ME/CFS Alert Episode 48: Deborah Waroff talks with Dr. Dan Peterson about treatments, research, and why has he stuck with it for all these years.
Q: You’ve been very aggressive about putting treatments forward for your patients. How many patients do you currently have on Ampligen, and how many have you treated with Ampligen in total?
A: I have 28 people on Ampligen, with a total of 300. With respect to aggressive treatment, for severely disabled patients, and evenly the moderately disabled, unless you introduce some sort of aggressive treatment they don’t spontaneously recover. Symptomatic therapy can be enormously beneficial, but patients don’t recover unless you attack the etiology and pathogenesis directly. We’ve stumbled upon Ampligen, which is very beneficial for a subset of patients.
Q: Vistide (cidofovir) is one of the most difficult drugs to manage. What is your protocol?
A: I have a subset of patients who have evidence of beta herpesvirus reactivation, either CMV or HHV6a or b, and for that subset of patients, particularly if they have it in their spinal fluid, they need a very potent antiviral. For beta herpesviruses we are somewhat limited to a few oral drugs that are not terribly effective, to foscarnet, which is very difficult to administer, and Vistide which is somewhat easier because the infusion is every two weeks. I have treated 65 people according to this protocol, which, relative to the world of chronic fatigue syndrome, is not very many people. But some of those people have had very dramatic responses. Some have been able to go back to work, and to normal lives.
Q: Most doctors do not want to deal with Vistide, isn’t that true?
A: Vistide has to be monitored. You have to monitor kidney function, and liver function, and white blood cell count. I don’t even think it is generally acknowledged that [beta herpesvirus] subsets of these patients are identifiable.
Q: Have you used Valcyte?
A: I have used Valcyte. I follow the protocol of Jose Montoya at Stanford, with a long course of therapy. It also has to be monitored very carefully, and there are significant side effects such as headache and nausea, etc.
Q: Would you use it again now that you have Vistide?
A: I still use it.
Q: From my personal experience [antivirals] do good for a while, then become ineffective. Is that universal?
A: With the herpesviruses, since we never really cure them, patients go into remission and then they relapse. This pattern also holds when patients are treated with Vistide. Most recently, I have been combining therapies, adding immunoglobulin, or Ampligen, or other agents, with some significant success.
Q: What is the longest you have been able to keep a patient in good shape?
A: So far, three or four years, but I’m talking about almost total remission. I frequently get asked the question, “Is this curable?” I can’t say that it’s curable, but [the combination of therapies] is able to relieve symptoms so that people can return to work full time, which is pretty dramatic.
Q: Are you looking forward to CMX001 [a lipid antiviral used to boost the effectiveness of Vistide]?
A: Biopharma is great when they see a market, so I look forward to better drugs for all the patients with CFS, not just the subsets with immunological abnormalities. But they are not terribly interested, I think because they don’t recognize the market potential. They can’t get their hands on a biological marker and endpoints. All those things are very important when you are trying to interest pharma. And for a drug that’s already licensed there is no incentive for them to do a study.
Q: Are there any other immune boosters you are interested in?
A: IV gammaglobulin. A new area I’m excited about is the cytokine blockers and the immune modulator rituximab, which has gotten lot of press. Hopefully, they will do a much larger rituximab study in the near future. My concern with rituximab is that I don’t know how to predict who will respond. It would be nice to have guidelines, for entrance criteria, etc. where we could give people an idea of whether or not they will respond. The side effects can be very rough.
Q: If you had all the money in the world, in what direction would you be going now?
A: I would invest the money in centers for excellence. The reason is that primary care physicians can’t manage this disease. It’s too complex, too time-consuming, and they have too many other things to do. If we could get primary care physicians to recognize the disease, to qualify the patient, then they must have some place to refer them to. I see a great need all over the world for people to seek specialty care, which is appropriate until the disease becomes simpler to manage. HIV, for example, has become a very manageable disease. CFS /ME is a long ways from that.
Q: What do we need to do to get there?
A: I think it’s clear this is not a homogeneous disease. I think the CDC is correct in trying to understand subsets and redefine the subsets both biologically and by symptoms. Things would move along more quickly if we did that. As far as a universal definition is concerned, that would be enormously helpful, but we seem to have a great deal of difficulty getting there.
Q: Do you see one or two subsets that predominate over the others?
A: There seems to a real different between people who have an acute onset versus a gradual onset. About 15% of the people I see have active [viral] infections of one sort or another. They are clearly treatable and should be identified. There are people who have had industrial exposures or heavy metal toxicities, or post-vaccination, or post-transfusion onset. Those are all potentially identifiable subsets that might best be treated differently.
Q: Why did chronic fatigue syndrome strike Lake Tahoe? Do you still have people coming in at a high rate?
A: Not locally. The local thing happened and disappeared. Some virus came through this community at that time, striking susceptible people, and then left. I mostly see people from distant places.
Q: Who do you need to set up centers for excellence?
A: The concept of translational medicine is very good, in which basic researchers work with clinicians – in this disease particularly, where there is not a lot of understanding between the scientists and the clinicians, or pharma for that matter. It would be doable because there are centers of excellence for breast cancer, for MS, for ALS, just go down the list. You can create that model if there is support for it.
Q: Wouldn’t major medical centers be a good place to start, like Stanford and Duke?
A: Traditionally, major medical centers have been great sources for centers of excellence. However, they operate very slowly, and they have very high overhead. And funding has been very short term. Some people have started these plans and run out of funds.
Q: As a disease, we get most of our research funding from private funding. Is this an advantage over government funding?
A: Private funding is very efficient. It can be targeted and it is easier to obtain in some circumstances. But this is a national problem that should be supported nationally. But I understand that with budget restrictions there is less and less available, particularly of these orphan diseases.
Q: Couldn’t the same researchers who do research on MS, or lymphoma, or HIV, be doing research on CFS/ME with very little extra salary?
A: That’s a hard sell. It goes back to the stigma of CFS/ME. The name just trivialized the disease. The lack of a clear-cut biological marker held off researchers, as well as short budget cycles, and low dollar amounts. A small grant gets you nowhere with this disease. You need large numbers of patients, which is why I totally support the OMI, with its idea of putting multiple physicians together, and adding all our patients. If you’re talking about things like genomic studies it takes a large number of patients in order to get a sufficient quantity for statistical validity. The same goes for treatment trials. With small treatment trials it’s very difficult to show efficacy.
Q: Is there any way to get researchers to focus on something other than blood? Lymph glands, for example?
A: The Ian Lipkin studies at Columbia are looking at other tissues – saliva, urine, cerebrospinal fluid. I think he may be one of the first ones to do that. I am really excited about that research. Hopefully, he will help us in terms of biological markers, or pathogens, and possibly autoimmunity, and chemokine and cytokine signaling. I know he is working on all those avenues. We need people with his kind of expertise and quality to be researchers in this field.
Q: How have you stood it all these years, plugging along in spite of an utter lack of support?
A: That’s a question I get asked frequently. The best answer I can give is that there is still an essential truth that we have to find. Remember, I saw perfectly healthy people become disabled, and nothing can ever convince me that that was not a pathophysiological process. I expected the answer long before now, but I am still looking for answers. The second thing is that discovery comes to the prepared mind. We need intellectual curiosity. We need people asking questions about this, pursuing it. I haven’t seen the end of this story yet, and that’s why I am still in the field.