SAT-783 - Milk, Minerals, and A Misstep: Postpartum Osteoporosis with A Low-Trauma Ankle Fracture

Introduction:

Pregnancy- and lactation-associated osteoporosis (PLO) is an uncommon but clinically important cause of fragility fractures in the postpartum period. During pregnancy and especially breastfeeding, maternal calcium is mobilized to meet fetal and neonatal skeletal demands. Most women compensate through increased calcium absorption and changes in bone turnover, with bone mineral density (BMD) recovering after weaning. However, in a subset—particularly those with low calcium and vitamin D intake, limited sun exposure, low pre-pregnancy BMD, low BMI, or other risk factors—bone loss can become pathologic and present with fractures. While vertebral compression fractures are most often reported, peripheral fractures can occur and may be misattributed to “routine” injuries.

Case:

35-year-old female, 4 months postpartum and breastfeeding, presented with left ankle pain after a fall from a standing height. She had not taken prenatal vitamins due to nausea during pregnancy. Postpartum, she continued without supplements and minimal dairy intake. She had no history of eating disorders, bariatric surgery, glucocorticoid use, thyroid disease, malabsorption, smoking, or alcohol use. Examination showed marked swelling over the left ankle with tenderness over the left inferior malleolus and inability to move the ankle. Imaging revealed a malleolar fracture of the left fibula.

Her last blood work done at 6-week post-partum showed iron deficiency anemia. Vitamin D level was not checked. She was diagnosed with clinical osteoporosis due to pregnancy and lactation. Management included analgesia, activity modification, physical therapy, and initiation of calcium (1,200 mg elemental/day) and vitamin D3 (2,000 IU/day). At 6-month follow-up, pain had resolved; no new fractures occurred. She later underwent a complete workup that showed normal Calcium, PTH and Vitamin D levels.



Discussion:

This case illustrates PLO presenting as a peripheral fragility fracture in the absence of calcium and vitamin D supplementation. Lactation increases skeletal resorption via hormonal shifts (low estrogen, elevated PTH-related peptide), and inadequate calcium/vitamin D intake may exacerbate compensatory bone loss. Evaluation should exclude secondary causes, assess vitamin D status, and consider DEXA when fractures occur with minimal trauma. Management typically includes optimizing calcium and vitamin D, activity modification and fall prevention, and counseling regarding lactation. Most patients experience substantial BMD recovery after weaning and nutritional correction, though recovery may be incomplete in severe cases. Clinicians should maintain suspicion for PLO when postpartum breastfeeding women sustain low-trauma fractures—especially if they are not taking calcium and vitamin D—so that deficiency is corrected early and future fractures prevented.

*Unless otherwise noted, all abstracts presented at ENDO must not be released to the press or the public until the date and time of presentation. For oral presentations, the abstracts are embargoed until the session begins. The Endocrine Society reserves the right to lift the embargo on specific abstracts that are selected for promotion prior to or during ENDO.*