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BACKGROUND: Because urinary low molecular weight protein (LMWP) measurement shows changes in renal integrity at an early stage, beta2-microglobulin (B2m), retinol-binding protein (RBP) and alpha1-microglobulin (A1m) were evaluated in 24-hour urine collection of 65 patients with pure monoclonal light chain (MLC) proteinuria and in 47 patients with different kidney diseases (DKDs) for comparison. METHODS AND RESULTS: Albumin, kappa, lambda, A1m and B2m were measured by immunonephelometry. RBP was determined by ELISA. The mean values of LMWP quantitation were significant for origin of the disease (MLC and DKD) (p<0.05) and renal failure (RF) (p<0.001) (MANOVA). Tukey HSD test only showed significant differences for LMWP between MLC patients with RF and DKD patients without RF. The mean value of A1m was different between patients with and without RF in each group (p<0.05 for MLC, and p<0.01 for DKD). In the group without RF, the frequency of A1m excretion above 12 mg/L differed between MLC patients and DKD patients (p<0.01). CONCLUSION: A tubular dysfunction occurred in a great number of patients excreting pure MLC even in those with well-preserved renal function, as it did in patients with DKDs. In patients with MLC without RF, A1m might be measured for the early recognition of tubular involvement.

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The majority of patients with hepatitis A have a benign course, but some may develop fulminant hepatitis and hematological complications. Peripheral stem cell transplantation (PSCT) is associated with loss of immunity. There are no data regarding loss of HAV antibodies (anti-HAV) after PSCT. We retrospectively evaluated the persistence of anti-HAV in a nonvaccinated population that underwent PSCT. Serum detection of anti-HAV was determined before and after PSCT using a qualitative commercially available enzyme immunoassay. From January 1997 to March 2001, 136 (68%) of 201 patients tested (+) for anti-HAV prior to PSCT. Subsequent investigation of anti-HAV was possible in 36 of these patients at a median of 12 months after PSCT. The median age of patients was 47 years old; they had diagnoses of hematological malignancies (33) and solid tumors (three), and underwent autologous (31) and allogenic (five) PSCT. A total of 31 (86%) of 36 patients remained anti-HAV (+) and five (14%) became (-) after PSCT. The variables age, sex, diagnosis, type of PSCT, time of testing, and number of CD34 cells infused were not predictors of loss of anti-HAV. In conclusion, 14% of 36 nonvaccinated anti-HAV (+) patients lost their antibodies at a median of 12 months after PSCT.

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Multiclonal gammopathies associated with multiple myeloma may result either from a neoplastic transformation of a cell clone undergoing immunoglobulin class switching or from independent transforming events yielding proliferation of unrelated plasma cell clones. The simultaneous presence of more than one neoplastic clone may possess regulatory implications in terms of cell proliferation, clonal expansion, secretion of M-components or response to chemotherapy. We report a patient, diagnosed with multiple myeloma stage IIIa, who presented with two well-defined homogeneous IgG1-kappa components in the serum (designated WER-1 and WER-2) with striking differences in their plasma concentration and response to the classic melphalan/prednisone treatment. Immunochemical characterization and amino terminal sequence analysis of both the heavy and light chains of each M-component undoubtedly determined their biclonal origin. WER-1 was identified as IgG1(VHII)-kappaI while WER-2 was classified as IgG1(VHIII)-kappaIII. The plateau phase was characterized by very low or undetectable levels of WER-2, a high, almost constant, concentration of WER-1 and the absence of Bence Jones proteinuria, whereas these parameters were completely reversed during the escape phase with levels resembling those observed at the time of diagnosis. The statistically significant negative correlation between the biclonal components and the different susceptibility to the treatment clearly suggests regulatory interactions between the clones WER-1 and WER-2.

