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#51 De:  Sergio V. Perrone <svperrone@interlink.com.ar>
Enviado:Martes 21de Diciembre de 1999 06:54
Asunto: Re: Chagas y Transplante/Re: Chagas and Transplantation
Interesante la revision bibliografica a travez de toda las publicaciones sobre Chagas y transplante que nos esta ofreciendo el colega. Especificamente en esta se hace referencia a la medicacion con Allopurinol para el tratamiento de la enfermedad de Chagas y quisiera hacer tres
comentarios:
1.- Se debe tener en cuenta que no todas las cepas responden al tratamiento con Allopurinol
2.- El allopurinol potencia significativamente la accion de la azathioprina ,por lo tanto es de hacer notar que los efectos indeseables de la droga son mas ostensibles (leucopenia e incluso aplasia medular) por lo cual es recomendable, en el caso de su utilizacion en pacientes que reciben ambas drogas disminuir la dosis a la mitad o mejor aun a 1/3 de la dosis habitual. En su defecto uno podria utilizar Micofenolato Mofetil que no ha mostrado interaccion con el allopurinol
3.- Ya que esta haciendo una revision bastante completa, que tal si nos provee de algun comentario sobre tratamiento de la parasitemia con Anfotericina B.

The bibliographical revision through all publications about Chagas and transplantation that our colleague is offering to us, is very interesting.
Specifically, in this reference is made to medication with Allopurinol for treatment of Chagas disease, and I would like to make three commentaries:
1- You must take into account that not all strains respond to treatment with Allopurinol
2- Allopurinol strengthens significantly the action of azathioprine, therefore it is necessary to make clear that the undesired  effects of the drug are more evident (leukopenia and even medullar aplasia), and because of this it is advisable, in the case of its use in patients that receive both drugs, to diminish the dose to a half, or even better, to a 1/3 of the usual dose. By default, one can use Micofenolate Mofetil, that has not displayed interaction with allopurinol
3- Since you are making a quite complete review: how about providing us with some commentary on treatment of parasitemia with
Anfotericine B
Dr. Sergio V. Perrone

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#52 De:  Enrique Manzullo
Enviado: Lunes 20de Diciembre de 1999 17:03
Asunto: Chagas y Trasplante/Chagas and transplantation
He leido las preguntas sobre terapeutica pariciticida en transplantes cardiaco. Tambien las respuestas de Jao Carlos Pinto Dias y de Roberto Michelson. Resulta claro que una terapeutica paraciticida eficaz, puede demostrarse porque un donante chagasico tratado y curado no deberia  trasmitir la infeccion al receptor, y un receptor chagasico tratado y curado no deberia infectar al organo recibido. Los colegas pueden sacar sus propias conclusiones de la bibliografia que presenta el Dr. Michelson. Tambien se puede destacar que en presencia de reagudizaciones el tratamiento paraciticida suele resultar eficaz. En Chagas agudo, los paraciticidas producen  curacion parasitologica y serologica, en reagudizaciones, por inmusupresion (transplantes, HIV, etc.)curacion del cuadro clinico frecuentemente, con mantenimiento de la serologia positiva. Que ocurre con la evolucion del cronico? Los resultados constituyen la mayor discusion en Chagas desde hace por lo menos treinta
anos. Creo importante destacar que no se puede descansar en el tratamiento paraciticida para transplantar tanto sea el chagasico donante o receptor. Se debe tratar pero tambien se debe estar muy alerta a las reagudizaciones que son frecuentes. El acto donacion- recepcion masfrecuente es la transfucion de sangre. Pregunto si el investigar  mas convencido de la utilidad de los paraciticidas permitiria que los chagasicos cronicos tratados fueran donantes de sangre.
Cordialmente.

