My Crohn’s Disease Adventure, Part II: Of Doctors and Death Panels

Continued from Part I

I finally was able to speak to a doctor the next day, a Friday. The conversation was enlightening in that it provided insight into what my Kaiser GI doctor considered “standard of care.” Here is how it went.

I checked in with the receptionist, politely declined to pay the co-pay that I fully intended to contest later, and patiently waited the customary 30 minutes minimum for the doctor to appear. After a pleasant hello, I asked what I should have been told far earlier.

Me: First I want to know if there’s anything from the biopsy…

Doctor: Yeah, they reported that earlier today. They see some — you heard from Dr. [Other] I imagine — your whole colon looked normal, until he got to the junction of the small and large intestine.

Me: Right.

Doctor: And he saw a little bit of inflammation right at the opening between the two on the valve that sits there between the small and large intestine, and he saw a little mild redness, maybe at the lining of the end of the small intestine. He took biopsies from that area and from the valve area, and some random biopsies from your colon. The biopsies from your colon looked normal. The biopsies from the end of your small intestine also looked normal — they didn’t see any significant inflammation even though it looked mildly red to him. They did see some inflammation on the biopsies from the valve… “Nonspecific inflammation…” Uh, they did, because of your concerns about uh, different forms of mycobacterium, they did a stain for TB that was negative…

Me: TB or para-TB?

Doctor: There’s no stain… It’s for AFB: acid-fast basilli, which is the whole family of…

Me: Right, but I’m pretty sure that MAP doesn’t show up with that stain.

Doctor: It may not show up — uh, it’s not a very sensitive stain, no.

Me: Right, but it doesn’t show up — at all — is my understanding.

Doctor: It was only done at your request, I mean we do that typically when we’re looking for mycobacterium.

Me: That wasn’t my request, to be clear. My request was that they do PCR.

Doctor: Yeah, well. That’s, that’s not a standard, uh, form of a test. Uh, you know.

Me: It depends what you mean by “standard,” but I understand, not here.

Doctor: Yeah. No, not anywhere in the United States, unless there’s a research protocol going on or something. I mean, if you read any of the mainstream gastroenterology — AGA, ASGE, ACG, Crohn’s and Colitis Foundation…

Me: Right.

Doctor: I mean, I know you’ve been reading a lot about this obviously, I saw your references there.

The doctor did indeed have a pile of the papers I had handed to the Kaiser administrator the day before.

Me: Yeah.

Doctor: And, you know I’d say, most people — you know there’s a lot of information out there and you’re a smart guy so you can access a lot of this information. The way people, at least in the United States, and a lot of the research comes from overseas obviously…

Me: Sure.

Doctor: …because perhaps they’re more open to looking into other avenues than the United States admittedly. The research has been skewed in the last couple decades because of the drug companies looking at drugs as opposed to underlying mechanisms and things, so a lot that research maybe is more overseas. But in the United States, the thinking about the, uh, MAP, if you want to call it that…

Me: It’s easier than the full name.

Doctor: …there certainly is an association. I think most everybody would believe that and buy the idea that there’s an association. There’s been a lot of research looking for that bacterium in people with Crohn’s, and you find it a lot more often than by chance.

Me: Right.

Doctor: Um, you know, I think the statistic is something like seven times — you’re seven times more likely to find it in someone with Crohn’s than someone with Ulcerative Colitis or someone who doesn’t have any either of the diseases. So there seems to be an association there. Now the tricky part is proving the cause and effect.

Me: Right.

Doctor: Um, and, and, part of that cause and effect if you thought it caused the disease would be, if you treated that, would it help? Is that a potential avenue for treating Crohn’s Disease? And those are the areas that are in a lot of controversy. I know you’ve got some of the references here that kind of support that. There’s, and my feeling — I know you’re in the [widget] business — uh, in my field, um, you know if you look at any issue you can find data on both sides of the issue.

Me: Right, and I’ve read…

Doctor: The question is, you know, what’s the…

Me: I’ve read both sides I think and the most recent reference I could find against the mycobacterium hypothesis was from 2001. And I couldn’t find a lot of research arguing against it that’s more recent. But I mean it could be out there. I guess my concern is not so much with the general field as my particular case. And so my question is — you know, if I didn’t have what is I think basically genital psoriasis — I would say that there’s probably a 50/50 chance that one hypothesis or the other is relevant to me. But, because I have psoriasis and because I have all of the other symptoms that you’d expect with Crohn’s — maybe not all but a lot of them — and because I’ve got…

Doctor: Have you had some sore joints?

