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Costenbader, K.

Publications and source records attributed to Costenbader, K..

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Using genetics to differentiate patients with similar symptoms: application to inflammatory arthritis in the rheumatology outpatient clinic

Slow developing complex diseases are a clinical diagnostic challenge. Since genetic information is increasingly available prior to a patients first visit to a clinic, it might improve diagnostic accuracy. We aimed to devise a method to convert genetic information into simple probabilities discriminating between multiple diagnoses in patients presenting with inflammatory arthritis.\n\nWe developed G-Prob, which calculates for each patient the genetic probability for each of multiple possible diseases. We tested this for inflammatory arthritis-causing diseases (rheumatoid arthritis, systemic lupus erythematosus, spondyloarthropathy, psoriatic arthritis and gout). After validating in simulated data, we tested G-Prob in biobank cohorts in which genetic data were linked to electronic medical records: - 1,200 patients identified by ICD-codes within the eMERGE database (n= 52,623);\n- 245 patients identified through ICD codes and review of medical records within the Partners Biobank (n=12,604);\n- 243 patients selected prospectively with final diagnoses by medical record review within the Partners Biobank (n=12,604).\nThe calibration of G-Prob with the disease status was high (with regression coefficients ranging from 0.90-1.08 (ideal would be 1.00) in all cohorts. G-Probs discriminative ability was high in all cohorts with pooled Area Under the Curve (AUC)=0.69 [95%CI 0.67-0.71], 0.81 [95%CI 0.76-0.84] and 0.84 [95%CI 0.81-0.86]. For all patients, at least one disease could be ruled out, and in 45% of patients a most likely diagnosis could be identified with an overall 64% positive predictive value. In 35% of instances the clinicians initial diagnosis was incorrect. Initial clinical diagnosis explained 39% of the variance in final disease prediction which improved to 51% (P<0.0001) by adding G-Prob genetic data.\n\nIn conclusion, by converting genotypes into an interpretable probability value for five different inflammatory arthritides, we can better discriminate and diagnose rheumatic diseases. Genotypes available prior to a clinical visit could be considered part of patients medical history and potentially used to improve precision and diagnostic efficiency in clinical practice.

genetics

Antibody against envelope protein from human endogenous retrovirus activates neutrophils in systemic lupus erythematosus

Neutrophil activation and the formation of neutrophil extracellular trap (NET) are hallmarks of innate immune activation in systemic lupus erythematosus (SLE) and contribute to the systemic interferon signature. Here we report that the expression of an endogenous retrovirus (ERV) locus ERV-K102, encoding an envelope protein, was significantly elevated in SLE patient blood and was correlated with higher interferon status. Induction of ERV-K102 expression most strongly correlated with reduced transcript levels of epigenetic silencing factors. SLE IgG promoted phagocytosis of ERV-K102 envelope protein by neutrophils through immune complex formation. ERV immune complex phagocytosis resulted in subsequent NET formation consisting of DNA, neutrophil elastase, and citrullinated histone H3. Finally, analysis of anti-ERV-K102 IgG in SLE patients showed that IgG2 likely mediates this effect. Together, we identified an immunostimulatory ERV-K envelope protein elevated in SLE that may be a target of SLE IgG and able to promote neutrophil activation.\n\neTOC summaryUsing ERVmap, the authors determined that the expression of ERV-K102 locus was elevated in SLE patient blood and correlated with the interferon signature. The envelope protein encoded by this locus activates human neutrophils through immune complex formation with SLE IgG.

immunology