Secretory immune response in patients with intestinal amoebiasis.

The secretory immune response in saliva from intestinal amoebiasis patients against antigens obtained from Entamoeba histolytica membranes was studied. Western blot analysis indicated that patient saliva contains secretory IgA antibodies against antigens with molecular masses ranging from 170 to 24 kDa, some of which were also recognized by saliva from healthy subjects. However, antigens of 170, 125, 46 and 37 kDa are recognized more frequently (> 90%) by the secretory IgA from patients with intestinal amoebiasis than by that from healthy subjects (< 10%).

Rapid screening test for tuberculosis using a 38-kDa antigen from Mycobacterium tuberculosis.

A screening test for the diagnosis of tuberculosis by immunodot (IDt) is described, using an antigen of Mycobacterium tuberculosis, namely, a 38-kDa glycoprotein which has shown great specificity in previous serologic analyses. The test was used to examine 28 sera from patients with lung tuberculosis. Of these, 85% were positive by micro-ELISA and by the IDt test herein described. Control sera from healthy subjects (n = 20) gave negative results for ELISA and for IDt, which indicates that the screening test is highly specific. The test is easy to handle and requires no equipment and is therefore particularly useful for field studies.

Secretory immune response to membrane antigens during Giardia lamblia infection in humans.

The secretory immune response in humans infected with Giardia lamblia was studied by using saliva samples and a membrane-rich protein fraction. The membrane fraction, studied by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, showed 24 antigen bands, ranging from 170 to 14 kDa. Saliva samples from giardiasis patients showed a heterogeneous response against the membrane fraction when they were assayed by immunoblotting. Among the antigens recognized by patient saliva samples, those of 170, 105, 92, 66, 32, 29, and 14 kDa stood out. These antigens were not recognized by saliva samples from healthy individuals. They may be of importance in future studies of protection from or diagnosis of G. lamblia infections.

[Metabolic changes in arachidonic acid during aspirin desensitization]. / Cambios metabólicos del ácido araquidónico en la desensibilización a la aspirina.

Aspirin sensitivity occurs in 10% of all asthmatics patients. In this subset of asthmatics, nasal congestion and bronchospasm occurs between 30-180 minutes after ingestion of aspirin. Following a respiratory reaction to aspirin, all patients can be desensitized to aspirin by repetitively introducing small and then larger doses of aspirin until the asthmatic subject can ingest 650 mg of aspirin without adverse effect. The mechanism of aspirin sensitivity are incompletely understood. And the reasons why ASA desensitization occurs universally are unknown. In this study, known ASA sensitive and control insensitive asthmatics were challenged with ASA. Urine was collected before, during induced bronchospasm, and after ingestion of 650 mg of ASA when the adverse effect (ie., acute desensitization) had subsided. Excretion levels of cyclo-oxygenase and lipoxygenase products in the urine were determined.

[Asthma induced by aspirin and arachidonic acid metabolites. II. The role of leukotrienes (part four)]. / Asma inducida por aspirina y metabolitos del ácido araquidónico. II. La participación de los leucotrienos (cuarta parte).

Although the mechanism of aspirin-induced asthma is unknown, it has be suggested that adverse nasal and bronchial reactions are caused by an increased production of lipoxygenase products. We have measured the release of urinary LTE4, TXB2 and 11-dehydro-TXB2 of aspirin induced asthmatics and controls by radioimmunoassay and HPLC methods during aspirin challenge and after desensitization. The overproduction demonstration of urinary LTE4 during aspirin challenge and the decrease after desensitization in inversal direct proportion manner with TXB2 suggest a "shunting" of the arachidonic acid metabolites of the target cells. Whichever theory is to be pursued further, it must also accommodate the clinical effect of aspirin densitization.

[Asthma induced by aspirin and arachidonic acid metabolites. Role of leukotrienes (third part)]. / Asma inducida por aspirina y metabolitos del ácido araquidónico. La participación de los leucotrienos (tercera parte).