I have read the questions about parasiticide therapeutics in heart transplantations. Also the answers by Joao Carlos Pinto Dias and Roberto Michelson. It is clear that an efficient parasiticide therapeutic may be proven because a treated and cured chagasic donor should not transmit
the infection to the receptor, and a treated and cured chagasic receptor should not infect the organ received. The colleagues may draw your own conclusions from the bibliography presented by Dr. Michelson. We can also emphasize that in the presence of new acuteness, the parasiticide treatment is usually efficient. In acute Chagas, parasiticides produce parasitologic and serologic healing, in new acuteness due to immunosuppression (transplantation, HIV, etc.), frequently healing of clinical manifestations, with maintenance of positive serology. What happens with evolution of chronic patients? Results constitute the greatest argument in Chagas since at least thirty years. I think it is important to emphasize that one cannot lay in parasiticide treatment to transplant, whether the chagasic patient is the donor or the receptor. It must be treated, but we must be very alert as well, to new acuteness that is frequent. The most frequent donation-reception act is blood transfusion. I wonder if we were to research more convinced of the usefulness of parasiticides, this would allow treated chronic chagasic patients to be blood donors.
Cordially,
Enrique Manzullo

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#53 De:  Joao Carlos Pinto Dias   <jcpdias@cpqrr.fiocruz.br>
Enviado: Jueves, 23 de Diciembre de 1999 07:22 p.m.
Asunto: Re: Chagas y Trasplante Medula Osea/Chagas and Bone Marrow transplantation
>Estimados colegas :
>Pregunta :
>Terapeutica profilactica en los pacientes que van a ser sometidos a trasplante de medula osea de tiopo autologo y alogenico en caso de  >receptor con serologia positiva o dador positivo: Momento, droga, duracion.
>Dr Alberto Cremona
En este caso, el mayor consenso es simplemente observar, desde que los dos son infectados. En el caso de acontecer una REACTIVACION, tratar como agudo (Benznid. 5mg/k/dias (en dos tomas) x 60 dias, para adulto. Ninos: 7 a 10 mg/k/dia). El mas probable es no pasar nada.
Joao Carlos Pinto Dias.
Fiocruz, Brasil.

>Dear colleagues:
>Question:
>Prophylactic therapy in patients that are going to undergo bone marrow transplantation, autologous and allogenic, in case of  receptor with >positive serology, or positive donor: time, drug, and duration.
>Dr Alberto Cremona
In this case, the greater consensus it just to observe, since both are infected. In case of a REACTIVATION, treat as acute (Benznid. mg/kg/day (twice) x 60 days, for adults. Children: 7 to 10mg/kg/day). The most probable, is that nothing happens.
Joao Carlos Pinto Dias.
Fiocruz, Brasil.

