Hello Dr Goswami

I read quite a few papers after reading your question and wondering if I could find any precise data, until I found this 2015 paper; have you come across it?:

Larsson, G., Shenoy, K. T., Ramasubramanian, R., Thayumanavan, L., Balakumaran, L. K., & Cvancarova, M. (2015). A Risk Matrix Model for the Prediction of Intestinal Tuberculosis and Differentiation from Crohn’s Disease. Austin J Gastroenterol, 2(5), 1052.

https://www.researchgate.net/profile/Geir_Larsson/publication/282354232_A_Risk_Matrix_Model_for_the_Prediction_of_Intestinal_Tuberculosis_and_Differentiation_from_Crohns_Disease/links/560d9e6b08aeed9d13753622.pdf

OR

http://austinpublishinggroup.com/gastroenterology/download.php?file=fulltext/ajg-v2-id1052.pdf

See Figure 1 at the top of the second column of p.03. This is more definitive than some of the papers that discuss the topic without any firm conclusions.

Very best wishes

Mary

Article A Risk Matrix Model for the Prediction of Intestinal Tubercu...

Dr. Goswami,

Thank you for the question.

I think so that it is quite impossible for the FCP (or another biochemical marker) to differenciate the small bowel Crohn's disease and the intestinal tuberculosis.

As for the paper provided by Dr.Wilson, let us read a little more careful what is written there:

A mean FCP level is 2.4 fold as higher in the ITB group than this in the CD group, indeed. On the other hand, on the page 3 of the article, one can notice the passage that the granuloma detection rate (GDR) are 33% and 6%, accordingly. So, the FCP is, seemingly, just a marker of the granuloma rate what is clear from the nature of the marker.

In case one can prove that the GDR is normally higher in patients with ITB than in these with CD, I could agree that the authors have a point, but I have not met such studies still.

Sincerely yours,

Andrey Borodach

Calprotectin is a protein contained in white blood cells. It is an excellent marker of intestinal inflammation, more sensitive for colonic than ileal site of flogosis. I think that it cannot diefferentiate the source of infection.

I agree with Dr Ierardi: to me calprotectin is just a marker of intestinal inflammation, whatever the cause.

Thanks Mary Wilson for sharing the article. Many thanks also to Andrew Borodach,Ieradi Enzo and Chantal C de Galocsy for giving such important opinions. I strongly feel for a good clinical trial with Fecal Calprotectin, CRP and ASCA and histological markers is needed in differentiating Crohn's and ITB. 

Dear Dr.Goswani,

Histological features are the same in both the CD and TBC, save for the caseouse necrosis what is specific for the latter. However, the absence of the caseouse necrosis does not mean the absence of TBC, unfortunately.

One of the old and wise physiceans said: "The terminal ileitis is a tuberculous lesion without a tuberculosis bacilla detection".

I believe, that the famous discovery of the H.pylori and Helicobacter-associated diseases may inspire some researchers to try and find again a bacterium which causes the Crohn's disease. There should be a bacterium in the root of this suffering. So to say, "Cherchez la bactérie" .

Secondly, the primer place for CD to develop is the submucosal layer of the intestinal wall. This layer is not only a room for the intrinsic intestinal immunity, but is the place where the intestinal glands (so called 'Lieberkuen's crypts') locate. To the best of my knowledge, no one has ever been investigating the glands from this point of view. It is sadly indeed that there is not the science of Exocrinology which would accumulate and integrate the sum of information about the exocrinal glands' physiology and pathology. This might shed some new light to the pathogenesis of various disease, from the acne to the acute and chronic pancreatitis, and - who knows! - Crohn's disease.

At any rate, best wishes in the Happy New Year!

Fecal calprotectin is a non-specific marker of inflammation. In combination with other markers it helps us to make a clinical decision. One can always calculate risk matrices. Within a different population with different prevalences of disease they may give other results. If for some reason I need to know without histological or microbiological prove that there might be Tb it might be better than nothing. Otherwise it might be interesting that another mycobacteria also have been implicated in the pathogenesis of Crohn's disease.

Fecal calprotectin is a marker of intestinal inflammation and or associated infection. So it is not possible to make a real diagnosis only by its measurement. It is helpful for distinguish intestinal inflammation from other functional ailments such as irritable bowel syndrome and so on.

Dr. Goswami

I can not help but Dr. David Diaz Jimenez who works for the Disciplinary Program of Immunology, Institute of Biomedical Sciences, Faculty of Medicine, Universidad de Chile, Santiago, Chile has presented  an abstract called "Serum ST2 and mucosal ST2 content as monitoring markers of Ulcerative Colitis outcome" which is available in the web site http://www.lasid2015.com/docs/abstractssai.pdf

Maybe he can help you

Sincerely yours

María Julia Traversa 

No. it just relfects the presence of infalmmation in GI tract. It is not specific. 

I fully agree with some comments that it is not useful to perform differential diagnosis. Just measure levels of intestinal inflammation, not more

It is possible if we use a diagnostic matrix

It is unspecific and only evaluate the degree of intestinal inflammation but doesn´t differentiate the cause

FCP can be comparable depending on the extend of disease like we can't compare FCP in ileocecal TB with extensive Ileocolonic CD.

I don't think so, because this test only evaluate degree of inflammation, not the cause of the disease

This is not a best test for this purpose