Bone Abstracts

Vitamin D (vit D) plays an important role in the regulation of mineral homeostasis. Vit D insufficiency leads to decreased calcium and phosphorous intestinal absorption, parathyroid glands (PG) stimulation with consequent development of secondary hyperparathyroidism (HPT) and bone mineralization defect. We present a clinical case of a patient with tertiary HPT as a consequence of severe vit D deficiency.

A clinical case: A woman 59 years old considered herself ill since childhood after nutritional rickets. She was receiving vit D occasionally, and for a long period of time was suffering from the pain in the lumbar spine, other bones, large joints, and progressing chest deformity. Between 50 and 56 years the above mentioned complaints intensified, which forced her to use a walking stick. Three Colles’ fractures also occurred. In 2012 a significant decrease in BMD was noted (T-score) at the radius −9.6 SD and the spine −8.1 SD, as well as an increased PTH level and hypercalcemia (verified twice). The diagnosis workup for primary HPT included Physical examination revealed kyphoscoliotic chest, bow-shaped thigh and crura deformities, and bone excrescence on the anterior surface of the left tibia. There were normal serum calcium and phosphorous levels and 24-h urine calcium, vit D deficiency 9.1 ng/ml, PTH 828.8 pg/ml (15.0–65.0), alkaline phosphatase 236 IU/l (10.0–150.0), osteocalcin 188.6 ng/ml (11.0–43.0) and b-crosslaps 2.29 (0.01–0.69). Ultrasound and CT imaging detected the enlargement of the upper left PG. Radiographs of the hands revealed osteoporosis, bow-shaped first metacarpal deformities, severe osteoporosis in the spine, compression fractures of all thoracic vertebrae, and kyphoscoliotic chest. CT imaging of the bones showed bow-shaped curvature of proximal thirds of both femoral bones, multiple Looser’s zones combined with bone cysts of the pelvis, both greater and lesser trochanters, right femoral bone and left tibia diaphyses. The condition was considered as tertiary HPT in the setting of severe vit D. Parathyroidectomy was performed. Follow-up in 6–12 months showed improvement in medical condition, normalization of mineral homeostasis, and significant increase in BMD.

Conclusion: The case presented is the outcome of non-compensated nutritional rickets since early childhood and illustrate the need most of early diagnosis and adequate treatment of deficiency of vitamin D.