What can falsely elevate calprotectin?

Calprotectin is a protein measured in stool to estimate inflammation in the digestive tract. It can help distinguish inflammatory conditions from functional bowel disorders and guide monitoring over time. But calprotectin results can be confusing: non-inflammatory issues, recent infections, medications, age, and even test variability can all push levels up without indicating chronic disease. This article explains what calprotectin is, why it rises, and what can falsely elevate calprotectin. You’ll learn how to interpret results in context, how the gut microbiome fits into the picture, and when additional evaluation—such as microbiome testing—may clarify what your numbers really mean.

Understanding Calprotectin: The Key Marker in Gut Health

What Is Calprotectin? Definitions and Biological Role

Calprotectin is a calcium- and zinc-binding protein (S100A8/A9) abundant in neutrophils, a type of white blood cell. When neutrophils migrate to the intestinal lining during inflammation, calprotectin is released into the gut lumen and becomes detectable in stool. Calprotectin has antimicrobial properties and participates in innate immune responses by limiting microbial access to trace metals and modulating inflammatory signaling. Because it is stable in feces for several days at room temperature, it serves as a practical, noninvasive marker of neutrophil-driven intestinal inflammation.

How Calprotectin Serves as an Indicator of Gut Inflammation

Fecal calprotectin reflects the degree of neutrophil activity at the mucosal surface. Elevated concentrations typically indicate mucosal inflammation originating from the intestine, not from systemic inflammation elsewhere. Unlike blood markers such as C-reactive protein, stool calprotectin is localized to the gut and tends to rise in conditions with epithelial disruption or active immune responses within the gastrointestinal tract, particularly the colon. In clinical practice, it helps distinguish inflammatory bowel diseases (IBD) such as Crohn’s disease and ulcerative colitis from non-inflammatory disorders like irritable bowel syndrome (IBS), where levels are usually normal or only slightly elevated.

The Standard Use of Calprotectin Testing in Clinical Practice

Clinicians order fecal calprotectin to support diagnostic decision-making when patients present with gastrointestinal symptoms. Common laboratory cutoffs (which vary by lab and patient age) often categorize results as: low/normal (<50 µg/g in many adult labs), borderline or indeterminate (50–200 µg/g), and elevated (>200–250 µg/g), where higher levels increase the likelihood of significant intestinal inflammation. Calprotectin is also used to monitor disease activity and response to therapy in known inflammatory conditions, assisting with decisions about escalating or de-escalating treatment. However, a single number rarely tells the full story; timing, context, and potential confounders matter.

Why Accurate Interpretation of Calprotectin Matters for Gut Health

Symptoms and Signals Associated with Elevated Calprotectin Levels

People with elevated fecal calprotectin may report abdominal pain, urgent or frequent bowel movements, diarrhea, visible or microscopic blood in stool, bloating, unintentional weight loss, fatigue, or low-grade fevers. Yet symptoms alone are imperfect guides. Some individuals with IBS can experience significant pain and diarrhea with normal calprotectin, while others with mild inflammation might notice few symptoms. Accurate interpretation of calprotectin requires integrating symptoms, test timing, age, recent infections, medication exposure, and comorbidities alongside other lab or imaging findings.

Differentiating inflammatory from non-inflammatory causes is essential. In IBD, active inflammation typically drives both symptoms and elevated calprotectin. In functional disorders such as IBS, calprotectin tends to remain low. Infections, polyps, diverticulitis, microscopic colitis, or celiac disease may elevate levels as well—often transiently or in patterns different from chronic IBD. Recognizing this nuance helps avoid over- or underestimating risk.

The Impact of Elevated Calprotectin on Diagnostic Decisions

Persistently high calprotectin generally prompts further evaluation, which may include repeat testing, stool cultures, celiac serology, imaging, or endoscopy. Elevated levels can support a working diagnosis of IBD or other inflammatory conditions, and a downward trend often reflects improvement. However, the differential diagnosis remains broad. For example, elevated levels after a bout of gastroenteritis are common and may not represent chronic disease. Likewise, medication exposures (notably nonsteroidal anti-inflammatory drugs, or NSAIDs) can transiently raise calprotectin. Knowing when to wait, repeat, or expand testing reduces unnecessary procedures while capturing clinically important disease.