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It is known that the receptors for the Fc portion of IgG molecules (Fc gamma R) are widely distributed in cells of the immune system. The expression of Fc gamma R enables monocytes and neutrophils to destroy antibody-coated target cells through the antibody-dependent cell-mediated cytotoxicity (ADCC) mechanism. In addition, the interaction of immune complexes or aggregated IgG with monocytes or neutrophils led to the lysis of nonsensitized target cells in a process known as nonspecific cytotoxicity (NSC). Despite that ADCC and NSC are both triggered through Fc gamma R, the cytolytic mechanism involved in each reaction is different. In this paper we analyze the ability of human monoclonal IgG1, IgG2, IgG3 and IgG4 to induce ADCC and NSC. Our results demonstrate that each IgG subclass is able to induce both, NSC and ADCC, mediated by monocytes or neutrophils, indicating that there is no correlation between IgG subclass specificity and the ability to activate both mechanisms.

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Four hundred ten previously untreated multiple myeloma patients entered onto two consecutive Grupo Argentino de Tratamiento de la Leucemia Aguda (GATLA) protocols were analyzed to identify significant prognostic factors influencing survival. The univariate analysis selected the following variables: performance status, renal function, percentage of bone marrow plasma cells at diagnosis, hemoglobin, and age. A multivariate analysis showed that performance status, renal function, percentage of bone marrow plasma cells, hemoglobin, and age were the best predictive variables for survival. A score was assigned to each patient according to these variables, which led to their classification in three groups: good, intermediate, and poor risk, with a probability of survival of 26% and 10% at 96 months, and 5% at 56 months, and median survival of 60, 37, and 14 months, respectively (P = .0000). In our patient population, this model proved to be superior to the Durie-Salmon staging system in defining prognostic risk groups, and separating patients with significantly different risks within each Durie-Salmon stage.

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Tratamos de corroborar el valor del clearence de alfa-antitripsina como una técnica eficaz para objetivar la pérdida de proteínas a través del tubo digestivo y su aplicación como método de diagnóstico en tal patología. Se estudiaron 22 individuos; 11 con patología intestinal capaz de producir pérdida proteica y 11 controles sin daño de la mucosa intestinal. Se determinó la concentración de alfa-1-antitripsina tanto en suero como en materia fecal en días consecutivos y pesando la materia fecal de 24 horas se pudo obtener el clearence intestinal de dicha proteína. En los pacientes con enfermedad perdedora de proteínas el valor del clearence fue siempre patológico mientras que en los controles se obtuvieron valores normales. Este método es útil para diagnosticar la pérdida proteica intestinal y tiene la ventaja de no utilizar material radioactivo para su determinación (AU)

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Tratamos de corroborar el valor del clearence de alfa-antitripsina como una técnica eficaz para objetivar la pérdida de proteínas a través del tubo digestivo y su aplicación como método de diagnóstico en tal patología. Se estudiaron 22 individuos; 11 con patología intestinal capaz de producir pérdida proteica y 11 controles sin daño de la mucosa intestinal. Se determinó la concentración de alfa-1-antitripsina tanto en suero como en materia fecal en días consecutivos y pesando la materia fecal de 24 horas se pudo obtener el clearence intestinal de dicha proteína. En los pacientes con enfermedad perdedora de proteínas el valor del clearence fue siempre patológico mientras que en los controles se obtuvieron valores normales. Este método es útil para diagnosticar la pérdida proteica intestinal y tiene la ventaja de no utilizar material radioactivo para su determinación

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We tried to evaluate the value of the alpha-1-antitrypsin clearance in order to search for the protein loss through the digestive tract. Twenty-two patients were studied, 11 with protein losing enteropathy and 11 normal controls. Alpha-1-antitrypsin concentration was determined in serum and feces to obtain the clearance of such protein. The values were always abnormal in patients with protein losing enteropathy, and normal in control patients. We consider this method simple and safe for the evaluation of intestinal protein loss, besides having the advantage of not using radioactive material.

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We tried to evaluate the value of the alpha-1-antitrypsin clearance in order to search for the protein loss through the digestive tract. Twenty-two patients were studied, 11 with protein losing enteropathy and 11 normal controls. Alpha-1-antitrypsin concentration was determined in serum and feces to obtain the clearance of such protein. The values were always abnormal in patients with protein losing enteropathy, and normal in control patients. We consider this method simple and safe for the evaluation of intestinal protein loss, besides having the advantage of not using radioactive material.

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