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Biomedical subjects

M L Baeza

Publications and source records attributed to M L Baeza.

At least 37 records · Page 2Linked to original sources
PubMed2001

Occupational asthma caused by exposure to cyanoacrylate.

BACKGROUND: Exposure to acrylates may give rise to rhinitis and asthma in both industrial and domestic environments. The mechanisms underlying these respiratory conditions caused by acrylates remain largely unknown. METHODS: We studied two assembly operators exposed to cyanoacrylate glue who developed rhinitis and asthma symptoms. The causal relationship of these symptoms to cyanoacrylate glue exposure was investigated by serial peak expiratory flow (PEF) monitoring at work and off work. Moreover, inhalation testing was performed by asking the patients to mimic exposure at work with the cyanoacrylate glue in a 7-m3 challenge chamber. RESULTS: Serial PEF monitoring at work and away from work was consistent with occupational asthma in both patients. The methacholine inhalation test was negative in patient 1 (off work) and showed bronchial hyperresponsiveness in patient 2. After 20-min exposure to cyanoacrylate, the patients had late and progressive asthmatic reactions, respectively, and the methacholine test became positive in patient 1. Induced-sputum samples obtained 3 and 24 h after the cyanoacrylate challenge showed a marked increase in sputum eosinophils. CONCLUSION: Exposure to cyanoacrylate in these patients provoked not only variable airflow limitation and bronchial hyperresponsiveness, but also pronounced eosinophilia in sputum.

Adult↗
PubMed2001

Allergy to grape: a case report.

We report a case of a 5-year-old child who suffered an oral allergy syndrome and lip angiedema after eating grapes. We obtained a positive prick test with commercial grape extract and a positive prick-by-prick test with pulp and peel of fresh white grape (Moscatel variety) and pulp and peel of blue grape. Sodium dodecyl sulphate-polyacrylamide gel electrophoresis followed by immunoblotting revealed specific immunoglobulin E (IgE) antibodies in the patient's serum against a 94,000 molecular-weight antigenic band. Lip open challenge was positive.

Angioedema↗
PubMed2001

Bezafibrate-induced anaphylactic shock: unusual clinical presentation.

We report a case of a patient who suffered generalized urticaria, chest tightness, wheezing, nausea, vomiting, hypotension, and loss of consciousness. Two hours earlier she had taken Eulitop Retard following lunch. She had tolerated all the implicated food after the reaction. Allergy evaluation revealed intense positive responses to intradermal tests with bezafibrate active component and Eulitop Retard (skin tests in control subjects were negative). Specific IgE tests (RAST) to Eulitop Retard were negative. An IgE mechanism is suggested to be responsible for this adverse reaction on the basis of the positive skin tets. The delayed onset (two hours) of this anaphylactic shock is unusual. Although infrequent, it may be caused by the specific pharmacokinetic characteristics of this drug, which is a slow releasing agent, mainly absorbed in the gut. The drug was taken just after lunch, and this concomitant food ingestion could also have produced a delay in gastric drainage and a retarded drug absorption. An IgE-mediated accelerated type reaction could also explain this delay. Apparently the patient reacted after the first contact to the drug, and the absence of a sensitization period is not usual in this type of immune reponse. Finally, we recommend the performance of prick and intradermal skin tests prior to any systemic challenge when allergic reactions to fibric acid derivatives are suspected.

Anaphylaxis↗
PubMed1999

Lupine-induced anaphylaxis.

BACKGROUND: Legumes are one of the most common foods causing allergic reactions in children and adults. Cross-reacting antibodies are frequently demonstrated in this family but the real clinical cross-reactivity is uncommon. OBJECTIVE: To report a case of lupine-induced anaphylaxis and to elucidate in vivo and in vitro cross-reactivity with some legumes. METHODS: Skin prick test (SPT) with some legumes were performed. Cap-IgE, ELISA-IgE, and immunoblotting were carried out. Open oral challenges with some legumes were performed. Cross-reactivity was studied by ELISA and immunoblotting inhibition. RESULTS: The results demonstrated type-I hypersensitivity reactions with lupine and some other legumes. Cap-IgE with peanut was positive but the SPT and ELISA-IgE were negative and the patient tolerated a peanut challenge. ELISA inhibition revealed a partial inhibition (62%) using lupine as the solid phase. Partial inhibition was demonstrated by immunoblotting inhibition. Open oral challenge with peanut and green bean were negative but positive with pea. CONCLUSION: We present a lupine sensitized patient with positive SPT and in vitro cross-reactivity with other legumes. Clinical cross-reactivity progressively developed over a 5-year period. Discrepancies were found between the clinical aspect and in vitro study of peanut allergy. Factors determining the wide variability in cross-reactivity among individuals are still obscure.

Adult↗
PubMed1999

Allergy to an occupational allergen (Sapelli wood) in a child.

The case is presented of a child who developed rhinoconjunctivitis, angioedema and asthma by sensitization to Sapelli wood, which was used in his father's carpentry. Positive skin-prick test, high levels of specific immunoglobulin E by ELISA and a positive conjunctival challenge test suggest a type I hypersensitivity mechanism to this wood. This is the first case report of sensitization to Sapelli wood and it confirms that occupational allergen exposure as Sapelli wood may also cause sensitization in a child.

Allergens↗
PubMed1998

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.

Aged↗
PubMed1997

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.

Anaphylaxis↗
PubMed1995

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.

Adult↗
PubMed1992

Connective tissue-activating peptide-III and its derivative, neutrophil-activating peptide-2, release histamine from human basophils.

