A hyper-coagulable state due to protein C deficiency has been postulated to be the cause of avascular necrosis of the capital femoral physes in Legg-Calve-Perthes disease (LCPD). In order to test this hypothesis, plasma protein C levels were analyzed from 51 unselected cases of LCPD. These were compared with a control group. Our findings showed that the levels were less than the mean for age in 38 (74.5%) of the cases, though were within the normal range. We conclude that clinical thrombosis could be triggered off in these susceptible individuals by prothrombotic insults such as passive smoking, ultimately leading to LCPD.

Hutchinson-Gilford progeria syndrome (HGPS) is a rare genetic disorder. The estimated incidence is one in 4 million births. Orthopaedic manifestations include abnormality of the hips occurring early in the disease process. Severe coxa valga can be apparent by the age of 2 years. We report two cases of HGPS, one in a 7-year-old girl with avascular necrosis of the left hip and the second in a 13-year-old girl with recurrent traumatic hip dislocations. We demonstrate the pathoanatomical changes in the hip with HGPS using a combination of imaging modalities including radiographic, computed tomographic and MRI scans. These include coxa magna, coxa valga and acetabular dysplasia. We also comment on how these would affect the surgical management of this high-risk group of patients.