IBD being of non specific etiology, could not be diagnosed beforehand. But, seeing that it has genetic background (mutations in genes related to the receptors in intestine) we might test people and tell them the chances of getting IBD

Faecal markers of inflammation - eg faecal calprotectin or faecal S100A2.

Sensitive but not specific - better for large bowel disease.

Useful test of exclusion - high negative predicitve value

Current guidelines indicate that faecal calprotectin values > 150-200 could be a good indicator for endoscopy performance. Nevertheless, this investigation needs to be suggested by the symptoms of the patients. I do not think that a screening population for IBD may be a useful tool.

faecal calprotectin is a marker that we are using to distinguish between inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS). Faecal calprotectin is a marker of neutrophilic intestinal inflammation and the test can help to distinguish patients who may have IBD from patients who have IBS. Faecal calprotectin can effectively triage which patients need referral to a Gastroenterologist for further investigation.

Joint hypermobility is very common in patients with IBD, especially to those who suffer from Crohn's disease. When symptoms of IBD and signs of joint hypermobity are present (according to Beighton's or Brighton's criteria) there is much possibility of an underlying IBD. This is so far an observation and it has not yet been standardized for sensitivity and specificity. I hope to give you further information in the near future.

For reference see: http://dx.doi.org/10.1155/2009/924138 and http://www.ncbi.nlm.nih.gov/pubmed/20334983#

I agree with others for calprotectin, but notice that only for triage purposes in diff it from IBS; ir for early detection of relapse in people with known disease. The same for the tradicional CRP. There are also some data on ultrasound of the bowel or terminal ileum, but, as you know, this is very operator dependent.

ASCA (for Crohn's) and pANCA (for Ulcerative colitis) can help to support the diagnosis of IBD.

Note that ASCA is positive in around 60% of patients with Crohn's disease patients especially those whose have ileal involvement.

Fecal calprotectin might be a good marker for patients with inflammatory bowel disease but is it better for Crohns disease or for ulcerative colits.. Also, there could be sampling error within a given stool specimen.

Faecal Calprotectin has been recommended by NICE to be a useful screening test to triage referrals to Gastroenterology for investigation of chrnoic diarrhoea, without rectal bleeding, in patients under the age of 60years. This excludes patients who would fit the criteria for a 2WW referral for excluding cancer, for a chnage in their bowel habit. Please refer to teh NICE Guidance, October 2013, for more information on the algorithm for Faecal Calprotectin testing.

Early detection of idiopathic inflammatory bowel disease seems to be important because it could lead to earlier treatment. Nutritional intervention with flavonoids (phytochemicals) might be effective when used as initial therapy before the chronic phase of the disease evolves.

Fecal Calprotectin testing in primary care could reduce the need for referral and colonoscopies. However, false positive results correspond to patients with gastrointestinal infections, systemic infections, ulcers or nonspecific histological alterations of the mucosa. Other false positive cases correspond to postsurgical samples, non-steroidal anti-inflammatory drugs and chronic liver diseases. Finally, false negatives may occur (e.g., in celiac disease). In conclusio the test has a high sensitivity, but a low specificity.

For the really early, before any clinical manifestations, diagnostics to perform, family history of the IBM and appropriate genes mutation (about 30) development are sufficient for a given patient to being referred on the colonoscopy/capsule investigation with biopsy. It is costly, though.

Further, the histological study is the golden standard for the IBM to be diagnosed positively.

The faecal calprotectin is non-specific, especially taking in mind a variety of possible intestinal infectious diseases in some regions and the seasons of the year and can hardly have overcome the clinical manifestations much. The intestine infiltrated by the neutrophils will not keep silence for long.

