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El lupino pertenece al género de las leguminosas, junto con el maní, las arvejas, las lentejas y los garbanzos. La harina de lupino ha sido ampliamente utilizada en algunos países por sus propiedades nutritivas y funcionales, destacando entre ellas su gran aporte proteico, adecuada proporción de fi bras, carbohidratos y bajo contenido graso, constituyendo para algunos grupos la "nueva soja". En relación al progresivo aumento en su consumo, han aumentado los reportes de reacciones adversas, destacando entre ellas las correspondientes a alergia alimentaria, que pueden ir desde el síndrome de alergia oral hasta la anafi laxia. Clínicamente la reacción cruzada más relevante se produciría con el consumo de maní y de almendra. En la actualidad existen pocos estudios acerca de la sensibilización a lupino en la población general, en la población atópica y conocemos parcialmente sus alérgenos. Ello, más la falta de incorporación de lupino en el etiquetado de los alimentos, son elementos que difi cultan conocer el real impacto que este alérgeno alimentario emergente cumple en el desarrollo de alergias alimentarias.(AU)

Lupine belongs to the leguminous family, along with peanut, peas, chickpeas and lentils. Lupine fl our has been widely used in some countries for its nutritional and functional properties, outstanding among them its great proteic value, appropriate proportion of fi ber and carbohydrate content, and its low percentage of fat, thus it has been named by some as the "new soy bean". As its consumption has increased, there has also been a raise in the report of adverse reactions, such as food allergy, that range from oral allergy syndrome to anaphylaxis. The most relevant clinical cross-reaction occurs with peanut and almond consumption. Now days there are few studies on general and on atopic population regarding lupine sensitization, furthermore, we hardly know its allergens. The lack of brand identifi cation of lupine in foods is a relevant fact that makes even more diffi cult to have a realistic knowledge of this emerging food allergen and its role in the production of food allergies(AU)

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Introducción: El síndrome Hiper IgE (SHIGE) autosómico dominante (SHIGE-AD) es una inmunodeficiencia primaria asociada a alteraciones del tejido conectivo, esqueléticas, cerebrales y vasculares. La patogénesis de la inmunodeficiencia reside en una alteración en la vía Th17 lo que explica la susceptibilidad especial de estos pacientes a infecciones por S. aureus y Candida. Objetivo: Describir tres niños diagnosticados como síndrome Hiper IgE y realizar una revisión sobre el tema, con especial foco en la forma dominante de la enfermedad. Casos clínicos: Se presentan 3 niños con SHIGE (2 varones), con rash eccematoso desde el período de recién nacido, infecciones cutáneas, óticas, pulmonares, ganglionares, con niveles de IgE sérica sobre 2.000 UI/ml y eosinofilia, tratados con antimicrobianos y tópicos, con seguimiento más de 7 años. Conclusiones: Es una entidad infrecuente, que requiere alto grado de sospecha y el manejo precoz de las infecciones. Uno de sus principales diagnósticos diferenciales está dado por el niño atópico con infecciones recurrentes pero difieren en el contexto, respuesta y resolución frente a las infecciones y la falta de las otras características fenotípicas.

Introduction: Autosomal dominant Hyper IgE syndrome (HIES-AD) is a primary immunodeficiency associated with connective tissue, skeletal, vascular and brain disorders. The pathogenesis of immune deficiency lies in an alteration of Th17 cells which explains the special susceptibility of these patients to S. aureus and Candida infections. Objective: To describe three children diagnosed with hyper IgE syndrome and conduct a study on the subject, with special focus on the dominant form of the disease. Case reports: 3 children with HIES-AD (2 males and one female) with eczema since birth, skin, ear, lung, and lymph node infections, and serum IgE levels over 2,000 IU/ml and eosinophilia values, treated with antibiotics and topically, and 7 year follow-up. Conclusions: It is a rare condition that requires a high index of suspicion and early management of infections. One of its main diagnoses is atopic syndrome with recurrent infections but both conditions differ in context, response and resolution against infections and lack of other phenotypic characteristics.

