Safety of Outpatient Surgical Abortion for Obese Patients in the First and Second Trimesters.

OBJECTIVE: To evaluate the relationship between obesity and surgical abortion complications in the outpatient setting. METHODS: We conducted a retrospective cohort study of 4,968 women undergoing surgical abortion at a large outpatient clinic network from September 2012 to July 2014. We used log-binomial regression to evaluate body mass index (BMI) as an independent risk factor for first- and second-trimester abortion complications. Body mass index was analyzed as both a continuous and categorical predictor. We assessed complications including need for uterine reaspiration (including same-day reaspiration), uterine perforation, cervical laceration, infection, emergency department visit or hospitalization, and excessive blood loss defined as estimated blood loss greater than or equal to 100 mL. RESULTS: The majority (77%) of procedures was performed in the first trimester. Forty-seven percent of women were normal weight or underweight, 28% were overweight, and 25% were obese, including 4% with BMI greater than or equal to 40. The overall complication rate was 1.7%; the most common complications were need for uterine reaspiration (1.0%) and excessive blood loss (0.6%). Obesity was not associated with increased risk of surgical complications, including when adjusting for age, gestational age, and history of prior cesarean delivery. CONCLUSION: In a high-volume outpatient abortion clinic with experienced health care providers, abortion is very safe. Obesity does not appear to be an independent predictor for abortion complications and should not be used in isolation to refer women to hospital-based facilities for abortion care in the first or second trimester.

Phosphate feeding induces arterial medial calcification in uremic mice: role of serum phosphorus, fibroblast growth factor-23, and osteopontin.

Arterial medial calcification is a major complication in patients with chronic kidney disease and is a strong predictor of cardiovascular and all-cause mortality. We sought to determine the role of dietary phosphorus and the severity of uremia on vascular calcification in calcification-prone DBA/2 mice. Severe and moderate uremia was induced by renal ablation of varying magnitudes. Extensive arterial-medial calcification developed only when the uremic mice were placed on a high-phosphate diet. Arterial calcification in the severely uremic mice fed a high-phosphate diet was significantly associated with hyperphosphatemia. Moderately uremic mice on this diet were not hyperphosphatemic but had a significant rise in their serum levels of fibroblast growth factor 23 (FGF-23) and osteopontin that significantly correlated with arterial medial calcification. Although there was widespread arterial medial calcification, there was no histological evidence of atherosclerosis. At early stages of calcification, the osteochondrogenic markers Runx2 and osteopontin were upregulated, but the smooth muscle cell marker SM22alpha decreased in medial cells, as did the number of smooth muscle cells in extensively calcified regions. These findings suggest that phosphate loading and the severity of uremia play critical roles in controlling arterial medial calcification in mice. Further, FGF-23 and osteopontin may be markers and/or inducers of this process.