What Calprotectin Levels Mean in Ulcerative Colitis

A faecal calprotectin result is a concentration. It says roughly how much calprotectin, a protein packed inside neutrophils, was present per gram of the stool you handed in. Neutrophils flood into an inflamed colon lining and spill their contents into the bowel, so the more inflamed colon surface you have at that moment, the more calprotectin ends up in the pot.

That is the whole of what the number measures. It is not a severity grade, not a percentage, not a stage, and not a score out of anything. Which is why the questions people actually ask, "is 145 high", "why was mine 1900 when I felt fine", "why did it drop from 800 to 31 without anything changing", do not have the tidy answers that the ranges printed on lab reports imply.

This guide is about reading the number itself: where the thresholds come from, why the same stool gives different answers in different laboratories, what disease extent does to the value, and what the best available trial found when people actually tried monitoring it at home.

The short answer: what the number is actually measuring

Calprotectin makes up a large share of the cytosol of neutrophils, the first-response white cells. When the colon lining is inflamed, neutrophils migrate across it into the bowel lumen, die, and release calprotectin, which resists degradation well enough to survive the trip and be measured in stool. So the value is a proxy for one specific thing: neutrophil traffic into your gut at the time you produced that stool.

That proxy is a good one. In a meta-analysis of 19 studies and 2,499 people with symptoms suggestive of active inflammatory bowel disease, faecal calprotectin detected endoscopically active disease with a pooled sensitivity of 0.88 and specificity of 0.73, against a CRP sensitivity of just 0.49, and it performed better in ulcerative colitis than in Crohn's disease (Mosli 2015). Colonic inflammation is close to the exit, which is part of why it shows up so reliably in UC.

But "good proxy" is not the same as "readable dial". Three things get between the inflammation in your colon and the number on the report: the assay the laboratory uses, how much of your colon is involved, and which bowel movement you happened to sample. All three are large enough to change the number by more than the difference between remission and mild activity.

Why "is 145 high?" has no single answer

The figure most people have absorbed is 50 micrograms per gram. It is on lab reports, it is the number community threads quote, and a common reply to someone posting a result of 145 is some version of "anything above 50 is not normal".

That 50 came from work establishing what healthy people produce. In 117 healthy children aged 4 to 17, the median was 13.6 micrograms per gram and 89% were below 50, which is where the paediatric use of the adult cutoff came from (Fagerberg 2003). It is a sensible screening line for deciding whether somebody with new bowel symptoms and no diagnosis needs a camera.

It is a much worse line for someone who already has ulcerative colitis, for two reasons.

First, the "normal" range moved when the assays did. In 382 healthy adults aged 50 to 65 from a Swedish population cohort, measured on a modern turbidimetric assay, the calculated reference interval was below 199 micrograms per gram when the samples were processed with an extraction device, and below 153 when they were weighed out by hand (Fall 2017). Same protein, same healthy people, an upper reference limit three to four times the familiar 50, purely because of the method.

Second, mildly raised values are common in people with nothing wrong. Among 590 outpatients who had a completely normal colonoscopy, 36% had a calprotectin above 50 micrograms per gram, and proton pump inhibitor use was one of the factors associated with the elevation (Lundgren 2019).

The practical reading of 145 is therefore: above the screening line, below the threshold the AGA uses to rule out active inflammation in symptomatic remission, in a band that carries measurable extra risk over years, and sensitive enough to method and sampling that a repeat is worth more than an interpretation.

Your number depends on which assay the lab runs

This is the part almost no patient-facing page mentions, and it explains more confusion than anything else on this list.

There is no international reference material that all calprotectin assays are calibrated against. Manufacturers use different antibodies, different extraction devices and different calibrators, and the results do not convert.

• A Belgian study ran six different calprotectin assays, three rapid immunochromatographic tests, two ELISAs and one automated fluoroimmunoassay, across 62 patients. All six correlated significantly with each other and had broadly comparable clinical performance, but the slopes and intercepts differed so much that there were up to five-fold quantitative differences between assays (Labaere 2014). The authors called for standardisation. That was more than a decade ago.
• A 2022 comparison of the first FDA-approved assay against four newer ones, on 50 stool samples, found correlation coefficients of 0.95 to 0.98, positive biases of 15% to 20% for three of them, and one widely used assay that ran approximately two-fold higher than the reference assay while still correlating at 0.98. The authors were explicit: the results correlated, but the assays are not standardised (Lin 2022).

