs. Cells from patients' parents exhibited in vitro toxicity that was intermediate between values for controls and patients. In vitro testing can help diagnose hypersensitivity to anticonvulsants. Cells from patients may also be used for prospective individualization of therapy to decrease risk of adverse reaction. Cross-reactivity among the major anticonvulsants is common and should be considered before deciding on alternative therapy.

The alveolitis of hypersensitivity pneumonitis

Abstract: In the pathogenesis of hypersensitivity pneumonitis (HP) several immune mechanisms are involved. The initial phase, 4-48 h after antigen inhalation, appears to be immune complex mediated and is characterized by an early increase in bronchoalveolar lavage (BAL) neutrophils and the histopathologic features of oedema, neutrophil infiltration of the alveolar wall, and vasculitis. After 12 h to several days, the immune response possibly shifts to a cell-mediated reaction, and the alveolitis consists of cytotoxic effector cells as well as suppressor cells which may be required to modulate the B cell response of antibody production by plasma cells. In this phase, lymphocytes of the OKT8 positive phenotype, natural killer cells, and occasionally a few plasma cells are increased in BAL fluid. The characteristic histopathologic finding is a mononuclear infiltrate consisting of lymphocytes, plasma cells, and foamy histiocytes. After weeks to months, a delayed type hypersensitivity reaction may lead to a slight predominance of OKT4 positive cells in BAL fluid and to granuloma formation. Finally, after months to years, repeated immune-mediated injury to the alveolar wall with release of proteolytic enzymes and fibroblast growth factors may result in pulmonary fibrosis and end stage lung with concomitant increase in BAL neutrophils as in other fibrotic diseases.

In Vitro Assessment of Risk

Abstract: Arene oxide metabolites of aromatic anticonvulsants (phenytoin, phenobarbital, and carbamazepine) may be involved in the pathogenesis of hypersensitivity reactions. We investigated 53 patients with clinical sensitivity to anticonvulsants by exposing their lymphocytes in vitro to drug metabolites generated by a murine hepatic microsomal system. The diagnosis of a hypersensitivity reaction was corroborated by in vitro rechallenge for each drug (phenytoin, n = 34; phenobarbital, n = 22; carbamazepine, n = 25) when cytotoxicity (% dead cells) exceeded 3 SD above the mean result for controls. Cross-reactivity among the drugs was noted. 7 out of 10 patients who had received all three anticonvulsants had adverse reactions to each. 40 out of 50 patients tested to all three drugs in vitro were positive to each. Adverse reactions were indistinguishable among anticonvulsants. Skin rash (87%), fever (94%), hepatitis (51%), and hematologic abnormalities (51%) were common clinical features of each drug. 62% of reactions involved more than two organs. Cells from patients' parents exhibited in vitro toxicity that was intermediate between values for controls and patients. In vitro testing can help diagnose hypersensitivity to anticonvulsants. Cells from patients may also be used for prospective individualization of therapy to decrease risk of adverse reaction. Cross-reactivity among the major anticonvulsants is common and should be considered before deciding on alternative therapy.

Severe hypersensitivity reaction upon rechallenge with trimethoprim-sulfamethoxazole in a patient with AIDS.

Abstract: A patient with acquired immunodeficiency syndrome (AIDS) developed rash, fever, neutropenia, and elevated liver function tests during an initial course of trimethoprim-sulfamethoxazole (TMP-SMX) therapy Upon reexposure to the drug, the patient experienced a severe anaphylactoid reaction associated with pulmonary edema and rhabdomyolysis Reactions associated with TMP-SMX rechallenge in this patient population have been previously reported but have not been associated with this degree of severity TMP-SMX therapy should be instituted with extreme caution in patients with AIDS who have demonstrated a prior hypersensitivity reaction to the drug

The laboratory evaluation of IgE antibody to metabisulfites in patients skin test positive to metabisulfites

Abstract: An immediate-type hypersensitivity reaction has been proposed as one possible mechanism in which metabisulfites (MBSs) cause reactions. As demonstrated with certain occupational chemicals, we proposed that MBS might conjugate with human proteins, such as human serum albumin, and then cause an immunologic response. Because we had identified no reactions to MBS at the Northwestern Allergy Service, we used sera from four patients reported elsewhere as having positive skin tests and positive oral challenges to sulfites. We attempted to demonstrate, both in vitro by ELISA and in vivo by passive cutaneous transfer to monkey, evidence for IgE-mediated hypersensitivity to MBSs. Our results demonstrated that there is evidence of IgE antibody by passive transfer for one patient studied, but no evidence of IgE antibody by ELISA to an MBS-albumin conjugate in any of the four patients. This study illustrates the complexities involved in the evaluation and mechanism of MBS-induced disease and the caution with which results must be interpreted.

Carbamazepine-Induced Severe Systemic Hypersensitivity Reaction with Eosinophilia

Abstract: Skin rash, fever, and eosinophilia developed in a previously healthy 35-year-old woman three weeks after starting carbamazepine. Fulminant respiratory and renal failure ensued. Autopsy showed pneumonitis, nephritis, serositis, pancreatitis, hepatitis, and carditis, characterized by an infiltrate of eosinophils and lymphocytes. The severity, duration, and extensive organ involvement of the reaction make this case unique.

