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!
- Glad to know that we are aware of major risk factors for HCC even in the absence of cirrhosis.
- No evidence as of yet to expand the risk pool to screen patients without evidence of cirrhosis.
- If chemoprevention is ever developed, now we know a good population to apply it in ( ex – Maybe Metformin?.
- It would be nice to have a large data dump of such patients on a national level, and include other variables in analysis, such as factors associated with good outcome or poor outcome. I suppose we can wait for the next paper.
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, infectious 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.
I have read this article back in July, and immediately found it interesting. One reason is that it is (albeit a poor one) an example of the use of “Big Data” type analysis where a large database of patient biopsy specimens can be searched.
Second reason – is the actual clinical finding – less polyps than expected in those with microscopic colitis – prevalence of ALL types of polyps was reduced.
Summary: 130,000 patients with symptoms of diarrhea had a colonoscopy with biopsies. Compared with 97,000 control cases. So, in this CASE-CONTROL study for patients with workup of diarrhea – less polyps (Odds ratios = 0.46 for hyperplastic, 0.24for serrated adenomas, and 0.35 for tubular adenomas).
Criticism: It would have been nice if the authors have age-matched the cases one for one from the beginning, even though these were adjusted for. There is no duration of disease, so the mechanism would remain elusive. Although it would be interesting to have someone do a database review of patients whose clinical history is known. It can even be compared to the current study, if the data is available, i.e. authors had 14% of colons have polyps in normals, and 8.3% in microscopic colitis, is there an influence of disease duration or is this an all or none phenomenon?