Two consequences follow directly.

Your number is only comparable with your own numbers from the same laboratory. A result of 300 at one hospital and 150 at another does not mean you halved your inflammation. It may mean you changed labs.

Units are not the confusing part. You will see micrograms per gram and milligrams per kilogram on different reports. These are the same quantity: 1 mg/kg equals 1 µg/g. A value of 440 mg/kg is a value of 440 µg/g. The assay, not the unit, is what changes the number.

There is also a ceiling to be aware of. Assays have a reportable range, and the first FDA-approved test reported between 16 and 1,250 micrograms per gram (Lin 2022). Laboratories handle results above the top of the range either by reporting "greater than" the limit or by diluting and re-running, which is why some people see a capped result and others see a specific five-figure number. Threads where people compare "records" of 9,000 or 14,000 are partly comparing laboratory policies.

Does a higher number mean more inflammation?

On average, yes. In an individual, only loosely.

The clearest demonstration comes from a prospective study of 228 people with ulcerative colitis and 52 healthy controls, all of whom had a complete colonoscopy scored on the modified Baron index. Calprotectin was the only marker tested that could separate every grade of endoscopic activity from the next.

Calprotectin correlated with endoscopic activity at r = 0.821, ahead of the clinical index at 0.682, CRP at 0.556 and haemoglobin at -0.388 (Schoepfer 2013).

Read that table the right way round. The medians climb cleanly. The ranges do not stay in their lanes: a value of 46 sits inside the interquartile range of both grade 1 and grade 2. So the table tells you that groups of people with worse endoscopic disease have higher calprotectin. It does not let you take your own 300 and read off a grade.

A common theme in r/UlcerativeColitis is exactly this mismatch. One widely read thread was started by someone whose calprotectin was 1,913 while they felt, in their words, as if they did not have UC at all, and who had read of other people flaring badly at around 100 (r/UlcerativeColitis thread). The most useful reply in that thread summarised it as: a good indicator of the presence of inflammation, a worse indicator of its severity, and a worse one still of how symptomatic somebody will be. That is close to what the data support.

The discordance in the other direction, a high number in someone who feels well, is common enough to have its own literature. We cover it in detail in high calprotectin but no symptoms, so it is not repeated here.

How much colon is involved changes the number

Here is the piece that most explains why one person's 150 and another's 1,500 can represent similar-looking mucosa.

A Norwegian single-centre study analysed 518 visits by 254 people with ulcerative colitis, scoring endoscopic activity with the Mayo endoscopic score and disease extent with the Montreal classification, using a fluoroenzyme immunoassay. Among people with endoscopically active disease (Mayo score 2 or more), median calprotectin was:

• Proctitis: 440 mg/kg (IQR 175 to 1,350)
• Left-sided colitis: 840 mg/kg (IQR 298 to 2,011)
• Pancolitis: 1,690 mg/kg (IQR 723 to 2,582)

The gradient persisted in the other direction too. Among people whose colon looked quiet (Mayo score 1 or less), median calprotectin was 24 in proctitis, 40 in left-sided disease and 85 in pancolitis (Steinsbo 2025).

The mechanism is simple arithmetic. Calprotectin is diluted into the whole stool volume, so it reflects total inflamed surface area rather than local intensity. Fifteen centimetres of furiously inflamed rectum contributes less protein to a whole day's stool than a metre of moderately inflamed colon.

A Japanese study reached the same conclusion from a different angle: across 136 colonoscopies in 102 people with UC, calprotectin correlated more strongly with the sum of the Mayo endoscopic subscores across five colonic segments (r = 0.86) than with the single worst segment score (r = 0.79), and the relationship held even among people whose maximum segment score was identical (Kawashima 2016).

Which remission are you asking about?

One of the sharpest replies in that same Reddit thread was a question rather than an answer: clinical remission, endoscopic remission, or histologic remission? The original poster had not realised there was a difference. Most people have not, and it matters here because each layer has a different calprotectin threshold.

The international STRIDE-II consensus, drawn from 89 IOIBD members after screening 11,278 papers, set clinical remission and endoscopic healing as long-term targets, with symptomatic relief and normalisation of serum and faecal markers as short-term targets. It noted that histological healing in ulcerative colitis is not a formal target but should be assessed as a measure of remission depth (Turner 2021).