Me: No, I haven’t had like arthritis… I’ve had episcleritis, I’ve had, as you can see, I have hair loss. I’ve had fatigue, I’ve had Vitamin D deficiency, I have fingernails that indicate Vitamin B deficiency and all these, well, ridges and things that aren’t totally normal I don’t think, and just a whole long — I’ve had all kinds of skin inflammation problems. I’ve had pain in my jaw that got inflamed spastically, and twitching muscles and things, so you know it’s hard for any one of these symptoms to necessarily prove cause and effect as you were saying, but, the constellation is consistent with what I’ve read about Crohn’s anyway. And then there’s the inflammation from the colonoscopy, so…

Doctor: Yeah, which is, you know, I think that’s the key question here, is do you have Crohn’s. I mean, that’s, to step back.

Me: Well, so I think before you even ask that question, it depends how you define it. Based on what I’m reading in the literature, I think the real question is do I have a mycobacterium infection? And that’s a more specific question. Whether or not you think it’s relevant, it’s at least more specific. And I’d like to answer that question first, because I think that is the primary hypothesis that makes sense to tackle.

Doctor: Well, you know, part of the reason why that hasn’t become the mainstream way of approaching this, is, what are you going to do about that?

Me: Well, what I would do is take Dapsone.

Doctor: There’s no — that’s the other problem. There is no established treatment that you know — I don’t know if you saw that Gastroenterology article from 2007 — the biggest study ever done looking at, if I treat MAP, if I treat it, am I going to help the disease, or cure the disease. And that’s the biggest thing I’m aware of, over 200 people in Australia that were treated, in a randomized study.

Me: With which drug?

Doctor: Combination of three…

Me: But not Dapsone.

Doctor: Not Dapsone. And again…

Me: I’m not interested in the three combo, I’m interested in Dapsone specifically because of the psoriasis.

Doctor: Yeah. Well, and again, and you bring up psoriasis, I was looking through the chart. I don’t know that a dermatologist had made the diagnosis of psoriasis.

Me: That’s because they’re wrong.

Doctor: Yeah, well. The last time I saw you talking about that rash was 2009. Is that the last time you saw somebody?

Me: Uh…

Doctor: I mean you’ve shown them pictures of moles and stuff since then but I think it was 2009 when they wanted to do a biopsy.

Me: I think I had at least four visits with dermatologists over the years, um — and I eventually — you have to pay a co-pay each time you go — there’s no point in going to an appointment where they tell you each time to put on hydrocortisone cream, which is not an effective treatment.

Doctor: Or do a biopsy, which is a more definitive way of…

Me: They looked, I can’t remember his name, but the head of dermatology looked at the skin shavings under a microscope, and perhaps doing a biopsy would shed more light but I really don’t think so. I’ve got red, flaky skin, which itches…

Doctor: I’m not saying you’re wrong. I’m just not a dermatologist, so I can’t be correct, you know, I mean I can’t be sure myself.

Me: I don’t think it’s an unreasonable hypothesis that it might be psoriasis instead of eczema especially because it spread to my elbow, which is…

Doctor: A common area.

Me: …a pretty common area for psoriasis, and now as you can probably see, it’s on the back of my head, which is brand new. And uh, you know, I’d like to prevent it from spreading any further at this point.

Doctor: Yeah. I mean, that’s the problem, is I don’t think you’re going to find any gastroenterologist to treat what they think could be Crohn’s, with Dapsone.

Me: That just isn’t true, because I’ve got two papers here that say…

Doctor: If you find someone, that’s great. But in the United States, that’s not an established treatment for Crohn’s Disease. Those are, let’s see, I saw your papers. Most of them were from outside the United States. One of them was from somebody with a private company…

Me: I guess I don’t understand why the origin of the paper would be a factor if it supports scientific method.

Doctor: Well, because, because I live and work in the United States. And in the United States…

Me: But to be clear, this isn’t like a regulatory issue… Like an FDA issue or something.

