No abstract

The reported in vivo bioinstability of sensors is likely to be caused by protein and cellular biofouling on the sensor membrane. Furthermore, the consistent finding of fibrinogen and fibrinogen fragments D and E at the sensor-tissue interface seems to play an important role in the pathogenesis as it possibly maintains the inflammation by promoting the recruitment of inflammatory cells to the implantation site.

The electrochemical enzyme-based glucose sensor for continuous glucose measurements in subcutis is acceptable from a biocompatibility point of view. Reducing the inserter needle in size reduces the trauma induced at sensor implantation to neglible levels. Furthermore, the tissue reaction to the sensor returns to near-normal 2 weeks after the sensor has been removed following a 3-day implantation period.

No abstract

No abstract