https://www.mdpi.com/2077-0383/9/8/2443/htm
Abstract
(1) Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a complex neuroimmunological disease. There is evidence for an autoimmune mechanism for ME/CFS with an infection-triggered onset and dysfunction of ß2-adrenoreceptor antibodies (ß2AR-AB). In a first proof-of-concept study, we could show that IA was effective to reduce ß2AR-AB and led to improvement of various symptoms. (2) Five of the ME/CFS patients who had clinical improvement following treatment with a five-day IA were retreated in the current study about two years later with a modified IA protocol. The severity of symptoms was assessed by disease specific scores during a follow-up period of 12 months. The antibodies were determined by ELISA. (3) The modified IA treatment protocol resulted in a remarkable similar clinical response. The treatment was well tolerated and 80–90% decline of total IgG and ß2AR-AB was achieved. Four patients showed a rapid improvement in several clinical symptoms during IA therapy, lasting for six to 12 months. One patient had no improvement. (4) We could provide further evidence that IA has clinical efficacy in patients with ME/CFS. Data from our pilot trial warrant further controlled studies in ME/CFS.
Conclusions
In summary, the current study provides further evidence that IA is effective in ME/CFS. This result warrants further studies of repeat IA therapy to maintain clinical remission, as shown for other autoimmune diseases [20]. Another option is to include IA in a therapy algorithm as initial therapy for autoantibody-positive ME/CFS patients in order to achieve rapid symptom relief and, therefore, shorten the known time latency of four months or longer until the onset of efficacy of B cell-targeting therapies.
Abstract
(1) Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a complex neuroimmunological disease. There is evidence for an autoimmune mechanism for ME/CFS with an infection-triggered onset and dysfunction of ß2-adrenoreceptor antibodies (ß2AR-AB). In a first proof-of-concept study, we could show that IA was effective to reduce ß2AR-AB and led to improvement of various symptoms. (2) Five of the ME/CFS patients who had clinical improvement following treatment with a five-day IA were retreated in the current study about two years later with a modified IA protocol. The severity of symptoms was assessed by disease specific scores during a follow-up period of 12 months. The antibodies were determined by ELISA. (3) The modified IA treatment protocol resulted in a remarkable similar clinical response. The treatment was well tolerated and 80–90% decline of total IgG and ß2AR-AB was achieved. Four patients showed a rapid improvement in several clinical symptoms during IA therapy, lasting for six to 12 months. One patient had no improvement. (4) We could provide further evidence that IA has clinical efficacy in patients with ME/CFS. Data from our pilot trial warrant further controlled studies in ME/CFS.
Conclusions
In summary, the current study provides further evidence that IA is effective in ME/CFS. This result warrants further studies of repeat IA therapy to maintain clinical remission, as shown for other autoimmune diseases [20]. Another option is to include IA in a therapy algorithm as initial therapy for autoantibody-positive ME/CFS patients in order to achieve rapid symptom relief and, therefore, shorten the known time latency of four months or longer until the onset of efficacy of B cell-targeting therapies.
