Denver Patient C: Part 2

D

Islet Transplantation as Theory

I have never liked science. At least not the learning of it. I simply have no hooks in my brain for that kind of information. High school chemistry inflicted a specific form of torture, the memory of which still triggers a facial tick to this day. The careful choice of lab partner was the only reason I didn’t fail the class. Yet, years later, I found myself at the center of a lab where I was not only the research subject but also its most fascinated and focused student. I suddenly transformed into a science geek and was completely drawn to the world in which I found myself. It was only other life circumstances that kept me from seriously seeking some small and insignificant corner of it where I could take up a new profession. And it is the science of this world where I pick up my story now.

At the end of part 1 of this tale, if you were listening, you might have heard me slowly exhale the heavy burden of anxiety and exhaustion. In November 2004, after 4 years of relentless blind pursuit, I was accepted into the islet cell transplant study at Denver’s Barbara Davis Center. I had absolutely no idea what lay ahead, but I didn’t care. I was in.

Once accepted, there was more paperwork—of course. An entire forest must have been sacrificed to explain exactly what I was signing on for. Clearly, the authors of HIPAA do not believe in the economy of words. And apparently innumerable signatures are required to demonstrate actual consent.

First, I had to understand how the procedure worked.

Islets cells are the insulin producers of the pancreas that are innocently and unjustly attacked in the body of a type 1 diabetic. But before we get any further in, this begs a correction to a widely held misconception.

Type 1 diabetes is not caused by a faulty or lazy pancreas. It’s the immune system that’s the culprit, the aggressor, which is why T1D is categorized as an autoimmune disease. But it doesn’t destroy the entire pancreas. It’s only the islet cells that wear the target on their chest. With that being the case, the theory of the transplant was that if the islets could be replaced and the immune system held in check, it might be possible to kick start insulin production.

But where to get the cells?

The technology did not, and does not yet, exist to grow them in a lab. And even though swine insulin was used to treat the disease prior to the evolution biosynthetic insulin, swine islets were not considered a viable option in the early days of this research. Human islets were the only choice. But islets can’t be kindly shared like blood or bone marrow, where the generous body that gave them up will simply make more. Nor do they come from an organ living as a nice couple, like the kidneys or the lungs, that can amicably break up, go their separate ways, and still lead a productive life—though perhaps less efficiently.

Just as with heart and liver transplants, islet cells had to come from human cadavers. And here’s the rub on that. A successful islet cell transplant did not require a single pancreas. It required three to gather the necessary number of cells. Three pancreases, three surgeries, ideally three weeks apart.

The way I understood it is that when a donor pancreas was received the cells would be harvested. This process involved the evisceration of the organ itself (I have no idea how that happened, nor do I want one), which was then put into a centrifuge of sorts to spin out the sought-after prize. Then, dizzy I’m sure, the cells were put into a slurry, for lack of a better description, for transplantation.

This is where things get interesting. The cells were not destined for the pancreas but rather the liver by way of the portal vein. A small incision would be made to locate said vein and the cell slurry would be infused by IV into the blood stream. Then, as the blood made its merry way through the liver, the body’s great filter, that organ would grab the cells for its own. Once there, they would get comfy and set up shop. Clearly, this is a ridiculous oversimplification of the process, but that’s the general idea.

Of course, there was the cheeky immune system to deal with. As with all type 1 diabetics, mine didn’t even like my own islets and would certainly not tolerate interlopers. So, it had to be dealt with, handcuffed, by immunosuppression therapy, aka anti-rejection drugs. Thus, countless pages of that mountain of paperwork listed every potential side effect these nasty-though-necessary drugs might impose. It was no joke. The list was long and unseemly, and I was instructed to read it carefully and consider it cautiously before signing on the dotted line.

I dutifully abided by the first directive. I read every word. But rather than seriously weighing the risks, I took a different tactic, though not consciously. As I read about all the unpleasant things that might lay ahead, I mentally sorted the side effects into two lists: one of those I could tolerate and another of those I could not. Then I simply told myself the second column was irrelevant because they wouldn’t happen to me. And, with a firm, though false, sense of confidence, I picked up my pen without a moment’s hesitation.

Was it blind naivety or was it a stubborn refusal to be deterred? Even now, I couldn’t say. What I do know is that on that day it all sounded so simple and so clinical on paper. It was theory. As it turns out, it was neither simple nor clinical when it became reality.

Today, I’m grateful I didn’t truly know what was in store for me. The next eight years were the hardest of my life—physically, mentally, emotionally, spiritually. And it all put a strain on many things that are precious to me. But those years were also the most fascinating, the most miraculous, the most valuable of my life. And they gave me many unexpected gifts.

But those are tales for another day.

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