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#54 De: Horacio Romero Villanueva <ramichel@intramed.net.ar >
Enviado: Lunes 27 de Diciembre de 1999 11:42
Asunto: Chagas y transplante de medula osea/Chagas and Bone Marrow transplantation
Quisiera referirme a la pregunta formulada por el Dr. Alberto Cremona, del Servicio de Transplante de Medula Osea del Hospital Italiano de La  Plata.
Los Dres. Dictar M, Sinagra A, Veron MT et al. (Recipients and donors of bone marrow transplants suffering from Chagas disease: management and preemptive therapy of parasitemia. Bone Marrow Transplantation, 1998, 21: 291-293) de la Unidad de Transplante de Medula Osea, del Servicio de Enfermedades Infecciosas, CP Independencia, del Instituto Nacional de Parasitologia Dr. Mario Fatala Chaben, de Buenos Aires, comunicaron el caso clinico de cinco pacientes adultos con enfermedad de Chagas que fueron sometidos a un transplante de medula osea durante un periodo comprendido entre 1989 y 1996. Dos pacientes tenian un linfoma no-Hodgkin y uno una leucemia linfoblastica aguda, recibiendo transplantes autologos.
Transplantes de medula osea halogenicos se realizaron en dos pacientes, uno con una leucemia mieloide aguda y el otro con una leucemia mieloide cronica respectivamente. Uno de los donantes presentaba una enfermedad chagasica cronica.
En todos los pacientes se extrajeron muestras de sangre periferica para investigacion del parasito por el metodo Strout, por hemocultivo, y mediante estudios inmunologicos por medio de analisis de inmunofluorescencia indirecta, ELISA y test de hemaglutinacion indirecta. Estos fueron realizados semanalmente desde el comienzo de la quimioterapia hasta mas alla del dia 60 para los transplantes autologos y durante el periodo de inmunosupresion en los transplantados alogenicos (cada 15 dias durante el tercer mes y mensualmente durante el periodo de inmunosupresion). No se hizo profilaxis para Chagas en ninguno de estos pacientes.
Solamente en un paciente con transplante autologo se pudo detectar tripomastigotes tempranamente por hemocultivo, sin que se observaran  signos de reactivacion
Se administro como tratamiento benznidazole durante 30 dias en dosis de 5-8 mg/kg/dia, comenzandose con 5 mg/kg/dia durante los tres primeros dias, y luego con una dosis de 8 mg/kg/dia durante 30 dias. La parasitemia fue rapidamente limpiada y al final de la terapia el xenodiagnostico fue negativo. En este paciente no se observaron efectos adversos de la terapia parasiticida. Los otros pacientes con enfermedad de Chagas no evidenciaron reaparicion de la parasitemia o signos y sintomas de reactivacion.
Los requisitos para definir una reactivacion fueron la deteccion de parasitos en la sangre, o bien en el liquido cefalorraquideo cuando estaban presentes signos neurologicos, y por biopsia cutanea y lesiones de organos profundos cuando existian signos de reactivacion.
Dos pacientes con transplantes alogenicos y un paciente con transplante autologo murieron despues del transplante, pero en ninguno de ellos se hicieron hallazgos sugestivos de reactivacion de la enfermedad de Chagas.
Con referencia a la parte de la pregunta del colega acerca de lo que ocurre cuando el donante es portador de la enfermedad de Chagas, permitaseme comentar el caso numero tres de esta serie, que es el de una mujer de 48 anios con una leucemia mieloide cronica. El donante tenia serologia positiva para Chagas, pero la parasitemia previa al transplante fue negativa. Durante la neutropenia no mostro ningun tipo de signos o sintomas sugestivos de enfermedad de Chagas. Durante el protocolo de seguimiento la serologia se definio como "discordante", lo cual significa negativizacion serologica y discordancia en los titulos de Ab anti-Cruzi, Strout negativo y cultivo de sangre negativo.
Por su parte, Altclas J, Jaimovich G et al. (Reactivation of chronic Chagas disease following allogenic bone marrow transplantation and successful preemptive therapy with benznidazole. Transplant Infectious Disease. 1999, 1:135-137) del Instituto de Criopreservacion y Transplante de Medula Osea, IMA, de Buenos Aires, y del Instituto Nacional de Parasitologia "Dr. Mario Fatala Chaben", comunicaron el caso de un paciente con enfermedad de Chagas de 27 anios de edad, con una leucemia mielogena cronica a quien se le realizo un transplante alogenico de medula osea. El paciente fue chequeado semanalmente por el metodo de Strout y cultivos de sangre los dos primeros meses, luego cada quince dias durante el tercer mes, y mensualmente durante el periodo de inmunosupresion. En el dia + 101, se detecto T.Cruzi en sangre periferica, iniciandose terapia con benznidazole a razon de 400 mg/dia.
La parasitemia fue limpiada el dia + 110, despues de siete semanas de tratamiento. La evolucion fue favorable y no se observaron efectos adversos inducidos por el benznidazole. El paciente continua libre de parasitemia dos anios despues de realizado el transplante.
Espero que esta informacion sea de alguna utilidad al colega, a quien aprovecho para enviar un saludo cordial.

