Erik A. Imel, MD
Associate Professor of Medicine
Bio
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.
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.
Serum fibroblast growth factor 23, serum iron and bone mineral density in premenopausal women.
The Case | Ectopic calcifications in a child.
Successful treatment of neonatal severe hyperparathyroidism with cinacalcet in two patients.
A Practical Clinical Approach to Paediatric Phosphate Disorders.
Disparities in osteoporosis treatments.
Hyperphosphatemic Familial Tumoral Calcinosis: Genetic Models of Deficient FGF23 Action.
Genome-wide association study of serum iron phenotypes in premenopausal women of European descent.
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.
FGF23 is elevated in multiple myeloma and increases heparanase expression by tumor cells.
Randomized trial of the anti-FGF23 antibody KRN23 in X-linked hypophosphatemia.
The changing face of hypophosphatemic disorders in the FGF-23 era.
Iron and fibroblast growth factor 23 in X-linked hypophosphatemia.
Approach to the hypophosphatemic patient.
Fluorosis because of prolonged voriconazole therapy in a teenager with acute myelogenous leukemia.
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.
Clinical variability of familial tumoral calcinosis caused by novel GALNT3 mutations.
Mutational survey of the PHEX gene in patients with X-linked hypophosphatemic rickets.
A homozygous missense mutation in human KLOTHO causes severe tumoral calcinosis.
A homozygous missense mutation in human KLOTHO causes severe tumoral calcinosis.
Novel GALNT3 mutations causing hyperostosis-hyperphosphatemia syndrome result in low intact fibroblast growth factor 23 concentrations.
Fibrous dysplasia, phosphate wasting and fibroblast growth factor 23.
FGF23 concentrations vary with disease status in autosomal dominant hypophosphatemic rickets.
Sensitivity of fibroblast growth factor 23 measurements in tumor-induced osteomalacia.
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.
Fibroblast growth factor 23: roles in health and disease.
Pediatric Endocrine Society
The Endocrine Society
Endocrinology
Pediatric Endocrinology