While most people returned to work for the first full week of 2014, I had Monday off. I returned to the hospital for a followup EGD, esophagogastroduodenoscopy, and a colonoscopy. These long words are very much like the German language – where there is no longest word; they can build compound words from individual words. The etymology of the EGD is 4 words: esophagus gastro duodenem endoscopy meaning – from the esophagus to the duodenem they’ll be looking with a scope. The gastro part might be because they add air, or because they’re GI doctors and add it where ever and whenever they can – like bathroom graffiti.
As follow-ups go, it was very routine. No more banding for the variceal bleeding and my colon looked remarkably good – even for someone who has Ulcerative Colitis and recent C. Diff issues. I don’t remember many negative diagnoses today, but lots of positives:
- The variceal backup has moved from the esophagus to a safer place; which means it still could bleed, but not life threatening. I don’t have leaky pipe syndrome–my term–which is replacing one leaky pipe and finding out the next weakest pipe is now leaking. Instead, my pipes seem strong.
- A good looking colon is a healthy colon. Anytime the doctor says ‘remarkably good’, it means they had set their expectations low and were pleasantly surprised.
- The doctor was familiar enough with the proton pump inhibitors (PPI) connection with C. Diff and told me to stop taking the stomach acid medication. Whenever a doctor agrees with LDAF (Logan Derek and Friends) Research Associates it’s good. (I’m laughing so hard about this! We need t-shirts, business cards, the works. -Logan)
- I didn’t feel sick after coming out of the hospital – this time they gave me Ondansetron (Zofran). This is unusual for me; even with medications that aren’t supposed to cause nausea, I still feel sick. I’m happy that there was no discomfort.
- It appears C. Diff is on it’s way out. Clean colon + antibiotics = get out of there! The doctor mentioned some people end up being carriers of C. Diff, but as long as the symptoms don’t return, it’s not a concern.
- Followup for varices is 3 months, 6 months, and then a year. I’m crossing my fingers there’s no GI followup until April!
The doctor, along with Logan, said my eyes look whiter than usual. Less jaundiced looking equals lower bilirubin levels (see FAQ post here). I have unintentionally done this ‘scientific study’ before – my colitis flares up, or I have bowel issues, and my bilirubin levels go down. I’ll wait for actual data from the blood test on my next MELD score – I expect to see a drop in bilirubin levels.
Could I single-handedly–with my sample of two flareups–be corroborating this study?
One hypothesis is that enterohepatic circulation of (as of yet undetermined) bacterially derived molecules plays a critical role in eliciting pro-inflammatory, pro-fibrotic hepatobiliary responses that lead to the development of PSC (hereinafter ‘PSC microbiota hypothesis’).[15–17] The entry of such molecules into the enterohepatic circulation may, in some patients, be related to the enteric dysbiosis and increased intestinal permeability associated with inflammatory bowel disease (IBD), a condition diagnosed in 75% of those with PSC.[18–22] Further supporting the PSC microbiota hypothesis is the observation, for example, that patients with PSC often have a leucocyte differential exhibiting increased neutrophils, even in the absence of signs or symptoms of acute cholangitis, suggesting circulation of endotoxins or other immunoactive molecules.Collectively, these and animal model[24, 25] findings point toward a role for bacteria and bacterially derived molecules in the aetiopathogenesis of PSC.[Source]
I interpret the preceding as saying: ‘The hypothesis is, PSC is related to bacteria and may be caused by backup/upstream flow into the bile ducts.’ Maybe a real specialist, instead of an electrical engineer, could better interpret the paper.