I would like to mention the question asked by Dr. Alberto Cremona, from the Service of Bone Marrow Transplantation from the "Hospital Italiano" in La Plata.
Drs. Dictar M, Sinagra A, Veron MT et al. (Recipients and donors of bone marrow transplants suffering from Chagas disease: management and preemptive therapy of parasitemia. Bone Marrow Transplantation,  1998, 21: 291-293) from the Unit of Bone Marrow Transplantation, from the Service on Infectious Diseases, CP Independencia, from the "Instituto Nacional de Parasitologia Dr. Mario Fatala Chaben", in Buenos Aires,  communicated the clinical case of five adult patients with Chagas disease that underwent a bone marrow transplantation during a period from 1989 and 1996. Two patients had no-Hodgkin lymphoma, and one had acute lymphoblastic leukemia, receiving autologous transplants. Halogenous bone marrow transplants were carried out in two patients, one with acute myeloid leukemia, and the other with chronic myeloid leukemia, respectively. One of the donors presented a chronic chagasic disease.
In all patients samples of peripheral blood were extracted to investigate the parasite by the Strout method, by blood culture, and by immunologic studies through analysis of indirect immunofluorescence, ELISA and indirect hemagglutination test. These were carried out weekly after the beginning of the chemotherapy until beyond the 60th day for autologous transplantation, and during the period of immunosuppression in the allogenic transplanted patients (each 15 days during the third month, and monthly during the period of immunosuppression). In none of these patients prophylaxis was carried out. 
Only in a patient with autologous transplantation we could detect tripomastigotes early by blood culture, without observing signs of reactivation. Benznidazole was administered as treatment during 30 days in doses of 5-8mg/kg/day, beginning with 5mg/kg/day during the first three days, and later with a dose of 8mg/kg/day during 30 days. The parasitemia was quickly cleaned, and at the end of the therapy the xenodiagnosis was negative. In this patient, adverse effects were not observed in the parasiticide therapy. The other patients with
Chagas disease did not display reappearance of parasitemia or signs and symptoms of reactivation.
The requisites to define a reactivation were the detection of parasites in blood, or else in the cerebrospinal fluid when neurological signs were present, and by cutaneous biopsy, and lesions in deep organs when there were reactivation signs. Two patients with allogenic transplants and a patient with autologous transplantation died after the transplantation, but in none of them significant finds of reactivation of Chagas disease were observed.
Concerning the part of the question by the colleague about what happens when the donor is a Chagas disease carrier, let me comment
on the case number three of this series, which is a female, 48 years old, with chronic myeloid leukemia. The donor had positive serology for Chagas, but the parasitemia previous to the transplantation was negative. During neutropenia the latter did not display any kind of significant signs or symptoms of Chagas disease. During the follow up protocol, the serology was defined as "discordant", which means serologic negativization, and discordance in titration of Ab anti-Cruzi, negative Strout, and negative blood culture.
As for Altclas J, Jaimovich G et al. (Reactivation of chronic Chagas disease following allogenic bone marrow transplantation and successful preemptive therapy with benznidazole. Transplant Infectious Disease. 1999, 1:135-137) from the "Instituto de Criopreservacion y Transplante de Medula Osea", IMA, in Buenos Aires, and the "Instituto Nacional de Parasitologia 'Dr. Mario Fatala Chaben'", communicated the case of a patient with Chagas disease, 27 years old, with a chronic myelogenic leukemia, in whom an allogenic bone marrow transplantation was performed. The patient was checked weekly by the Strout method, and blood cultures during the first two months, after each fifteen days during the third month, and monthly during the period of immunosuppression. On the day + 101, T. Cruzi was detected in peripheral blood, beginning then a therapy with benznidazole in doses of 400mg/day. The parasitemia was cleaned on the day + 110, after seven weeks of treatment. The evolution was favorable, and no adverse effects induced by benznidazole were observed. The patient remains free of parasitemia two years after the transplantation.
I hope that this information is somehow useful for my colleague, to whom I send my warm regards.
DR. HORACIO ROMERO VILLANUEVA

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#55 De:  Alberto Cremona
Enviado: Lunes 10 de Enero de 2000 22:09
Asunto:Megavisceras/Megaviscera
Sponsored by: Pfizer
Estimados colegas :
Experiencia en tratamiento de los pacientes con serología positiva con afectación viseral: Momento, droga, evaluación del tratamiento.

Dear colleagues:
Experience in treatment of the patients with positive serology with viscera involvement: Moment, drug, evaluation of treatment.
Dr. Alberto Cremona
Infectologo
Hospital Italiano La Plata