Doctor: No, no, no, Dapsone is a drug that’s out in the United States. It’s used predominantly to treat pneumocystis carinii pneumonia, it’s a form of treating leprosy…

Me: Right, which — leprosy is also caused by mycobacteria.

Doctor: Yeah, exactly. But I mean so it’s out there but a rarely-used drug these days. And in the United States, I mean the standard of care is to practice what’s called evidence-based medicine. So you practice a form of medicine that’s based on the availble evidence and the predominant thinking.

Me: I’m all for that, which is why I would like to be tested for the pathogen. That seems like evidence.

Doctor: Well, that’s… There’s no evidence. If you go to the Crohn’s and Colitis Foundation or a doctor at gastroenterology at [nearby universities] or Kaiser nobody routinely, or to my knowledge, is rarely even checking for that. Because nobody would know what to do with the information even if they spent the extra money on an already-expensive procedure, colonoscopy, every time they saw some inflammation and checked the PCR for MAP…

Me: Well I actually don’t think you’d have to do the colonoscopy necessarily if you already went just direct to PCR you could tell if they have that or not.

Doctor: You can tell that, but again, that does not equal Crohn’s Disease. It’s…

Me: Well, that depends on your definition of Crohn’s Disease.

Doctor: It’s suspected of being potentially associated with Crohn’s Disease. And again the current thinking in kind of mainstream GI circles about Crohn’s Disease is there are genetic predispositions…

Me: That, that theory is like 30 years old.

Doctor: That’s what you hear at meetings you go to in 2015, 2014… That’s there’s genetic predispostions, there are genes that have been associated…

Me: I understand that there are adherents to that theory. But the more recent papers do not support that hypothesis.

Doctor: Well, I don’t know. I can’t... You can find papers… That’s the mainstream thinking about this.

Me: I understand that you’re representing what you see. But I want to know if you agree with me that these papers don’t support that.

Doctor: Oh yeah. Like I’ve said, you can find information on both sides of pretty much every issue in medicine.

Me: Okay.

Doctor: And admittedly Crohn’s Disease is a disease that many people spent 50 years researching so there’s a lot of information out there…

Me: Sure.

Doctor: …from all around the world. And this issue of the cause, the association… I mean I could give you a stack that big too of papers trying to associate measles virus with Crohn’s. I’m sure you’ve seen those as you look around. Um, you know, the thinking is that people are predisposed to it, genetically. Again, over 200 genes have now been sort of tied in loose ways to colitis and Crohn’s. And that something, some exposure, be it infectious, be it environmental or dietary, triggers that predisposed individual to cause this inflammatory response. And again, you know, and that was a very hot theory in the 90s, the MAP, but the more they looked at it, they were like okay we find it fairly often, but not everybody that we call “Crohn’s”.

Me: Well isn’t there also the possibility that there’s different diseases that look similar, especially given that the gut is full of bacteria. So…

Doctor: Yeah, well, and again, that’s the other question. Because you know, even in that paper from Australia, in the early stages of people taking that triple antibiotic combination, people felt a little bit better. But as they followed them, and they were treating them for a couple of years, after a couple years in some cases, there was no difference between treatment or not. And again, were they changing their microfluora in the gut? And that was maybe helping or hurting Crohn’s…

Me: It’s certainly complicated, I’m not denying that. I certainly don’t deny the immense complexity between the genetics and the microfluora issues but, um, again, for my particular case…

Doctor: You’re interested in MAP.

Me: I’m interested in MAP because of the psoriasis. The psoriasis seems to be very closely correlated with MAP.

Doctor: There’s a number of skin conditons — in fact we have a dermatologist here who has a kind of special interest, Dr. [Name] — she’s found a couple of unusual rashses in my Crohn’s patients, not psoriasis but other conditions that people have had that there’s some literature associated with, too. Um, in that avenue you might, I would think you might want to see another derm, maybe her in particular because I know she has this particular interest in IBD skin issues. You know I could talk to our pathologists and see whether they could find a place that does PCR for MAP…

Me: Yeah, if it isn’t prohibitively expensive for some reason — and even if it is I’d like to know.

Doctor: They’d have to look. They’d have to look I mean again ’cause again it’s not standard.

Me: I get that it isn’t standard, but I feel like, um, you know this isn’t something where it’s one paper. This a lot of papers.

