Primary antiphospholipid syndrome in premenopausal women: low vitamin D, high fat mass and maintained bone mineral mass

Abstract

The aim of this study was to analyze vitamin D levels and their association with bone mineral density and body composition in primary antiphospholipid syndrome. For this cross-sectional study 23 premenopausal women with primary antiphospholipid syndrome (Sapporo criteria) and 23 age- and race-matched healthy controls were enrolled. Demographic, anthropometric, clinical and laboratorial data were collected using clinical interview and chart review. Serum 25-hydroxyvitamin D levels, parathormone, calcium and 24-hour urinary calcium were evaluated in all subjects. Bone mineral density and body composition were studied by dual X-ray absorptiometry. The mean age of patients and controls was 33 years. Weight (75.61 [20.73] vs. 63.14 [7.34] kg, p = 0.009), body mass index (29.57 [7.17] vs. 25.35 [3.37] kg, p = 0.014) and caloric ingestion (2493 [1005.6] vs. 1990 [384.1] kcal/day, p = 0.03) were higher in PAPS than controls. All PAPS were under oral anticoagulant with INR within therapeutic range. Interestingly, biochemical bone parameters revealed lower levels of 25-hydroxyvitamin D [21.64 (11.26) vs. 28.59 (10.67) mg/dl, p = 0.039], serum calcium [9.04 (0.46) vs. 9.3 (0.46) mg/dl, p = 0.013] and 24-hour urinary calcium [106.55 (83.71) vs. 172.92 (119.05) mg/d, p = 0.027] in patients than in controls. Supporting these findings, parathormone levels were higher in primary antiphospholipid syndrome than in controls [64.82 (37.83) vs. 44.53 (19.62) pg/ml, p = 0.028]. The analysis of osteoporosis risk factors revealed that the two groups were comparable (p > 0.05). Lumbar spine, femoral neck, total femur and whole body bone mineral density were similar in both groups (p > 0.05). Higher fat mass [28.51 (12.93) vs. 20.01 (4.68) kg, p = 0.005] and higher percentage of fat [36.08 (7.37) vs. 31.23 (4.64)%, p = 0.010] were observed in PAPS in comparison with controls; although no difference was seen regarding lean mass. In summary, low vitamin D in primary antiphospholipid syndrome could be secondary to higher weight and fat mass herein observed most likely due to adipocyte sequestration. This weight gain may also justify the maintenance of bone mineral density even with altered biochemical bone parameters.

Vitamin D and antiphospholipid syndrome

“…VitD levels above 30 ng/ ml were considered sufficient, according to international guidelines. 10 Insufficiency was defined as values between 10 and 30 ng/ml and deficiency when values fell below 10 ng/ml.…”

“…[9][10][11][12] In all studies, the average value for APS patients was below 30 ng/ml, a cut-off value suggested by international guidelines. 13 Although they lack data on race, seasonality, nutrition and sun exposure, overall these studies suggest that APS patients are comparably as affected by hypovitaminosis D as they are by other systemic autoimmune diseases.…”

Juvenile onset systemic lupus erythematosus: a possible role for vitamin D in disease status and bone health

“…23,28 Regarding body composition, fat mass was a relevant factor for hypovitaminosis D in autoimmune diseases. 29 In Juvenile onset SLE (JoSLE) there is no data regarding the influence of vitamin D status in bone health and the risk of deficiency was recently demonstrated to be higher in autoimmune conditions. 30 Moreover, glucocorticoid (GC) may have a regulatory effect on vitamin D metabolism 31 aggravating this deficit.…”

Antiphospholipid (Hughes) syndrome: insights for orthopedics

“…Conflicting reports were published about the association of osteoporosis to APS, 20,21 but the more common conclusion was that longstanding anticoagulation in APS patients is an indirect risk factor to develop osteoporosis, 21,22 possibly related to the consequential vitamin D deficiency in anticoagulated APS patients. 21 Among many of the above-mentioned reports, the most striking piece of evidence suggesting a strong link between APS and its orthopedic complications is the symptomatic and radiologic improvement upon initiation of anticoagulation.…”