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E Losada Cosmes

Publications and source records attributed to E Losada Cosmes.

10 recordsLinked to original sources
PubMed2001

Chronic urticaria and Helicobacter pylori.

BACKGROUND: Although the clinical manifestations of chronic urticaria (CU) are similar in most patients, a variety of factors should be taken into consideration. In general, the cause of CU cannot be determined in most patients, and it is considered idiopathic. In the past several years, relationships between some patients with CU and hepatitis C or autoimmune thyroid diseases have been established. Similarly, other factors may also be considered as possible causes to explain certain patients with CU. Previously, some patients with CU have had their disease attributed to Helicobacter pylori (HP), but the relationship was only clinical. OBJECTIVE: None of the patients previously described included an immunological study. Thus, we studied a patient with CU, who showed marked clinical improvement after eradication of HP, to demonstrate an IgE relationship with this skin disease. METHODS: First, blood analytical parameters, roentgenograms, fecal examination for parasites, and skin tests were performed to try to establish an etiology. In addition, endoscopy with gastric biopsy confirmed HP colonization, and eradication treatment was prescribed. To investigate an immunological relationship, other tests performed included the following: HP-specific IgG, histamine release induced by HP, HP-specific IgE, and sodium dodecyl sulfate-polyacrylamide gel electrophoresis with immunoblotting. RESULTS: The blood analytical parameters, roentgenograms, fecal examination for parasites, and skin tests were all negative. In contrast, the tests for HP-specific IgG, histamine release induced by HP, and HP-specific IgE were all positive. In addition, the sulfate-polyacrylamide gel electrophoresis with immunoblotting showed specific IgE binding to an extract of HP. CONCLUSIONS: Our results may indicate an immunological IgE relationship between HP colonization and CU in this particular patient.

Antibodies, Bacterial↗
PubMedDate not supplied

[Value of eosinophilia in blood and nasal exudate in the diagnosis of different types of rhinitis].

162 patients with different patterns of rhinitis were studied. In 94 a diagnosis of allergic rhinitis was made. The remaining 68 were considered as nonallergic rhinitis. In the allergic group, 64 had seasonal allergic rhinitis. 24 of them were studied during the hay fever season and 40 out of the hay fever season. Positive nasal smear eosinophilia (up to 10%) was found in 56 of 96 patients from the allergic group (59.5%), 21 of them had perenneal allergic rhinitis and 35 had seasonal allergic, of those 20 were studied during the hay fever season. In the non allergic group, 35 were diagnosed as intrinsic rhinitis and 33 as cholinergic rhinitis. Positive nasal smear eosinophilia could be demonstrated in 15 out of 35 cases of intrinsic rhinitis (42.8%), but could not be shown in patients suffering from cholinergic rhinitis. Peripheral blood eosinophilic cells were found in normal values in all patients in spite of the character of the rhinitis. These results suggest that nasal smear eosinophilic cells count is a useful orientative datum in the diagnosis of allergic and intrinsic rhinitis (59.5% and 42.8% respectively in our cases) but is not useful in the diagnosis of cholinergic rhinitis (not one out of 33 cases). Blood eosinophil cells count had no value in nasal allergy diagnosis.

Adolescent↗
PubMedDate not supplied

[Syndrome due to acetylsalicylic acid intolerance. What should be prescribed as substitutes for aspirin?].

In the daily practice of allergology, one of our commonest problems concerns the prescription of nonsteroidal anti-inflammatory drugs for our patients who are intolerant of acetylsalicylic acid, whose basic clinical expression of this intolerance is primary bronchial asthma. Our problem is the high frequency with which the syndrome appears after the administration of other analgesics chemically unrelated to acetylsalicylic acid. Most authors accept that derivatives of pyrazolones and indoles, and of phenylisopropionic and anthranilic acids must be avoided. This avoidance is based on collected clinical experience and the currently accepted hypothesis concerning the pathogenesis of the syndrome (pyrazolones, indoles, etc. are inhibitors of the byosynthesis of the E series of prostaglandins, particularly PG synthetase). On the other hand there is no agreement concerning what type of analgesics, anti-inflammatory drugs and antipyretics we should prescribe for these patients. The conclusions of the protocol which we carried out are as follows. Dextropropoxyphene chlorhydrate, diviminol, tilidine chlorhydrate, salicylamide, benzidamine, pentazocine, isonixine, hyoscine bromide and ergotamine tartrate can be prescribed safely for these patients in the usual therapeutic dosage. To the list of prohibitions should be added the derivatives of glaphenine and phenylacetic acid. As regards paracetamol, our opinion is that its use should be restricted to those cases in which the previously listed drugs cannot be substituted for it, and always after administration under medical supervision in a hospital setting.

Analgesics↗