Doctor: There’s clearly… There’s clearly… Like I said, I think almost everybody would agree there seems to be association. Cause…

Me: It may not be everyone. But if it is in me, and it’s curable, I want it cured.

Doctor: That’s a totally other question.

Me: I realize that’s a separate issue.

Doctor: Even if the PCR was positive…

Me: But that’s an important piece of information. Because the anti-TNF drugs, if I have a mycobacterium infection, and the anti-TNF agents make me more susceptible to that, I don’t want to take them.

Doctor: Well, that’s one of the key dilemmas with your — the hypothesis actually, about MAP. Is, if that’s a big cause in a lot of people, um, of the disease, why is it we’re using all of these drugs to suppress people’s immune systems, and a lot of them get better with their symptoms when we give them immune suppressant drugs, like TNF-alpha? Like some of the other immunosuppressants, prednisone, things that we commonly use to treat most of their cases. Um, because that argues against it being an active infection at least.

Me: Right.

Doctor: You know, maybe it was a triggering event. Maybe it was a triggering event in the individual but if it was an active ongoing infection you would expect it to get worse when you use these immunosuppressant drugs which we use all the time in people with Crohn’s.

Me: Well, but it seems like some people get better, and some people do get worse.

[Discussion of symptoms getting worse, family history.]

Doctor: As you have probably read, there is no one test you can do that proves somebody actually has Crohn’s. But if you see…

Me: Well, I’m not sure I agree with that.

Doctor: Well, your test would prove MAP.

Me: Well, but that’s my point. I’ve run into this issue before. My brother has Dandy-Walker Variant, which is a relatively unknown condition among even neurologists, and uh, it is referred to commonly as “autism.” Autism is really a collection of tons of discrete neurological conditions. I’m getting the sense that Crohn’s is kind of similar. Maybe not as broad, but still pretty broad.

Doctor: I’m just saying, the longer we see signs of inflammation in somebody’s gut over time, uh, the more comfortable we are saying “OK, yeah, this is Crohn’s.” Now this is the first time we’ve seen the inflammation, so.

Me: Right.

Doctor: And it’s nonspecific. But there’s nothing you see on biopsy that’s 100% conclusive of Crohn’s, even if you see these things called granulomas, which they didn’t see. They only see those in about 20% of Crohn’s people. And those aren’t specific to Crohn’s although they’re commonly seen. So right now we know that you have at least a little bit of inflammation. I mean one question would be whether we should look for any other signs of inflammation in the small bowel, which is a common area for Crohn’s to hang out, especially that area, right around there…

Me: So when you say “a common area for Crohn’s to hang out,” what are they actually looking for? I mean, inflammation showing up on a slide, or a particular something…

Doctor: Signs of inflammation in someone’s intestine, especially over time, you know again because you can get acute inflammation from any number of infectious things, or blood flow drugs… You don’t take a lot of aspirin or motrin or any of those things?

Me: I don’t do any drugs and I don’t take anything regularly except for vitamin supplements.

Doctor: What about an inhaler?

Me: I haven’t used an inhaler for decades.

Doctor: So uh, but yeah, so there are a lot of things that cause acute inflammation. But if over months or years you’re seeing signs of inflammation more chronically — there are only a couple of things that cause chronic inflammation in the gut as far as we know — and uh, so yeah, you’re looking for erosions or inflammation like we saw right around that opening, um, and those are things that can be subtle, unfortunately. We have scopes that reach up into the end of the small intestine and that can reach below into the beginning of the small intestine, but there’s about 16–18 feet there of the small intestine that we can’t reach and visualize directly. You can do scans, MRIs, and CT scans of people’s small intestines looking for signs of thickening or inflammation…

[Description of my particular symptoms]

There’s ways of seeing this area is all I’m saying, if you want to look for more — there’s capsule endoscopy, you might have heard of.

Me: The camera you swallow?

Doctor: The camera that you swallow.

Me: I think the most obvious — and those are not unreasonable things to try I think if it gets worse, and hopefully it won’t — but, um, I think still the most obvious thing to try would be PCR.

