Largely due to the use of corticosteroids, osteoporosis in young patients with SLE is not uncommon. Bone mineral density (BMD) is decreased in premenopausal women with SLE when compared with healthy women without lupus, and the prevalence of osteoporosis (as defined by T-score > 2.5) is as high as 18% in some studies. Specific data on fractures before menopause is sparse; however incidence of (self-reported) fracture in patients with SLE of all ages is five times that of normals.
Most studies find loss of BMD in lupus patients (especially in the lumbar spine) to be associated with prednisone use of > 7.5 mg/day: corticosteroid use is by far the greatest risk factor for osteopenia and osteoporosis. The bone loss from steroid therapy occurs rapidly -- within the first six months of treatment - and slows somewhat after this early drop. Other factors that contribute to increased osteoporosis risk in SLE include decreased vitamin D metabolism, decrease in weight-bearing exercise, ovarian dysfunction related to medications or disease activity, and a potential direct effect of inflammation on bone turnover.
Prevention and therapy of osteoporosis in young women with SLE of child-bearing age who are not yet pregnant is difficult despite availability of the bisphosphonates. The recommendation for anti-resorptive therapy with steroid use - given its demonstrated protective effect - is not an issue for women who do not plan further pregnancies. The half-life of the bisphosphonates is extremely long, however, and many rheumatologists are hesitant to give these drugs to patients before child-bearing is completed. Transplacental effects of bisphosphonates on fetal skeletal ossification have been shown in rats: alendronate, for example, passes through rat placenta and accumulates in fetal bones, with demonstrated changes histomorphologic studies. Alternate therapy for women planning child-bearing includes adequate calcium and vitamin D, weight-bearing exercise, minimal dose of steroid, and nasal calcitonin(Miacalcin). In corticosteroidexposed SLE patients, regular exercise has been shown to be protective of femoral neck bone loss. Hoever, long-term vitamin D and calcium in those on extended corticosteroid therapy is not necessarily protective.
Pregnancy and lactation contribute further to the problem of osteoporosis in young women with SLE. Bone mineral density normally decreases slightly (3 - 7%) during pregnancy; breast-feeding causes a more significant decrease. Fracture is, fortunately, extremely rare. Pregnancy-related decrease in BMD is lessened, and the return to baseline more rapid (about 6 months on average), in the absence of lactation.
Unfortunately, additional calcium intake does not prevent bone loss during pregnancy or lactation and does not enhance recovery after weaning (although obviously adequate calcium intake is important). The recovery of bone is complete for most women, however, once pregnancy or lactation ceases, and recovery in normal women occurs even with shortly spaced pregnancies. Bone loss is not significantly worse after prolonged vs. shorter duration breast-feeding as the rate of lactation-related bone loss is maximal in the first five months of breastfeeding and slows considerably after that.
The expected mild drop in BMD with pregnancy should not be confused with transient, or regional, osteoporosis, the idiopathic localized osteoporosis that rarely presents during pregnancy, primarily in the hip or spine. This usually presents in the third trimester with thigh and groin pain, or back pain, and gradually resolves (without therapy) over about six months. Etiology is not known. Spine involvement may result in vertebral collapse. This disorder is unpredictable, although most common in first pregnancies, and is not more likely to occur in patients with SLE or preexisting osteoporosis.
Risk factors for osteoporosis in the SLE patient during pregnancy may be additive. Preexisting osteoporosis (starting at a lower baseline) may present a greater risk for fracture during or after pregnancy. It is not known whether patients with preexisting osteoporosis are as likely to return to their baseline after pregnancy or lactation is completed.
While glucocorticoid dose is almost always minimized and prophylactic steroid generally not given, maintaining a low dosage during pregnancy represents more of a challenge than in the nonpregnant patient since there is a real absence of alternative therapies. NSAIDS or other immunosuppressives are often avoided in pregnancy (although hydroxychloroquine is now generally continued), and prednisone substituted, for fetal safety.
In addition, other medications may impact bone density in patients with SLE. Heparin therapy is recommended for patients with antiphospholipid-related fetal loss and for patients with any history of prior thrombosis, since pregnancy exerts a strong (additional) prothrombotic effect. In the general (non-lupus) population, the risk of DVT increases five times during pregnancy and the post-partum period. Heparin is safe for the fetus, as its large size prevents placental passage. The most significant maternal risk, however, is osteoporosis related to long-term use. Coumadin is contraindicated during much of pregnancy due to risk of teratogenic effects.
The incidence of symptomatic osteoporosis associated with (unfractionated) heparin during pregnancy in a woman with previously normal BMD may be as high as 2%, and there are case reports of vertebral collapse in women treated with heparin during pregnancy. It is unclear if the risk is dose related, as studies are conflicting. Significant reduction in BMD is often seen even in the absence of true osteoporosis. There is no evidence that additional calcium prevents bone loss. Recovery in most patients on heparin alone is complete by six months post-partum, if the mother does not breastfeed. With breastfeeding, a further drop in BMD occurs post-partum.
Low molecular weight heparin - LMWH - appears to present a lower risk of osteoporosis, with a .2% incidence of vertebral fracture. A randomized study comparing unfractionated heparin (UH) with LMWH during pregnancy found lumbar spine BMD to be lower in the UH group for up to 52 weeks postpartum. There was no difference in BMD between the LMWH and the control groups.
A baseline BMD before pregnancy should be done for the patient with known osteoporosis or osteopenia, and, if not previously performed, for a patient with lupus and a history of long-term steroid or heparin use. These data may be of most use in making decisions post-partum, as there is little change that can be recommended during the pregnancy itself. All patients should have adequate calcium and vitamin D (1500 mg calcium/day). Weight-bearing exercise may be one intervention that can help to preserve BMD during the pregnancy itself, if the patient is able to undertake or continue such a program. Pregnancy related complications (preeclampsia, preterm labor, etc.) may prohibit such exercise.
Corticosteroid dose is obviously maintained as low as possible.
For the patient at greatest risk of fracture (known osteoporosis, especially on steroid or heparin), breastfeeding is contraindicated. In a patient where the desire to breastfeed is strong, and without preexisting osteoporosis, a repeat BMD test may be done post-partum. A significant decrease in BMD (whether pregnancy-, steroid- or heparin-related) should preclude lactation. Minimal or no decline on post-partum BMD testing is reassuring, and breastfeeding is reasonable for these patients.
Forgoing breastfeeding in the osteoporotic patient will minimize pregnancy-related bone loss and allow recovery to begin. Treatment for osteoporosis may also be initiated at this time. Nasal calcinonin (Miacalcin) does not pose the same long-term questions for safety of future pregnancies that bisphosphonates do.
 Ramsey-Goldman R, Dunn JE, Cheng-Fang H et al. Frequency of fractures in women with systemic lupus erythematosus. Arthritis Rheum. 1999;42:882-890.
 Pettila V, Leinonen P, Markkola A, et al. Post-partum bone mineral density in women treated for thromboprophylaxis with unfractionated heparin or LMW heparin. Thromb Haemost .2002;87:182-186.