A 2026 pooled analysis of 741 people with UC from four academic centres tried to pin down the thresholds. Using receiver operating characteristic curves with cross-validation, it found:

The authors proposed 170 µg/g as a practical threshold for the Mayo 0 to 1 versus 2 to 3 question, giving sensitivity of 0.801 but specificity of 0.648 and overall accuracy of 67.6% (Dube 2026). Worth reading alongside that: the paper's disclosures record that one senior author has received funding from Buhlmann, a manufacturer of calprotectin assays, among many other companies, and several co-authors report extensive pharmaceutical industry relationships.

Two honest conclusions come out of that table. The first is that the threshold moves with the question, and the question a patient usually means ("is my colon completely normal?") is the one calprotectin answers worst: an AUC of 0.716 and a sensitivity of 0.64 is modest performance. The second is that anyone quoting a single number as "the remission level" is compressing four different answers into one.

An earlier study made the same point from inside endoscopic remission. Seventy people with a total Mayo score of 1 or less and a Mayo endoscopic score of exactly 0 were followed for a year. Almost 12% had histological inflammatory activity despite the endoscopically normal appearance, and their calprotectin was higher: median 236.5 versus 56 mg/kg. A baseline value above 321 mg/kg predicted relapse at both 6 and 12 months, while a value at or below 40.5 mg/kg was the threshold that best predicted a histological activity score of zero (Theede 2016).

So within a single group of people who all looked healed on camera, the useful thresholds ranged from about 40 to about 320 depending on what you wanted to know.

For what the guidelines themselves say, the AGA's UC biomarker guideline suggests using a faecal calprotectin below 150 micrograms per gram, a normal faecal lactoferrin or a normal CRP to rule out active inflammation and avoid routine endoscopy in someone in symptomatic remission, and makes all seven of its recommendations conditional (Singh 2023). Our companion post on knowing whether your ulcerative colitis is flaring works through how those thresholds sit alongside symptom scoring, so this post does not rebuild it.

One sample is a noisy sample

Two studies published in 2015, both in people with active ulcerative colitis, both with 18 participants, looked at how much calprotectin varies within a single person over a single day. They found large variation and drew opposite practical conclusions, and the disagreement has never been resolved by a larger study that we could find.

Study one. Patients collected two samples at every bowel movement over two days, 287 samples in all. The median individual coefficient of variation within the same day was 52% (range 4% to 178%). Calprotectin correlated with the time elapsed since the previous bowel movement (r = 0.5, p = 0.013), which led the authors to conclude that the first bowel movement of the morning was the most appropriate one to analyse. They also found concentrations unchanged after three days at room temperature but significantly reduced by seven days, by a mean of 28% (Lasson 2015).

Study two. Patients admitted with active UC, most with extensive disease and severe activity, collected samples from several bowel movements in chronological order, 56 samples in all. The median coefficient of variation was 40% (range 5% to 114%), with a median range of variation across the day of 3,887 mg/kg. Crucially, the first stool of the morning was the highest value of the day in 33.3% of cases and the lowest in 38.9%. The authors concluded that a single determination should not be the basis for a therapeutic decision in overt active UC (Calafat 2015). If you are trying to work out whether you are at that point, our guide to when to go to the hospital for a UC flare covers the thresholds, and why calprotectin is a poor triage test for this particular question.

A third study helps narrow where the noise comes from. In 31 people starting remission-induction treatment for UC, within-day variability was described as remarkably wide, while within-stool variability was extremely small (Toyonaga 2017). In other words, it barely matters which bit of the sample you scoop. It matters a lot which bowel movement you scoop it from.

That study also found something useful about timing. Among people who responded by week 4, the two-item patient-reported outcome fell significantly from day 3, while calprotectin showed no significant reduction until week 2 (Toyonaga 2017). If you start a new treatment and retest after a week, a flat number is not evidence of failure. The marker is slower than you are.