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#56 De: Enrique Manzullo
Enviado: Lunes 10 de  Enero de 2000 17:03
Asunto: Chagas y Trasplante/Chagas and transplantation
Sponsored by: Pfizer
He leido las preguntas sobre terapeutica pariciticida en transplantes cardiaco. Tambien las respuestas de Joao Carlos Pinto Dias y de Roberto Michelson.
Resulta claro que una terapeutica paraciticida eficaz, puede demostrarse porque un donante chagasico tratado y curado no deberia trasmitir la infeccion al receptor, y un receptor chagasico tratado y curado no deberia infectar al organo recibido.
Los colegas pueden sacar sus propias conclusiones de la bibliografia que presenta el Dr. Michelson. Tambien se puede destacar que en presencia de reagudizaciones el tratamiento paraciticida suele resultar eficaz.
En Chagas agudo, los paraciticidas producen curacion parasitologica y serologica, en reagudizaciones, por inmusupresion (transplantes, HIV, etc.)curacion del cuadro clinico frecuentemente, con mantenimiento de la serologia positiva. Que ocurre con la evolucion del cronico? Los resultados constituyen la mayor discusion en Chagas desde hace por lo menos treinta anos.
Creo importante destacar que no se puede descansar en el tratamiento paraciticida para transplantar tanto sea el chagasico donante o receptor. Se debe tratar pero tambien se debe estar muy alerta a las reagudizaciones que son frecuentes.
El acto donacion- recepcion mas frecuente es la transfucion de sangre. Pregunto si el investigar mas convencido de la utilidad de los paraciticidas permitiria que los chagasicos cronicos tratados fueran donantes de sangre.
Cordialmente.

I have read the questions about parasiticide therapeutics in heart transplantation. Also the answers by Joao Carlos Pinto Dias, and Roberto Michelson. It is clear that an efficient parasiticide therapeutics may be proven because a treated and cured chagasic donor should not transmit
the infection to the receptor, and a treated and cured chagasic receptor, should not infect the received organ. The colleagues may draw their own conclusions about the bibliography presented by Dr. Michelson.
It may be emphasized also that in the presence of new worsening, the parasiticide treatment is usually efficient.
In acute Chagas, the parasiticides produce parasitologic and serologic healing, in new worsenings, by immunosupression (transplantation, HIV, etc.) healing of clinical manifestations frequently, with maintenance of positive serology. What happens with the evolution of the chronic patient? Results have constituted the greatest discussion in Chagas for at least thirty years.
I think it is important to emphasize that there should be no rest in the parasiticide treatment for transplantation, both in chagasic donors or receptors. We must treat, but we must also be very alert to new worsening, that is frequent.
The most frequent donation-reception act is blood transfusion. I wonder if researching more convinced of the usefulness of parasiticides would allow treated chronic chagasic patients to be blood donors.
Cordially,
Enrique Manzullo

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#57 De: Sergio V. Perrone <svperrone@interlink.com.ar>
Enviado: Jueves 23 de Diciembre de 1999 00:54
Asunto: Re: Chagas y Trasplante/Re: Chagas and transplantation
Sponsored by: Bayer SA
Respuesta al Caso Clinico enviado por la Dra Paola Koslowski:
Mas que respuesta desearia obtener mas datos sobre la paciente de referencia:
1.- Cuales fueron las dosis de azathioprina y Cyclosporina (CsA) a las que Ud refire como menores y que niveles T0 de CsA fueron alcanzados durante el post operatorio?
2.- Se utilizaron terapia de induccion?
3.- Resultado del Cross match contra Pannel y del Cross match Directo?
3.- La profilaxis con Gancyclovir (DHPG) se debi=F3 a miss match donante receptor?
4.- Que grado de episodios de rechazo (ISHLT) presento la paciente, al cuanto tiempo post-Transplante se presentaron y como fueron tratados?
5.- Se coloco profilaxis antiparasitaria ante la administracion de GAT o el incremento de los esteroides para el tratamiento de los episodios de rechazo?
6.- Cual fue la evolucion de la paciente? no parece ser muy favorable!.

