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Predictors of Usage of a Web-based Asthma Education Program
Abstracts S139
J ALLERGY CLIN IMMUNOL VOLUME 121, NUMBER 2
Reasons for Discontinuation of Omalizumab Therapy in the Treatment of Patients With Moderate to Severe Persistent Asthma L. E. Sheinkopf1, A. W. Rafi2, L. T. Do2, W. B. Klaustermeyer1, R. M. Katz2; 1VA Greater Los Angeles Healthcare System/UCLA, Los Angeles, CA, 2Allergy, Asthma Care Center, Inc., Santa Monica, CA. RATIONALE: Omalizumab is a humanized monoclonal anti-IgE antibody and has been available since 2003 for the treatment of moderate to severe persistent allergic asthma. This study highlights reasons patients discontinue omalizumab. METHODS: An IRB approved prospective analysis was performed. Ninety-six patients with moderate to severe persistent allergic asthma were treated with omalizumab. Dosages were administered subcutaneously every 2 - 4 weeks. Adverse events were documented at each injection visit and follow up visit. Reasons for discontinuation of therapy were documented. RESULTS: Twenty-five patients (ages 14-84), discontinued treatment during a 4 year period. One patient experienced coughing and angioedema after the first injection and therapy was discontinued. Five patients discontinued therapy due to the expense of the medication. Four patients discontinued therapy when no overall improvement occurred within 5 to 9 doses. Three patients moved to a new location and discontinued therapy within 3 to 12 doses. Four patients started omalizumab because of experiencing anaphylaxis during immunotherapy. These patients required only 6 to 8 doses of omalizumab to continue immunotherapy without symptoms. Eight patients discontinued therapy due to excellent results with no further need for controller medications within 6 to 35 doses. One of these patients discontinued therapy and started immune globulin to treat a new diagnosis of immune deficiency. These eight patients continued doing well while off omalizumab during follow-up at 2 years. CONCLUSIONS: Reasons for discontinuation of omalizumab include side effects, costliness, inconvenience, and success. This data may provide practical guidance along with the established criteria when starting patients on omalizumab.
538
Predictors of Usage of a Web-based Asthma Education Program P. A. Richardson1, S. Hollman1, K. K. Shanovich1, A. D. Pulvermacher1, A. Bhattacharya2, E. Y. Lee1, C. A. Sorkness3, D. H. Gustafson1; 1Center for Health Enhancement Systems Studies, University of Wisconsin-Madison, Madison, WI, 2Quality Resources, University of Wisconsin Hospital and Clinics, Madison, WI, 3Schools of Pharmacy and Medicine, University of Wisconsin-Madison, Madison, WI. RATIONALE: The ‘‘Internet Telehealth for Pediatric Asthma Case Management’’ project was an NIH-funded, randomized-control trial that integrated asthma nurse case management with Center for Health Enhancement Systems Studies (CHESS) technology. The year-long study was developed to test the effectiveness of a web-based, interactive computer program designed to help participant’s manage their child’s asthma when compared to usual medical care. This abstract evaluates which sub-groups of the intervention arm best utilized this program. METHODS: 305 participants whose children had poorly-controlled asthma were enrolled. Computer use data of the intervention arm was tracked and compiled on a weekly basis. Intake and exit questionnaires provided additional information about Medicaid status, education level, prior computer experience and access, and self-reported reasons for utilization of CHESS. RESULTS: Among 152 participants randomized to the intervention arm, 45% were Medicaid recipients who logged-on to CHESS an average of 53 times, compared to 27 times (p < 0.05) of their counterpart. Participants with high school education or more (33%), logged-on significantly fewer times, (36 to 41) then those who had less than high school education. With an even distribution regarding prior computer access, significantly higher number of log-ins were observed among those who lacked prior computer access (54 to 25). Similarly, the participants who did not have prior computer experience (45%) logged-in an average of 47 times, higher than their counterpart (33 times), though not significant.