Things that raise calprotectin that are not your colitis

Calprotectin measures neutrophils in the gut. It has no opinion about why they are there. The commonest confounders in ulcerative colitis are:

• Gut infections. In 153 children aged 3 months to 10 years with infectious diarrhoea, median calprotectin was 765 µg/g with Salmonella and 689 with Campylobacter, against 89 for rotavirus, 93 for norovirus and 95 for adenovirus (Chen 2012). That study was in children with infection, not adults with IBD, but the direction is the point: a bacterial gut infection produces numbers that look exactly like active colitis.
• Clostridioides difficile. This is worth its own line because it is both common and consequential in UC. A Finnish case-control study of 279 people with IBD and C. difficile infection found, from symptoms and calprotectin levels, that IBD activity was typically already raised in the three months before the infection. Recurrence occurred in 30% of episodes, and 79% of those with recurrent infection had ulcerative colitis. Corticosteroid use frequently preceded episodes, and in 30% of episodes no antibiotic exposure was recorded at all (Vitikainen 2025). So it runs both ways: active disease invites the infection, and the infection pushes the number up.
• NSAID painkillers. Faecal calprotectin was used to establish that NSAID enteropathy is common in the first place: among 312 people taking 18 different NSAIDs, mostly for rheumatoid arthritis and osteoarthritis, the prevalence of enteropathy by this method was 44% (Tibble 1999).
• Proton pump inhibitors, as above (Lundgren 2019).

This is why an IBD team faced with a sudden change in symptoms and a jump in calprotectin will usually want a stool pathogen panel, including C. difficile toxin, before assuming the disease itself has escalated.

The blood-in-the-sample question

A recurring claim in community threads is that visible blood or haemorrhoids inflate a calprotectin result. It appears alongside confident counter-examples in the same threads: people describing years of bleeding haemorrhoids with consistently normal results, and people whose numbers rose only after the bleeding stopped.

We looked for a study measuring the effect of luminal blood or haemorrhoidal bleeding on faecal calprotectin in people with UC and did not find one we could read, so we are not going to state a number in either direction. What can be said is the mechanism: calprotectin comes from neutrophils, and whole blood contains neutrophils, so contamination is biologically plausible, but the concentrations in an inflamed mucosa are far higher than in circulating blood. Treat the claim as unsettled. If you are bleeding, that is worth reporting to your IBD team regardless of what the stool test says.

A worked example: two people, both 450

Two people get an identical result on the same assay at the same laboratory in the same week.

Person A has proctitis diagnosed four years ago. Her last three results were 38, 52 and 61 over eighteen months. She has been well, but for the past fortnight she has had more urgency and streaks of blood twice.

Person B has pancolitis diagnosed eleven years ago, treated with a biologic. His last three results were 890, 520 and 470 over a year, falling steadily since a treatment change. He feels the best he has in two years and has no bleeding.

The same 450 means almost opposite things:

• For A, it is a seven-fold rise from her own baseline, in a disease extent where the ceiling is lower, alongside a symptom change. That combination is a reason to contact her IBD team this week.
• For B, it is the fourth consecutive fall, in a disease extent where the same amount of inflammation produces bigger numbers, alongside clinical improvement. It is consistent with a treatment that is working and has not finished working.

Neither reading comes from the number. Both come from the number plus the trend, the extent and the symptoms. This is the single most useful habit to build: your own previous results are the reference range that matters.

Does watching the number actually help?

Here is where the evidence diverges sharply from what most pages on this keyword imply.

The case for monitoring is genuinely good as prediction:

• In 79 people with clinically quiescent IBD followed for a year, median baseline calprotectin in ulcerative colitis was 220.6 µg/g in those who relapsed versus 67 in those who did not. In Crohn's disease, there was no difference at all between relapsers and non-relapsers (220.1 versus 220.5, p = 0.395) (Costa 2005).
• A meta-analysis of six prospective studies and 672 people with IBD found pooled sensitivity of 78% and specificity of 73% for predicting relapse, with an area under the summary ROC curve of 0.83 (Mao 2012).
• A systematic review of studies with repeated measurements found that asymptomatic people with two consecutive results above the study cutoff, tested one to three months apart, had a 53% to 83% probability of relapsing (Heida 2017).

The case for monitoring as an intervention is much weaker, and 2026 delivered the clearest test of it yet.

Two footnotes on that trial, in the interests of being straight about it. The primary endpoint was missed, and a missed primary endpoint is a miss, not a "trend". And the registry entry for the trial (NCT03549988, sponsored by the University of British Columbia with no listed industry collaborators) records 726 participants enrolled against the 716 in the paper; we could not reconcile that difference from the abstract, and it does not change the result.