In ulcerative colitis (UC), persistent bloody diarrhea is the presenting symptom in the majority of patients, so colonoscopy is promptly performed and, usually, diagnostic delay is of no matter. Conversely, symptoms and signs of Crohn's disease often overlap with irribable bowel syndrome (IBS), a condition 4-500 fold more common, at least in Italy. There is now compelling evidence that early start of new highly effective therapy (immunosuppresive, antiTNF, and so on) may favourably modify the natural history of the disease and early diagnosis in patients with IBS-like symptoms may be desirable. I agree with most colleagues in the present forum on the usefulness of fecal calprotectin as a screening tool to address patients wit high values to ileocolonoscopy, however bowel sonography, in experienced hands, is an excellent screening tool I successufully perform from 20 years in clinical practice. Unfortunately, only one old published study by Astegiano and coworkers (http://www.ncbi.nlm.nih.gov/pubmed/11507357) addressed this topic obtaining good sensitivity and specificity values (with first generation instruments)

It depends on which situation you are considering.

If you are looking for a screening tool, to be used in large populations, there is currently no test with enough sensitivity.

If you are thinking about a clinical situation in which the suspicion of IBD can arise, the discussion is different.

Genetics (mentioned in other commentd) do not play any role at all in diagnostics.

The determination of ASCAs/ANCAs may be of some value in differentiating Crohn's from UC, but again they are not very specific.

Then what is left? Make a good clinical interview with the patient, search for anemia and for inflammatory markers (C reactive protein and calprotectin), rule out other possibilities (infections, parasites, hyperthyroidism,...). If there is inflammation and you rule out other possibilities, proceed to ileocolonoscopy and add some technique to see the small bowel, probably US in slim people with ileocecal disease and some other (MRI, barium studies...) in the rest, depending on which country and situation you are practicing in.

"From another commentator":

The question of this topic is' Is there any early detection method of the inflammatory bowel disease?' (as it follows from further context, before severe manifestations have already occured).

Those patients with the ulcerative colitis are rather lucky from this point of view if it would be correct to use the term 'lucky' for incurable still a disease. An onset of diarrhea brings the patient to an infectious hospital at once. Not more than in a week, the infectionists will rule out 'their' disease so that the diagnosis becomes more or less evident. So, we can assume that the early diagnostics of the UC exists these days (what does not exclude another major problem, namely, that the onset may be severe from the very beginning).

The Crohn's disease and indifferenciate form of the IBD are quite another business, so that one can speak of the 'earliness' just nominally.

It takes several years to find proper a diagnosis for them usually if they are not operated upon by mistake due to the acute appendicitis suspition (or, much rarer, for the diffuse peritonitis, gastrointestinal bleeding, or ileus). The surgeon must being wise enough to take the appropriate mesentery lymph node up during the operation so that the histological examination and the Crohn's granulomas are to possible. This way may be entitiled as nominally 'early diagnostics' of the CD, before the fistula and strictures formation.

The second possibility for the CD to be diagnosed 'early' is 'visual' location with biopsy (those that can be reached through routine endoscopic studies, or even 'true' visual. They all take less than 5 per cent of our casualty).

The third and, perhaps, the best possibility for the 'earliness' is the family history of the CD. Recently, our specialists from the City Centers of Coloproctology and Gastroenterology those deal with those patients get used to refer their young relatives to the Institute of Cytology and Genetics of the Siberian Branch of the Russian Academy of Sciences (http://www.bionet.nsc.ru/en) for genetic examination before become manifested.

Unfortunately, the capsule endoscopy is still unavaible for us for reasons beyond this discussion. To perform the procedure, a physician has to refer the given patient to Moscow or St.Petersburg. Our place is a rather remote one as any person can easily imagine if recall where Lara Croft met the Planetary Alignment.

As for the ileocolonoscopy, this procedure is a heavy and dangerous to perform as a screening. Further, the US, MRI, and barium studies can provide nothing until complications have come forth already. I must confess that there are few exceptions, though, and might depend on the visual diagnost personal experience.

The irritable bowel disease is a condition defined very loosely and, if it is really functional a condition, than it cannot be manifestatied by ANCAs, calprotectins levels, and other markers of autoimmunity and acute inflammation (see at 'Irritable bowel syndrome: are intestinal bacteria the cause?' https://www.researchgate.net/post/Irritable_bowel_syndrome_are_intestinal_bacteria_the_cause ).

Ceterum censeo, Carthaginem esse delendam, and it is Genetics that seemingly is the most promising pathway for the IBD early diagnostics, or so it looks like for now at any rate.