CONCLUSION: Our findings suggest that CHESS was most likely helping participants who had less education, lacked previous computer access and were of lower socio-economic status. Funding: National Institute of Nursing Research
539
Single Non-Viral Antigen Exposure During a Paramyxoviral Respiratory Infection is Sufficient to Drive Specific IgE Production S. S. Park, R. T. Kitchens, M. H. Grayson; Washington University School of Medicine, St. Louis, MO. RATIONALE: Severe paramyxoviral respiratory infections are known to induce viral-specific IgE responses and increase risk for atopic disease development. Whether IgE can be induced against non-viral antigens during a respiratory viral infection is unknown. For this study, we assessed the ability to induce non-viral antigen-specific IgE in mice acutely infected with a mouse paramyxovirus, Sendai virus (SeV). METHODS: C57BL6 mice were inoculated with either SeV or UVinactivated SeV (UV-SeV). On day 8 post-inoculation (PI), ovalbumin (30 ml; 1 mg/ml) was given intranasally (i.n.), and sera evaluated for ovalbumin-specific IgE at day 21 PI. As a control, uninfected mice were injected intraperitoneally (i.p.) with 20 ml ovalbumin and alum (1:1) weekly for 2 weeks prior to intranasal ovalbumin challenge. Anti-ovalbumin specific IgE in the sera was determined by ELISA one week later. RESULTS: Administration of ovalbumin i.n. at day 8 PI led to production of ovalbumin-specific IgE (1463 6 950 ng/ml; mean 6 sem). This response depended upon a productive viral infection, as administration of ovalbumin to UV-SeV inoculated mice led to minimal anti-ovalbumin IgE (172 6 39 ng/ml). The level of anti-ovalbumin IgE generated during the productive viral infection was similar to that induced by two i.p. injections of antigen plus adjuvant and a subsequent i.n. antigen challenge (1033 6 687 ng/ml). CONCLUSIONS: Exposure to non-viral antigens during a severe paramyxoviral respiratory infection can drive specific IgE production against these non-viral antigens. These data suggest a potential mechanism linking severe paramyxoviral infections to the development of post-viral atopic disease. Funding: Washington University School of Medicine, Dept. of Internal Medicine
540
The Expansion of Airway Mast Cells during Allergic Inflammation is Mediated by IgE Antibodies C. B. Mathias1,2, E. Freyschmidt1,2, B. Caplan1, T. Jones3, K. L. Harrison1, M. F. Gurish3,2, H. C. Oettgen1,2; 1Children’s Hospital Boston, Boston, MA, 2Harvard Medical School, Boston, MA, 3The Brigham and Women’s Hospital, Boston, MA. RATIONALE: In light of recent observations that IgE can support the expansion and survival of cultured mast cells, we examined the role of IgE in the homeostasis of airway mast cells in a mouse model of allergic asthma. METHODS: Mice were subjected to repeated inhalations of an aqueous extract of Aspergillus fumigatus (Af) and the number, function and phenotype of mast cells was studied by histological and flow cytometric techniques. RESULTS: Repeated inhalation of Af induces a significant expansion of mast cells in the airways of wild-type mice. Mast cell expansion is accompanied by increased expression of FcepsilonRI and elevated levels of mouse mast cell protease-1 (mMCP-1) and IL-5. In contrast, both mast cell expansion and the levels of FcepsilonRI, mMCP-1 and IL-5 were significantly reduced in IgE-/- mice. IgE is not required for the recruitment of mast cell progenitors to the airways, but enhances the survival of differentiated mast cells in vivo. Mast cell-driven migration of allergen-specific T cells is also reduced in the absence of IgE. Decreased mast cell expansion in IL-3-/- mice suggests that IgE-induced mast cell expansion may occur via an IL-3-dependent mechanism. CONCLUSIONS: Our data identify a critical role for IgE in mast cell homeostasis during allergic inflammation in vivo and suggest novel mechanisms whereby therapeutic blockade of IgE may provide clinical benefit for patients with asthma. Funding: NIH
SUNDAY
537
J ALLERGY CLIN IMMUNOL VOLUME 121, NUMBER 2