The Pitfalls of Relying Solely on Calprotectin Results

Individual Variability and Uncertain Significance of Elevated Levels

Interpreting calprotectin is complicated by biological variability. Calprotectin levels can fluctuate day to day by 20–40% in the same person, and values differ among laboratories and assay kits. Age plays a role: infants and toddlers naturally have higher baseline levels, and older adults can run slightly higher than younger adults. Stool consistency can affect extraction and measured concentration. A “borderline” value in one setting may be normal or elevated in another. Repeating the test and considering trends is often more informative than acting on one isolated measurement.

Common Causes of Elevated Calprotectin Beyond Inflammatory Conditions

Not all elevations signal chronic inflammatory disease. Transient infections, recent antibiotic-associated dysbiosis, strenuous endurance exercise, NSAID-related mucosal injury, gastrointestinal bleeding from non-inflammatory sources, colorectal neoplasia, diverticulitis, or even recent invasive procedures can push values upward. In these scenarios, calprotectin is acting as a sensitive barometer of mucosal stress or neutrophil presence—not necessarily as a specific indicator of IBD. Recognizing fecal calprotectin false positives is crucial to avoid unnecessary alarm or invasive testing.

Calprotectin Levels Misinterpretation—Potential Diagnostic Pitfalls

Misinterpretation happens in two directions. First, calprotectin levels misinterpretation can lead to overattributing a moderate rise to IBD when an infection or medication effect is more plausible. Second, a mild result might be dismissed in someone with concerning symptoms and weight loss, leading to delayed evaluation. Calprotectin diagnostic pitfalls also arise from using a single cutoff across all ages or from assuming that normalization always equals remission (steroids, for example, may lower calprotectin rapidly but not address underlying drivers in every case). The key is context, clinical judgment, and sometimes additional testing.

Understanding False Elevations: What Can Falsely Elevate Calprotectin?

Factors Contributing to Fecal Calprotectin False Positives

Several scenarios can produce elevated calprotectin without indicating chronic inflammatory bowel disease. While these elevations often reflect some degree of mucosal irritation or neutrophil activity, they can be considered “false positives” with respect to IBD suspicion. Common contributors include:

• Recent gastrointestinal infections: Bacterial enteritis (e.g., Salmonella, Campylobacter), viral gastroenteritis, or Clostridioides difficile can cause marked, short-lived increases. Levels typically trend down as the infection resolves.
• Use of NSAIDs: Agents like ibuprofen, naproxen, or diclofenac can injure the small bowel and colon mucosa, leading to raised calprotectin. Even short courses may affect results in susceptible individuals.
• Proton pump inhibitors (PPIs): Some studies, particularly in pediatric populations, suggest PPIs may be associated with higher calprotectin, potentially via microbiome shifts or subtle mucosal effects. The signal is inconsistent in adults, but PPIs are a potential confounder.
• Recent antibiotic use: Antibiotics can disrupt the microbiome (dysbiosis), occasionally triggering transient inflammation or overgrowth by opportunistic microbes, which may raise calprotectin for weeks.
• Strenuous exercise and heat stress: Endurance events can transiently increase gut permeability (“leaky gut”), enabling neutrophil activation and elevated calprotectin in the days after intense exertion.
• Gastrointestinal bleeding: Bleeding due to hemorrhoids, fissures, or upper GI sources does not always increase calprotectin by itself, but mucosal injury causing neutrophil recruitment can. Contamination with menstrual blood is best avoided when collecting a sample.
• Age-related variation: Infants and young children naturally have higher baselines, and older adults can show modest elevations even without overt disease. Lab-specific pediatric cutoffs and age interpretation are essential.
• Non-IBD inflammatory conditions: Diverticulitis, celiac disease, microscopic colitis, colorectal cancer or polyps, radiation proctitis, and ischemic colitis can all raise levels, often variably and sometimes transiently.
• Recent colonoscopy, biopsies, or bowel infections: Mucosal manipulation or residual inflammation post-procedure may temporarily elevate readings.

It is worth noting that corticosteroids usually decrease inflammation and tend to lower calprotectin rather than elevate it. If anything, they can mask active disease and contribute to false reassurance (a different pitfall addressed below).

