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Lani · 05-22-2006, 12:23 AM

used vs. Lymphoma

Herceptin can cause dry eyes (previous posts) but I ran across the following article which may interest you--all you need is the extra expense of a second monoclonal antibody, of course!

1: Arthritis Rheum. 2005 Sep;52(9):2740-50.
Related Articles, Links

Rituximab treatment in patients with primary Sjogren's syndrome: an open-label phase II study.

Pijpe J, van Imhoff GW, Spijkervet FK, Roodenburg JL, Wolbink GJ, Mansour K, Vissink A, Kallenberg CG, Bootsma H.

Department of Oral and Maxillofacial Surgery, University Medical Center Groningen, Groningen, The Netherlands. j.pijpe@kchir.umcg.nl

OBJECTIVE: To investigate the safety and efficacy of B cell depletion treatment of patients with active primary Sjogren's syndrome of short duration (early primary SS) and patients with primary SS and mucosa-associated lymphoid tissue (MALT)-type lymphoma (MALT/primary SS). METHODS: Fifteen patients with primary SS were included in this phase II trial. Inclusion criteria for the early primary SS group were B cell hyperactivity (IgG >15 gm/liter), presence of autoantibodies (IgM rheumatoid factor, anti-SSA/SSB), and short disease duration (<4 years). Inclusion criteria for the MALT/primary SS group were primary SS and an associated MALT-type lymphoma (Ann Arbor stage IE) localized in the parotid gland. Patients were treated with 4 infusions of rituximab (375 mg/m2) given weekly after pretreatment with prednisone (25 mg) and clemastine. Patients were evaluated, using immunologic, salivary/lacrimal function, and subjective parameters, at baseline and at 5 and 12 weeks after the first infusion. RESULTS: Significant improvement of subjective symptoms and an increase in salivary gland function was observed in patients with residual salivary gland function. Immunologic analysis showed a rapid decrease of peripheral B cells and stable levels of IgG. Human anti-chimeric antibodies (HACAs) developed in 4 of 15 patients (27%), all with early primary SS. Three of these patients developed a serum sickness-like disorder. Of the 7 patients with MALT/primary SS, complete remission was achieved in 3, and disease was stable in 3 and progressive in 1. CONCLUSION: Findings of this phase II study suggest that rituximab is effective in the treatment of primary SS. The high incidence of HACAs and associated side effects observed in this study needs further evaluation.

Publication Types:
Clinical Trial
Clinical Trial, Phase II
PMID: 16142737 [PubMed - indexed for MEDLINE]

PS as far as I can tell HACAs are antibodies which tend to develop to the antibodies when monoclonal antibodies which are not purely human are used(there is a tiny bit of mouse antibody in Herceptin). There have been reports of antibodies to a monoclonal antibody used for rheumatoid arthritis (and those patients developing that antibody experience ineffectiveness of the monoclonal antibody) Perhaps it is something inherent in the immune system of rheumatoid arthritis patients, and maybe there is something similar in SOME sjoegren's patients.

05-22-2006, 12:23 AM	#4
Lani Senior Member Join Date: Mar 2006 Posts: 4,778	Rina--have I got an article for you! Rituximab is a monoclonal antibody used vs. Lymphoma Herceptin can cause dry eyes (previous posts) but I ran across the following article which may interest you--all you need is the extra expense of a second monoclonal antibody, of course! 1: Arthritis Rheum. 2005 Sep;52(9):2740-50. Related Articles, Links Rituximab treatment in patients with primary Sjogren's syndrome: an open-label phase II study. Pijpe J, van Imhoff GW, Spijkervet FK, Roodenburg JL, Wolbink GJ, Mansour K, Vissink A, Kallenberg CG, Bootsma H. Department of Oral and Maxillofacial Surgery, University Medical Center Groningen, Groningen, The Netherlands. j.pijpe@kchir.umcg.nl OBJECTIVE: To investigate the safety and efficacy of B cell depletion treatment of patients with active primary Sjogren's syndrome of short duration (early primary SS) and patients with primary SS and mucosa-associated lymphoid tissue (MALT)-type lymphoma (MALT/primary SS). METHODS: Fifteen patients with primary SS were included in this phase II trial. Inclusion criteria for the early primary SS group were B cell hyperactivity (IgG >15 gm/liter), presence of autoantibodies (IgM rheumatoid factor, anti-SSA/SSB), and short disease duration (<4 years). Inclusion criteria for the MALT/primary SS group were primary SS and an associated MALT-type lymphoma (Ann Arbor stage IE) localized in the parotid gland. Patients were treated with 4 infusions of rituximab (375 mg/m2) given weekly after pretreatment with prednisone (25 mg) and clemastine. Patients were evaluated, using immunologic, salivary/lacrimal function, and subjective parameters, at baseline and at 5 and 12 weeks after the first infusion. RESULTS: Significant improvement of subjective symptoms and an increase in salivary gland function was observed in patients with residual salivary gland function. Immunologic analysis showed a rapid decrease of peripheral B cells and stable levels of IgG. Human anti-chimeric antibodies (HACAs) developed in 4 of 15 patients (27%), all with early primary SS. Three of these patients developed a serum sickness-like disorder. Of the 7 patients with MALT/primary SS, complete remission was achieved in 3, and disease was stable in 3 and progressive in 1. CONCLUSION: Findings of this phase II study suggest that rituximab is effective in the treatment of primary SS. The high incidence of HACAs and associated side effects observed in this study needs further evaluation. Publication Types: Clinical Trial Clinical Trial, Phase II PMID: 16142737 [PubMed - indexed for MEDLINE] PS as far as I can tell HACAs are antibodies which tend to develop to the antibodies when monoclonal antibodies which are not purely human are used(there is a tiny bit of mouse antibody in Herceptin). There have been reports of antibodies to a monoclonal antibody used for rheumatoid arthritis (and those patients developing that antibody experience ineffectiveness of the monoclonal antibody) Perhaps it is something inherent in the immune system of rheumatoid arthritis patients, and maybe there is something similar in SOME sjoegren's patients.