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Relationship of Interferon Beta Use in Multiple Sclerosis and Development of Pulmonary Arterial Hypertension
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A2122 - Relationship of Interferon Beta Use in Multiple Sclerosis and Development of Pulmonary Arterial Hypertension
Author Block: Z. Safdar; Pulmonary-Critical Care Medicine, Houston Methodist Hospital/Weill Cornell College fo Medicine, Houston, TX, United States.
Introduction: Pulmonary Arterial Hypertension (PAH) has been reported in patients treated with interferon beta (IFN β) and in patients with multiple sclerosis (MS). Interferons are commonly used for a number of conditions such as malignancies, chronic viral infections, and chronic neurological conditions. We present a case series of patients who developed PAH after undergoing treatment with IFN β for MS. Method: Four PAH patients who previously were treated with IFN β for MS and later diagnosed with PAH were identified at Pulmonary Hypertension Center at Houston Methodist Hospital. Baseline demographics, duration of PAH in years, duration of MS in years, duration of IFN β treatment in years, historical right heart catheterization, hemodynamics from echocardiogram (ECHO), six minute walk distance (6MWD) and Borg dyspnea score (BDS) were recorded for each patient. Results: Mean age was 51±9 years, all were females, 3 were Caucasians and 1 was Hispanic. Age at MS diagnosis was 35±6 years and age at PAH diagnosis was 47±10 years. All received IFN β prior to developing PAH. There was a lag of 12±5 years between developing PAH after IFN β treatment. Two were on intravenous prostacyclin therapy plus oral agents (epoprostenol + tadalafil and treprostinil+macitentan) whereas 2 were on oral PAH medications (ambrissentan+tadalafil and macitentan + tadalafil). Hemodynamics from right heart catheterization done at the time of diagnosis showed a mean pulmonary artery pressure of 53±11 mmHg, right atrial pressure (RAP) of 7±2 mmHg, mixed venous saturation was 71±3%, pulmonary capillary wedge pressure was 12±7 mmHg, thermodilution cardiac output (CO) was 4.66 ±1.7 ml/min and cardiac index (CI) was 2.55±0.8 ml/min/m2. Hemodynamics from recent echo showed a right ventricular systolic pressure of 70±16 mmHg, RAP of 6±2 mmHg, CO of 6.2±2.1 L/min, CI of 3.5±0.73 L/min/m2. The recent 6MWD was 435±115 meters and BDS ranged from 0.5 to 4. All were alive at the time of last follow up that was 16±3 years from MS diagnosis. Conclusions: We present this case series to provide further evidence of the possible relationship between interferon beta treatment, MS and PAH development. In our cohort there was a lag of 12 ± 5 years from IFN β therapy before developing PAH. In contrast to other reports, none of our PAH patients had a reversibility of PAH with cessation of IFN β treatment suggesting early screening of MS patients for PAH.
Author Block: Z. Safdar; Pulmonary-Critical Care Medicine, Houston Methodist Hospital/Weill Cornell College fo Medicine, Houston, TX, United States.
Introduction: Pulmonary Arterial Hypertension (PAH) has been reported in patients treated with interferon beta (IFN β) and in patients with multiple sclerosis (MS). Interferons are commonly used for a number of conditions such as malignancies, chronic viral infections, and chronic neurological conditions. We present a case series of patients who developed PAH after undergoing treatment with IFN β for MS. Method: Four PAH patients who previously were treated with IFN β for MS and later diagnosed with PAH were identified at Pulmonary Hypertension Center at Houston Methodist Hospital. Baseline demographics, duration of PAH in years, duration of MS in years, duration of IFN β treatment in years, historical right heart catheterization, hemodynamics from echocardiogram (ECHO), six minute walk distance (6MWD) and Borg dyspnea score (BDS) were recorded for each patient. Results: Mean age was 51±9 years, all were females, 3 were Caucasians and 1 was Hispanic. Age at MS diagnosis was 35±6 years and age at PAH diagnosis was 47±10 years. All received IFN β prior to developing PAH. There was a lag of 12±5 years between developing PAH after IFN β treatment. Two were on intravenous prostacyclin therapy plus oral agents (epoprostenol + tadalafil and treprostinil+macitentan) whereas 2 were on oral PAH medications (ambrissentan+tadalafil and macitentan + tadalafil). Hemodynamics from right heart catheterization done at the time of diagnosis showed a mean pulmonary artery pressure of 53±11 mmHg, right atrial pressure (RAP) of 7±2 mmHg, mixed venous saturation was 71±3%, pulmonary capillary wedge pressure was 12±7 mmHg, thermodilution cardiac output (CO) was 4.66 ±1.7 ml/min and cardiac index (CI) was 2.55±0.8 ml/min/m2. Hemodynamics from recent echo showed a right ventricular systolic pressure of 70±16 mmHg, RAP of 6±2 mmHg, CO of 6.2±2.1 L/min, CI of 3.5±0.73 L/min/m2. The recent 6MWD was 435±115 meters and BDS ranged from 0.5 to 4. All were alive at the time of last follow up that was 16±3 years from MS diagnosis. Conclusions: We present this case series to provide further evidence of the possible relationship between interferon beta treatment, MS and PAH development. In our cohort there was a lag of 12 ± 5 years from IFN β therapy before developing PAH. In contrast to other reports, none of our PAH patients had a reversibility of PAH with cessation of IFN β treatment suggesting early screening of MS patients for PAH.
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