Answer to the Clinical Case submitted by Dr. Paola Koslowski:
More than an answer, I would like to obtain more data about the mentioned patient:
1. Which were the doses of azathioprine and cyclosporine (CsA) that you mentioned as lower, and what T0 levels of CsA were reached during the post-operative?
2. Was induction therapy used?
3. Result of the Cross match against Pannel, and Direct Cross match?
3. Prophylaxis with Gancyclovir (DHPG) was due to donor-receptor miss match?
4. What degree of episodes of rejection (ISHLT) did the patient present, how long after post-transplantation did they present, and how were treated?
5. Was anti-parasite prophylaxis used before administration of GAT, or increase of steroids for treatment of episodes of rejection?
6. How was the evolution of the patient? It does not seem very favorable!
Dr. Sergio V. Perrone

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#58 De:  Paola Koslowski
Enviado: Lunes 17 de Enero de 2000 11:50
Asunto: Chagas y Trasplante/Chagas and transplantation
Sponsored by: Bayer SA
En relacion a las preguntas del Dr. Sergio Perrone referentes al caso clinico comentado:
> 1.- Cuales fueron las dosis de azathioprina y Cyclosporina (CsA) a las que  Ud refire como menores y que niveles T0 de CsA fueron >alcanzados durante el  post operatorio?
1) La dosis de Azotioprina utilizada en principio fue: 150 mg/dia; y la de Ciclosporina:150 mg/dia.
> 2.- Se utilizaron terapia de induccion?
2) no se utilizo terapia de induccion.
> 4.- Que grado de episodios de rechazo (ISHLT) presento la paciente, al  cuanto tiempo post-Transplante se presentaron y como fueron >tratados?
4) El primer episodio de rechazo fue Grado IIIA, se desarrollo a los 21 dias del transplante y se inicio tratamiento con: Linfoglobulina 2.5 mg/dia, y se aumento la dosis de Ciclosporina a 300 mg/dia. El segundo a los 43 dias y se evidencio por BEM (biopsia endomiocardica) Rechazo IA-IB, donde no hubo modificaciones en el tratamiento. El tercer episodio se diagnostica a los 60 dias y fue grado IIIA, se reemplaza el tratamiento de Micofenolato-mofetil (que se habia reemplazado por la Azatioprina a los 5 dias post-transplante) por Ciclofosfamida 100 mg/dia, se administra bolo de Metilprednisolona 1 gr/dia por tres dias (continuando con deltisona 60 mg/dia). A los 110 dias se constata Rechazo II donde se continua con el mismo tratamiento. Finalmente a los 120 dias aparece en la BEM control Rechazo IA-IB, continuando en tratamiento con Ciclofosfamida 50 mg/dia, Ciclosporina 300 mg/día, Deltisona B 60 mg/dia.
> 5.- Se coloco profilaxis antiparasitaria ante la administracion de GAT o el   incremento de los esteroides para el tratamiento de los episodios de
> rechazo?
5) No.
> 6.- Cual fue la evolucion de la paciente? no parece ser muy favorable!.
La evolucion posterior fue buena; no volvio a presentar episodios de rechazo.
Un resumen ampliado de la Historia clinica, en castellano, se halla disponible para quienes lo soliciten.

About the questions by Dr. Sergio Perrone in regard to the commented clinical case:
>"1. Which were the doses of azathioprine and cyclosporine (CsA) that you mentioned as lower, and what T0 levels of CsA were reached
during the post-operative?"
1) The dose of Azathioprine used initially was: 150mg/day; and Cyclosporine: 150mg/day
>"2. Was induction therapy used? "
2) We did not use an induction therapy.
>"4. What degree of episodes of rejection (ISHLT) did the patient present, how long after post-transplantation did they present, and how were treated?"
4) The first episode of rejection was degree IIIA, it developed 21 days after transplantation, and we began treatment with: Lymphoglobulin 2.5mg/day, and the dose of Cyclosporine at 300mg/day was increased. The second at the 43 days, and became evident through EMB (emdomyocardial biopsy). Rejection IA-IB, where there were no modifications in treatment. The third episode was diagnosed at the 60 days, and was degree IIIA, the treatment of Mycophenolate mofetil was replaced (that was replaced by Azathioprine after 5 days post-transplantation) due to Cyclophosphamide 100mg/day, bolus of Methylprednisolone 1gr/day is administered for three days (continuing with deltisone 60mg/day). After 110 days Rejection II was verified, and the same treatment is continued.
Finally, after 120 days the EMB of control displays Rejection IA-IB, continuing under treatment with Cyclophosphamide 50mg/day, Cyclosporine 300mg/day, Deltisone B 60mg/day.
>"5. Was anti-parasite prophylaxis used before administration of GAT, or increase of steroids for treatment of episodes of rejection?"
5) No
>"6. How was the evolution of the patient? It does not seem very favorable!"
Afterwards evolution was good: she did not present episodes of rejection.
An expanded summary of the clinical History, in Spanish, is available for those who ask for it.