Doctor: If — you know, I will call our pathologist and say “OK, if we want to do that on the tissue that we have, is there a place that you know of that does that?” I mean, you know there’s research labs and these places that are doing research on this obviously developed the technology or get it acquired and have it available in their lab. It’s not standardly done, you know the question is, is there a place that they know of around here that does PCR for MAP, and could they send the tissue that was obtained from your biopsies for MAP testing. But possibly that’s going to lead to another argument because you’re going to have a hard time finding people willing to try to then treat — treat, you know…

Me: You could be totally right; I still think it’s worth asking.

Doctor: Yeah… So, so you know I think that’s out there. So if I was going to do another test, just to talk about that part of it, again you’re a young person, so we try to avoid radiation and things like CT scans as much as we can — but MRI.

Me: MRI is fine but I will not have another CT scan. I’ve had six CTs, so I’m not really up for more of those.

[Discussion of medical history.]

Doctor: Um, yeah, well so there is something called MRE, Magnetic Resonance Enterography, where they try to get a good image of the small intestine with the MRI without any exposure to radiation.

Me: Yeah, I’m totally happy to do that.

Doctor: With the CT scan or MRI you’re looking for particular areas that look inflamed basically, and to make sure there’s no narrowed areas. Because if you think someone has Crohn’s and they have narrowed areas, which Crohn’s could cause, you wouldn’t want to do a capsule test.

Me: Right.

Doctor: The capsule test is — again is not something that exposes you to any radiation, it sends out the little pictures via radio frequency, um, you do have to drink some of that same nasty stuff you drank for a colonoscopy to get the debris and bubbles out of the way so you get quality pictures, but then you swallow the capsule and go home with a monitor around your waist or on your belt for six hours or so. And then you come back late in the afternoon to download them and see if we can see mild erosions or things you wouldn’t see on a CT scan. Then we might have more evidence that you have inflammation sort of chronically in your small intestine.

Me: I still think, I mean, that sounds like a secondary measure. So.

Doctor: I understand. Just ways of trying to kind of firm up the thought that you have Crohn’s. Then again, there’s suspicion certainly, a pretty strong suspicion.

Me: There’s no competing hypothesis, like if it’s not Crohn’s then it’s…?

Doctor: No clear thing. You don’t have a recent infection, doesn’t sound like you had recent bout of gastroenteritis, anything that sounded different from your chronic symptoms’ wax and wane, because you can see that kind of mild, non-specific inflammation.

Me: No. For a while I thought maybe it was the kind of food I was eating but I really don’t think it is. It seems to be kind of independent. And I eat a pretty healthy diet, generally speaking. I never eat fast food. I do eat at restaurants, which aren’t always great, but uh, generally I try to eat pretty healthy.

Doctor: Yeah, I mean I could refer you — like I said, in terms of the rash, it wouldn’t hurt to have it… How has it changed over the years?

Me: It’s been getting bigger.

Doctor: Since 200 — ?

Me: Six.

Doctor: So nine years or so. GI issues also began roughly around that time?

Me: The exact same time.

Doctor: And the rash is in the groin area you mentioned, a little spot on the back of the neck now, and also both elbows? Or one elbow?

Me: Just the right elbow for some reason. I’ve put all kinds of things on it.

Doctor: Steroids, or other things?

Me: No, nothing with steroids. Colloidal oatmeal cream, I got something on Amazon that claimed to be for psoriasis which is more like a herbal plant extract-type-thing. But none of them really do anything.

Doctor: Do you think it looks a little bit better?

Me: Actually, that’s not true. The colloidal oatmeal has helped with the flaking.

Doctor: Was it redder at one point?

Me: The groin rash is always red. It never goes away. And it’s definitely spread, it started out smaller and it’s gotten bigger and bigger.

Doctor: I mean I think that would be another question. The funny thing… Psoriasis and Crohn’s… I wonder, I’m curious if she would — I don’t think of those as two connected diseases.

Me: Oh, I think they’re absolutely connected.

Doctor: Well, again, there’s a number of different things: erythema nodosum, erethma multiforme, these reddish spots and ulcerated lesions on the legs are clearly associated with Crohn’s. She has pointed out a couple of rare things, dermatitis herpetiformis, inflammation that’s different from what you have that there’s some association with. I mean, we do similar drugs sometimes to treat psoriasis as Crohn’s Disease, mainly things like Remicade.

