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--- acr2026 [2026/09/21 13:06] – admin
+++ acr2026 [2026/09/30 19:52] (current) – admin
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-**Poster presenter (name, credentials, title, institution)**
+====== Admin Details ======
-Eric W. Robbins, MD
+{{ :itinerary_pwzf4p_28sep_robbins.pdf |itinerary}}
-Clinical Fellow
+^ place                                    ^ Map ^ Address ^ Phone^
+| Hotel                                | [[ https://maps.app.goo.gl/YD9W4zZMc1fFaBEU9| Hilton Chicago]] | 720 S Michigan Ave, Chicago, IL 60605| 312-922-4400|
+| Conference Venue|[[https://maps.app.goo.gl/waGyp1qzgnBwcURt5 | McCormick Place]]|2301 S Martin Luther King Dr, Chicago, IL 60616|312-791-7000|
-Critical Care Medicine and Pulmonary Branch; National Heart, Lung, and Blood Institute
+^Origin ^ Destination ^ Flight ID^
+| DCA |ORD |AA 1165|
+| ORD | DCA| AA 2249|
-National Institutes of Health
+====== Transit ======
-**Poster title:**
+App: [[https://www.ventrachicago.com/ | Ventra]]
-Serial Quantitative Changes in Anti-Scl-70 Autoantibodies Are Associated with Lung Function Decline in Systemic Sclerosis
+<todo>At O'Hare, purchase a 3-day disposable Ventra pass</todo>
-**What is your poster about?**
+=== From Airport to Hotel ===
-Our study investigates whether serial, quantitative changes in anti-Scl-70 autoantibody levels can provide information about subsequent lung function decline and disease progression in systemic sclerosis (SSc). Using a research assay known as luciferase immunoprecipitation systems (LIPS), we evaluated patients from the multicenter CONQUER registry.
+CTA Blue line from _O'Hare_ to _Jackson_
-We found that greater early increases in anti-Scl-70 levels were consistently associated with subsequent forced vital capacity (FVC) decline. For example, a greater than 30% increase in anti-Scl-70 levels was associated with nearly a four-fold higher risk of pulmonary progression over two years. These findings suggest that the trajectory of an autoantibody level may provide prognostic information beyond a single baseline measurement.
+=== From Hotel to Venue ===
-**Why did you decide to investigate this topic?**
+  * Option 1:
+    * [[https://maps.app.goo.gl/7ToNXXqLJGKFngcN6 | Take bus 3 from directly in front of hotel to venue]]
+  * Option 2:
+    * [[https://maps.app.goo.gl/w5rKjyFAurhTronY8 | Walk to Museum Campus / 11th street stop and take Orange line]]
-Our group previously studied myositis-associated interstitial lung disease (ILD), and we wanted to expand our work to other rheumatic diseases that can lead to pulmonary fibrosis. Anti-Scl-70 autoantibodies are a well-established risk factor for SSc-ILD, but prior studies have largely focused on whether the antibody is present or on a single baseline measurement.
-We were interested in whether quantitative changes over time might provide additional information about a patient's disease trajectory.
+====== Schedule ======
-Our goal was to determine whether serial antibody measurements could serve as a dynamic biomarker to help identify patients at greater risk for future pulmonary worsening.
-**What are you working on next related to this research?**
+  * Sun, Oct 26
+    * 09:59 flight, DCA to ORD
-Broadly, we are investigating shared proteomic profiles of pulmonary fibrosis across a spectrum of autoimmune rheumatic diseases, including myositis, SSc, and Sjögren's syndrome.
+    * 11:06 arrival in ORD
+  * Mon, Oct 27
-We are hoping to extend our work within the CONQUER cohort using high-breadth proteomic profiling.
+    * 10:30 - 12:30, Marce poster
-By expanding the number of analytes we can measure, we hope to develop a more comprehensive picture of the biological pathways associated with clinical progression and identify molecular signatures that correlate closely with pulmonary outcomes.
+      * Hall F1
+  * Tue, Oct 28
-**What excites you most about your work?**
+    * 10:30 - 12:30, My abstract
+      * Hall F1, 1949
-I'm excited by the possibility of developing tools that enable more dynamic and proactive monitoring of SSc-ILD, rather than relying solely on static risk assessments.
+    * 17:19 flight, ORD to DCA
-If we can identify biomarker trajectories that precede measurable clinical decline, we may ultimately be able to give rheumatologists and pulmonologists an earlier signal that a patient's disease is changing.
+    * 20:16 arrival in DCA
-The broader goal is to move toward more personalized monitoring and, eventually, better-informed treatment decisions before substantial and potentially irreversible lung injury occurs.
-**What are you most looking forward to at ACR Convergence 2026 in Orlando?**
-As a pulmonologist, I'm especially looking forward to connecting with rheumatology colleagues, translational researchers, and other ILD specialists.
-There is exciting work underway in the rheumatic disease biomarker field, as well as ongoing trials evaluating new therapeutic approaches for refractory rheumatologic disease.
-I'm eager to share what we have learned from the CONQUER cohort, hear how other investigators are approaching biomarkers and ILD, and see which emerging discoveries might ultimately translate into clinical practice.

ewrobbins.com

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