Anaphylactic shock caused by impurities in orgotein preparations

Previously reported allergic reactions to orgotein (superoxide dismutase) injections has assigned responsibility to this molecule, which is obtained from bovine liver. We report an anaphylactic shock probably caused by impurities contained in an orgotein preparation. Prick test to Peroxinorm¿ (orgotein), BSA, and cow liver extract were positive but resulted negative with chymotrypsin, milk, meat and cow epithelium extracts. Tryptase levels determined 3, 24 hours and 15 days after the shock measured 6.32, 0.81 and 0.84 U/L respectively. Detection of specific IgE to Peroxinorm¿, BSA and chymotrypsin by ELISA was negative and positive to cow liver. Specific IgE to milk and cow epithelium by Pharmacia CAP system was negative. Immunoblotting with Peroxinorm¿ revealed IgE specific bands at an apparent M.W of 67, 51, 56 and 16 kDa; immunoblotting with cow liver revealed bands at 72, 56, 50 and 36 kDa; immunoblotting with BSA and chymotypsin were negative. This case emphasises the role that 20 % of impurities of the pharmaceutical preparation may have in immediate hypersensitivity reactions (AU)

Hasta la fecha, las reacciones alérgicas por infiltraciones de orgoteína (superóxido dismutasa) se han atribuido a esta molécula, que es obtenida del hígado de vaca. Presentamos un choque anafiláctico que fue causado probablemente por impurezas presentes en un preparado de orgoteína. Las pruebas de prick con Peroxinorm (orgoteína), BSA e hígado de vaca resultaron positivas, pero fueron negativas con quimiotripsina y con extractos de leche, carne y epitelio de vaca. Los niveles de triptasa medidos a las 3, 24 horas y 15 días después de la anafilaxia fueron de 6,32, 0,81 y 0,84 U/L, respectivamente. Mediante ELISA no se detectó IgE específica para Peroxinorm , BSA ni quimiotripsina, pero el resultado fue positivo para hígado de vaca. La detección de IgE específica para leche y epitelio de vaca fue negativa mediante sistema CAP de Pharmacia. El immunoblotting con Peroxinorm mostró bandas de IgE específica en los P.M aparentes de 67, 51, 56 y 16 kDa; el immunoblotting con hígado de vaca mostró bandas en 72, 56, 50 y 36 kDa; los immunoblotting con BSA y quimiotripsina resultaron negativos. En este caso se destaca el papel que pueden tener el 20 por ciento de impurezas de este preparado en las reacciones de hipersensibilidad inmediata. (AU)

Anisakis simplex-sensitized patients: should fish be excluded from their diet?

BACKGROUND: Anisakis simplex (A.s.) allergy is an emerging disease. The third-stage larvae of this nematode are a source of hidden allergens in fish. There are no clear guidelines concerning dietary restrictions for patients with serum-specific IgE to this parasite. OBJECTIVE: To follow up the clinical data and immunological parameters of patients sensitized to A.s. during 6 to 23 months. METHODS: The clinical symptoms and serologic status of 17 patients with specific IgE and positive skin prick test results to A.s. were studied prospectively. Six of these had anaphylaxis (ANA) attributed to A.s. and 11 patients experienced concomitant chronic urticaria (CU). All patients were advised not to eat fish for 6 months. RESULTS: Four patients from the ANA group excluded fish, and ANA did not recur. Two other patients with ANA refused to exclude fish; one remained free of symptoms and the other experienced several urticarial episodes. During this 6-month period total IgE levels decreased in all six ANA patients; specific IgE for A.s. decreased in four patients and increased in two. Two patients from the CU group did not exclude fish, and symptoms persisted in these two patients. Clinical improvement was observed in 78% of the patients with CU who excluded fish. Total and specific IgE levels decreased in all the patients with CU. CONCLUSIONS: Because ANA symptoms are very severe, patients should always be advised to exclude fish until specific food allergens are identified. However, in patients with CU and specific IgE to A.s., only the clinical response to fish ingestion will determine the need for strict fish avoidance.

Anaphylactic shock caused by impurities in orgotein preparations.

Previously reported allergic reactions to orgotein (superoxide dismutase) injections has assigned responsibility to this molecule, which is obtained from bovine liver. We report an anaphylactic shock probably caused by impurities contained in an orgotein preparation. Prick test to Peroxinorm (orgotein), BSA, and cow liver extract were positive but resulted negative with chymotrypsin, milk, meat and cow epithelium extracts. Tryptase levels determined 3, 24 hours and 15 days after the shock measured 6.32, 0.81 and 0.84 U/L respectively. Detection of specific IgE to Peroxinorm, BSA and chymotrypsin by ELISA was negative and positive to cow liver. Specific IgE to milk and cow epithelium by Pharmacia CAP system was negative. Immunoblotting with Peroxinorm revealed IgE specific bands at an apparent M.W of 67, 51, 56 and 16 kDa; immunoblotting with cow liver revealed bands at 72, 56, 50 and 36 kDa; immunoblotting with BSA and chymotypsin were negative. This case emphasises the role that 20 % of impurities of the pharmaceutical preparation may have in immediate hypersensitivity reactions.