Reasons for Discontinuation of Omalizumab Therapy in the Treatment of Patients With Moderate to Severe Persistent Asthma L. E. Sheinkopf1, A. W. Rafi2, L. T. Do2, W. B. Klaustermeyer1, R. M. Katz2; 1VA Greater Los Angeles Healthcare System/UCLA, Los Angeles, CA, 2Allergy, Asthma Care Center, Inc., Santa Monica, CA. RATIONALE: Omalizumab is a humanized monoclonal anti-IgE antibody and has been available since 2003 for the treatment of moderate to severe persistent allergic asthma. This study highlights reasons patients discontinue omalizumab. METHODS: An IRB approved prospective analysis was performed. Ninety-six patients with moderate to severe persistent allergic asthma were treated with omalizumab. Dosages were administered subcutaneously every 2 - 4 weeks. Adverse events were documented at each injection visit and follow up visit. Reasons for discontinuation of therapy were documented. RESULTS: Twenty-five patients (ages 14-84), discontinued treatment during a 4 year period. One patient experienced coughing and angioedema after the first injection and therapy was discontinued. Five patients discontinued therapy due to the expense of the medication. Four patients discontinued therapy when no overall improvement occurred within 5 to 9 doses. Three patients moved to a new location and discontinued therapy within 3 to 12 doses. Four patients started omalizumab because of experiencing anaphylaxis during immunotherapy. These patients required only 6 to 8 doses of omalizumab to continue immunotherapy without symptoms. Eight patients discontinued therapy due to excellent results with no further need for controller medications within 6 to 35 doses. One of these patients discontinued therapy and started immune globulin to treat a new diagnosis of immune deficiency. These eight patients continued doing well while off omalizumab during follow-up at 2 years. CONCLUSIONS: Reasons for discontinuation of omalizumab include side effects, costliness, inconvenience, and success. This data may provide practical guidance along with the established criteria when starting patients on omalizumab.
538
Predictors of Usage of a Web-based Asthma Education Program P. A. Richardson1, S. Hollman1, K. K. Shanovich1, A. D. Pulvermacher1, A. Bhattacharya2, E. Y. Lee1, C. A. Sorkness3, D. H. Gustafson1; 1Center for Health Enhancement Systems Studies, University of Wisconsin-Madison, Madison, WI, 2Quality Resources, University of Wisconsin Hospital and Clinics, Madison, WI, 3Schools of Pharmacy and Medicine, University of Wisconsin-Madison, Madison, WI. RATIONALE: The ‘‘Internet Telehealth for Pediatric Asthma Case Management’’ project was an NIH-funded, randomized-control trial that integrated asthma nurse case management with Center for Health Enhancement Systems Studies (CHESS) technology. The year-long study was developed to test the effectiveness of a web-based, interactive computer program designed to help participant’s manage their child’s asthma when compared to usual medical care. This abstract evaluates which sub-groups of the intervention arm best utilized this program. METHODS: 305 participants whose children had poorly-controlled asthma were enrolled. Computer use data of the intervention arm was tracked and compiled on a weekly basis. Intake and exit questionnaires provided additional information about Medicaid status, education level, prior computer experience and access, and self-reported reasons for utilization of CHESS. RESULTS: Among 152 participants randomized to the intervention arm, 45% were Medicaid recipients who logged-on to CHESS an average of 53 times, compared to 27 times (p < 0.05) of their counterpart. Participants with high school education or more (33%), logged-on significantly fewer times, (36 to 41) then those who had less than high school education. With an even distribution regarding prior computer access, significantly higher number of log-ins were observed among those who lacked prior computer access (54 to 25). Similarly, the participants who did not have prior computer experience (45%) logged-in an average of 47 times, higher than their counterpart (33 times), though not significant.