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#59 De:  Leonardo Feldman
Enviado: Viernes 14 de Enero de 2000 04:56 PM
Asunto: Dr.Feldman: Trasplante de médula ósea en pacientes con Chagas/Dr. Feldman: bone marrow transplantation in patients with chagas.
Sponsored by: Laboratorios Bago
Pacientes inmunocomprometidos, como aquellos que reciben un Trasplante de médula ósea,tienen riesgo de enfermedad de Chagas por reactivación o por las múltiples transfusiones recibidas especialmente en países donde esta enfermedad es endemica.Nuestro grupo describió recientemente el caso de un paciente femenino que recibió un TAMO (Trasplante Medula Osea) alogénico de un hermano histo idéntico por una Leucemia Mieloide Cronica.El paciente y donante presentaron, previo al transplante, test de chagas por Elisa negativos. Y todos los productos sanguíneos infundidos, fueron negativos para chagas.El día + 23 presentó un engraftment adecuado. El día + 48 fue readmitida por un GVHD. II-III y tratada con methylprednisona 30 mg kg.día. El día +65 observamos en los extendidos de sangre periférica formas morfológicas que identificamos como trypomastigotes del trypanosoma cruzi. La paciente presentó severa pancitopenia complicada con una sepsis por seudomona aeruginosa.El aspirado de médula ósea, mostró un cuadro aplásico y múltiples tripanosomas. La paciente fallece el día + 74 por hemorragia y sepsis no controlada mientras realizaba tratamiento con nifurtimox 10mg. kg., durante al menos 8 días.-(Case Report. CHAGAS DISEASEA AFTER BONE MORROW TRANSPLANTATION, J. Altlas,G. Jaimovich, V. Milovik, F. Klein,and L.Feldman.Bone Marrow Transplantation (1996) 18-447-448).
Además hemos reportado más recientemente, la detección precoz de reactivación en un hombre de 27 con Leucemia Mieloide Crónica sometido a transplante alogénico de médula, y en el que la terapia preventiva, con benznidazole durante un período de 7 semanas,llevó a una rápida recuperación del paciente, el que continúa libre de parasitemia dos años después del transplante.( J. Altlas, A. Sinagra, A. Requejo, L. Feldman, A. Riarte. Transpl. Infect Dis.1999 1, 135-137) Por lo tanto nosotros sugerimos el uso de dos diferentes test específicos para evitar los resultados falsos negativos, y el uso profiláctico de drogas antitripanosómicas, como nifurtimox o benznidazole ( que son potenciamente mielotóxicas) o interferon gama en pacientes serológicamente positivos que van a realizar TAMO.-
Dr. Leonardo Feldman
Hematologo

Immuno-endangered patients, like those that receive a bone marrow transplantation, are under risk of Chagas disease due to reactivation, or due to multiple transfusions received, especially in countries where this disease is endemic. Our group recently described the case of a female patient that received an allogenic BMT (Bone Marrow Transplantation) from a histo-identical brother due to a Chronic Myeloid Leukemia. The  patient and donor presented, prior to the transplantation, negative test of chagas by Elisa. And all administered blood products, were negative for chagas. On day + 23, she presented a proper engraftment. On day + 48 she was readmitted due to a GVHD II-III, and treated with methylprednisone, 30mg/kg/day. On day + 65 we observed in the samples of peripheral blood, morphological forms that we identified as trypomastigotes of trypanosoma cruzi. The patient presented severe pancytopenia, complicated with a sepsis due to seudonoma aeruginosa. Aspiration of bone marrow displayed aplastic manifestations, and multiple tripanosomas. The patient died on day + 74 due to hemorrhage and non-controlled sepsis while under treatment with  nifurtimox 10mg/kg, during at least 8 days.-( Case Report. CHAGAS DISEASE AFTER BONE MORROW TRANSPLANTATION, J. Altlas,G. Jaimovich, V. Milovik, F. Klein,and L.Feldman.Bone Marrow Transplantation (1996) 18-447-448).
Besides, we have reported more recently, the early detection of reactivation in a 27-year-old man with Chronic Myeloid Leukemia that underwent an allogenic transplantation of medulla, and in whom preventive therapy with benznidazole during a period of 7 weeks, lead to a quick recovery of the patient, who remains free of parasitemia two years after transplantation. (J. Altlas, A. Sinagra, A. Requejo, L. Feldman, A. Riarte. Transpl. Infect Dis.1999 1, 135-137). Therefore, we suggest use of two different specific tests to prevent the negative false results, and the prophylactic use of anti-tripanosomic drugs, such as nifurtimox or benznidazole (that are potentially myelotoxic) or interferon gamma in  serologic positive patients that will undergo BMT.
Dr. Leonardo Feldman
Hematologo
Bs As .Argentina