External Influences and Technical Limitations: Assay Interference and Testing Variability

Beyond biology, measurement issues can influence results. Pre-analytical factors—such as stool sampling from a highly watery area, prolonged delays before extraction in very hot conditions, or inconsistent sample mass—can alter measured concentration. Inter-assay variability among different calprotectin kits is well-documented; numeric values can differ despite representing a similar inflammatory state. This leads to potential calprotectin assay interference and testing variability, especially when patients switch labs.

Other sources of variability include:

• Extraction device differences: Home collection tubes and extraction kits can produce small but meaningful variation in recovery.
• Diarrheal dilution: Watery stools dilute concentration, potentially underestimating peaks or, conversely, producing uneven distribution of calprotectin within the sample.
• Heterogeneity within a single stool: Calprotectin can vary across different parts of the same bowel movement; repeat or composite sampling improves reliability.
• Inter-laboratory calibration: Not all labs align to identical standards. Tracking trends is most accurate when using the same laboratory and assay method over time.

Common Misinterpretations and the Need for Contextual Analysis

Common misinterpretations include assuming that any elevation equals IBD, or that a normal result excludes all important disease. Some infections can generate very high values; conversely, segmental small bowel inflammation may yield less dramatic rises. A single borderline result after a viral illness may not justify invasive testing, whereas persistent values above lab thresholds with alarm features (e.g., bleeding, weight loss) typically warrant further evaluation. Interpreting calprotectin wisely means triangulating between clinical features, repeat measurements, age-appropriate cutoffs, and potential confounders such as medications and exercise habits.

The Role of the Gut Microbiome in Calprotectin Levels and Gut Inflammation

How Microbiome Imbalances Contribute to Gut Inflammation and Elevated Calprotectin

The gut microbiome—trillions of microbes and their genes—plays a central role in immune education, epithelial barrier maintenance, and metabolic signaling. When this ecosystem is disrupted (dysbiosis), the mucosal immune system may respond with heightened vigilance, recruiting neutrophils and increasing calprotectin. Dysbiosis can be triggered by infections, antibiotics, dietary shifts, stress, or medications like PPIs, and can persist even after an acute trigger is gone.

Mechanistically, an imbalanced microbiome may increase production of pro-inflammatory metabolites, reduce short-chain fatty acid (SCFA) levels that normally nourish colonocytes, and compromise tight junction integrity. Microbial overgrowth in the small intestine (SIBO), colonization by pathobionts, or loss of keystone commensals can complicate symptoms and mimic inflammatory disorders. The result may be mild to moderate calprotectin elevations that sit in the “borderline” range, obscuring whether findings reflect transient dysbiosis or a chronic immune-mediated disease.

The Spectrum of Microbiome-Related Factors That May Mimic or Mask Inflammatory Conditions

Microbiome-related changes can both mimic and mask inflammation:

• Post-infectious states: After gastroenteritis, altered microbial communities can sustain symptoms like bloating, urgency, and loose stools even as overt inflammation wanes. Calprotectin may remain mildly elevated.
• Opportunistic overgrowth: Certain taxa can drive low-grade immune activation and barrier dysfunction. The pattern may resemble IBD in symptoms yet yield lower calprotectin peaks.
• Antibiotic-associated dysbiosis: Reduced diversity and loss of beneficial bacteria can prolong recovery and produce lingering GI symptoms with borderline calprotectin.
• Protective microbiome patterns: Conversely, robust SCFA-producers and balanced microbial communities may keep calprotectin low even when symptoms stem from non-inflammatory mechanisms like visceral hypersensitivity (as in IBS).

Understanding these nuances helps explain why people with similar symptoms can have very different calprotectin readings—and why results sometimes appear to “contradict” how a person feels on a given day.

Leveraging Microbiome Testing to Clarify Calprotectin Interpretation

Why Microbiome Testing Offers Valuable Diagnostic Insights

Because symptoms do not always reveal the root cause, complementary stool microbiome testing can provide context for confusing calprotectin results. By profiling microbial diversity, relative abundance, potential pathogens, and functional potentials (e.g., SCFA pathways, bile acid metabolism), testing can highlight whether dysbiosis or specific microbial patterns may contribute to symptoms and low-grade inflammation. This is especially valuable when calprotectin is persistently borderline, fluctuates widely without an obvious trigger, or remains elevated after an infection has clinically resolved.

