Letters to the Editors: Prednisone and Microglia Modulators
Use of Prednisone
I find the articles on stress hormones by Dr. Tennant and others to be a big help to my pain practice.1 When replacing low cortisol levels, you avoid oral prednisone—I was wondering why? I have been using it with great success. I find that prednisone, at a dose of 5 to 10 mg/day, works well in restoring morning cortisol levels and always has a very positive effect on the patient’s pain. My main problem is with primary care physicians who always want to take the patient off the prednisone.
Thomas B. Brummett, MD
Piasa Pain Center
Dear Dr. Brummett,
Your use of prednisone to replace low cortisol levels is a most welcome and timely bit of news. I have pushed the use of plain hydrocortisone because the vast majority of our readers are unaccustomed to hormone replacement.
For the inexperienced, plain hydrocortisone 5 mg twice a day or three times a day is simple and safe. As one becomes experienced with cortisol replacement, alternatives as you have discovered may provide superior results. Quite frankly, I personally have patients on hydrocortisone, compounded cortisol, prednisone, and methylprednisolone. Some patients don’t convert hydrocortisone to cortisol, so alternatives are essential.
As time is marching on, I’m developing the belief that low-dose, sub-replacement of a corticoid (take your pick) may almost be essential in controlling and ameliorating centralized pain. Modulation and suppression of microglial cells and neuroinflammation may require on-going, low dose corticosteroids.
I suspect your use of prednisone is doing this, and that is the reason for your excellent results. Keep up the good progress.
Forest Tennant, MD, DrPH
I read with interest your article on microglial modulators as it refers to centralized pain.2 For several years I have treated chronic pain patients within my general osteopathic practice. I, like others, have clinically observed the wide range of non-opioid medications that chronic pain patients seem to need and demand. Until my understanding of centralized pain, microglial activation, and neuroinflammation in these patients, I reluctantly participated in the polypharmacy that typically characterize these patients.
I write to briefly give some of my clinical experiences.
First, chronic pain patients who have come to me have usually been through the workup of adjunctive medicines, anti-seizure agents, mood elevators, muscle relaxants, and the WHO ladder Steps 2 and 3. Now the patients are at the very top of the ladder in pain management. Long-acting/extended-release (LA/ER) opioids have primarily been used for these patients, and the short-acting opioids have been used for breakthrough pain.
Many of these patients desire carisoprodol (Soma). While I suspected abuse in some patients, the great majority benefitted from its use. I, therefore, read with great interest, that carisoprodol acts at GABA receptors, which provide a rationale for their desire by chronic pain patients. The addition of centrally acting agents (ie, amphetamine salts and oxytocin) have been of great benefit in this group.
I now read with interest how the dopamine and the adrenergic nervous systems must also be covered to treat descending pain pathways. Anxiolytic medications have been used episodically. I have noted with great interest that hormone therapies have great benefit. I routinely use vitamin C therapy at 1 gram per day and then vitamin D therapy for those with low 25-OH D in the serum. I have continued using NSAIDS, mood elevators, and anti-convulsants if, indeed, necessary. My use of opioids has diminished as I’ve learned to treat alternate pathways.
In summary, medical decision-making in centralized pain patients appear to need coverage for multiplicity of receptors and pathways to achieve pain control. As an osteopathic physician, I would like the readers not to forget our hands-on neuromusculoskeletal fascial release techniques, along with our therapies such as acupuncture and the modalities of physical medicine.
Martin J. Porcelli, DO
Dear Dr. Porcelli,
You make a point that needs to be heard. The “polypharmacy” or use of multiple, seemingly disparate drugs that pain patients require is not a random act of drug seeking, but one which the patient needs to control the multiple biologic mechanisms that control pain. It does little good to criticize polypharmacy since a lot of good pain control can be obtained in centralized pain patients by fitting a specific pharmacologic agent with a specific clinical need. In the recent past we’ve had to rely too extensively on opioids to achieve pain control.
The new scientific understanding of these multiple, biologic pain control mechanisms allows us to decrease the use of opioids.
Forest Tennant, MD, DrPH