La rinitis a la luz de los consensos internacionales / Rhinitis in the light of international consensuses

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What does Anisakis simplex parasitism in gastro-allergic anisakiasis teach us about interpreting specific and total IgE values?

BACKGROUND: gastro-allergic Anisakiasis is a mostly transitory clinical entity caused by Anisakis simplex (A. simplex) and can be suspected by history and confirmed by fiberoptic gastroscopy and specific IgE. OBJECTIVE: we report a case of gastro-allergic Anisakiasis, in which the parasite induces a high specific and total IgE response, and want to follow the specific and total IgE values by a serologic follow up over 10 months. METHODS: an analysis of total IgE and specific IgE against. A. simplex was performed within 24 hours, after 1, 4, 6 and 10 months. At month 4 and month 10 specific IgE against Ascaris lumbricoides and Echinococcus granulosus was determined in order to value cross-reactivity. RESULTS: there is an important raise in specific IgE against Anisakis simplex (up to 903 kU/l) after 6 months and total IgE (up to 15,258 kU/l) after one month. Cross-reactive specific IgE against Ascaris lumbricoides and Echinococcus granulosus can be detected. CONCLUSIONS: we consider a raise of total and specific IgE as a typical feature of helminth infestation and learn that specific and total IgE values are highly variable in the months following the allergic and parasite-specific reaction. The amount of specific IgE against other cross reactive parasites depends directly on the total IgE values.

What does Anisakis simplex parasitism in gastro-allergic Anisakiasis teach us about interpretating specific and total IgE values?

Background: gastro-allergic Anisakiasis is a mostly transitory clinical entity caused by Anisakis simplex (A. simplex) and can be suspected by history and confirmed by fiberoptic gastroscopy and specific IgE. Objective: we report a case of gastro-allergic Anisakiasis, in which the parasite induces a high specific and total IgE response, and want to follow the specific and total IgE values by a serologic follow up over 10 months. Methods: an analysis of total IgE and specific IgE against. A. simplex was performed within 24 hours, after 1, 4, 6 and 10 months. At month 4 and month 10 specific IgE against Ascaris lumbricoides and Echinococcus granulosus was determined in order to value cross-reactivity. Results: there is an important raise in specific IgE against Anisakis simplex (up to 903 kU/l) after 6 months and total IgE (up to 15,258 kU/l) after one month. Cross-reactive specific IgE against Ascaris lumbricoides and Echinococcus granulosus can be detected. Conclusions: we consider a raise of total and specific IgE as a typical feature of helminth infestation and learn that specific and total IgE values are highly variable in the months following the allergic and parasite-specific reaction. The amount of specific IgE against other cross reactive parasites depends directly on the total IgE values (AU)

Antecedentes: la anisakiasis gastroalérgica es una entidad clínica, generalmente transitoria, producida por Anisakis simplex. La historia clínica sugiere su presencia y el diagnóstico se confirma por gastroscopia e IgE específica. Objetivo: describir un caso de anisakiasis gastroalérgica con una respuesta de IgE específica y total importante y los resultados de 10 meses de seguimiento serológico de la IgE específica y total. Métodos: la IgE total e IgE específica contra A. simplex se analizaron a las 24 horas y después de 1, 4, 6 y 10 meses. En los meses 4 y 10, se determinó la IgE específica frente a Ascaris lumbricoides y Echinococcus granulosus para valorar la sensibilidad cruzada. Resultados: se observó una elevación importante de IgE específica frente a Anisakis simplex (hasta 903 kU/l) a los seis meses y de IgE total (hasta 15.258 kU/l) al mes. Se detectó IgE específica con reactividad cruzada a Ascaris lumbricoides y Echinococcus granulosus.Conclusiones: consideramos que la elevación de IgE total y específica es una característica de la infestación por helmintos y encontramos una gran variabilidad en los valores de la IgE específica y total en los meses después de la reacción alérgica y parasitaria. La cantidad de IgE específica contra otros parásitos que pueden producir reactividad cruzada depende directamente del nivel de IgE total. (AU)

Exposure to parakeets and bronchiolitis obliterans.

Case report of a 64-year-old woman with increasing dyspnea and cough. She cared at home for 8 parakeets (Melopsittacus undulatus). Subsequent studies revealed a restrictive pulmonary defect and transbronchial biopsy, a histological bronchiolitis obliterans (BO). No significant elevated anti-avian IgG could be detected, probably because of a transient hypogammaglobulinaemia. The implication of antigenic exposure to avian antigens in the pathogenesis of BO is discussed.

Delayed hypersensitivity to beta-lactams.

We present nine patients with delayed allergic reactions to beta-lactams. Four of them developed reactions to ampicillin; the diagnostic studies suggested the involvement of a type IV hypersensitivity mechanism to an antigenic determinant in the side-chain structure, with intradermal and patch tests positive to ampicillin but good tolerance to benzylpenicillin. Three patients showed delayed hypersensitivity reactions to benzylpenicillin (positive delayed skin tests and/or challenges). Arthus-type reactions were seen in two other patients. Specific IgE of uncertain relationship to benzylpenicillin and ampicillin was later detected in four cases.

Analysis of cross-reactivity between sunflower pollen and other pollens of the Compositae family.

The sera of 20 patients with Compositae pollen allergy were investigated for the presence of IgE antibodies reacting against sunflower pollen by means of RAST and immunoblotting studies. Thirteen IgE-binding bands were detected with molecular weights ranging from 14.4 to 94 kd. Two of these bands, with molecular weights of 24 and 25 kd, contained major allergens that reacted strongly with 100% (24 kd) and 95% (25 kd) of the sera, respectively. Cross-reactivity between sunflower and other Compositae pollens (mugwort, marguerite, dandelion, golden rod, and short ragweed) was revealed by RAST and immunoblotting inhibition experiments. Mugwort pollen exhibited the greatest degree of allergenic homology (cross-reactivity) with sunflower pollen, whereas at the other end of the spectrum, short ragweed showed less cross-reactive epitopes.

