Hasan Jilaihawi.

All serious adverse events were adjudicated by an independent scientific events committee. All data were analyzed by a biostatistician who was paid by the sponsor and by an academic biostatistician. An independent primary laboratory analyzed all echocardiograms. Procedure The SAPIEN heart-valve system , that was used in this scholarly study, consisted of a balloon-expandable, stainless-steel stent frame housing a tri-leaflet bovine pericardial valve within a deflectable delivery catheter. The operational system was inserted into the common femoral artery under aseptic conditions, with the use of both transesophageal and fluoroscopic assistance, while the affected individual was under general anesthesia.2 End Points The prespecified primary end point of the PARTNER trial was all-trigger mortality, over the duration of the trial.Sulfation appears to be the predominant direction of the interconversion between DHEAS and DHEA,13 which implies that improved DHEA sulfation would limit the amount of DHEA designed for androgen synthesis. Conversely, impaired sulfation would increase the amount of obtainable DHEA and the degrees of active androgens thus. SULT2A1 is the major enzyme responsible for DHEA sulfation, converting DHEA to DHEAS mainly in the adrenal glands and the liver.14 The sulfate donor PAPS is required by all sulfotransferases, including SULT2A1.14 In human beings, PAPS is synthesized by both isoforms of PAPS synthase, PAPSS2 and PAPSS1.14 A homozygous PAPSS2 mutation that is within spondyloepimetaphyseal dysplasia, Pakistani type ,15 is thought to be caused by impaired proteoglycan sulfation in growth-plate chondrocytes.15-17 Here we report on the case of a girl with androgen excess, premature pubarche, hyperandrogenic anovulation, and serum DHEAS levels beneath the limit of detection.