What the trial does not show is that calprotectin is useless. It shows that handing people a test, without a rule for what happens when it is high, does not by itself change outcomes. Among the 88 participants who did change therapy after a confirmed elevated result, flare frequency was 49% versus 55%, a difference the trial was not powered to detect and which did not translate into a different flare risk (Rosenfeld 2026).

The honest summary: calprotectin is a good early-warning signal and a poor intervention on its own. What you and your team do with a rising number is where any benefit has to come from.

Home tests, and why the brand matters more than you would expect

Smartphone-read home calprotectin tests exist and are broadly accurate, within limits that are worth knowing.

A head-to-head study compared three home tests against their own manufacturers' ELISAs, using untrained medical students and four different phone models, across 1,440 smartphone readings and 120 ELISA tests. In the low range, at or below 500 µg/g, agreement was 87%, 82% and 76% for the three tests. Above 500 µg/g, agreement collapsed to 37%, 19% and 37%. Reading error rates differed by device, with 43% of errors on a single Android handset. The authors' conclusion was blunt: to avoid misreading changes over time, always use the home test and the companion ELISA from one and the same manufacturer (Haisma 2019).

A separate Canadian evaluation of one home test in 61 people with IBD found 88% agreement with laboratory ELISA on the same stool sample, with no qualitative false positives or negatives, and 79% of participants finding it easy to use (Moore 2019). That study evaluated a single manufacturer's device; we did not read its funding statement, and one of its authors also led the 2026 monitoring trial above, so treat it as evidence about usability and agreement rather than about clinical benefit.

The practical upshot: home testing is reasonable for tracking a value in the lower range, where treatment decisions in remission are usually made. It is least reliable exactly where the numbers are most alarming.

Why a colonoscopy is still on the plan

People sometimes hope a good calprotectin will let them skip a scope indefinitely. In symptomatic remission, guidelines do support using a biomarker to avoid routine endoscopy (Singh 2023). That is not the same as replacing colonoscopy altogether, for two reasons.

Surveillance is looking for something else. Ulcerative colitis carries an increased risk of colorectal cancer, roughly 1.7-fold higher than the general population, with a risk of about 4.5% after 20 years of disease, and colonoscopy for dysplasia surveillance is recommended from about eight years after diagnosis (Gros 2023). Calprotectin measures neutrophils. Dysplasia is not neutrophils. A perfect stool result tells you nothing about it. If you are due a scope, the colonoscopy preparation guide covers the practical side, including how prep differs when you have IBD.

Calprotectin's accuracy is moderate at the strictest targets. As the pooled analysis above showed, the AUC for separating a Mayo endoscopic score of 0 from anything higher was 0.716 (Dube 2026). When the question is deep healing rather than obvious activity, the stool test is helping, not deciding.

There are non-invasive tools that add to it. A small prospective cohort of 29 paired same-day assessments found that intestinal ultrasound activity was associated with histological activity, and that a composite of ultrasound plus calprotectin predicted histological activity accurately in 88% of cases, better than either alone, although its negative predictive value was only 57% (Goodsall 2024). Twenty-nine cases is small, and ultrasound access varies enormously by country, so treat that as a direction of travel rather than a current standard.

How to read your own run of numbers

None of the above is much use unless it changes what you do with the result when it lands. A short protocol that respects what the evidence actually supports:

1. Write down which laboratory and, if your report states it, which assay. If either changes, your series has a break in it and old numbers are not directly comparable.
2. Record the collection conditions you can control. Which bowel movement of the day, and how long the sample sat before it reached the lab. Concentrations were stable at room temperature for three days but had fallen by a mean of 28% at seven days (Lasson 2015).
3. Log a symptom snapshot on the same day. Stool frequency against your own normal, and whether there was blood. Those two items are what the PRO-2 score is built from, and how PRO-2 is calculated and what it misses is worth understanding before you pair it with a lab value.
4. Compare with your own last two or three results, not with a population range. A doubling from your own baseline is more informative than crossing an arbitrary line.
5. Repeat before you react. Given within-day coefficients of variation of 40% to 52% in active disease, a single unexpected result is a prompt to test again, not a verdict (Calafat 2015, Lasson 2015).
6. Take the series to the appointment, not the single value. A trend line with dates, your stool frequency and blood days, and which lab did each test, is far more use in a ten-minute slot than one number read aloud.

