A case of postpregnancy osteoporosis

A case of postpregnancy osteoporosis

European Journal of Obstetrics & Gynecology and Reproductive Biology 88 (2000) 107–109 www.elsevier.com / locate / ejogrb Case Report A case of pos...

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European Journal of Obstetrics & Gynecology and Reproductive Biology 88 (2000) 107–109

www.elsevier.com / locate / ejogrb

Case Report

A case of postpregnancy osteoporosis a, a a b Akihiro Yamaga *, Michiyoshi Taga , Tsuneo Takahashi , Toshiaki Shirai a

Department of Obstetrics and Gynecology, Yokohama City University School of Medicine 3 – 9 Fukuura, Kanazawa-ku, Yokohama, 236 -0004 Japan b Department of Orthopedic Surgery, Yokohama City University School of Medicine 3 – 9 Fukuura, Kanazawa-ku, Yokohama, 236 -0004 Japan Received 11 February 1999; received in revised form 23 March 1999; accepted 10 May 1999

Abstract A puerperant woman, who was previously healthy and had no disease known to affect bone metabolism, experienced lower back pain and lumbar vertebral fractures during lactation. Both bone formation markers and resorption markers were markedly elevated. Bone mineral density of the lumbar spine as measured by dual energy X-ray absorptiometry was extremely low. She stopped lactation through the use of bromocriptine because of the large volume of milk secretion. After treatment with calcitonin injections and the use of a corset, her back pain gradually disappeared. This case appears to be postpregnancy osteoporosis.  2000 Elsevier Science Ireland Ltd. All rights reserved. Keywords: Pregnancy; Osteoporosis; Puerperium; Bone fracture

1. Introduction While osteoporosis is usually associated with postmenopause, postpregnancy osteoporosis is very rare in young women. Its etiology and pathogenesis remain unclear. We report a young woman who experienced lower back pain and had vertebral compression fractures during lactation. Bone mineral density in the lumbar spine was markedly decreased and biochemical markers of bone turnover were elevated.

2. Case report A 25-year-old woman, who was previously healthy and had no disease known to affect bone metabolism, developed lower back pain 5 weeks after her first delivery by Cesarean section following a normal pregnancy. She consulted an orthopedic clinic 11 weeks postpartum. *Corresponding author. Correspondence address: Department of Obstetrics and Gynecology, Kanagawa Prefectural Ashigarakami Hospital, 866-1 Matsudasoryo, Matsuda-machi, Ashigarakami-gun 258-0003, Japan. Tel.: 181-465-83-0351; fax: 181-465-82-5377.

Spinal X-ray films revealed compression fractures of L1 and L2 with osteoporosis (Fig. 1). The serum alkaline phosphatase (ALP) level was 206 I.U. / l, with 33% ALP-2 and 67% ALP-3. She was instructed to wear a corset and was prescribed calcium, vitamin D, and diclofenac sodium for osteoporosis and bromocriptine for suppression of lactation. She had breast-fed her infant for 10 weeks and then weaned the infant because of the large volume of milk. She came to our hospital 14 weeks postpartum. Serum free triiod-thyronin, free thyroxin, thyroid-stimulating hormone, follicular stimulating hormone, luteinizing hormone, prolactin, and cortisol were within normal levels. The serum estradiol level was 10 pg / ml. The levels of the markers of bone metabolism are shown in Table 1. The serum intact-osteocalcin (I-OC) and bone specific ALP levels were high, indicating increased bone formation. The urine pyridinoline (Pyr), deoxypyridinoline (D-Pyr), Ctelopeptide of type I collagen (CTX), and cross-linked N-telopeptide of type I collagen (NTX) values were also high, suggesting a state of increased bone resorption. Bone mineral density (BMD) was markedly decreased: BMD of the lumbar spine (L2–L4) measured by dual energy X-ray absorptiometry (Hologic QDR 2000) was 0.546 g / cm 2 . The mean value of BMD in 25–29-year-old Japanese

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3. Discussion

Fig. 1. Right lateral view of spinal X-ray film of this patient taken at 11 weeks postpartum. Compression fractures are seen in spine of L1 and L2 with osteoporosis.

women is 1.00360.110 g / cm 2 (mean6SD). The T- and Z-scores were 24.19 and 24.25, respectively. For the treatment of back pain, 20 units of elcatonin was injected intramuscularly once a week. Thereafter, back pain gradually disappeared.

Table 1 Biochemical markers of bone turnover in this patient a

Serum I-OC Serum bone specific ALP Urine Pyr Urine D-Pyr Urine CTX Urine NTX

Patient

Normal range

11.2 ng / ml 32.6 mU / ml 79 nmol / mmol ? Cr 13 nmol / mmol ? Cr 409 mmol / mmol ? Cr 96.9 nmol BCE / mmol ? Cr

2.2–5.4 ,9.6 13–36 2.8–7.6 159691 8.3–69.9

a Abbreviations: I-OC, intact-osteocalcin; ALP, alkaline phosphatase; PYR, pyridinoline; D-Pyr, deoxypyridinoline; CTX, C-telopeptide of type I collagen; NTX, cross-linked N-teleopeptide of type I collagen; Cr, creatinine.