Urticaria from erythromycin.

We report an adverse cutaneous reaction (urticaria) due to erythromycin. A positive skin prick and leukocyte histamine release tests, as well as a positive single-blind, placebo controlled oral challenge to erythromycin, strongly suggest an IgE mediated hypersensitivity mechanism.

Sulfite-induced urticaria.

Metabisulfite sensitivity is being described with growing frequency. Sulfites are used in food, drinks, and drugs. Adverse reactions to apparently nontoxic doses have been described. Exposure of sensitive persons to sulfites has produced asthma, and occasionally other adverse reactions in nonasthmatic patients. We present a case of urticaria induced by metabisulfites. During the previous 2 years the patient had suffered episodes of urticaria and angioedema limited to the face, neck, upper thorax, and dysphonia without asthma after the ingestion of food and drinks containing sulfites. Oral challenge with 25 mg of potassium metabisulfite elicited urticaria on the face and neck, nasal itching, rhinorrhea, and dysphonia. Prick and intradermal tests were negative. Two further challenges with the same doses were also positive. One of these was controlled with placebo, 30 minutes after oral administration of 400 mg sodium cromolyn; the second was carried out 90 minutes after oral administration of 5000 micrograms cyanocobalamin. We have been unable to identify a pathogenic mechanism.

Short-term treatment of asthma with budesonide versus placebo.

The effects of the topical steroid budesonide on bronchial hyperreactivity were evaluated in a patient group (A, n = 17) and a placebo-controlled patient group (B, n = 11). Group A was given budesonide 400 micrograms/12 h for 4 weeks and 200 micrograms/12 h for four more weeks. The drug proved efficient in controlling asthma clinically and improving the spirometric parameters: FVC (p < 0.05), FEF50 (p < 0.05) and FEV1 (p < 0.01). Bronchial hyperreactivity (PD20) decreased moderately in the treatment group (p < 0.1). On the contrary, basal spirometry and PD20 worsened in the control group. Some patients in group A showed peripheric eosinophilia (2/15) or in secretions (9/15), which persisted in one patient at end of treatment. Budesonide was effective in the clinical and spirometric control of asthma. We conclude that for a better assessment of the treatment of bronchial hyperreactivity with budesonide, the drug must be administered for a longer period of time. The differences between this study and previous ones is that the improvement in PD20 can be explained by the different characteristics of the patients selected for this study.

Hypocomplementemic urticarial vasculitic syndrome, asthma and anaphylactic reaction with ampicillin.

A patient with hypocomplementemic urticarial vasculitic syndrome (HUV) is presented. This is an immunological pathology, limited to skin or multisystemic, that requires a differential diagnosis with erythematosus systemic lupus on the same occasions. The ever-present symptom is skin participation, such as urticaria-angioedema or fixed exanthema; biopsy shows necrotizing venulitis with polymorphonuclear infiltration and leukocytoclastic powder. Typical laboratory data are: diminished C3, C4 and C1q; C1 inhibition can be low or normal; the more characteristic finding is the presence of C1q associated immunocomplexes. Leukocytoclastic necrotizing vasculitis was found in the skin biopsy. During the course of illness (three years) the patient presented moderate cutaneous symptoms and asthma, without other systemic participation. During this period, antihistamines and, occasionally, corticoids were administered with improvement. Moreover, the patient presented urticaria related to ampicillin ingestion, and furthermore, the presence of anaphylaxis to beta-lactam was diagnosed in vivo and specific IgE was found in the laboratory study. This feature was previously observed by other authors; however, we cannot determine why the IgE-mediated allergy to beta-lactam and a complement pathology like HUV are related.

Hypersensitivity to mercuric fluorescein compounds.

The mercurial compounds are known to be a common cause of allergic contact dermatitis. Immediate hypersensitivity is rarely induced by mercurial organic derivatives. However, none of the published cases showed both immediate and delayed hypersensitivity as was the case of one of our two patients. A boy and a woman experienced urticaria and anaphylaxis, respectively after topical application of Merchromine (Merbromine). We were able to demonstrate immediate hypersensitivity in both patients to mercuric fluorescein compounds by skin test and histamine liberation. In addition, the child but not the woman, showed delayed hypersensitivity to mercurial compounds.

[Cold urticaria associated with serologic markers of hepatitis B and cryoglobulinemia]. / Urticaria a frigore asociada a marcadores serológicos de la hepatitis B y a crioglobulinemia.

The acquired form of cold induced urticarial syndrome can be found associated with serum cryoproteins, in idiopathic form (generally IgE mediated) and transitory forms associated with other factors. The viral infections, specially infectious mononucleosis and hepatitis B can cause urticaria, mostly chronic, although infrequently produces cold urticaria. We present a case of a 13 year old patient with history suggestive of cold urticaria wherein we have found the existence of a mixed polyclonal cryoglobulinemia, IgG-IgA (exceptionally associated) and serologic markers of hepatitis B, HBsAb and HBsAb (the last being suggestive of a recent infection) 3 months from the urticaria, without recent or past history of hepatitis B infection. We also observed an elevated total serum IgE and peripheral blood eosinophilia. The provocation test presented an evolution similar to the cryoglobulinemia and markers of hepatitis B (after 18 months were negative) but serum IgE and eosinophilia remain elevated until the present time. All of this make us think that the patient could have suffered a subclinical form of hepatitis B which triggered off a cryoglobulinemia, presenting as cold urticaria.