Familial Thrombophilia Is Associated With Primary Multifocal Osteonecrosis: A Case-Control Study of 40 Patients.

To characterize pathoetiologic associations of heritable thrombophilia-hypofibrinolysis with idiopathic (primary) multifocal osteonecrosis (ON) (≥3 ON anatomic sites), we prospectively studied 28 women and 12 men with primary multifocal ON compared with 27 women and 24 men with primary nonmultifocal ON (<3 sites) and 110 healthy controls without ON. The 40 cases with primary multifocal ON differed from controls for 3 familial thrombophilias: Factor V Leiden heterozygosity (6 of 40 [15%] vs 2 of 109 [2%], =.002), G20210A prothrombin gene heterozygosity (6 of 40 [15%] vs 3 of 110 [3%], =.

Long-term Anticoagulation Prevents Progression of Stages I and II Primary Osteonecrosis of the Hip in Patients With Familial Thrombophilia.

The authors prospectively assessed long-term anticoagulation outcomes (≥3 years) for 9 patients meeting 4 inclusion criteria: pretreatment Ficat stage I or II primary hip osteonecrosis (ON), factor V Leiden or prothrombin G20210A heterozygosity, no contraindication to anticoagulation, and 90-day participation in an initial enoxaparin 60 mg/d protocol. The primary endpoint was prevention of hip collapse (Ficat stage III or IV). The secondary endpoint was pain relief.

Testosterone Therapy, Thrombophilia, Venous Thromboembolism, and Thrombotic Events.

In our sequential studies of 67 and 21 patients, testosterone therapy (TT) interacted with thrombophilia⁻hypofibrinolysis, leading to venous thromboembolism (VTE). Compared to 111 VTE controls not taking TT (VTE-no TT), the 67 and 21 cases were more likely ( < 0.05 for all) to have Factor V Leiden (FVL) heterogeneity (24% and 33% vs.

Characteristics of obesity in polycystic ovary syndrome: Etiology, treatment, and genetics.

Polycystic ovary syndrome (PCOS) has multiple etiologies including ovarian and adrenal hyperandrogenism, neuro-endocrine and hypothalamic-pituitary dysfunction, and disorders of peripheral insulin resistance. Obesity is neither necessary nor sufficient for the PCOS phenotype, and the association of PCOS with obesity is not universal, with national, cultural, and ethnic differences. Obesity, particularly visceral adiposity which is common in obese and non-obese women with PCOS, amplifies and worsens all metabolic and reproductive outcomes in PCOS.