PDF(Pubmed)
Abstract：
UNASSIGNED: Hyperammonemic encephalopathy caused by Ureaplasma spp. and Mycoplasma hominis infection has been reported in immunocompromised patients undergoing lung transplant, but data are scarce in patients with hematological malignancies.
UNASSIGNED: We describe the cases of 3 female patients aged 11-16 years old, developing initially mild neurologic symptoms, rapidly evolving to coma and associated with very high ammonia levels, while undergoing intensive treatment for acute leukemia (chemotherapy: 2 and hematopoietic stem cell transplant: 1). Brain imaging displayed cerebral edema and/or microbleeding. Electroencephalograms showed diffuse slowing patterns. One patient had moderate renal failure. Extensive liver and metabolic functions were all normal. Ureaplasma spp. and M. hominis were detected by PCR and specific culture in two patients, resulting in prompt initiation of combined antibiotics therapy by fluoroquinolones and macrolides. For these 2 patients, the improvement of the neurological status and ammonia levels were observed within 96 h, without any long-term sequelae. M. hominis was detected post-mortem in vagina, using 16S rRNA PCR for the third patient who died of cerebral edema.
UNASSIGNED: Hyperammonemic encephalopathy linked to Ureaplasma spp. and M. hominis is a rare complication encountered in immunocompromised patients treated for acute leukemia, which can lead to death if unrecognized. Combining our experience with the few published cases (n=4), we observed a strong trend among female patients and very high levels of ammonia, consistently uncontrolled by classical measures (ammonia-scavenging agents and/or continuous kidney replacement therapy). The reversibility of the encephalopathy without sequelae is possible with prompt diagnosis and adequate combined specific antibiotherapy. Any neurological symptoms in an immunocompromised host should lead to the measurement of ammonia levels. If increased, and in the absence of an obvious cause, it should prompt to perform a search for Ureaplasma spp. and M. hominis by PCR as well as an immediate empirical initiation of combined specific antibiotherapy.
UNASSIGNED: We describe the cases of 3 female patients aged 11-16 years old, developing initially mild neurologic symptoms, rapidly evolving to coma and associated with very high ammonia levels, while undergoing intensive treatment for acute leukemia (chemotherapy: 2 and hematopoietic stem cell transplant: 1). Brain imaging displayed cerebral edema and/or microbleeding. Electroencephalograms showed diffuse slowing patterns. One patient had moderate renal failure. Extensive liver and metabolic functions were all normal. Ureaplasma spp. and M. hominis were detected by PCR and specific culture in two patients, resulting in prompt initiation of combined antibiotics therapy by fluoroquinolones and macrolides. For these 2 patients, the improvement of the neurological status and ammonia levels were observed within 96 h, without any long-term sequelae. M. hominis was detected post-mortem in vagina, using 16S rRNA PCR for the third patient who died of cerebral edema.
UNASSIGNED: Hyperammonemic encephalopathy linked to Ureaplasma spp. and M. hominis is a rare complication encountered in immunocompromised patients treated for acute leukemia, which can lead to death if unrecognized. Combining our experience with the few published cases (n=4), we observed a strong trend among female patients and very high levels of ammonia, consistently uncontrolled by classical measures (ammonia-scavenging agents and/or continuous kidney replacement therapy). The reversibility of the encephalopathy without sequelae is possible with prompt diagnosis and adequate combined specific antibiotherapy. Any neurological symptoms in an immunocompromised host should lead to the measurement of ammonia levels. If increased, and in the absence of an obvious cause, it should prompt to perform a search for Ureaplasma spp. and M. hominis by PCR as well as an immediate empirical initiation of combined specific antibiotherapy.
摘要：
■由脲原体引起的高氨血症性脑病。在接受肺移植的免疫功能低下的患者中，已经报道了人支原体感染，但是血液系统恶性肿瘤患者的数据很少。
■我们描述了3名年龄在11-16岁的女性患者的病例，最初发展为轻微的神经系统症状，迅速演变为昏迷，并伴有非常高的氨水平，同时接受急性白血病的强化治疗（化疗：2和造血干细胞移植：1）。脑成像显示脑水肿和/或微出血。脑电图显示弥漫性减慢模式。一名患者患有中度肾功能衰竭。广泛的肝脏和代谢功能均正常。脲原体属。并通过PCR和特异性培养检测了两名患者的人源支原体，迅速启动氟喹诺酮类和大环内酯类联合抗生素治疗。对于这两个病人来说，在96小时内观察到神经状态和氨水平的改善，没有任何长期后遗症。人类分枝杆菌在阴道死后被检测到，对第三例死于脑水肿的患者使用16SrRNAPCR。
■高氨血症性脑病与脲原体属有关。人型支原体是一种罕见的并发症，在接受急性白血病治疗的免疫功能低下患者中，如果不被识别就会导致死亡.结合我们的经验和少数已发表的案例(n=4)，我们观察到女性患者的强烈趋势和非常高的氨水平，始终不受经典措施（氨清除剂和/或连续肾脏替代疗法）的控制。通过及时诊断和适当的联合特异性抗菌治疗，可以逆转无后遗症的脑病。免疫受损宿主的任何神经症状都应导致氨水平的测量。如果增加,在没有明显原因的情况下，它应该提示执行脲原体属的搜索。通过PCR以及立即经验启动联合特异性抗菌疗法。
■我们描述了3名年龄在11-16岁的女性患者的病例，最初发展为轻微的神经系统症状，迅速演变为昏迷，并伴有非常高的氨水平，同时接受急性白血病的强化治疗（化疗：2和造血干细胞移植：1）。脑成像显示脑水肿和/或微出血。脑电图显示弥漫性减慢模式。一名患者患有中度肾功能衰竭。广泛的肝脏和代谢功能均正常。脲原体属。并通过PCR和特异性培养检测了两名患者的人源支原体，迅速启动氟喹诺酮类和大环内酯类联合抗生素治疗。对于这两个病人来说，在96小时内观察到神经状态和氨水平的改善，没有任何长期后遗症。人类分枝杆菌在阴道死后被检测到，对第三例死于脑水肿的患者使用16SrRNAPCR。
■高氨血症性脑病与脲原体属有关。人型支原体是一种罕见的并发症，在接受急性白血病治疗的免疫功能低下患者中，如果不被识别就会导致死亡.结合我们的经验和少数已发表的案例(n=4)，我们观察到女性患者的强烈趋势和非常高的氨水平，始终不受经典措施（氨清除剂和/或连续肾脏替代疗法）的控制。通过及时诊断和适当的联合特异性抗菌治疗，可以逆转无后遗症的脑病。免疫受损宿主的任何神经症状都应导致氨水平的测量。如果增加,在没有明显原因的情况下，它应该提示执行脲原体属的搜索。通过PCR以及立即经验启动联合特异性抗菌疗法。