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Microbiome analysis does not diagnose IBD or replace clinical evaluation. Instead, it offers an additional lens to interpret what calprotectin might be “detecting,” uncovering hidden drivers such as opportunistic overgrowth, reduced beneficial species, or patterns consistent with post-infectious states. For readers seeking structured insight, see how a dedicated microbiome test can complement calprotectin trends by identifying microbial imbalances that might explain subtle inflammation or ongoing digestive symptoms.

What a Microbiome Test Can Reveal in the Context of Elevated Calprotectin

In individuals with elevated or borderline calprotectin, stool microbiome testing may reveal:

• Reduced diversity: Lower microbial richness has been linked to barrier dysfunction and susceptibility to inflammation.
• Opportunistic or pathogenic taxa: Findings suggestive of recent or smoldering infection, or overgrowth that could sustain symptoms and inflammatory signaling.
• Functional deficits: Diminished SCFA-related microbes or pathways potentially associated with impaired mucosal nutrition and resilience.
• Signs of dysbiosis from medications: Patterns sometimes seen with repeated antibiotic courses or prolonged acid suppression, which can align with calprotectin fluctuations.

While not diagnostic, these insights create a more complete picture—guiding discussions with healthcare professionals about whether a transient cause is likely, if retesting timing should change, or if further conventional evaluation is warranted.

Who Should Consider Microbiome and Gut Testing?

Individuals with Repeatedly Elevated Calprotectin Yet Unclear Diagnosis

When calprotectin remains elevated without a clear structural explanation on imaging or endoscopy, microbiome profiling may help identify dysbiosis or overlooked infectious contributors. A data-informed approach reduces guesswork about whether levels represent inflammation-in-transition versus an ongoing stimulus from the microbial environment.

Patients with Symptoms Suggestive of Gut Issues but Inconclusive Standard Tests

People with bloating, abdominal discomfort, and irregular stools may have normal or borderline calprotectin. In such cases, microbiome testing can uncover patterns consistent with functional disturbances, post-infectious changes, or small intestinal overgrowth that may not be visible on standard tests. A noninvasive test can add clarity before deciding on more invasive procedures.

Those Who Want to Understand and Support Their Gut Microbiome for Better Digestive Health

Even without a clinical diagnosis, some individuals prefer a proactive, personalized perspective. Identifying microbial imbalances or strengths can guide discussions about diet, lifestyle, and monitoring strategies with a clinician. For an example of how structured stool profiling can inform these conversations, consider stool microbiome testing as an educational tool to contextualize calprotectin and symptom patterns over time.

Situations Where Microbiome Testing Adds Diagnostic Confidence and Guides Management

Microbiome testing adds value when standard results are ambiguous, when symptoms persist despite otherwise “normal” studies, or when fluctuations in calprotectin do not fit clinical impressions. By characterizing the gut ecosystem, clinicians and patients can better judge whether the next step is watchful waiting, retesting at a different interval, or coordinating additional targeted investigations.

Decision Support: When to Pursue Further Testing for Better Clarity

Indicators That Calprotectin Results May Be Misleading

Consider a broader workup or repeat testing if:

• Persistent symptoms despite normal or borderline calprotectin: Weight loss, blood in stool, anemia, or nocturnal diarrhea warrant attention regardless of calprotectin.
• Confounding factors are present: Recent infections, NSAID or PPI use, heavy endurance exercise, or recent antibiotics can distort results. Temporary discontinuation (if safe and advised by a clinician) and retesting may clarify the picture.
• Age or assay differences complicate interpretation: Pediatric and older adult cutoffs vary; switching labs mid-evaluation can shift numeric ranges and complicate comparisons.
• Post-procedural timing is suboptimal: Testing too soon after colonoscopy, biopsy, or gastroenteritis may capture transient elevations.

Integrating Microbiome Testing into the Diagnostic Roadmap

When uncertainty persists, integrating stool microbiome analysis with calprotectin can yield a more nuanced view. For example, a borderline calprotectin result alongside evidence of low microbial diversity and recent antibiotic exposure may support retesting after a defined interval rather than immediate invasive studies. In contrast, high or rising calprotectin with concerning symptoms should prompt standard medical evaluation regardless of microbiome findings. To see what such an approach entails in practice, review a comprehensive microbiome analysis that can be interpreted alongside clinical history and lab trends.

