User login
BARCELONA — Clinical improvement in a small series of patients with inflammatory myopathies treated with rituximab suggests that B-cell depletion may prove useful in these disorders, according to Dr. Marlies Blom of the department of rheumatology, Radboud University Nijmegen Medical Centre (the Netherlands).
Among seven patients who had either dermatomyositis, polymyositis, or antisynthetase syndrome, two infusions of 1,000 mg rituximab 2 weeks apart resulted in a mean 30% increase in muscle strength at 3 months, Dr. Blom reported in a poster session at the annual European Congress of Rheumatology.
The patients' subjective reports of improvement in muscle strength were later confirmed by using handheld dynamometry.
The patients ranged in age from 38 to 58 years, and the duration of their disease ranged from 3 to 16 years. Four of the seven were female.
Previous treatments included oral and intravenous prednisone, methotrexate, azathioprine, cyclophosphamide, interferon, etanercept, and intravenous immunoglobulin.
A mean 13% improvement was reported on Health Assessment Questionnaire (HAQ) scores, and improvements also were also seen in levels of creatine phosphokinase, a marker of disease activity.
In one patient, a muscle biopsy taken 4 months after treatment showed a total absence of CD20+ B cells. This patient's Disease Activity Score-28 (DAS28) score fell from 6.83 to 4.46 after 3 months, according to Dr. Blom.
After initial good response, three patients required retreatment for exacerbations of myositis at about 6 months.
No serious adverse events were observed and immunoglobulin levels remained within normal ranges.
These results suggest that B cells play an important role in the pathogenesis of inflammatory myopathies, Dr. Blom noted.
Another recent report suggested that a possible rationale for considering B-cell depletion as a therapeutic strategy in dermatomyositis was that treatment with rituximab had previously been shown to result in improvements in muscle strength in humorally mediated autoimmune peripheral neuropathies (Arthritis Rheum. 2005;52:601-7).
The importance of humoral immunity in dermatomyositis also is suggested by the observation that perifascicular endothelial immunoglobulin and complement deposition are thought to result in the muscle ischemia and atrophy (J. Rheumatol. 2006;33:1021-6).
Furthermore, the observation that there are antibodies specific for myositis also supports the concept of B-cell-mediated humoral abnormality in dermatomyositis (Medicine [Baltimore]. 1991;70:360-74).
BARCELONA — Clinical improvement in a small series of patients with inflammatory myopathies treated with rituximab suggests that B-cell depletion may prove useful in these disorders, according to Dr. Marlies Blom of the department of rheumatology, Radboud University Nijmegen Medical Centre (the Netherlands).
Among seven patients who had either dermatomyositis, polymyositis, or antisynthetase syndrome, two infusions of 1,000 mg rituximab 2 weeks apart resulted in a mean 30% increase in muscle strength at 3 months, Dr. Blom reported in a poster session at the annual European Congress of Rheumatology.
The patients' subjective reports of improvement in muscle strength were later confirmed by using handheld dynamometry.
The patients ranged in age from 38 to 58 years, and the duration of their disease ranged from 3 to 16 years. Four of the seven were female.
Previous treatments included oral and intravenous prednisone, methotrexate, azathioprine, cyclophosphamide, interferon, etanercept, and intravenous immunoglobulin.
A mean 13% improvement was reported on Health Assessment Questionnaire (HAQ) scores, and improvements also were also seen in levels of creatine phosphokinase, a marker of disease activity.
In one patient, a muscle biopsy taken 4 months after treatment showed a total absence of CD20+ B cells. This patient's Disease Activity Score-28 (DAS28) score fell from 6.83 to 4.46 after 3 months, according to Dr. Blom.
After initial good response, three patients required retreatment for exacerbations of myositis at about 6 months.
No serious adverse events were observed and immunoglobulin levels remained within normal ranges.
These results suggest that B cells play an important role in the pathogenesis of inflammatory myopathies, Dr. Blom noted.
Another recent report suggested that a possible rationale for considering B-cell depletion as a therapeutic strategy in dermatomyositis was that treatment with rituximab had previously been shown to result in improvements in muscle strength in humorally mediated autoimmune peripheral neuropathies (Arthritis Rheum. 2005;52:601-7).
The importance of humoral immunity in dermatomyositis also is suggested by the observation that perifascicular endothelial immunoglobulin and complement deposition are thought to result in the muscle ischemia and atrophy (J. Rheumatol. 2006;33:1021-6).
Furthermore, the observation that there are antibodies specific for myositis also supports the concept of B-cell-mediated humoral abnormality in dermatomyositis (Medicine [Baltimore]. 1991;70:360-74).
BARCELONA — Clinical improvement in a small series of patients with inflammatory myopathies treated with rituximab suggests that B-cell depletion may prove useful in these disorders, according to Dr. Marlies Blom of the department of rheumatology, Radboud University Nijmegen Medical Centre (the Netherlands).
Among seven patients who had either dermatomyositis, polymyositis, or antisynthetase syndrome, two infusions of 1,000 mg rituximab 2 weeks apart resulted in a mean 30% increase in muscle strength at 3 months, Dr. Blom reported in a poster session at the annual European Congress of Rheumatology.
The patients' subjective reports of improvement in muscle strength were later confirmed by using handheld dynamometry.
The patients ranged in age from 38 to 58 years, and the duration of their disease ranged from 3 to 16 years. Four of the seven were female.
Previous treatments included oral and intravenous prednisone, methotrexate, azathioprine, cyclophosphamide, interferon, etanercept, and intravenous immunoglobulin.
A mean 13% improvement was reported on Health Assessment Questionnaire (HAQ) scores, and improvements also were also seen in levels of creatine phosphokinase, a marker of disease activity.
In one patient, a muscle biopsy taken 4 months after treatment showed a total absence of CD20+ B cells. This patient's Disease Activity Score-28 (DAS28) score fell from 6.83 to 4.46 after 3 months, according to Dr. Blom.
After initial good response, three patients required retreatment for exacerbations of myositis at about 6 months.
No serious adverse events were observed and immunoglobulin levels remained within normal ranges.
These results suggest that B cells play an important role in the pathogenesis of inflammatory myopathies, Dr. Blom noted.
Another recent report suggested that a possible rationale for considering B-cell depletion as a therapeutic strategy in dermatomyositis was that treatment with rituximab had previously been shown to result in improvements in muscle strength in humorally mediated autoimmune peripheral neuropathies (Arthritis Rheum. 2005;52:601-7).
The importance of humoral immunity in dermatomyositis also is suggested by the observation that perifascicular endothelial immunoglobulin and complement deposition are thought to result in the muscle ischemia and atrophy (J. Rheumatol. 2006;33:1021-6).
Furthermore, the observation that there are antibodies specific for myositis also supports the concept of B-cell-mediated humoral abnormality in dermatomyositis (Medicine [Baltimore]. 1991;70:360-74).