Treatment in Hodgkin Lymphoma and Guillian-Barre Syndrome
Treatment in Hodgkin Lymphoma and Guillian-Barre Syndrome
A 37-year-old Caucasian man with a history of hypertension presented to his primary care physician with rhinorrhea, a cough and an enlarged lymph node in the left posterior neck that had been worsening over the past one to two months. Our patient was initially treated with a course of oral antibiotics, but had no improvement in his symptoms. He then developed intermittent numbness and tingling in his bilateral feet, which progressed to involve both of his legs and his fingertips. After a few more days, he developed weakness in his bilateral lower extremities and his hands. A computed tomography (CT) scan of his head revealed no significant abnormalities. A fine-needle aspiration of the neck lymph node was suggestive of, but not definitive for, HL. Excisional biopsy of a left supraclavicular lymph node was consistent with classical HL, nodular sclerosis-type.
Further workup with a positron emission tomography (PET)/CT scan revealed small volume left cervical, supraclavicular, axillary and mediastinal lymphadenopathy. A bone marrow biopsy demonstrated a cellular bone marrow with a slight increase in eosinophils, but no evidence of lymphoma, so our patient was given a diagnosis of stage IIB classical HL. By that time, the weakness in his arms and legs had become worse and our patient had experienced at least two episodes of falling with difficulty getting up without assistance. Our patient had right facial weakness, three out of five strength in his bilateral shoulders and hip flexors, four out of five strength in his knee flexors and decreased vibratory sensation up to the knees bilaterally. Patellar and Achilles reflexes were not present.
A magnetic resonance imaging (MRI) scan of his brain showed no intracranial abnormality. An MRI scan of his spine showed subtle nerve root enhancement of the cauda equine, but cerebrospinal fluid was negative for any evidence of malignant cells with only one white blood cell present (CSF protein = 205). Findings from an electromyelogram and nerve conduction study were consistent with an AIDP or GBS. Our patient received two days of intravenous immune globulin (IVIG) at a dose of 1g per kg with complete resolution of his sensory complaints and improvement in his weakness. Three days later, his neurologic symptoms had worsened along with development of some mild shortness of breath. Plasma exchange was initiated for a course of five days with resolution of his shortness of breath and mild improvement of his weakness and sensory deficit.
The following week, chemotherapy with doxorubicin, bleomycin and dacarbazine was initiated (Table 1). Vinblastine was originally omitted from the standard doxorubicin, bleomycin, vinblastine, and dacarbazine (ABVD) regimen to avoid exacerbation of our patient's neuropathy. It was added back during cycle 2 and again held after our patient developed redness and tenderness in his fingertips following 3a. It was reintroduced at a reduced dose after cycle 4 and at full dose for cycle 5.
Bleomycin was omitted for cycle 1b and cycle 2a due to the development of cough and a 20% reduction in diffusion lung capacity for carbon monoxide (DLCO) on repeat pulmonary function tests (PFTs), but then reintroduced once our patient's cough resolved. It was again omitted after cycle 5a due to worsening shortness of breath and further decrease in DLCO on PFTs.
Our patient was then treated with ifosfamide, carboplatin, etoposide (ICE) for two cycles with persistent disease, gemcitabine and vinorelbine for two cycles with persistent disease followed by brentuximab vendotin for three cycles with progressive disease. Note that brentuximab can cause peripheral sensory neuropathy; our patient experienced numbness and tingling in the lower extremities that resolved after four days.
Since our patient still only had localized disease at that point, intensity-modulated radiation therapy (IMRT) was given to the mediastinum, neck and axilla at a total dose of 30.6Gray (Gy) in 17 fractions with an additional 5.4Gy boost to the mediastinum and neck. He then underwent an autologous stem cell transplant with carmustine, etoposide, cytarabine and melphalan conditioning.
Our patient went into remission for about six months, but then developed recurrent disease in his right lower lung. He is currently undergoing chemotherapy with bendamustine with plans for an allogeneic stem cell transplant. Interestingly, his neurologic symptoms had mostly resolved despite the persistence of his HL.