Collaboration with healthcare providers remains essential. Microbiome insights are most useful when integrated thoughtfully with clinical assessment, imaging, and, when indicated, endoscopy. A careful, stepwise plan reduces both missed conditions and unnecessary procedures.

Practical Guidance: Minimizing False Positives and Making Sense of Results

Before Testing: How to Plan for a Clearer Readout

• Discuss medications: Ask your clinician whether NSAIDs or PPIs could be paused safely before testing. Never stop prescribed medications without medical guidance.
• Time your test appropriately: If possible and safe, avoid testing during acute gastroenteritis or immediately after colonoscopy/biopsy; retest after recovery for baseline assessment.
• Consider activity: Avoid unusually strenuous endurance exercise in the day or two before sampling.
• Sample handling: Follow instructions carefully. Avoid contamination with urine or menstrual blood and ensure proper storage and mailing as directed by the lab.

After Testing: Interpreting Results in Context

• Look at trends, not just one value: A single borderline result may be less meaningful than a persistent rise over time.
• Align with symptoms: Discrepancies between how you feel and what the number shows are signals to reassess timing, confounders, or add complementary testing.
• Account for age and lab-specific ranges: Pediatric and older adult values require age-appropriate interpretation; try to use the same lab for repeat tests.
• Use a decision tree: High or rising levels with alarm features usually mean timely medical evaluation. Borderline levels after infection may justify watchful waiting and repeat testing.

Case Scenarios: How False Elevations Can Appear

Post-Marathon Spike

A healthy adult runs an ultramarathon, develops two days of diarrhea and cramps, and tests fecal calprotectin at 220 µg/g. With rest and hydration, symptoms resolve and calprotectin falls to 45 µg/g two weeks later. The initial elevation likely reflects exercise-induced permeability and transient inflammation—not chronic disease.

NSAID-Related Elevation

An individual uses high-dose NSAIDs for a musculoskeletal injury and has calprotectin of 180 µg/g. After discontinuation (under medical guidance) and two weeks of recovery, calprotectin drops to 60 µg/g. The transient rise is medication-related rather than IBD.

Post-Infectious Borderline Results

Following bacterial gastroenteritis, calprotectin measures 260 µg/g, then 120 µg/g at four weeks, and 75 µg/g at eight weeks, with lingering bloating. Microbiome testing shows reduced diversity and low SCFA-associated taxa consistent with post-infectious dysbiosis. Gradually improving trends and contextual data guide conservative follow-up rather than immediate invasive testing.

How the Microbiome Shapes Personalized Gut Health

Why Symptoms Don’t Always Reveal the Root Cause

Abdominal pain, diarrhea, and bloating can arise from many mechanisms: active mucosal inflammation, altered motility, visceral hypersensitivity, bile acid malabsorption, or microbial imbalance. Two people with similar symptoms may have very different underlying biology. Calprotectin helps narrow the field, but borderline or inconsistent results leave questions. Guesswork can prolong frustration and delay targeted care.

How Microbiome Testing Provides Deeper Insight

By evaluating the gut’s microbial community, stool testing brings otherwise hidden patterns to light—dysbiosis, overgrowth, or loss of beneficial fermenters—that can explain low-grade inflammation or non-inflammatory symptoms. These insights are educational, helping individuals and clinicians choose whether to retest calprotectin later, pursue additional conventional diagnostics, or focus on supportive strategies appropriate to the clinical context. For those exploring a data-informed approach, microbiome testing can anchor conversations about what your calprotectin result may mean for your unique gut ecosystem.

Conclusion: Moving Toward Personalized Understanding of Gut Health

Calprotectin is a valuable, noninvasive marker of intestinal inflammation, but its interpretation is nuanced. Elevated results can reflect many situations—from recent infections and medications to age-related differences and benign, transient mucosal stress. Understanding potential false elevations and calprotectin diagnostic pitfalls reduces unnecessary alarm and helps direct appropriate follow-up. The gut microbiome adds another dimension, clarifying whether dysbiosis or post-infectious changes may be driving symptoms or subtle inflammatory signals.

Personalized interpretation—incorporating clinical features, repeat measurements, age-specific ranges, and microbiome context—builds trust in the numbers and supports better decision-making. When used thoughtfully, calprotectin and complementary tools can guide a clear, stepwise path to understanding what’s happening in the gut and how to navigate the next, most appropriate step.

