Ascites is rare in patients with multiple myeloma (MM). It may be due to diverse mechanisms, most frequently because of an increased permeability of the peritoneum or because of portal hypertension due to liver infiltration. Myelomatous ascites occurs more frequently in patients having Ig-G or Ig-A paraprotein and their prognosis is poor. It is submitted the case of a female patient aged 50 years with IgA-kappa MM, who evolved with cardiac failure (CF), plasma cells leukemia and ascites of mixed cause, because of peritoneal infiltrate of myelomatous cells, hepatic compromise and CF. A review of the different causes of ascites in patients with MM is performed. There are also summarized all myelomatous ascites cases published in the literature. Our report presents the first case of myelomatous ascites in a patient with plasma cells leukemia.

Los pacientes con mieloma múltiple (MM) raramente presentan ascitis. La misma puede responder a diversos mecanismos, siendo las causas más frecuentes el aumento de permeabilidad del peritoneo y la hipertensión portal por infiltración hepática. La ascitis mielomatosa (AM) ocurre con más frecuencia en pacientes con paraproteína de tipo Ig-G e Ig-A y su pronóstico es sombrío. Se presenta el caso de una paciente de sexo femenino de 50 años con diagnóstico de MM IgA-kappa que evoluciona con insuficiencia cardíaca (IC), leucemia de células plasmáticas y ascitis de causa mixta, por infiltración peritoneal por células mielomatosas, compromiso hepático e IC. Se realiza una revisión de las distintas causas de ascitis en pacientes con MM. Asimismo se resumen todos los casos publicados en la literatura mundial de AM. Nuestro reporte representa el primer caso de AM en un paciente con leucemia de células plasmáticas.

Primary systemic amyloidosis with clinical and histopathologic features of giant cell arteritis has already been described. The association of multiple myeloma (with primary amyloidosis) and giant cell arteritis is also known. We present the first case in the literature of a patient with multiple myeloma and giant cell arteritis without systemic amyloidosis, suggesting a pathogenic relationship between the two diseases.

La amiloidosis sistémica primaria y el mieloma múltiple con amiloidosis primaria se han presentado con características clínicas e histopatológicas que simulan una arteritis de células gigantes. Hasta el momento la asociación se basaba en el rol antigénico del depósito de amiloide sobre las arterias, desencadenando la respuesta inmune que finaliza con una arteritis. Presentamos el primer caso en la literatura de un paciente con mieloma múltiple y arteritis de células gigantes sin amiloidosis sistémica, sugiriendo una relación patogénica entre estas dos entidades. En el caso de nuestro paciente se descartó la presencia de amiloide en la pared arterial, por lo que proponemos que el estímulo para el desarrollo de la arteritis podría ser una excesiva producción de interleuquina 6 fabricada por las células mielomatosas.

ABO incompatibility in allogeneic bone marrow transplantation may be associated with incomplete or delayed erythroid engraftment, being pure red cell aplasia (PRCA) the most severe complication in this setting. Attempts for the treatment of PRCA have been made with erythropoietin or with plasmapheresis with relative success, and some authors have reported the reversibility of PRCA with antilymphocyte globulin (ALG or ATG), based on the assumption that PRCA might be immunologically mediated. We report herewith a patient with acute leukemia who developed post - BMT pure red cell aplasia. His sibling donor (sister) was HLA identical and ABO incompatible, having low agglutinin titers against donor's blood group. PRCA did not improve after treatment with erythropoietin or a boost of hematopoietic progenitor cells obtained from donor's peripheral blood but the problem was resolved completely after treatment with ALG.

El trasplante alogeneico de células progenitoras hematopoyéticas (TCPH) con incompatibilidad ABO entre el donante y el receptor puede en ocasiones asociarse a trastornos en la progenie eritroide desarrollada a partir de la médula ósea trasplantada, caracterizado por un funcionamiento tardío, inadecuado e incompleto de la misma. En este contexto, la aplasia pura de serie roja es la complicación más severa. Se han intentado tratamientos para la aplasia pura de serie roja post-TCPH con eritropoyetina o plasmaféresis, con relativo éxito. Algunos autores han informado también la utilización de globulina antilinfocitaria, asumiendo que dicha aplasia selectiva de la serie roja en la médula ósea trasplantada es mediada por un mecanismo inmune. En este trabajo se describe un paciente portador de una leucemia aguda en quien se realizó un TCPH alogeneico (ABO incompatible con su donante). Teniendo niveles bajos de aglutininas contra el grupo sanguíneo de la donante, desarrolló una aplasia pura de serie roja post - TCPH. La misma no mejoró con tratamiento con eritropoyetina o con un refuerzo de progenitores hematopoyéticos de sangre periférica de la misma donante (boost), resolviéndose totalmente luego de un tratamiento exitoso con globulina antilinfocitaria de origen equino.

In a previous study we demonstrated that the incidence of fibroblast colony-forming units (CFU-F) was very low in bone marrow primary cultures from the majority of untreated advanced non-small lung cancer patients (LCP) compared to normal controls (NC). For this reason, we studied the ability of bone marrow stromal cells to achieve confluence in primary cultures and their proliferative capacity following four continuous subcultures in consecutive untreated LCP and NC. We also evaluated the production of interleukin-1ß (IL-1ß) and prostaglandin E2 (PGE2) by pure fibroblasts. Bone marrow was obtained from 20 LCP and 20 NC. A CFU-F assay was used to investigate the proliferative and confluence capacity. Levels of IL-1ß and PGE2 in conditioned medium (CM) of pure fibroblast cultures were measured with an ELISA kit and RIA kit, respectively. Only fibroblasts from 6/13 (46%) LCP confluent primary cultures had the capacity to proliferate following four subcultures (NC = 100%). Levels of spontaneously released IL-1ß were below 10 pg/ml in the CM of LCP, while NC had a mean value of 1,217 ± 74 pg/ml. In contrast, levels of PGE2 in these CM of LCP were higher (77.5 ± 23.6 pg/ml) compared to NC (18.5 ± 0.9 pg/ml). In conclusion, bone marrow fibroblasts from LCP presented a defective proliferative and confluence capacity, and this deficiency may be associated with the alteration of IL-1ß and PGE2 production.