Me: Well, and Dapsone. The other thing that has me fairly interested in this is that there are case reports of people taking Dapsone and curing both Crohn’s and psoriasis simultnaeously. Which is pretty compelling.

Doctor: I mean I’m not a psoriasis expert. If they thought it was psoriasis, do they ever use Dapsone for that? And maybe they do.

Me: I think, well I don’t know. The reports I’ve seen about Crohn’s seem to be more focused on genital psoriasis but I don’t know if it’s broader. The other thing that’s a link is that psoriasis is tied to Vitamin D deficiency, and so is Crohn’s. So…

Doctor: And uh, I think I saw [we] did a bunch of labs last September that all looked pretty good. You’ve been taking some extra vitamin pills..

Me: So those labs, I wasn’t sure how much faith to put in them. At least the Vitamin B tests, he tested for B-12 and -6 but not -9. And I’m pretty sure at least before I started taking the multi-vitamin I was definitely deficient in -9. Because that can cause gray hair, and I have gray hair, and when I started taking the vitamins it started turning black. And I don’t take them religiously, I only take them every now and then because I didn’t want to over-do it, but I definitely was shocked to see gray hair growing in black. In fact, I can show you…

Doctor: Alright, well, I guess, you know, I’ll start by asking the pathologist, “can you find a place where you can send the tissue to check for that.” And see.

Me: That would be great. Someone must do it. It’s a big country.

Doctor: Well, yeah. If any of these people were local, that would be a place to start. But like I said, Australia, I saw New Zealand, England on one…

Me: The English one was from ’04, then there’s Chile which isn’t particularly close.

Doctor: Like I said, you know, there’s a reason why you see more of these kind of esoteric things overseas, which is that the drug companies… You know, that’s where the money is for research these days, it comes from industry. And they’re not so much interested in making or using old drugs that are already out there. They’re interested in new drugs that they can charge a lot for.

Me: Unfortunately that has a pretty perverse effect.

Doctor: It’s a vicious cycle. Yes, it’s a vicious cycle. You don’t get a lot of basic science research unless it’s funded by the government. Which is… Anyway, I’ll let you know as soon as I hear back from them what they’re suggesting.

Me: I don’t know how common Dapsone is as a drug in the pharmacopeia, but they said yes, we can find a place, and yes we can test it, and yes it’s positive, at that point would you be able to prescribe Dapsone?

Doctor: Well, able to and willing to are two different things. Like I said, I mean, you have to practice within the standard of care for your field. And I’d have to look around — I’d probably ask some of the experts in my field, I know some of the experts at [various places] who see IBD all day — I see a lot of IBD, but they do it all day some of these people I know — and ask “have you ever done that, or would you be willing to do that?” Dapsone exists. I’ve given it, uh you know, for PCP, pneumocystis pneumonia, as one of the things that it’s used for, and I’ve given some of my transplant patients that drug. So I have written prescriptions for Dapsone in my life. So I have. It’s out there, it’s not a drug that’s not available. But again it’s an avenue I’ve never gone, and my understanding is it’s an avenue that few if any people in this country go. Uh now, the question is if I heard from some of the people that I respect in the field if they wouldn’t think that’s unreasonable, maybe they haven’t done it, that would give me some reassurance at that approach…

Me: That seems like a reasonable approach.

Doctor: And especially again, another reason maybe if we can find a place that does PCR and they say they see evidence of MAP we could also talk to one of the dermatologists. If they agree with your diagnosis of the rash, and say that Dapsone is potentially the way they could treat that, that would be a double reason to consider it. You know, and it might be a more mainstream reason to use it.

Me: Well, so this something that actually concerns me. You have these brochures on the wall here, and I looked at the Crohn’s one. And it doesn’t mention anything about frankly either mainstream hypothesis, you know…

Doctor: Well, this is not for people who have been reading hours and days… It’s pretty basic information.

Me: No, but it’s for people who are sick, and I feel like — you don’t have to overwhlem them acronyms and things, but you know it’s incredibly basic. It doesn’t tell you anything.

Doctor: It is. I mean a lot of people don’t delve into this as deeply as you have. I mean there’s the Crohn’s and Colitis Foundation, is an organization for people who are more interested in these things, I kind of mentioned them. They do a lot of good stuff and have different levels of information for people and stuff, so.

