Repository corticotropin injection’s nearly six-decade history as a therapy has been tumultuous, but has most recently resulted in its use as an auto-immune drug.
Repository corticotropin injection’s nearly six-decade history as a therapy has been tumultuous. From widespread use in the 1960s, to clinical concern in the 2000s, the therapy’s prevalence has twisted and turned to become a common drug in the auto-immune space.
In an interview with MD Magazine® while at the American College of Rheumatology (ACR) annual meeting in Chicago, IL, W. Hayes Wilson, MD, a rheumatologist at Piedmont Hospital, Atlanta, GA, tracked the clinical history of repository corticotropin injection.
MD Mag: What is the clinical history of repository corticotropin injection?
Wilson: Repository corticotropin injection came out in 1952, and in the 1960s, it had [about] 51 indications. Recently, in the 2000s, there was more information that was found out about repository corticotropin injection, specifically that it affects melanocortin receptors. Consequently, the indications were revised and now there are 19 indications as of the late 2000s.
Why did its use fall out of favor with clinicians?
It’s an injection and its cousin—prednisone or prednisolone—actually became more popular, because it was easier to offer [an oral medication] to a patient and say, ‘here’s a medication, take it home,’ [instead of coming in] and getting an injection.
[Today,] we have become more familiar with giving injections to our patients and our patients giving themselves an injection. It was probably more common in the 1950s and 1960s to hand someone a pill. The injectable medication was available, and was being used, it just was not as popular as oral steroids.
The interesting thing is that in the 1990s, we learned more about repository corticotropin injection, and what we found out was that there are 5 melanocortin receptors [and] only the second receptor is the one that has steroid genetic effects. The other 4 were directly on different cells like B-cells or T-cells, microglia cells, and have a direct effect.
For instance, in dermatomyositis and polymyositis, the melanocortin receptors are on the myocyte, the muscle cell, and so there is a direct effect on the muscle cell. That’s why, in the year 2012, it was promoted for dermatomyositis and polymyositis, and that’s when I started using it more in our more complicated auto-immune diseases.