Postpregnancy osteoporosis, which is not clearly defined, was first described as a clinical syndrome by Nordin and Roper [1]. They stated that the main cause of this condition was the high level of circulating plasma corticosteroids during pregnancy. After that, several investigators reported postpregnancy osteoporosis or pregnancy-associated osteoporosis [2–7]. The etiology of this condition is unknown. Low BMD and fractures may be due to increased bone metabolism during the perinatal period. However, we do not think that postpregnancy osteoporosis occurs due only to pregnancy or lactation itself because there is no recorded case of rapid loss of more than a few percent of bone mass during pregnancy and because this disease usually occurs about 1.5 months postpartum, whereas the loss of BMD induced by lactation usually appears after 3 months postpartum. Aspects of changes in BMD and bone metabolism during pregnancy and puerperium are still controversial. Previous studies have shown bone mass during these periods to be decreased, unchanged, or increased, depending on differences in study design, measurement techniques, or skeletal sites [8–14]. The serum level of total calcium is gradually decreased with increases in gestational age [15]. This phenomenon is mainly caused by a decrease of calcium-binding protein, but the level of serum ionized calcium is unchanged during pregnancy. While changes of serum parathyroid hormone and calcitonin are slight, serum total 1,25 (OH)2D is greatly increased during pregnancy [15]. According to our recent studies [8,9], both bone formation markers and resorption markers are increased in the latter half of pregnancy and puerperium, and these markers are higher in women who breast feed than those who formula feed, indicating that bone turnover is accelerated by breast feeding. Considering the symptoms that this patient presented with, our case reported here may be diagnosed as postpregnancy osteoporosis. One of the possible causes of the marked bone loss found in this case is probably excess secretion of milk. The patient had to use bromocriptine to suppress lactation. Long-term follow-up and treatment are necessary in such cases, although recovery usually occurs between 3 months and 1 year after the first symptom [6].

References [1] Nordin BEC, Roper A. Post-pregnancy osteoporosis: a syndrome? Lancet 1955;I:431–4. [2] Gruper HE, Grutteridge DH, Baylink DJ. Osteoporosis associated with pregnancy and lactation: Bone biopsy and skeletal features in 3 patients. Metab Bone Dis Relat Res 1984;5:159–65. [3] Dunne F, Walters B, Marshall T, Heath DA. Pregnancy associated osteoporosis. Clin Endcrinol 1993;39:487–90. [4] Yamamoto N, Takahasi HE, Tanizawa T, Kawashima T, Endo N.

A. Yamaga et al. / European Journal of Obstetrics & Gynecology and Reproductive Biology 88 (2000) 107 – 109

[5] [6]

[7] [8]

[9]

Bone mineral density and bone histomorphometric assessments of postpregnancy osteoporosis: a report of five patients. Calcif Tissue Int 1994;54:20–5. Khastgir G. Pregnancy-associated osteoporosis. Br J Obstet Gynaecol 1994;101:836–8. Carbone LD, Palmieri GMA, Graves SC. Osteoporosis of pregnancy: long-term follow-up of patients and their offspring. Obstet Gynecol 1995;86:664–6. Smith R, Athanasou NA, Ostlere SJ, Vipond SE. Pregnancy-associated osteoporosis. Q J Med 1995;88:865–78. Yamaga A, Taga M, Minaguchi H, Sato K. Changes in bone mass as determined by ultrasound and biochemical markers of bone turnover during pregnancy and puerperium: a longitudinal study. J Clin Endocrinol Metab 1996;81:752–6. Yamaga A, Taga M, Minaguchi H. Changes in urinary excretions of C-telopeptide and cross-linked N-telopeptide of type I collagen during pregnancy and puerperium. Endocrine J 1997;44:733–8.

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[10] Drinkwater BL, Charles H. Bone density changes during pregnancy and lactation in active women: a longitudinal study. Bone Miner 1991;14:153–60. [11] Sowers MF, Crutchfield M, Jannausch M, Updike S, Corton G. A prospective evaluation of bone mineral change in pregnancy. Obstet Gynecol 1991;77:841–5. [12] Cross NA, Hillman LS, Allen SH, Krause GF, Vieira NE. Calcium homeostasis and bone metabolism during pregnancy, lactation, and postweaning: a longitudinal study. Am J Clin Nutr 1995;61:514–23. [13] Hayslip CC, Klein TA, Wray HL, Duncan WE. The effects of lactation on bone mineral content in healthy postpartum women. Obstet Gynecol 1989;73:588–92. [14] Prentice A. Maternal calcium requirements during pregnancy and lactation. Am J Clin Nutr 1994;59(suppl):477S–83S. [15] Seki K, Makimura N, Mitsui C, Hirata J, Nagata I. Calciumregulating hormones and osteocalcin levels during pregnancy: a longitudinal study. Am J Obstet Gynecol 1991;164:1248–52.