ABSTRACT
Thyroid antibodies are frequently observed in urticaria patients, but their roles in urticaria are not clearly elucidated. We investigated the role of serum specific IgE to thyroid peroxidase (TPO) in patients with aspirin intolerant acute urticaria (AIAU) and aspirin intolerant chronic urticaria (AICU). We recruited 59 AIAU and 96 AICU patients with 69 normal controls (NC). Serum specific IgE to TPO was measured by manual direct ELISA, and CD203c expressions on basophil with additions of TPO were measured to prove a direct role of TPO in effector cells. The prevalences of serum specific IgE to TPO were significantly higher in AIAU (15.2%) and AICU groups (7.5%) compared to NC (0%, P=0.018: P=0.013, respectively). Flow cytometry showed CD203c induction in a dose dependent manner with serial additions of TPO in some AIAU and AICU patients having high specific IgE to TPO. Our findings show that the prevalence of serum specific IgE to TPO was significantly higher in both AIAU and AICU patients than in NC. It is suggested that specific IgE to TPO play a pathogenic role in AIAU and AICU.
Subject(s)
Adult , Humans , Anti-Inflammatory Agents, Non-Steroidal/adverse effects , Aspirin/adverse effects , Autoantibodies/immunology , Basophils/drug effects , Immunoglobulin E/blood , Iodide Peroxidase/blood , Urticaria/chemically inducedABSTRACT
La tríada de la aspirina, caracterizada por intolerancia a la aspirina, asma bronquial y poliposis nasal, fue descrita inicialmente por Widal en 1922. La prevalencia de intolerancia a la aspirina en la población general es de aproximadamente 6 por ciento, pero estudios han revelado que hasta 78 por ciento de los pacientes con poliposis nasal padecen la triada. La presentación clínica consiste en un patrón característico evolutivo de la aparición de los síntomas, presentándose en primer lugar rinitis, luego poliposis nasal, asma bronquial y finalmente IA. Si bien es sabido que esta patología corresponde a una pseudoalergia, donde ocurre una degranulación inespecífica de los mastocitos, los mecanismos fisiopatológicos que gatillan esta degranulación no están totalmente dilucidados, siendo la hipótesis más aceptada actualmente aquella que guarda relación con las modificaciones en el metabolismo del ácido araquidónico causadas por la aspirina. Actualmente no existen exámenes de laboratorio para la confirmación diagnóstica de intolerancia a la aspirina, por lo que frente a la sospecha clínica de esta patología debe someterse al paciente a pruebas de provocación para hacer el diagnóstico certero de esta enfermedad, siendo la más utilizada la prueba de provocación con aspirina oral.
The aspirin triad, characterized by aspirin intolerance, bronchial asthma and nasal polyposis was first described by Widal in 1922. Prevalence of aspirin intolerance in the general population is near 6 percent, but studies have shown that 78 percent of the patients with nasal polyps suffer from the triad. Clinical presentation consists of a characteristic evolutive pattern, with rhinitis appearing first, then nasal polyps, bronchial asthma and finally aspirin intolerance. Even though it is well known that this pathology corresponds to pseudoallergy where unspecific mast cell degranulation occurs, the physiopathologic mechanisms that trigger this degranulation are not completely understood. The most accepted hypothesis involves aspirin-induced modifications in the metabolism of arachidonic acid. Currently there are no in vitro tests available for aspirin intolerance diagnosis, so if this pathology is suspected, a provocation test with aspirin is necessary to confirm the diagnosis, oral provocation test being the most frequently used in clinical practice.
Subject(s)
Humans , Aspirin/adverse effects , Drug Hypersensitivity/diagnosis , Drug Hypersensitivity/physiopathology , Drug Hypersensitivity/therapy , Nasal Polyps/chemically inducedABSTRACT
Aspirin intolerance is defined as acute urticaria-angioedema, bronchospasm, severe rhinitis, or shock occuring within three hours of aspirin ingestion. Aspirin intolerance occurs most frequently in individuals with chronic urticaria, asthma, chronic rhinitis, and normal individual in order of decreasing frequency. NSAIDs frequently cross-react with aspirin in intolerant individuals. We report a case of aspirin intolerance, which cross-reacts with naproxen, in a 42-year-old male with chronic urticaria. He experienced angioedema within 20 minutes after ingesting aspirin (700mg) and within 2 hours after ingesting naproxen (125mg). He has also experienced itching, wheal, chest tightness, and nausea during oral challenge test with aspirin.