Me: I would expect — I would expect more. I feel like this stuff has been out there. Even if it’s not from the U.S. it’s real work.

Doctor: Most of the United States people would give a balance of information…

Me: Actually, this [paper] is Baylor…

Doctor: Yeah there was one person from Las Vegas from someone who runs a company.

Me: Actually, this happened as well. In 2006, a ton of my hair fell out. And I was very stressed at the time and I was attributing it to stress, but that did happen… So there’s some U.S. focus I guess. Alright, well, thank you.

Doctor: At some point next week I should hear from them about whether they can find someone to do that.

There were several takeaways from this conversation:

1. It is no one’s job to consider a patient’s well-being as a whole. Gastroenterologists consider it inappropriate and liability-prone to even provide an opinion on a skin condition that is part of a GI disease, and dermatologists routinely refuse to offer any thoughts about a GI disease that manifests partly through skin. The hyperspecialization of medicine is directly at odds with the hippocratic oath: first do no harm. Patients, most of whom are not more educated on their conditions than their doctors and thus unable to synthesize data from multiple fields, are caught in the middle. PCPs exist in Kaiser’s medical-MBA matrix merely to “defer” to specialists, so that they may safely know next to nothing about anything;
2. Despite Dr. Burrill B. Crohn himself believing that MAP was responsible for the disease he was seeing in humans, today Crohn’s Disease is apparently diagnosed with one subjective evaluation of intestinal inflammation after another, which always provides an incentive to keep on scheduling increasingly invasive and expensive diagnostic procedures that can, by definition, never bring about absolute clarity;
3. Modern treatment of Crohn’s Disease is about management of symptoms, rather than finding the underlying cause, which no MRI, CT, swallowable pill or colonoscopy is designed to identify;
4. Apparently, American doctors do not believe in the MAP hypothesis on account of a single study from 2007, and don’t even mention it to patients unless specifically asked;
5. My doctor didn’t seem to be aware that Crohn’s Disease is associated with all kinds of skin disorders, including but not limited to psoriasis (which is, in fact, sometimes treated with Dapsone);
6. My doctor was blaming the pharmaceutical industry for general disinterest in curing a disease with an old drug (which is certainly possible), but not explaining why Kaiser Permanente or any doctor necessarily had to follow the drug companies’ lead;
7. My doctor wanted confirmation from another doctor he knew personally before prescribing Dapsone, despite having supplied him with case reports on Dapsone and Crohn’s which were written by doctors;
8. At the end of the day, it was possible to at least look into ordering a PCR test for MAP; but
9. Had I not persisted, I would have just been expected to believe that I did not have a MAP infection because it did not appear on a slide with a standard AFB stain, which some papers have described getting to work as “impossible;”
10. The 2007 Selby study from Australia had clearly had a big impact on the field — but what went unsaid was that Selby and his co-authors never actually tested any of their participants for MAP with PCR ahead of time. Instead, they used an arbitrary index of Crohn’s symptoms to identify who might and might not have the disease. Yet their conclusion definitively ruled out MAP’s significance. (And other doctors have posted other critiques of the Selby study.)

Fortunately, I had already set up a “derm in medicine” appointment for the following Tuesday, where I could see both my Primary Care Physician and a dermatologist at the same time in the same room. That appointment began poorly: with my PCP, who had previously advised me against being tested for Vitamin D even after it showed that I was deficient, telling me that I didn’t have a MAP infection because it didn’t appear on a slide in pathology. I quickly told him that it never could or would, and he seemed to be completely unaware and taken aback. When he responded that the pathology department had used a stain, I gave him my stack of journal articles to read, confirming that MAP does not appear with the typical Ziehl-Neelsen stain. He refused to accept them, and actually handed the papers back. I was furious. The rest of the appointment was contentious.

In addition, my PCP had sent me the pathology report from my colonoscopy in an Epic message literally only seconds before he entered the exam room, so that I did not have time to read it. When I later opened it, that report stated the following:

The ileocecal valve specimen consists of multiple mucosal fragments, one of which shows focal minimal architectural distortion along with a few small neutrophilic crypt abscesses. No granulomas are seen. The findings are nonspecific. The differential diagnosis includes and is not limited to etiologies such as infection, NSAID injury, ischemia, and also possibly mild Crohn’s
disease. AFB stain was performed because of the patient’s concern for possible infection with Mycobacterium avium sub-species paratuberculosis, which has been reported to be found more often in patients with Crohn’s disease than in other patients, and no acid-fast bacilli are seen.

