Osteoporosis of pregnancy: Long-term follow-up of patients and their offspring

Carbone, Laura D.; Palmieri, Genaro M. A.; Graves, Stanley C.; Smull, Katherine

doi:10.1016/0029-7844(95)00226-h

Cited by 37 publications

(15 citation statements)

References 7 publications

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“…Low bone density, initially shown by single photon absorptiometry of the distal radius, was still present 10 years later and the BMD of the offspring of these women (measured by DXA) was also low at the ages of 11 and 13 years. This led the authors to suggest that osteoporosis associated with pregnancy should not be regarded as a transient process and may be familial [12]; this view is supported by previous work which showed a higher prevalence of adult-related fractures in mothers of some subjects with pregnancy-associated osteoporosis [1]. Although the spine and hip are the areas where fractures most often occur in pregnancy-associated osteoporosis, an insufficiency fracture in the sacrum in a vitamin-D-deficient woman has been reported [13].…”

Section: Previous Observationsmentioning

confidence: 96%

Pregnancy-Associated Osteoporosis: Does the Skeleton Recover?

Phillips¹,

Ostlere²,

Smith

2000

Osteoporosis International

183

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Osteoporosis in pregnancy is a rare clinical problem of unknown cause. If the bone loss results from the pregnancy alone it should improve toward normal after delivery; in contrast, where bone density was low before pregnancy, due to some other secondary cause, significant postpartum improvement might not be expected. Thirteen women (age 23-37 years) with pregnancy-associated osteoporosis presenting with either pain in the back and vertebral collapse (8 subjects) or pain in the hip (5 subjects) had consecutive dual-energy X-ray absorptiometry measurements of bone mineral density (BMD) for up to 8 years after an affected pregnancy. The BMD results were expressed as a Z-score in relation to an age-matched mean. The mean initial (0-6 months postpartum) BMD was low in both groups and at both sites. In the back pain group the mean spine Z-score (Ll-L4) was -3.34 (range -2.25 to -4.66) and mean total hip Z-score was -2.41 (range -1.44 to -3.82). In the hip pain group the mean spine Z-score was -2.00 (range -1.48 to -2.65) and mean hip Z-score was -2.19 (range -1.12 to -3.26). Subsequent mean hip and spine BMD increased significantly toward the lower end of the normal range. We conclude that a reversible part of the bone loss is related to the pregnancy itself. A low BMD before pregnancy cannot be excluded. Knowledge that the bone density increases after an affected pregnancy, combined with the known rarity of recurrent symptoms in subsequent pregnancies, is important in prognosis.

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Section: Previous Observationsmentioning

confidence: 96%

Pregnancy-Associated Osteoporosis: Does the Skeleton Recover?

Phillips¹,

Ostlere²,

Smith

2000

Osteoporosis International

183

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“…The rationale of using established clinical risk factors for fragility fracture, such as thin complexion, or others included in the risk assessment scales (81), may be an option, but it has not been tested. A possible genetic background has been suggested after some reports of familial aggregation (79,82,83).…”

Section: Clinical Presentationmentioning

confidence: 99%

ENDOCRINOLOGY IN PREGNANCY: Bone metabolic changes during pregnancy: a period of vulnerability to osteoporosis and fracture

Sanz-Salvador

Garcı́a-Pérez

Tarı́n

et al. 2015

European Journal of Endocrinology

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Changes in bone density and bone markers suggest that pregnancy is associated with deterioration of bone mass in the mother. The metabolism of calcium resets to allow for the needs imposed by the building of the fetal skeleton. The fetus contributes to the process through the output of regulators from the placenta. Understanding of the whole process is limited, but some changes are unambiguous. There is an increase in the circulating levels of vitamin D, but its functional impact is unclear. Fetal parathyroid hormone (PTH) and PTH-related peptide (PTHrp) play an indirect role through support of a calcium gradient that creates hypercalcemia in the fetus. Placental GH, which increases up to the end of pregnancy, may exert some anabolic effects, either directly or through the regulation of the IGF1 production. Other key regulators of bone metabolism, such as estrogens or prolactin, are elevated during pregnancy, but their role is uncertain. An increase in the ratio of receptor activator of nuclear factor kappa B ligand (RANKL) to osteoprotegerin (OPG) acts as an additional pro-resorbing factor in bone. The increase in bone resorption may lead to osteoporosis and fragility fracture, which have been diagnosed, although rarely. However, the condition is transitory as long-term studies do not link the number of pregnancies with osteoporosis. Prevention is limited by the lack of identifiable risk factors. When fractures are diagnosed, rest, analgesics, or, when indicated, orthopedic intervention have demonstrated efficacy. Systemic treatment with anti-osteoporotic drugs is effective, but the potential harm to the fetus imposes caution in their use.

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“…Yapılan çalışmalarda GİO tanısı alan hastaların annelerinde yüksek kırık prevalansı olması altta yatan bir genetik komponentin olduğunu düşündürmektedir (4,5). Diğer bir çalışmada GİO tanılı hastaların akrabalarında kemik kütle analizi yapılmış ve hastaların kendi yaş grubuna göre düşük kemik kitlesi değerleri saptanmıştır (6).…”

Section: Tanımunclassified