Gastroenterology Literature Review
After a Long long hiatus on posting, and inspired by many GI folks out there producing content that is extremely useful and entertaining, I’ve spent a couple of dollars on a new microphone setup and will be producing two episodes a month of a GI literature review podcast.
Still trying to figure out how to host it etc. So stay tuned…
Always great stuff, from Jay Hochman
Great review by @gutsandgrowth of the latest Regueiro article
While I am contemplating 
to actually starting a podcast that would review the GI literature in some detail on a monthly basis, i will prepare myself by posting a few reviews of the articles that sparked my interest/I feel are important for a gastroenterologist to be aware of.
I start with the March 10th Issue of NEJM, which has a nice summary article on Mesenteric Ischemia. Now if you are looking for a quick-guide to how to diagnose it or how to treat it – this is NOT the article for you. But if you want the details on exact specificity/sensitivity of different imaging modalities ( it happens to be 85% Sensitive-90% specific on Ultrasound, for example, and CTA is 95-100% Accurate) – then this is the article for you – you can download it and file it away for when you need the info. It is too bad that the authors did not want to make a table such as this (found and cited elsewhere):(which they cite as reference 26)
But I understand that the aim here was to give a more “comprehensive” view on what mesenteric ischemia is for the general reader. It has nice figures with examples of CTA with acute embolus to SMA, as well as chronic mesenteric ischemia with occlusion of SMA in setting of a celiac stent occlusion.
For the endoscopists amongst us, nothing is more true:”…endoscopic examination does not reach the majority of sections of the small bowel that are most frequently involved in mesenteric ischemia…” so dont scope of VCE these patients for no reason.
And now for clinical pearl:
Lawrence Brandt – a professor at Albert Einstein College of Medicine – one of the first persons to expose me to the wonderful world of gastroenterology loves to talk about non-occlusive mesenteric ischemia – NOMI – Overall mortality is 50% – Mostly in patients with cardiac disease/complications/recent cardiac surgery. Papaverine hydrochloride through a catheter infusion can be considered. Not sure where else we can use Papaverine for a GI condition (let me know if you know).
To remember NOMI, Dr. Brandt usually brings up is a person in their 70s, with HTN, has an MI with hypotension, then stented, was put on beta blocker, and clopidogrel/aspirin, then develops severe abdominal pain. Exam is with mild tenderness, labs are unhelpful. INR is 2.1, everything else is ok. What’s the diagnosis? – NOMI! Why? – vasoconstriction that is persistent,as a reaction to a previous insult, even if precipitating event is gone.
References as cited or linked.
We often talk to
our patients with cirrhosis regarding the risk of HCC, and putting aside the debate as to the efficacy of screening for such, most of our patients get the ultrasound twice yearly, +/- AFP every so often, and we cross our fingers and hope for the best, given how non-existent effective therapy for HCC is (other than resection).
This article in CGH – which regained the title of my second most favorite GI journal this week, is an article from the Texan folks, discussing HCC in the absence of cirrhosis.
This is a review of the Veteran’s Affairs database (boy would I love to get my hands on that!), 2005-2011 diagnoses of HCC, which was limited to 1500 random charts (obtained from a total of 10,695 HCC diagnoses).
~80% of the patients diagnosed with HCC had cirrhosis. Which means ~20% did not. Who are these remaining folks?
Many had metabolic syndrome, NAFLD, but some had no risk factors whatsoever. It is interesting that in the cohort of 43 patients with what authors defined as “No cirrhosis – very high probability” – many still had some fibrosis.
In any case, logistic regression to look for associations and risk factors for HCC in absence of cirrhosis was conducted. Results:
NAFLD, HCV, HBV, Alcohol abuse, Metabolic syndrome, Others (hemochromatosis, autoimmune hepatitis, A1-AT deficiency). Idiopathic – only in 13 out of 194 patients!
Conclusions:
I am surprised that there are so few new oral drugs coming out for IBD. I guess Infusions are all the rage due to potential profits. AJM300 has been around for a while, and I remember seeing an abstract for it at DDW last year.
This Article – in Gastroenterology, which has been online for a while, finally came out in print edition.
AJM300 is an alpha4 integrin antagonist. In their paper describing a double-blind, placebo-controlled phase 2a study, AJM300 was shown to be well tolerated and more effective than placebo including both clinical response, remission and mucosal healing.
For those of you like me, who do not remember what Phase 2a is – Pilot clinical trials to evaluate efficacy ( and safety) in selected populations of patients with the disease or condition to be treated, diagnosed, or prevented. Objectives may focus on dose-response, type of patient, frequency of dosing, or numerous other characteristics of safety and efficacy. (2B being a larger study showing efficacy, the so-called “Pivotal trial”).
Another interesting statement in the article made me aware of the number of cases of PML as a result of Natalizumab treatment – 2.1 cases per 1000 (total of 212 cases out of 99,751 patients treated). Two take aways for me – I had no idea that many patients were treated with Ntalizumab!!!I had no idea that there was a registry, but that makes sense.
Once again, remember, JCV negative patients never get PML.
Lastly, efficacy in this group: I will only mention mucosal healing which is most important for these pilot studies: 58.8% – AJM300 versus 29.4% in placebo group. – another reminder that a third of patients with UC will just get better.
This Article in December issue of Gastroenterology summarizes the findings from the Gastroparesis Clinical Research Consortium (7 tertiary care centers). Out of 262 patients- only 28% had a reduction in symptoms that was significant.
They also tabulated factors that are associated with reduction in symptoms – male sex, older age, infect
ious prodrome, antidepressant use, and 4-hr retention greater than 20%.
This is bad news for those with gastroparesis. Most importantly there was no difference in those with and without diabetes.
Most notably there is no post-treatment gastric emptying, which would be interesting to see who actually improved, and who just “felt” better, and whether there is a correlation between these.