Connective tissue-activating peptide-III (CTAP-III) is a 9 kd platelet alpha-granule-derived growth factor. It stimulates the synthesis of DNA, hyaluronic acid, glycosaminoglycans, and proteoglycan core protein in human fibroblasts. Human mononuclear cell-derived proteases have been previously demonstrated to digest the N-terminal 15 residues of CTAP-III (total, 85 residues) to produce neutrophil-activating peptide-2 (NAP-2). CTAP-III and NAP-2 belong to a class of proteins (platelet factor 4, interleukin-8/NAP-1, etc.) associated with inflammation and wound repair. In our efforts to purify human mononuclear cells and platelet-derived histamine-releasing factors, we had previously discovered that mixtures of CTAP-III and NAP-2 released histamine from human basophils. We have now developed simple protocols for the purification of CTAP-III and NAP-2, independently, from calcium ionophore (A23187)-stimulated platelet supernatants by affinity chromatography and have established their identity by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and N-terminal sequence analysis. Each of these related histamine between 2 and 10 micrograms/ml, a range identical to that obtained with CTAP-III/NAP-2 mixtures that we reported earlier. Thus, our data suggest that CTAP-III and NAP-2 independently release histamine from human basophils in dose ranges similar to ranges required for fibroblast stimulation by each.

Basophils↗
PubMed1990

Relationship of one form of human histamine-releasing factor to connective tissue activating peptide-III.

We have previously reported purification of three forms of histamine-releasing factors (HRFs) from mixtures of streptokinase-streptodornase stimulated human mononuclear cells and platelets with apparent molecular masses of 10-12, 15-17, and 40-41 kD (1989. J. Clin. Invest. 83:1204-1210). We have also prepared mouse MAbs against the 10-12-kD HRF (1989. J. Allergy Clin. Immunol. 83:281). Affinity-purified 10-12-kD HRF appears as a broad band upon polyacrylamide gel electrophoresis in the presence of SDS. We determined the NH2-terminal amino acid sequence of the top and bottom halves of this broad band. Sequence analysis revealed striking homology between this HRF and connective tissue activating peptide-III (CTAP-III), a platelet-derived 8-10-kD protein known to cause mitogenesis and extracellular matrix formation in fibroblast cultures. 19 of 21 NH2-terminal residues in the top half of the HRF band were identical to the NH2-terminal sequence of CTAP-III. 20 of 21 NH2-terminal residues in the bottom half were identical to the NH2-terminal sequence of neutrophil-activating peptide-2, which is derived from CTAP-III by proteolytic cleavage between residues 15 and 16. Purified CTAP-III also released histamine from basophils. Rabbit antiserum raised against either native or recombinant CTAP-III recognized affinity-purified HRF in immunodot blot assays, and MAb against HRF recognized CTAP-III in both dot blot and microtiter plate based immunoassays. These data demonstrate the first structural, functional, and immunologic relationship between one form of human HRF and a previously described cell product.

Amino Acid Sequence↗
PubMed1989

Purification and further characterization of human mononuclear cell histamine-releasing factor.

We have purified and further characterized a histamine releasing factor (HRF) derived from human mononuclear cells using gel-filtration HPLC, reverse-phase HPLC, anion exchange chromatography, and elution from SDS gels after electrophoresis. Considerable heterogeneity is seen, far exceeding that published in prior reports. Gel filtration HPLC yielded a major peak at molecular weight 30,000 and minor peaks at 50,000 and 12,000. Reverse-phase HPLC gave one major fraction in the void volume and an eluted peak at 50-60% acetonitrile. Accell QMA anion exchange HPLC revealed three peaks of activity; one in the void volume similar to that published previously using QAE-Sephadex, and peaks that eluted at 0.5 and 0.8 M ammonium acetate, respectively. Electroelution following SDS-PAGE yielded peaks at MW 12,000 and 15-17,000 plus variable peaks at 25-27,000, 31-34,000, and 80-90,000 D. Using a combination of the aforementioned procedures, we have purified molecular species of HRF at 41,000 and 17,000 D to apparent homogeneity, as judged by SDS PAGE and autoradiography. Since human interleukin 3 and granulocyte-macrophage colony-stimulating factor possess histamine-releasing capability, it is clear that multiple cytokines can share this activity. However, the major HRF we isolate from human mononuclear cells appears, thus far, to be unique.

Biomarkers, Tumor↗
PubMed1988

Responsiveness to human mononuclear cell-derived histamine-releasing factor. Studies of allergic status and the role of IgE.

Human mononuclear cell-derived histamine-releasing factor (MNC-HRF) has m.w. of 29,000 and 23,000 and two charge species isoelectric at pH 6.9 and 7.3. Minor forms of HRF are also seen at m.w. of 12,000 to 15,000 and 60,000 to 80,000. In this manuscript we have further defined the response of human basophils to MNC-HRF in terms of atopic status of cell donors and the role of IgE antibody. We found that basophils of allergic persons, nonallergic controls, or donors who have positive skin tests but no symptoms, cannot be distinguished based upon responsiveness to HRF. Further, the response of basophils that have been desensitized to anti-IgE is retained when they are subsequently stimulated with HRF derived from human MNC. Thus an interaction with cell-surface IgE to cause histamine release is not evident. Nevertheless, one of two IgE myeloma proteins tested were capable of binding HRF and such binding could be utilized as a purification step. We conclude that MNC-HRF is heterogeneous in terms of size, charge, and affinity for a subpopulation of IgE. Histamine release is more prominent in atopic individuals but does not appear to require an interaction with IgE.

Basophils↗