Clairop's visit report is built for that last step: it puts your activity score trend, your movements per day against your own baseline, days with blood and your lab results on a single page, with a note above the numbers saying the data was entered by you rather than measured in clinic. You can see how that is assembled on the how it works page.

Myths about calprotectin numbers

"Anything above 50 means my UC is active." Fifty is a screening threshold derived from healthy populations and older assays. On a modern assay in a healthy middle-aged cohort, the upper reference limit was below 199 with an extraction device (Fall 2017), and 36% of people with a completely normal colonoscopy were above 50 (Lundgren 2019).

"My 800 is worse than their 400, so I am sicker." Not necessarily. Disease extent alone shifted medians from 440 in proctitis to 1,690 in pancolitis among people with the same category of endoscopic activity (Steinsbo 2025), and different assays can differ five-fold (Labaere 2014).

"A normal calprotectin means nothing else can be wrong." It means neutrophil-driven gut inflammation is unlikely at that moment. It does not address fatigue, anaemia, joint symptoms, bile acid diarrhoea, an overlapping functional disorder or dysplasia. Persistent fatigue during remission in particular usually has explanations other than hidden inflammation.

"Food I ate must have pushed the number up." There is no good evidence that a single meal moves faecal calprotectin. Over years, habitual diet has been linked to flare risk in UC, and the evidence on that is covered in can food trigger a UC flare. A day's eating is not what your stool test is registering.

"If the number is dropping I can stop my maintenance treatment." A falling number is usually evidence that the treatment is doing its job, which is a reason to continue it rather than stop it. Any change to maintenance therapy is a conversation with your IBD team, never something to do on the strength of a stool test.

"Calprotectin replaces colonoscopy." It can reduce routine endoscopy in symptomatic remission (Singh 2023), but it cannot detect dysplasia, which is the point of surveillance colonoscopy in longstanding UC (Gros 2023).

When to see a doctor promptly

A calprotectin result never overrides how you are actually doing. Contact your IBD team promptly if you have:

• New or increasing blood in your stool, or blood that has returned after a period without it
• Unexplained weight loss
• Fever alongside a change in bowel symptoms
• Night-time symptoms that wake you from sleep
• Symptoms of anaemia such as breathlessness on stairs, unusual pallor or a racing heart
• Severe or persistent abdominal pain
• New symptoms starting after the age of 50, or a family history of bowel cancer or IBD, if these have not already been assessed
• Diarrhoea starting after a course of antibiotics or a hospital stay, which raises the possibility of C. difficile (Vitikainen 2025)

Seek same-day help for more than six bloody stools a day with fever, a racing heart, faintness or severe abdominal pain.

On the test itself, contact your team rather than waiting for the next routine appointment if a result has risen substantially above your own usual range, if two consecutive results are raised, or if a result is raised and your symptoms have changed. Two consecutive elevated results in an asymptomatic person carried a 53% to 83% probability of relapse in the studies reviewed (Heida 2017), which is a good reason for a conversation.

This guide describes what published research shows about a laboratory measurement. It is not a substitute for your own IBD team, who have your history, your disease extent, your previous results and your endoscopy findings, none of which a general article can have.

The honest bottom line

A faecal calprotectin number in ulcerative colitis is an estimate of how much neutrophil traffic is crossing into your bowel, diluted into whatever you produced that day. It is the best non-invasive marker available for colonic inflammation, more sensitive than CRP and better in UC than in Crohn's (Mosli 2015). It is also noisier and more context-dependent than the confident tables on most pages suggest.

Higher does mean more inflamed surface on average (Schoepfer 2013), but the value shifts with how much colon is involved (Steinsbo 2025), with which assay ran it (Labaere 2014, Lin 2022), and with which bowel movement you sampled (Calafat 2015, Lasson 2015). The threshold for "remission" is not one number but at least four, depending on whether you mean symptoms, endoscopy, histology or the strictest version of each (Dube 2026, Theede 2016).

And the thing most pages assert, that keeping an eye on your calprotectin keeps you out of flares, is exactly what the largest randomised trial in ulcerative colitis failed to show: 32% flared in both arms, with a hazard ratio of 1.05 (Rosenfeld 2026). The test earns its place as an early warning that something is changing before you feel it. What happens next is a decision, and decisions are made by you and your IBD team, not by a stool sample.