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INTRODUCTION: Autosomal dominant Hyper IgE syndrome (HIES-AD) is a primary immunodeficiency associated with connective tissue, skeletal, vascular and brain disorders. The pathogenesis of immune deficiency lies in an alteration of Th17 cells which explains the special susceptibility of these patients to S. aureus and Candida infections. OBJECTIVE: To describe three children diagnosed with hyper IgE syndrome and conduct a study on the subject, with special focus on the dominant form of the disease. CASE REPORTS: 3 children with HIES-AD (2 males and one female) with eczema since birth, skin, ear, lung, and lymph node infections, and serum IgE levels over 2,000 IU/ml and eosinophilia values, treated with antibiotics and topically, and 7 year follow-up. CONCLUSIONS: It is a rare condition that requires a high index of suspicion and early management of infections. One of its main diagnoses is atopic syndrome with recurrent infections but both conditions differ in context, response and resolution against infections and lack of other phenotypic characteristics.

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A multiplex polymerase chain reaction (PCR) was initially developed to detect the presence of mycoplasma genus DNA sequences in cell cultures and to differentiate between three human pathogenic mycoplasma species simultaneously. The assay in turn, proved to be a useful tool for the detection of mycoplasma infection in human DNA samples. One set of oligonucleotide primers which are specific for a highly conserved region among all members of the genus mycoplasma along with three other primer sets which are specific for Mycoplasma fermentans, Mycoplasma hominis andMycoplasma penetrans species were used in this assay. The sensitivity of detection was determined by infecting peripheral blood mononuclear cells (PBMC) of healthy individuals with known bacterial copy numbers from each species, extracting the DNA, and subjecting 1 microgram of DNA from each sample to 40 cycles of amplification. By using agarose gel electrophoresis the detection level was determined to be 7, 7, 9 and 15 mycoplasma cells per microgram of human genomic DNA for M. genus,M. fermentans, M. hominis and M. penetrans, respectively. The assay was applied to DNA extracted from the PBMCs of individuals suffering from chronic fatigue syndrome (CFS) (n=100) as determined by the Center for Disease Control (CDC) criteria, and compared to healthy individuals (n=100). The percentage of M. genus infection was found to be 52% in CFS patients and only 15% in healthy individuals. Mycoplasma fermentans, M. hominis andM. penetrans were detected in 32, 9 and 6% of the CFS patients while they were detected in 8, 3 and 2% of the healthy control subjects, respectively. This assay provides a rapid and cost efficient procedure to screen either cell cultures or clinical samples for the presence of three potentially pathogenic species of mycoplasma with a high level of sensitivity and specificity.

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Mycoplasma fermentans and other Mycoplasma species are colonizers of human mucosal surfaces and may be associated with human immunodeficiency virus infection. While many infectious agents have been described in different percentages of patients with Chronic Fatigue Syndrome (CFS), little is known about the prevalence of mycoplasmas and especially M. fermentans in CFS patients. A polymerase chain reaction (PCR)-based assay was used to detect Mycoplasma genus and M. fermentans genomes in peripheral blood mononuclear cells (PBMC) of CFS patients. Blood was collected from 100 patients with CFS and 50 control subjects. The amplified products of 717 bp of Mycoplasma genus, and 206 bp of M. fermentans were detected in DNA purified from blood samples in 52% and 34% of CFS samples, respectively. In contrast, these genomes were found in only 14% and 8% of healthy control subjects respectively (P < 0.0001). All samples were confirmed by Southern blot with a specific probe based on internal sequences of the expected amplification product. Several samples, which were positive for Mycoplasma genus, were negative for M. fermentans indicating that other Mycoplasma species are involved. A quantitative PCR was developed to determine the number of M. fermentans genome copies present in 1 microg of DNA for controls and CFS patients. Mycoplasma copy numbers ranging from 130 to 880 and from 264 to 2400 were detected in controls and CFS positive subjects, respectively. An enzyme immunoassay was applied for the detection of antibodies against p29 surface lipoprotein of M. fermentans to determine the relationship between M. fermentans genome copy numbers and antibody levels. Individuals with high genome copy numbers exhibited higher IgG and IgM antibodies against M. fermentans specific peptides. Isolation of this organism by culture from clinical specimens is needed in order to demonstrate specificity of signal detected by PCR in this study.

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