Erik A. Imel, MD
Associate Professor of Medicine
Dr. Imel's clinical and research interests include pediatric metabolic bone and mineral disorders, especially hypophosphatemic disorders, calcium disorders, and disorders of low bone density. After completing his medical degree at the University of Cincinnati, Dr. Imel engaged in a combined internal medicine and pediatrics residency program at the University of Rochester. Then he completed combined training in both pediatric and adult endocrinology, with a special focus on metabolic bone and mineral disorders. He is engaged at the national level with the American Society for Bone and Mineral Research, the Endocrine Society and the Pediatric Endocrine Society. Dr. Imel's clinical and research interests include pediatric metabolic bone and mineral disorders, especially hypophosphatemic disorders, calcium disorders, and disorders of low bone density. As a Regenstrief Institute Affiliate Scientist, he also conducts research into "real-world" application and effects of osteoporosis treatment in clinical populations. Dr. Imel also sees patients as adolescents and young adults in his adult endocrinology clinic for bone and mineral disorders and also other endocrine disorders such as congenital adrenal hyperplasia, Turner syndrome, hypopituitarism and McCune-Albright syndrome.
Gatch Hall, Suite 380 F 1120 W. Michigan St.
Indianapolis, IN 46202-5111
Titles & Appointments
- Associate Professor of Pediatrics
Metabolic bone diseases in adults and children, including osteoporosis, osteogenesis imperfecta, calcium and phosphorus disorders, including X-linked hypophosphatemia and related disorders;
Infants With Congenital Adrenal Hyperplasia Are at Risk for Hypercalcemia, Hypercalciuria, and Nephrocalcinosis.
Proportion of osteoporotic women remaining at risk for fracture despite adherence to oral bisphosphonates.
Population pharmacokinetic and pharmacodynamic analyses from a 4-month intradose escalation and its subsequent 12-month dose titration studies for a human monoclonal anti-FGF23 antibody (KRN23) in adults with X-linked hypophosphatemia.
Pharmacokinetics and pharmacodynamics of a human monoclonal anti-FGF23 antibody (KRN23) in the first multiple ascending-dose trial treating adults with X-linked hypophosphatemia.
Prolonged correction of serum phosphorus in adults with X-linked hypophosphatemia using monthly doses of KRN23.
Miscellaneous non-inflammatory musculoskeletal conditions. Hyperphosphatemic familial tumoral calcinosis (FGF23, GALNT3 and aKlotho).
Iron modifies plasma FGF23 differently in autosomal dominant hypophosphatemic rickets and healthy humans.
Treatment of X-linked hypophosphatemia with calcitriol and phosphate increases circulating fibroblast growth factor 23 concentrations.
Novel GALNT3 mutations causing hyperostosis-hyperphosphatemia syndrome result in low intact fibroblast growth factor 23 concentrations.
Intronic deletions in the SLC34A3 gene cause hereditary hypophosphatemic rickets with hypercalciuria.
Tumoral calcinosis presenting with eyelid calcifications due to novel missense mutations in the glycosyl transferase domain of the GALNT3 gene.
The Endocrine Society
American Society for Bone and Mineral Research