Reduced bone mass in women with premenstrual syndrome Academic Article uri icon

Overview

MeSH Major

  • Neuroendocrine Tumors
  • Radiopharmaceuticals
  • Tomography, Emission-Computed, Single-Photon

abstract

  • Recent evidence has demonstrated the efficacy of calcium in the relief of premenstrual syndrome (PMS) symptomatology. We therefore, hypothesized that PMS might be a clinical manifestation of a calcium deficiency state resulting in potential bone loss. The present study was designed to determine whether women with established PMS have reduced bone mineral density (BMD) measurements compared to asymptomatic controls. Women with PMS and asymptomatic controls were evaluated with dual-photon absorptiometry at two sites, the lumbar vertebrae and the proximal femur. During the luteal phase, concentrations of the calciotropic hormones iPTH, 1,25(OH) 2D, 25OHD, and total serum calcium were obtained. Dietary calcium intake and 24-hour urine calcium excretion were measured as well in all participants. Controls and women with PMS had similar age, race, body mass index (BMI), and physical activity, Compared to controls, women with PMS had significantly lower vertebral bone mass measurements at L2-4 (1.18 ± 0.11 vs. 1.28 ± 0.11 g/cm 2, p = 0.0016), and at the femur in Ward's triangle (0.84 ± 0.10 g/cm 2 vs. 0.91 ± 0.16 g/cm 2, p = 0.0458). In contrast, BMD at the femoral neck and trochanter was not different between groups. Women with PMS also had significantly lower 25OHD concentrations (19.5 ± 7.5 vs. 25.3 ± 8.3 ng/mL, p = 0.018) than controls. There were no differences between the two groups in the mean concentrations of iPTH, 1,25(OH) 2D, calcium excretion, or dietary calcium intake. These data suggest that PMS is associated with reduced bone mass measurements and a calcium deficiency state. Further research in calcium metabolism may be worthwhile in elucidating the pathophysiology of PMS.

publication date

  • August 21, 1995

Research

keywords

  • Academic Article

Additional Document Info

start page

  • 161

end page

  • 168

volume

  • 4

number

  • 2