SUN-795 - A Young Mother with Lactation-Associated Fractures

Introduction

There are significant changes to the skeletal system that occur during pregnancy and lactation, but these changes almost never lead to pathologic outcomes. We present a case of a young mother who presented with lumbar spine fractures believed to be due to lactation.

Background

Lactation is accompanied by a high calcium demand for adequate breast milk production. Calcium demands typically cannot be met with dietary calcium intake alone, and significant strain is placed on the maternal skeleton to meet these demands. Parathyroid hormone-related protein (PTHrP) produced by breast tissue leads to maternal bone resorption, and bone mineral density loss of 5-10% in the spine is typically seen during lactation. However, these changes rarely lead to fractures and usually reverse soon after weaning.

Case

A 25-year-old female with no notable medical problems presented to the emergency department with severe back pain six weeks after delivering her first child. Magnetic resonance imaging revealed acute compression fractures of the thoracic and lumbar spine at T9, T11, T12, L1 and L4. The patient reported a subjective overproduction of breast milk since delivering her child. The workup for secondary causes of osteoporosis was not remarkable. She was offered cabergoline to lower prolactin and speed weaning, as well as teriparatide, but the patient declined both.

Discussion

Fracture is an uncommon complication of lactation. While normal physiology often leads to significant decreases in bone mineral density during lactation, this rarely leads to fracture and typically reverses rapidly after cessation of lactation. In some cases, lactation-associated fracture may uncover an underlying secondary cause of osteoporosis that becomes exacerbated by lactation and leads to fracture.

Pharmacologic treatment of lactation-associated fractures remains controversial. Antiresorptive therapies may blunt the spontaneous recovery phase of bone reformation that occurs after weaning and are generally not recommended. Small studies have shown that teriparatide leads to increased bone density but lacked controls and cannot be directly compared to spontaneous bone mineral density recovery. Unlike postmenopausal women, patients with lactation-associated fractures have shown the ability to maintain their bone mineral density gains after treatment with teriparatide even when it is not followed by an antiresorptive. The risk of fracture with future pregnancies is thought to be about 10-20% in patients with a pregnancy or lactation-associated fracture.

Conclusion

Lactation places significant strain on the maternal skeleton, but fracture is an uncommon complication of this process. Pharmacologic treatment in these cases is often not needed, and bone mineral density typically recovers spontaneously.

*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.*