Fever and Septicemia

Abstract: Fever is the hallmark of infection but is not specific for it. Infection can begin and progress in the absence of fever. When fever occurs in the immunocompromised host, the single major challenge in clinical decision making is to ascertain whether the onset of temperature elevation is a reliable indication of the onset of infection rather than a manifestation of the underlying disease, a hypersensitivity reaction, or a factitious development. Another major issue that frequently stirs acrimonious bedside debate involves the clinical wisdom of suppressing fever with or without evidence of documented infection. Despite many decades of controversy, it has not been conclusively established whether fever is “good” for the patient or just adds to patient discomfort without benefitting host defenses against infection or the underlying disease.

Hypersensitivity reaction with intravenous GnRH after pulsatile subcutaneous GnRH treatment in male hypogonadotrophic hypogonadism.

Abstract: Chronic pulsatile subcutaneous administration of low doses of gonadotrophin releasing hormone (GnRH) is an effective therapy for men with hypogonadotrophic hypogonadism. Hypersensitivity reactions to GnRH are rare. We wish to report hypersensitivity reactions with intravenous GnRH after low dose subcutaneous pulsatile GnRH treatment in two men with hypogonadotrophic hypogonadism due to suprasellar disease.

Role of cytokines in the restoration of the delayed-type hypersensitivity reaction of anergic patients.

Abstract: Soluble mediators from peripheral blood lymphocytes activated either by skin test antigens or by alloantigens restored the delayed type hypersensitivity (DTH) reaction in the majority of anergic surgical patients who are at increased risk for sepsis and mortality. Antigen had to be injected together with the mediators and the individual had to be reactive to the antigen for restoration. These results suggest that restoration of the DTH response depends on the ability of cytokines produced and acting in a non-specific manner to promote the response of the anergic patients' specific antigen-sensitive cells to antigen.

Enzyme-linked Immunossays for Detection of Anti-drug Antibodies

Abstract: Adverse reactions to drugs constitute a serious problem in clinical practice, with respect to both their unpredictability and their sometimes life-threatening consequences. A large proportion of adverse drug reactions (estimates range from 10–50%) are labelled as ‘allergic’ or ‘hypersensitivity’ reactions, with the implication that the reaction is mediated by a specific immune response directed against the drug. Such classification of adverse reactions is based largely on symptoms alone, which may include skin rashes, fever, taste disturbance, and occasionally more serious disorders such as anaphylaxis, kidney dysfunction and cytopenias, all of which certainly can be caused by hypersensitivity reactions. For example, anaphylactic reactions and skin inflammation can be caused by cross-linking of cell-bound IgE by antigen, leading to release of histamine and other mast-cell-dependent chemical mediators (type I hypersensitivity); blood cells can be destroyed by antibody-dependent cytotoxic reactions (type II); inflammatory reactions and kidney dysfunction can be caused by immune complex deposition (type III); and inflammatory tissue reactions can also be T-cell-mediated (type IV). However, although certain symptoms may point to an immune aetiology, an adverse drug reaction can only be classified with certainty as a ‘hypersensitivity reaction’ or ‘drug allergy’ when drug-specific antibodies or sensitized T cells can be demonstrated. Even so, convincing evidence that an adverse reaction is immunologically mediated will only be obtained when the severity of the reaction is shown to relate to levels of circulating or tissue antibody or sensitized T cells. Hence, diagnosis of drug hypersensitivity depends on the development and correct use of appropriate laboratory tests for humoral and cellular indices of specific immune responses. Only when these immunological parameters are monitored in a quantitative manner will it be possible to relate drug dosage, distribution, disposition and metabolism to the induction of hypersensitivity.

Poppy seed allergy

Abstract: A patient with an immediate type hypersensitivity reaction against poppy seed is reported. Clinical symptoms consisted of swelling of the oral mucosa, vomiting, respiratory distress, and urticaria. Specific IgE antibodies were demonstrable by RAST.

Methyldopa hypersensitivity can mimic acute toxic enterocolitis.

Abstract: The most widely known hypersensitivity reaction of methyldopa, a drug commonly used in the treatment of hypertension, is seroconversion to a positive result of a direct Coombs' test that may lead to a hemolytic anemia. The authors report a case of an infrequently noted, but serious, hypersensitivity reaction to methyldopa, manifesting primarily as acute toxic enterocolitis. A 63-year-old woman was admitted to hospital and underwent aggressive and prolonged investigation of enterocolitis. Withdrawal of methyldopa gave immediate relief of intestinal problems. Rechallenge precipitated a return of symptoms within 14 hours. It is recommended that periodic blood counts and liver function tests be done on patients treated with methyldopa for hypertension. If any abnormalities are noted the drug should be discontinued.

Hypersensitivity reaction after barium meal examination

Abstract: Hypersensitivity reactions can occur after the administration of barium products and all caused by one of the many additives. These reactions are extremely unusual. Authors report on a patient who developed urticaria shortly after a conventional barium examination.

The granulocyte factor abrogates the alloantigen-induced delayed type hypersensitivity suppression in mice.

Abstract: Adherent granulocytes secrete granulocyte factor (GF) in the course of the first 60 min of adherence. GF abolishes suppressor cell generation in mice induced by intravenous injection of irradiated allogeneic lymphoid cells. The effect of such induced suppressors was measured in delayed type hypersensitivity reaction induced by subcutaneously injected irradiated allogeneic spleen cells and evaluated in the foodpad test. Suppressor cell induction or GF treatment had no effect on antigen- or phytohaemagglutinin-induced production of migration inhibitory factor.