CONCLUSION: Our findings suggest that CHESS was most likely helping participants who had less education, lacked previous computer access and were of lower socio-economic status. Funding: National Institute of Nursing Research
539
Single Non-Viral Antigen Exposure During a Paramyxoviral Respiratory Infection is Sufficient to Drive Specific IgE Production S. S. Park, R. T. Kitchens, M. H. Grayson; Washington University School of Medicine, St. Louis, MO. RATIONALE: Severe paramyxoviral respiratory infections are known to induce viral-specific IgE responses and increase risk for atopic disease development. Whether IgE can be induced against non-viral antigens during a respiratory viral infection is unknown. For this study, we assessed the ability to induce non-viral antigen-specific IgE in mice acutely infected with a mouse paramyxovirus, Sendai virus (SeV). METHODS: C57BL6 mice were inoculated with either SeV or UVinactivated SeV (UV-SeV). On day 8 post-inoculation (PI), ovalbumin (30 ml; 1 mg/ml) was given intranasally (i.n.), and sera evaluated for ovalbumin-specific IgE at day 21 PI. As a control, uninfected mice were injected intraperitoneally (i.p.) with 20 ml ovalbumin and alum (1:1) weekly for 2 weeks prior to intranasal ovalbumin challenge. Anti-ovalbumin specific IgE in the sera was determined by ELISA one week later. RESULTS: Administration of ovalbumin i.n. at day 8 PI led to production of ovalbumin-specific IgE (1463 6 950 ng/ml; mean 6 sem). This response depended upon a productive viral infection, as administration of ovalbumin to UV-SeV inoculated mice led to minimal anti-ovalbumin IgE (172 6 39 ng/ml). The level of anti-ovalbumin IgE generated during the productive viral infection was similar to that induced by two i.p. injections of antigen plus adjuvant and a subsequent i.n. antigen challenge (1033 6 687 ng/ml). CONCLUSIONS: Exposure to non-viral antigens during a severe paramyxoviral respiratory infection can drive specific IgE production against these non-viral antigens. These data suggest a potential mechanism linking severe paramyxoviral infections to the development of post-viral atopic disease. Funding: Washington University School of Medicine, Dept. of Internal Medicine
540
The Expansion of Airway Mast Cells during Allergic Inflammation is Mediated by IgE Antibodies C. B. Mathias1,2, E. Freyschmidt1,2, B. Caplan1, T. Jones3, K. L. Harrison1, M. F. Gurish3,2, H. C. Oettgen1,2; 1Children’s Hospital Boston, Boston, MA, 2Harvard Medical School, Boston, MA, 3The Brigham and Women’s Hospital, Boston, MA. RATIONALE: In light of recent observations that IgE can support the expansion and survival of cultured mast cells, we examined the role of IgE in the homeostasis of airway mast cells in a mouse model of allergic asthma. METHODS: Mice were subjected to repeated inhalations of an aqueous extract of Aspergillus fumigatus (Af) and the number, function and phenotype of mast cells was studied by histological and flow cytometric techniques. RESULTS: Repeated inhalation of Af induces a significant expansion of mast cells in the airways of wild-type mice. Mast cell expansion is accompanied by increased expression of FcepsilonRI and elevated levels of mouse mast cell protease-1 (mMCP-1) and IL-5. In contrast, both mast cell expansion and the levels of FcepsilonRI, mMCP-1 and IL-5 were significantly reduced in IgE-/- mice. IgE is not required for the recruitment of mast cell progenitors to the airways, but enhances the survival of differentiated mast cells in vivo. Mast cell-driven migration of allergen-specific T cells is also reduced in the absence of IgE. Decreased mast cell expansion in IL-3-/- mice suggests that IgE-induced mast cell expansion may occur via an IL-3-dependent mechanism. CONCLUSIONS: Our data identify a critical role for IgE in mast cell homeostasis during allergic inflammation in vivo and suggest novel mechanisms whereby therapeutic blockade of IgE may provide clinical benefit for patients with asthma. Funding: NIH
SUNDAY
537