Yet despite having read this, and despite knowing that I did not have an unrelated infection, or NSAID injury, or ischemia, my PCP refused to acknowledge that I might have Crohn’s Disease — something I had suggested to him as a possibility six months prior. His refusal was adamant. When pressed, he would only defer, defer, and defer some more, until he finally admitted, “I sent you the full report just now. It showed a little bit of inflammation in the colon around the ileum, which sometimes can be a sign of…” I waited for him to say Crohn’s Disease. Instead, he finished after a pause, with “somethin’ goin’ on.”

The dermatologist finally arrived, and after looking at my rash for no more than 15 seconds concluded that it was “probably” psoriasis, and that he would not be nervous about prescribing Dapsone for it. But he wouldn’t actually do it without the approval of GI, and my PCP certainly would not under any circumstances, because he said he was not comfortable doing so (likely because he had not read any of the scientific literature). When I asked if the rash could be anything else, the dermatologist said no. And when I asked why he said “probably,” he said that he just meant he had seen worse cases of psoriasis, which I didn’t doubt. I also verified that he didn’t see anything that would rule out psoriasis, and he agreed that nothing ruled it out. I left with no prescription, but at least confirmation that ten years of visits to Kaiser dermatologists had “probably” yielded one misdiagnosis after another, as I had thought.

By Thursday night, my symptoms had worsened again and I was worried. I e-mailed Bernard J. Tyson, the CEO of Kaiser Permanente, demanding a prescription for Dapsone, since at this point I had been left with no treatment options. I heard nothing all day on Friday, and sent another two e-mails. The nurse advice line finally yielded a doctor who insisted that even though she technically could issue prescriptions, she would not, because I needed to see a dermatologist, even though I just had. I was dumbfounded. Saturday morning, I received a call back from someone who sounded like an administrative assistant. She offered a new option I had never heard of: a committee of Kaiser doctors would review my request over the phone if I could be ready in roughly two hours. No problem, I told her.

I enlisted the help of a family member, an MD/PhD who agreed that Dapsone seemed like a very reasonable treatment option. Via conference call, we had ten minutes exactly to tell the committee of anonymous doctors on the phone why I was making the request, and why it made sense. I spoke clearly and articulately about my symptoms and the research. My supporting MD/PhD pointed out that a very similar situation had transpired not long ago regarding H. pylori, which we now know — but didn’t always — causes gastric ulcers. At the end of the ten minutes, the assistant asked if anyone on the panel had any questions.

“No.”

“No.”

“No.”

That’s all I heard from them. Suddenly I realized what I had just participated in — something that until that moment I hadn’t really thought existed. But here it was, in real life: a Death Panel. And the potential Death being evaluated, even if a ways off, was mine.

There was no way that Kaiser’s doctors were going to approve my request. An informed patient and a practicing MD/PhD had just presented a concise but technical recommendation that even if controversial begged all kinds of questions, and between the three of them, they had not one. I was sure it meant denial.

And I was right. The next morning, the assistant called back to let me know that my request had been denied. I was furious. It really did seem like Kaiser could care less if I keeled over and died. I still had no medicine and asked her what she expected me to do. She clearly didn’t care. The assistant reassured me that one of the doctors had read one of the abstracts of one of the eleven paper citations I had sent them by fax (since they refused to accept the papers via e-mail). I was given the option to appeal the decision to a state government agency which serves as Kaiser’s regulator, and within 20 minutes, I had, hoping that my symptoms would not get even worse within the 30-day waiting period.

A few hours went by before I was reminded of something.

Another family member, a doctor, had once lived in my state, and was still a licensed physician here. None of us thought it was a good idea for family members to be prescribing drugs for other family members, but he also saw the seriousness of the situation. After a series of short discussions, he called in a prescription for 100mg Dapsone daily to a nearby pharmacy, and miracurously, I had my drug, whether Kaiser liked it or not, and no matter what the Death Panel had to say.

The only question now was whether or not it would actually work.

Continued in Part III.