Although the mechanism of aspirin-induced asthma is unknown, it has been suggested that adverse nasal and bronchial reactions are caused by an increased production of lipoxigenase products. In examining the hypothesis of inhibition on cycloxigenase, we support evidence in favor of this theory. We have measure the release of urinary LTE4, TXB2 and 11-dehydro-TXB2 of aspirin-induced asthmatics and controls by radioimmunoassay and HPLC methods during aspirin challenge and after desensitization. The over production demonstration of urinary LTE4 during aspirin challenge and the decrease after desensitization in inversal direct proportion manner with TXB2 suggest a "shunting" of the arachidonic acid metabolites of the target cells. Whichever theory is to be pursed further, it must also accommodate the clinical effect of aspirin desensitization.

[Aspirin-induced asthma and arachidonic acid metabolites. In search of answers to an enigma. Part 2]. / Asma inducida por aspirina y metabolitos del ácido araquidónico. En búsqueda de respuestas a un enigma (segunda parte).

Acetylsalicylic acid is one of the most commonly used drugs and high on the list of causes of drug reactions. Since early publication on 1902 by Hirschberg, a great deal of information has emerged on aspirin sensitivity, including data on epidemiology, further characterization of the two major subtypes of sensitivity (bronchospastic and urticarial types), hereditary aspects, cross-reactions to other nonsteroidal antiinflammatory drugs, and methods of desensitization. Although the pathogenesis of aspirin-sensitive asthma remains unknown, several theories has been proposed to explain the disease enigma.

[Asthma induced by aspirin and arachidonic acid metabolites. I. In search of answers to an enigma (first part)]. / Asma inducida por aspirina y metabolitos del ácido araquidónico. I. En busca de respuestas a un enigma (primera parte).

Acetylsalicylic acid, one of the most commonly used drugs and high on the list of causes of drug reactions. Since early publication on 1902 by Hirschberg, a great deal of information has emerged on aspirin sensitivity, including data on epidemiology, further characterization of the two major subtypes of sensitivity (bronchospastic and urticarial types), hereditary aspects, cross-reactions to other nonsteroidal antiinflammatory drugs, and methods of desensitization. Although the pathogenesis of aspirin-sensitive asthma remains unknown, several theories has been proposed to explain the disease enigma.

[Symptomatic dermatographism and HLA antigens]. / Dermografismo sintomático y antígenos HLA.

This research reports the unique case of manifestation of symptomatic dermographism which includes all of its twenty five members of the family. Probing a genetic transmission autosomal dominant manner and taking into account the highly probable role of HLA in this illness. The symptomatic dermographism correspond to a group of physical familiar urticarias with symptoms appearing in early childhood and evolving throughout adulthood with seldom periods of remission. Due to the fact that all patients were affected, it was not possible to realize a typification of HLA antigens with persons not affected, to establish a relationship with the data obtained. However, results show a significant association of haplotypes; HLA A2 (78.95), B16 (68.4%), A1 (47.3%), and B5 (42.5%) among the most important. This is the first research that reports the analysis of HLA within the physical familial urticarias.

Trasplante renal. / Kidney transplantation

Se presentan los resultados de 15 pacientes trasplantados en el Hospital de Especialidades del CMO del Instituto Mexicano del Seguro Social. Con donador relacionado vivo y siguiendo la tecnica quirurgica de Harrison y Murray y con inmunodepresion en base de azathioprina con ciclos de ciclosfosfamida y metil-prednisolona. 14 de los 15 pacientes estan vivos con el trasplante de rinon, uno de ellos fallecio en el postrasplante a causa de neumonia por pseudomona. 10 de los 15 pacientes fueron compatibilidad "A", segun el sistema H.L.A., los otros 5 fueron compatibilidad "B". Las complicaciones fueron fundamentalmente: 5 casos con insuficiencia de rinon aguda normalizandose posteriormente. Tuvimos tambien 3 infecciones como linfocele, y no ha habido ni complicaciones angiologicas ni urologicas