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#60 De: Edgardo Schapachnik  <edgardo@schapachnik.com.ar>
Enviado: Miercoles 26 de Enero de 2000, 11:11
Asunto: Chagas con serologia no reactiva?/Chagas with non reactive serology?
Sponsored by: IntraMed
Estimados colegas y amigos:
En mi caracter de Moderador alterno (Marcelo Bassino disfruta de sus vacaciones) me parecio de interes hacerles llegar una consulta que hoy me hicieron los medicos residentes del Hospital.
Se trata de un paciente joven (42 anios) sin factores de riesgo coronario, nacido en la Banda, Provincia de Santiago del Estero, Argentina, que como todos ustedes conocen es una de las mas alta endemicidad para la enfermedad que nos ocupa.
Sintetizando en muy pocas lineas el resumen de Historia clinica, este paciente es internado con un cuadro de insuficiencia cardiaca a predominio derecho. El ECG muestra un ritmo sinusal predominante, aunque alternan breves periodos de fibrilacion auricular, bloqueo completo de rama derecha, hemibloqueo anterior izquierdo, arritmia ventricular caracterizada por extrasistoles muy frecuentes, duplas y tripletas, diurnas y nocturnas. En el ecocardiograma presenta signos claros de miocardiopatia dilatada con un microaneurisma apical.
Hasta aqui, el caso parece sacado de un libro.
Tres serologias realizadas en el INDIECH (Instituto Nacional de Investigacion de Enfermedad de Chagas), -inmunoensayo enzimatico, inmunofluorecencia indirecta y hemoaglutinacion indirecta- han sido NO REACTIVAS.
La pregunta que me hicieron los colegas residentes y que comparto con ustedes es si a pesar de estos resultados serologicos se puede sostener el diagnostico de miocardiopatia dilatada chagasica teniendo en cuenta los demas elementos. Que otros estudios sugeririan? Cambiarian ellos la conducta?
Un abrazo.

Dear colleagues and friends:
As the substitute Moderator (Marcelo Bassino is enjoying his holidays), I considered it would be interesting to send you a consult that I was made today by the residents of the Hospital.
This is a young patient (42 years), without coronary risk factors, who was born in la Banda, in the Province of Santiago del Estero, Argentina, that as you may know is an area with highest endemicity for the disease we are dealing with.
Summarizing his clinical history in a few lines, this patient was admitted with clinical manifestations of heart failure with right predominance.  The ECG displays predominant sinusal rhythm, though there are brief alternate periods of atrial fibrillation, complete block of right ramus, left anterior hemi-block, ventricular arrhythmia characterized by very frequent extrasystoles, double and triple, during daytime and night-time.
In the echocardiogram, he shows clear signs of dilated cardiomyopathy with an apical microaneurysm.
Up to here, the case seems to be taken from a book.
Three serologies were carried out at the INDIECH (Instituto Nacional de Investigacion de Enfermedad de Chagas-National Institute for Research of Chagas Disease), -enzymatic immunoassay, indirect immunofluorescence, and indirect hemoagglutination- and they were NON REACTIVE.
The question I was made by my resident colleagues, and that I share with you is, if in spite of these serologic results, the diagnosis of chagasic dilated cardiomyopathy can be sustained, taking into account the rest of the elements. What other studies would you suggest? Would they change management?
Hugs,
Edgardo

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Feb/01/2000