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CLEVELAND — Treatment with a tumor necrosis factor-α inhibitor may trigger a demyelinating polyneuropathy with Guillain-Barré-like symptoms, according to MaryAnn Mays, M.D., of the Cleveland Clinic Foundation.
The case in point, presented in a poster at a symposium on the treatment of autoimmune and inflammatory disorders sponsored by the clinic, was that of a 56-year-old man with seropositive rheumatoid arthritis who became severely disabled after infliximab infusions were added to his methotrexate therapy.
Dr. Mays, a neurologist, said in an interview that following his first anti-TNF treatment in 2002, the patient's rheumatoid arthritis symptoms lessened dramatically, but following an infusion in late 2003, he had dizziness and hearing loss for a week. The symptoms recurred and lasted longer following a third infusion 2 months later.
The next infliximab infusion in April 2004 produced worsening neurologic symptoms, including blurred vision, headaches, dysarthria, hearing loss, ataxia, dysphagia requiring percutaneous endoscopic gastrostomy for nutrition, and progressive weakness, according to Dr. Mays.
“Initial evaluation included cerebrospinal fluid WBC of 123, protein 79, and electromyograph consistent with demyelinating polyneuropathy. But the overall pattern was not typical of Guillain-Barré syndrome [GBS],” Dr. Mays said. “He had high white count and normal protein. Auditory evoked potentials showed a right central conduction disturbance. His detrusor urinae muscle were unresponsive, which is typical of GBS. His right Babinski sign was atypical of GBS.”
Feyrouz Al-Ashkar, M.D., the lead investigator and a rheumatologist, noted in an interview that by the time the patient was brought to the clinic, he “could not walk, use his hands, lift his head, or feed himself, although he could still breathe on his own.”
“He received intravenous immunoglobulin [IVIg] and steroids before we saw him. When he got here, he again received intravenous steroids and another course of intravenous immunoglobulin, and slowly but surely, he recovered completely,” Dr. Al-Ashkar said.
Dr. Mays noted that the patient's response to IVIg supports the diagnosis of a demyelinating polyneuropathy other than GBS.”
Dr. Al-Ashkar said that the onset of neurologic deficits or demyelinating diseases in patients on infliximab is a red flag to stop TNF blockade. “In such cases, our experience would suggest that there is potential for worsening of neurologic deficits with each infliximab treatment, and that continuing treatments after onset of neurologic symptoms would be relatively contraindicated,” according to the poster.
CLEVELAND — Treatment with a tumor necrosis factor-α inhibitor may trigger a demyelinating polyneuropathy with Guillain-Barré-like symptoms, according to MaryAnn Mays, M.D., of the Cleveland Clinic Foundation.
The case in point, presented in a poster at a symposium on the treatment of autoimmune and inflammatory disorders sponsored by the clinic, was that of a 56-year-old man with seropositive rheumatoid arthritis who became severely disabled after infliximab infusions were added to his methotrexate therapy.
Dr. Mays, a neurologist, said in an interview that following his first anti-TNF treatment in 2002, the patient's rheumatoid arthritis symptoms lessened dramatically, but following an infusion in late 2003, he had dizziness and hearing loss for a week. The symptoms recurred and lasted longer following a third infusion 2 months later.
The next infliximab infusion in April 2004 produced worsening neurologic symptoms, including blurred vision, headaches, dysarthria, hearing loss, ataxia, dysphagia requiring percutaneous endoscopic gastrostomy for nutrition, and progressive weakness, according to Dr. Mays.
“Initial evaluation included cerebrospinal fluid WBC of 123, protein 79, and electromyograph consistent with demyelinating polyneuropathy. But the overall pattern was not typical of Guillain-Barré syndrome [GBS],” Dr. Mays said. “He had high white count and normal protein. Auditory evoked potentials showed a right central conduction disturbance. His detrusor urinae muscle were unresponsive, which is typical of GBS. His right Babinski sign was atypical of GBS.”
Feyrouz Al-Ashkar, M.D., the lead investigator and a rheumatologist, noted in an interview that by the time the patient was brought to the clinic, he “could not walk, use his hands, lift his head, or feed himself, although he could still breathe on his own.”
“He received intravenous immunoglobulin [IVIg] and steroids before we saw him. When he got here, he again received intravenous steroids and another course of intravenous immunoglobulin, and slowly but surely, he recovered completely,” Dr. Al-Ashkar said.
Dr. Mays noted that the patient's response to IVIg supports the diagnosis of a demyelinating polyneuropathy other than GBS.”
Dr. Al-Ashkar said that the onset of neurologic deficits or demyelinating diseases in patients on infliximab is a red flag to stop TNF blockade. “In such cases, our experience would suggest that there is potential for worsening of neurologic deficits with each infliximab treatment, and that continuing treatments after onset of neurologic symptoms would be relatively contraindicated,” according to the poster.
CLEVELAND — Treatment with a tumor necrosis factor-α inhibitor may trigger a demyelinating polyneuropathy with Guillain-Barré-like symptoms, according to MaryAnn Mays, M.D., of the Cleveland Clinic Foundation.
The case in point, presented in a poster at a symposium on the treatment of autoimmune and inflammatory disorders sponsored by the clinic, was that of a 56-year-old man with seropositive rheumatoid arthritis who became severely disabled after infliximab infusions were added to his methotrexate therapy.
Dr. Mays, a neurologist, said in an interview that following his first anti-TNF treatment in 2002, the patient's rheumatoid arthritis symptoms lessened dramatically, but following an infusion in late 2003, he had dizziness and hearing loss for a week. The symptoms recurred and lasted longer following a third infusion 2 months later.
The next infliximab infusion in April 2004 produced worsening neurologic symptoms, including blurred vision, headaches, dysarthria, hearing loss, ataxia, dysphagia requiring percutaneous endoscopic gastrostomy for nutrition, and progressive weakness, according to Dr. Mays.
“Initial evaluation included cerebrospinal fluid WBC of 123, protein 79, and electromyograph consistent with demyelinating polyneuropathy. But the overall pattern was not typical of Guillain-Barré syndrome [GBS],” Dr. Mays said. “He had high white count and normal protein. Auditory evoked potentials showed a right central conduction disturbance. His detrusor urinae muscle were unresponsive, which is typical of GBS. His right Babinski sign was atypical of GBS.”
Feyrouz Al-Ashkar, M.D., the lead investigator and a rheumatologist, noted in an interview that by the time the patient was brought to the clinic, he “could not walk, use his hands, lift his head, or feed himself, although he could still breathe on his own.”
“He received intravenous immunoglobulin [IVIg] and steroids before we saw him. When he got here, he again received intravenous steroids and another course of intravenous immunoglobulin, and slowly but surely, he recovered completely,” Dr. Al-Ashkar said.
Dr. Mays noted that the patient's response to IVIg supports the diagnosis of a demyelinating polyneuropathy other than GBS.”
Dr. Al-Ashkar said that the onset of neurologic deficits or demyelinating diseases in patients on infliximab is a red flag to stop TNF blockade. “In such cases, our experience would suggest that there is potential for worsening of neurologic deficits with each infliximab treatment, and that continuing treatments after onset of neurologic symptoms would be relatively contraindicated,” according to the poster.