Do patients with ehlers-danlos syndrome and a history of fractures have calcium and phosphate metabolism disturbances?

- Łapan Aleksandra Żuk; Ivan Rychlik; Jan Domański; Jakub Podstawka; Bernadetta Kałuża; Edward Franek

doi:10.1530/endoabs.110.EP213

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Endocrine Abstracts (2025) 110 EP213 | DOI: 10.1530/endoabs.110.EP213

ECEESPE2025 ePoster Presentations Bone and Mineral Metabolism (142 abstracts)

Do patients with ehlers–danlos syndrome and a history of fractures have calcium and phosphate metabolism disturbances?

Aleksandra Żuk - Łapan ^1,2 , Ivan Rychlik ³ , Jan Domański ^1,2 , Jakub Podstawka ^1,2 , Bernadetta Kałuża ^1,2 & Edward Franek ^1,4

Author affiliations

¹Department of Internal Medicine, Endocrinology, and Diabetology, National Medical Institute of the Ministry of the Interior and Administration, Warsaw, Poland; ²Students Scientific Group of the Medical University of Warsaw at the Department of Internal Medicine, Endocrinology, and Diabetology, National Medical Institute of the Ministry of the Interior and Administration, Warsaw, Poland; ³Department of Internal Medicine, Third Faculty of Medicine, Charles University, and Královské Vinohrady University Hospital, Prague, Czech Republic; ⁴Department of Human Epigenetics, Mossakowski Medical Research Institute, Polish Academy of Sciences, Warsaw, Poland

JOINT2317

Background: Patients with Ehlers–Danlos syndrome (EDS) are at an increased risk of fractures whose etiology is chiefly associated with joint hypermobility and instability. One of the possible risk factors for fractures are calcium and phosphate metabolic disorders. The purpose of this study was to investigate calcium and phosphate metabolic disorders in patients with a hypermobile or classical EDS subtype and a history of fractures.

Material and Methods: The study involved a prospective assessment of 30 female patients, with either hypermobile or classical EDS. The patients were divided into two groups based on their fracture history. Group 1 comprised patients with no history of fractures (n =13); group 2 comprised patients with a history of fractures (n =17). All patients were evaluated for parameters of calcium and phosphate metabolism.

Results: The two study groups showed no differences either in terms of such parameters as total calcium (2.41±0.09 vs. 2.39±0.08, P = 0.691 [mmol/l]), parathyroid hormone (41.68±15.63 vs. 43.73±15.19, P = 0.805 [pg/ml]), vitamin 25OH-D (28.2±10.8 vs. 32.44±20.35, P = 0.786 [ng/ml]), alkaline phosphatase (8.6±2.33 vs. 10.24±2.78, P = 0.133 [µg/l]), beta-CrossLabsCTX (0.43±0.2 vs. 0.36±0.2, P = 0.336 [ng/ml]), and osteocalcin (21.7±6.59 vs. 19.72±8.04, P= 0.341 [ng/ml]) levels, or in terms of EDS subtypes: classical (n =5 (38.5%) vs. n =6 (35.3%), P = 0.901) and hypermobile (n =8 (61.5%) vs. n =13 (76.5%), P = 0.399) EDS. Inorganic phosphorus levels were significantly lower in group 2 than in group 1 patients (3.19±0.51 vs. 3.85±0.59, P = 0.003). There was a significant negative correlation between a history of fractures and inorganic phosphorus levels (Spearman’s R -0.559, P = 0.001).

Conclusions: Patients with EDS and fracture history may exhibit abnormal calcium and phosphate metabolism manifesting in the form of low phosphorus levels.