Pregnancy-associated osteoporosis revisited

To the Editor, A 23-year-old female was seen due to severe back pain for 3 months after delivering her first child. On detailed questioning, she declared that her pain started during the last trimester of pregnancy and that it was worse during activities. She denied having any numbness, weakness or pain in the lower limbs. She had recently stopped breastfeeding and the medical history was otherwise noncontributory. Questioning for osteoporosis (OP) risk factors only yielded inadequate calcium intake. On physical examination, her height was 160 cm, body weight was 50 kg (BMI 19.5 kg/m). Posture analysis revealed increased dorsal kyphosis and thoracolumbar scoliosis. Thoracic vertebrae were tender to compression. Neurological evaluation was unremarkable. Plain radiographs showed compression fractures at T8–T12 and scoliosis (Fig. 1). Dual energy X-ray absorptiometry (DXA) (Hologic QDR-4500) was performed for the evaluation of bone mineral density (BMD) (Table 1). Laboratory tests (inclusing serum calcium, phosphate, alkaline phosphatase, parathyroid hormone levels and thyroid, liver and renal function tests) were all normal except decreased 25-OH vitamin D level (12.2 ng/ml = 30.45 nmol/L, N [ 20 ng/ ml). Overall, she was diagnosed to have pregnancyassociated osteoporosis (PAO). Medical treatment comprised daily intake of calcium carbonate (1,200 mg ionized calcium), 800 IU vitamin D3 and 200 IU nasal calcitonin. She was additionally prescribed analgesics, bed rest and a thoracolumbar brace at the initial stage. Thereafter, she was commenced on a physical therapy program (superficial and deep heat for the low back region; isometric strengthening exercises for the trunk muscles and scoliosis exercises). PAO is an uncommon disorder characterized by painful vertebral fractures (generally more than one) in late pregnancy or early postpartum periods [1, 2]. The incidence is estimated to be only 0.4 cases per 100,000 women whereas the number of undiagnosed cases is probably higher [3]. Despite the skepticism on its etiology and pathogenesis, the condition has been linked to insufficient calcium intake and increased mechanical stress throughout the course of pregnancy (hyperlordosis). Significant calcium transfer from the mother to the fetus and the infant (during rapid mineralization) occurs during pregnancy and lactation, theoretically placing the mother at an increased risk for OP later in life [4]. Further, it is also reflected on the maternal BMD, as a decrease of 2–4% depending on the site of measurement [5]. It is well known that peak bone mass (the basis of the latter calcium reservoir) is achieved between 20 and 30 years of age and depends on genetic disposition, gender, age at menarche, nutrition, lifestyle, level of physical activity and consumption of alcohol, tobacco and caffeine. Accordingly, the lower the peak bone mass before pregnancy is, the higher the risk of PAO development becomes [3]. In our primagravid female patient, the risks for PAO with nontraumatic vertebral fractures seemed to be poor calcium and vitamin D intake prior and throughout her pregnancy. Management of PAO is not well established but should definitely not be confined to medical treatment only. Recent studies have shown that the bone loss should improve toward normal after the delivery; however, this G. Kara L. Ozcakar F. U. Malas A. Akinci O. Basgoze Department of Physical Medicine and Rehabilitation, Hacettepe University Medical School, Ankara, Turkey e-mail: gkara2005@yahoo.com.tr