Abdulrahman Nasiri, Tamam Alshammari, Alanood Alsolaihim, Huda Alfattah, Ali Alahmri
{"title":"他克莫司相关格林-巴利综合征。","authors":"Abdulrahman Nasiri, Tamam Alshammari, Alanood Alsolaihim, Huda Alfattah, Ali Alahmri","doi":"10.22551/2025.47.1202.10317","DOIUrl":null,"url":null,"abstract":"<p><p>Guillain-Barré syndrome (GBS) is a rare but serious neuropathy in hematopoietic stem cell transplant recipients. Immunosuppressants, particularly tacrolimus, have been implicated as potential triggers. We present a 27-year-old man with BCR-ABL-positive acute myeloid leukemia who developed an acute demyelinating polyneuropathy possibly related to tacrolimus therapy post-transplantation, highlighting diagnostic challenges and management considerations. The patient developed progressive ascending weakness, areflexia, sensory loss, and bulbar symptoms 58 days after an allogeneic stem cell transplant from an HLA-matched sibling donor. Cerebrospinal fluid (CSF) analysis showed elevated protein (1,900 mg/L) with lymphocytic pleocytosis (51 cells/μL), an atypical finding for GBS. Magnetic resonance imaging revealed subtle nerve root enhancement, and nerve conduction studies demonstrated markedly slowed conduction velocities and prolonged distal latencies consistent with an acute inflammatory demyelinating polyneuropathy. Extensive infectious work-up (including viral PCR panels and cultures) was negative, and no leukemic cells were seen in CSF. Tacrolimus was discontinued (trough level 3.1 ng/mL, below therapeutic range) and intravenous immunoglobulin (2 g/kg total over five days) initiated. The patient's neurological deficits improved rapidly, with near-complete recovery within four weeks. Notably, withdrawal of tacrolimus immunosuppression did not precipitate graft-versus-host disease, and the patient's acute leukemia remained in remission on ponatinib monotherapy. This case illustrates an acute demyelinating polyneuropathy in a post-transplant patient, associated with tacrolimus. It underscores the importance of careful diagnostic assessment of GBS in transplant recipients, including consideration of atypical CSF findings and alternative diagnoses. Prompt recognition and management - including immunosuppressant adjustment and immunotherapy - can achieve full neurological recovery without compromising transplant outcomes.</p>","PeriodicalId":72274,"journal":{"name":"Archive of clinical cases","volume":"12 2","pages":"75-79"},"PeriodicalIF":0.6000,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12096302/pdf/","citationCount":"0","resultStr":"{\"title\":\"Tacrolimus associated Guillain-Barre syndrome.\",\"authors\":\"Abdulrahman Nasiri, Tamam Alshammari, Alanood Alsolaihim, Huda Alfattah, Ali Alahmri\",\"doi\":\"10.22551/2025.47.1202.10317\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Guillain-Barré syndrome (GBS) is a rare but serious neuropathy in hematopoietic stem cell transplant recipients. Immunosuppressants, particularly tacrolimus, have been implicated as potential triggers. We present a 27-year-old man with BCR-ABL-positive acute myeloid leukemia who developed an acute demyelinating polyneuropathy possibly related to tacrolimus therapy post-transplantation, highlighting diagnostic challenges and management considerations. The patient developed progressive ascending weakness, areflexia, sensory loss, and bulbar symptoms 58 days after an allogeneic stem cell transplant from an HLA-matched sibling donor. Cerebrospinal fluid (CSF) analysis showed elevated protein (1,900 mg/L) with lymphocytic pleocytosis (51 cells/μL), an atypical finding for GBS. Magnetic resonance imaging revealed subtle nerve root enhancement, and nerve conduction studies demonstrated markedly slowed conduction velocities and prolonged distal latencies consistent with an acute inflammatory demyelinating polyneuropathy. Extensive infectious work-up (including viral PCR panels and cultures) was negative, and no leukemic cells were seen in CSF. Tacrolimus was discontinued (trough level 3.1 ng/mL, below therapeutic range) and intravenous immunoglobulin (2 g/kg total over five days) initiated. The patient's neurological deficits improved rapidly, with near-complete recovery within four weeks. Notably, withdrawal of tacrolimus immunosuppression did not precipitate graft-versus-host disease, and the patient's acute leukemia remained in remission on ponatinib monotherapy. This case illustrates an acute demyelinating polyneuropathy in a post-transplant patient, associated with tacrolimus. It underscores the importance of careful diagnostic assessment of GBS in transplant recipients, including consideration of atypical CSF findings and alternative diagnoses. Prompt recognition and management - including immunosuppressant adjustment and immunotherapy - can achieve full neurological recovery without compromising transplant outcomes.</p>\",\"PeriodicalId\":72274,\"journal\":{\"name\":\"Archive of clinical cases\",\"volume\":\"12 2\",\"pages\":\"75-79\"},\"PeriodicalIF\":0.6000,\"publicationDate\":\"2025-05-22\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12096302/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Archive of clinical cases\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.22551/2025.47.1202.10317\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/1/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"Q3\",\"JCRName\":\"MEDICINE, GENERAL & INTERNAL\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Archive of clinical cases","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.22551/2025.47.1202.10317","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/1/1 0:00:00","PubModel":"eCollection","JCR":"Q3","JCRName":"MEDICINE, GENERAL & INTERNAL","Score":null,"Total":0}
Guillain-Barré syndrome (GBS) is a rare but serious neuropathy in hematopoietic stem cell transplant recipients. Immunosuppressants, particularly tacrolimus, have been implicated as potential triggers. We present a 27-year-old man with BCR-ABL-positive acute myeloid leukemia who developed an acute demyelinating polyneuropathy possibly related to tacrolimus therapy post-transplantation, highlighting diagnostic challenges and management considerations. The patient developed progressive ascending weakness, areflexia, sensory loss, and bulbar symptoms 58 days after an allogeneic stem cell transplant from an HLA-matched sibling donor. Cerebrospinal fluid (CSF) analysis showed elevated protein (1,900 mg/L) with lymphocytic pleocytosis (51 cells/μL), an atypical finding for GBS. Magnetic resonance imaging revealed subtle nerve root enhancement, and nerve conduction studies demonstrated markedly slowed conduction velocities and prolonged distal latencies consistent with an acute inflammatory demyelinating polyneuropathy. Extensive infectious work-up (including viral PCR panels and cultures) was negative, and no leukemic cells were seen in CSF. Tacrolimus was discontinued (trough level 3.1 ng/mL, below therapeutic range) and intravenous immunoglobulin (2 g/kg total over five days) initiated. The patient's neurological deficits improved rapidly, with near-complete recovery within four weeks. Notably, withdrawal of tacrolimus immunosuppression did not precipitate graft-versus-host disease, and the patient's acute leukemia remained in remission on ponatinib monotherapy. This case illustrates an acute demyelinating polyneuropathy in a post-transplant patient, associated with tacrolimus. It underscores the importance of careful diagnostic assessment of GBS in transplant recipients, including consideration of atypical CSF findings and alternative diagnoses. Prompt recognition and management - including immunosuppressant adjustment and immunotherapy - can achieve full neurological recovery without compromising transplant outcomes.