Summary: My endo thinks that my D is caused by hepatitis C. I think that this is possible but not certain. I've searched TU carefully (with Google), and this topic hasn't been covered, so I thought it would be useful to post about it. The longwinded version:
I haven't posted much since mid-May, when many of you were very helpful in replying to my initial post. There are several reasons for this. One is that once I got traction with Novolog, I've had excellent control. At the same time, the hard core of experienced posters here are so good that it wasn't clear I had anything unique to say in discussions, so I decided to spend a lot of time reading old posts (a treasure chest, from Funny Hypo Stories to The Good Wifeabetes?)
The main reason, though, was that I was digesting a hepatitis C Dx. I found out about this as a consequence of asking my internist for pancreatic CT scan the day I was Dx'ed, as I explained elsewhere. The scan showed that my pancreas had a few calcifications, kidneys had a cyst or two, and 'mild nodularity of the hepatic contour'. I now understand that nodularity is associated with scarring and cirrhoses. In any case, during the same dramatic initial 90 minute visit with my endo where I first got my hands on some Novolog, he persuaded me to take a hepC antibody test, which came out positive. This was followed by a PCR test for the virus: positive. DNA sequencing revealed I have genotype 1b. Finally, as a substitute for liver biopsies, current practice is to test for a panel of markers for liver damage. Unfortunately these tests unequivocally show only 'normal liver' and 'cirrhosis'. Intermediate results showing damage short of cirrhosis--I had a FibroSpect score of 59--are uninterpretable in terms of safety margin. At this point I will interrupt this narrative for a few words about hepatitis C.
hepC is caused by an RNA virus, so-called because the viral genes are encoded in RNA not DNA. HepC is not caused by a retrovirus. Retroviruses, such as HIV, also have an RNA genome, but they transcribe DNA from it which becomes permanently inserted in the host's chomosome. HepC virus replicates in the cytoplasm and has no DNA stage in its life cycle. HepC is blood borne through contaminated needles, transfusion sets, etc. It's existence began to be suspected in the 1970s, but the virus was not conclusively identified until 1989. The typical type of infection is chronic, and people may be asymptomatic for decades. Sometimes the latency is so long that an infected person dies of other causes; sometimes a chronically infected person develops cirrhoses, which frequently progresses to hepatic cancer. End stage disease can sometimes be cured by a transplant; one prominent hepC/hepatic cancer survivor is former Grateful Dead bassist Phil Lesh, who now gives a little rap about organ donation before the encore at all his shows.
Before 2011, the treatment prospects were pretty grim. The major treatment was PEGylated interferon and ribivarin. This had a 50% success rate and usually took 24 weeks, during which the interferon caused fever, diarrhea, and exhaustion characterized by sleeping 14hrs/day. Since 2011, however, new treatments have become available that are 99% effective and have no side effects except photosensitivity. The 'official medical guidelines' are here. These treatments appear to be safe and highly effective, but they are currently new and very expensive and will require heavy advocacy with your insurance company/medicare/medicaid.
This is not a hepC board; what about the D? My endo believes that I have type 2, and I am about 95% certain I agree with him. Let's recap:
Arguments in favor of slow onset type 1: Never obese, loss of weight prior to Dx, BMI 20-21, TDD 40U at 60kg--high but not impossible for type 1. No auto-antibodies, but as Melitta points out, 5% of bona fide Type 1's don't have them.
Arguments in favor of type 2: I show signs of insulin resistance. My I:C has varied from 2.5:1 recovering from major periodontal surgery to 1:5 after regular aerobic exercise. The TDD of 20U basal / 20U bolus only applies to days with low carb breakfast and lunch, 70carb total. At 100carb/day bolus total more like 30, and on a carby day (130-140carb) 40. That's a TDD of 40-60U with basal always 20U. Finally, C-peptide is 3.4 ng/ml, normal for this lab given as 1.1-4.4. This test was given in late April, when I was testing a lot but had levemir only with good fasting BG and ugly post-meal spikes. My log says I tested BG at 84 right before the C-peptide test late in the afternoon and hadn't had lunch. This seems high for fasting at this BG at (then) 23U/day basal.
My endo, like me, thought for for sure I had type 1 at first. He thought that in part because I'd be 'among the 10% of non-obese type 2's and probably among the 5% without metabolic syndrome'. After the hepC Dx, his opinion shifted to type 2 from hepC caused insulin resistance. My hepatologist thinks the evidence is only epidemiological and pooh-poohs the whole notion. I had intended to make this post only after doing thorough research, but the day job takes a lot of time, so I'll share what I know.
I just got the 14th edition of "Joslin's Diabetes Mellitus", which seems to be a top textbook but this edition dates from 2005. It makes no mention of hepatitis C in Chapter 27 "Secondary causes of diabetes", which is where it would be mentioned. I have found numerous (low quality) papers that are, in fact, epidemiological, and show a higher frequency of type 2 among hepC patients. One review that has a useful paragraph about diabetes and is open access is here. Unfotunately, some interesting references therein are behind paywalls. One paper that isn't is this one by Milner at al.. The authors used a euglycemic clamp to measure insulin resistance in a group of uninfected and hepC infected non-diabetic subjects. They found significant insulin resisrance in the hepC subjects, and by indirect means concluded that it was in muscle and not in liver. Maybe this is why metformin does nothing for me?
In any case, this post is now WAY too long. I'm interested in any comments, experiences, about this here at TU. If you'd like to correspond privately with me about hepC, please send a friend request. I'll try to do more reading and report what i find. Should I actually get treated (not clear at this point), the effects of treatment on my D will be useful data. Apologies for the length of this post.
-ZZ