Case Presentation
A 37-year-old Caucasian man with a history of hypertension presented to his primary care physician with rhinorrhea, a cough and an enlarged lymph node in the left posterior neck that had been worsening over the past one to two months. Our patient was initially treated with a course of oral antibiotics, but had no improvement in his symptoms. He then developed intermittent numbness and tingling in his bilateral feet, which progressed to involve both of his legs and his fingertips. After a few more days, he developed weakness in his bilateral lower extremities and his hands. A computed tomography (CT) scan of his head revealed no significant abnormalities. A fine-needle aspiration of the neck lymph node was suggestive of, but not definitive for, HL. Excisional biopsy of a left supraclavicular lymph node was consistent with classical HL, nodular sclerosis-type.
Further workup with a positron emission tomography (PET)/CT scan revealed small volume left cervical, supraclavicular, axillary and mediastinal lymphadenopathy. A bone marrow biopsy demonstrated a cellular bone marrow with a slight increase in eosinophils, but no evidence of lymphoma, so our patient was given a diagnosis of stage IIB classical HL. By that time, the weakness in his arms and legs had become worse and our patient had experienced at least two episodes of falling with difficulty getting up without assistance. Our patient had right facial weakness, three out of five strength in his bilateral shoulders and hip flexors, four out of five strength in his knee flexors and decreased vibratory sensation up to the knees bilaterally. Patellar and Achilles reflexes were not present.
A magnetic resonance imaging (MRI) scan of his brain showed no intracranial abnormality. An MRI scan of his spine showed subtle nerve root enhancement of the cauda equine, but cerebrospinal fluid was negative for any evidence of malignant cells with only one white blood cell present (CSF protein = 205). Findings from an electromyelogram and nerve conduction study were consistent with an AIDP or GBS. Our patient received two days of intravenous immune globulin (IVIG) at a dose of 1g per kg with complete resolution of his sensory complaints and improvement in his weakness. Three days later, his neurologic symptoms had worsened along with development of some mild shortness of breath. Plasma exchange was initiated for a course of five days with resolution of his shortness of breath and mild improvement of his weakness and sensory deficit.
The following week, chemotherapy with doxorubicin, bleomycin and dacarbazine was initiated (Table 1). Vinblastine was originally omitted from the standard doxorubicin, bleomycin, vinblastine, and dacarbazine (ABVD) regimen to avoid exacerbation of our patient's neuropathy. It was added back during cycle 2 and again held after our patient developed redness and tenderness in his fingertips following 3a. It was reintroduced at a reduced dose after cycle 4 and at full dose for cycle 5.
Bleomycin was omitted for cycle 1b and cycle 2a due to the development of cough and a 20% reduction in diffusion lung capacity for carbon monoxide (DLCO) on repeat pulmonary function tests (PFTs), but then reintroduced once our patient's cough resolved. It was again omitted after cycle 5a due to worsening shortness of breath and further decrease in DLCO on PFTs.
Our patient was then treated with ifosfamide, carboplatin, etoposide (ICE) for two cycles with persistent disease, gemcitabine and vinorelbine for two cycles with persistent disease followed by brentuximab vendotin for three cycles with progressive disease. Note that brentuximab can cause peripheral sensory neuropathy; our patient experienced numbness and tingling in the lower extremities that resolved after four days.
Since our patient still only had localized disease at that point, intensity-modulated radiation therapy (IMRT) was given to the mediastinum, neck and axilla at a total dose of 30.6Gray (Gy) in 17 fractions with an additional 5.4Gy boost to the mediastinum and neck. He then underwent an autologous stem cell transplant with carmustine, etoposide, cytarabine and melphalan conditioning.
Our patient went into remission for about six months, but then developed recurrent disease in his right lower lung. He is currently undergoing chemotherapy with bendamustine with plans for an allogeneic stem cell transplant. Interestingly, his neurologic symptoms had mostly resolved despite the persistence of his HL.