Alveolitis alérgica extrínseca por exposición a un humidificador ultrasónico / Extrinsic allergic alveolitis due to exposure to an ultrasound humidifier

La alveolitis alérgica extrínseca es una entidad con frecuencia de origen ocupacional, que afecta al parénquima pulmonar y progresa hacia fibrosis en estadios avanzados si no se diagnostica de forma precoz. Requiere para su diagnóstico una anamnesis detallada en la búsqueda del agente etiológico. Se ha estudiado a un paciente con cuadros repetidos de infiltrados pulmonares que simulaban neumonías y se trataban con antibióticos. El diagnóstico, tras realizar un detallado estudio, fue el de alveolitis alérgica extrínseca desencadenada por un antígeno de origen no ocupacional debido a los contaminantes probablemente fúngicos de un humidificador ultrasónico en el domicilio del paciente, utilizado para el tratamiento de cuadros de bronquiolitis de repetición de su hijo. Se objetivó infiltración bibasal en la tomografía computadorizada, restricción acusada en la espirometría y anticuerpos precipitantes contra los restos del humidificador; el paciente realizó una provocación involuntaria con exposición al humidificador en su domicilio tras ser dado de alta del último episodio. En el cultivo realizado con los residuos del humidificador crecieron varios hongos: Candida albicans, Aspergillus fumigatus y Rhodotorula rubra. Se obtuvo anticuerpos precipitantes frente a C. albicans. En el ELISA inhibición la IgG específica frente a componentes del humidificador se inhibió el 10 por ciento por C. albicans y no se obtuvo inhibición por R. rubra. Dada la ubicuidad de C. albicans y su escasa participación en los anticuerpos contra los contaminantes del humidificador, no puede confirmarse como agente etiológico. El paciente quedó totalmente asintomático al retirar el aparato de su domicilio. (AU)

Fluorescein-induced allergic reaction.

BACKGROUND: Adverse reactions following intravenous sodium fluorescein are very unusual and their mechanism is still uncertain. We report the case of a patient who suffered an adverse reaction during a fluorescein ocular angiography. Positive allergy tests to fluorescein suggest an IgE-mediated mechanism. OBJECTIVE: Report the allergy evaluation performed in a patient who suffered an adverse reaction during an intravenous fluorescein administration. METHODS: We selected the case of a patient who suffered dizziness, diaphoresis, generalized pallor, nausea, sphincter relaxation, hypotension, and intense malaise during a fluorescein ocular angiography and compared the results to other nonreactive subjects. Allergy evaluation: Prick and intradermal skin tests and serial determinations of serum tryptase were performed on the patient and four control subjects who underwent and tolerated the same procedure as well as on a patient who developed an intense vagal reaction during blood extraction. RESULTS: Positive skin tests and dramatic increase of serum tryptase (67U/I) were observed in our patient. The rest of the patients had negative skin tests and did not have any variation in their serum tryptase. CONCLUSIONS: An IgE-mediated mechanism is suggested as responsible for this adverse reaction. We recommend that a complete allergy evaluation should be performed in all patients who have adverse reactions to fluorescein in order to differentiate true allergic reactions from other types of reactions.

Serum tryptase levels in adverse drug reactions.

We evaluated the usefulness of individual tryptase levels and variations after adverse drug reactions in 64 patients. Our aim was to find a tool for the diagnosis of drug allergy. Thirty-seven subjects were confirmed to have drug allergy, 12 had nonsteroidal anti-inflammatory drug (NSAID) reactions, five had negative controlled drug challenges (NAAR), and 10 had symptoms after placebo intake (PLA). Serum tryptase levels greatly increased after anaphylactic shocks (2242%) and anaphylaxis (710.5%). Patients with allergic urticaria and those with idiosyncratic responses to acetylsalicylic acid (ASA) exhibited a small increase in serum tryptase (49.5% and 38.2%, respectively). In the other two groups (NAAR and PLA), no variation in this serum protease was observed. The time of appearance of the serum tryptase peak differed considerably among patients with similar clinical reactions (from 30 min to 6 h) and was independent of the latent period, severity of symptoms, or the amount of tryptase released. We conclude that serum tryptase determinations are helpful in the diagnosis of anaphylactic shock and anaphylaxis, but serial measurements may be needed to confirm mast-cell participation in milder reactions.

Cross-sensitivity among oxicams in piroxicam-caused fixed drug eruption: two case reports.

Fixed drug eruption (FDE) caused by oxicams is very rare. There are few reports of FDE induced by piroxicam, and this explains why cross-sensitivity among oxicams (piroxicam, tenoxicam, and droxicam) has been studied in only one patient. The patch test on residual lesions has lately been used by some authors in FDE diagnosis with variable results. We describe two cases of piroxicam-caused FDE and demonstrate cross-sensitivity among piroxicam, tenoxicam, and droxicam in both of them. One patient had residual lesions and the patch test was useful for diagnosis and cross-sensitization studies. The second patient had no residual lesions, and the patch test was negative on normal but previously affected skin; therefore, the study was performed by single-blind controlled oral challenge.