Key Takeaways

• Calprotectin is a stool marker of neutrophil-driven gut inflammation; it’s helpful but not definitive on its own.
• False or misleading elevations can occur with infections, NSAID use, strenuous exercise, age-related variation, and recent procedures.
• Assay variability and sampling issues can influence results; repeat testing and using the same lab improve reliability.
• Non-IBD conditions (diverticulitis, celiac disease, microscopic colitis, colorectal neoplasia) can elevate calprotectin.
• Corticosteroids typically lower calprotectin and can mask active disease, contributing to false reassurance.
• Symptoms alone don’t define the cause; borderline values should be interpreted in clinical context.
• The microbiome can drive or dampen mucosal inflammation; dysbiosis may sustain borderline elevations.
• Microbiome testing is an educational tool that adds context to ambiguous calprotectin readings.
• When calprotectin and symptoms disagree, a stepwise plan—considering timing, confounders, and complementary tests—is best.
• Personalized assessment, not one-size-fits-all cutoffs, leads to more accurate and actionable insights.

Q&A

What does calprotectin measure exactly?

Calprotectin is a protein released by neutrophils during intestinal inflammation. Measuring it in stool provides a noninvasive estimate of mucosal immune activity, especially in the colon. High levels suggest active neutrophil presence in the gut lining.

What can falsely elevate calprotectin besides IBD?

Common non-IBD contributors include recent gastroenteritis, NSAID use, strenuous endurance exercise, diverticulitis, colorectal polyps or cancer, microscopic colitis, celiac disease, and age-related variations. PPIs and recent antibiotics may also play a role through microbiome changes.

Do proton pump inhibitors really raise calprotectin?

Evidence is mixed. Some studies—more so in children—report higher levels with PPIs, potentially related to microbiome shifts or subtle mucosal effects. In adults, the association is less consistent. If results are unclear, discuss timing and potential retesting with your clinician.

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Can gastrointestinal bleeding alone increase calprotectin?

Bleeding without mucosal inflammation does not always raise calprotectin, because the marker reflects neutrophil activity, not red blood cells. However, many causes of GI bleeding involve mucosal injury and neutrophil recruitment, which can elevate levels.

How reliable is a single calprotectin test?

It’s informative but imperfect. Biological variability, sampling differences, and inter-lab assay variability can shift values by 20–40%. Trends over time and clinical context are more reliable than a single measurement.

What are typical cutoffs for adults?

Many labs consider <50 µg/g normal, 50–200 µg/g borderline, and >200–250 µg/g suggestive of active inflammation. Cutoffs vary by laboratory and assay, and pediatric ranges are higher. Always interpret results using your lab’s reference intervals.

Should I stop NSAIDs before testing?

NSAIDs can raise calprotectin in some people. Do not stop any medication without medical advice, but discuss with your clinician whether a pause is appropriate and safe before testing or retesting to reduce confounding.

How soon after an infection should I test or retest?

Calprotectin can remain elevated for weeks after gastroenteritis. If clinically safe, retesting 2–8 weeks after symptom resolution can yield a more stable baseline. The exact timing depends on severity, ongoing symptoms, and clinical guidance.

Can exercise affect calprotectin results?

Yes. Intense endurance exercise can transiently increase intestinal permeability and raise calprotectin for a short period. Avoid unusually strenuous activity immediately before sampling when possible.

Where does the microbiome fit into calprotectin interpretation?

Microbiome composition influences barrier function and immune tone. Dysbiosis can perpetuate low-grade inflammation, yielding borderline or fluctuating calprotectin levels, while balanced microbiota may correspond with normal levels even when symptoms stem from non-inflammatory mechanisms.

How can microbiome testing help if my calprotectin is borderline?

Microbiome testing can reveal dysbiosis, potential pathogens, or functional deficits (like low SCFA-associated microbes) that provide context for borderline results. These insights can guide discussions about retesting and whether to pursue further evaluation.

Does a normal calprotectin rule out all important disease?

No. While a normal result lowers the likelihood of active mucosal inflammation, it doesn’t exclude all conditions. Alarm features—such as rectal bleeding, anemia, or significant weight loss—warrant medical evaluation regardless of calprotectin.

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