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GastroAGI flagship

1
MASLD–MASH NITIntegrated non-invasive assessment of MASLD fibrosis and at-risk MASH — FIB-4, APRI, NFS, FAST, Agile 3+, Agile 4, ELF and ADAPT in one pass

Most used

21
MELD-NaAssesses the severity of chronic liver diseaseChild-Pugh ScoreAssesses the prognosis of chronic liver disease, mainly cirrhosisFIB-4 IndexLiver fibrosis scoring indexAPRIAST to platelet ratio — liver fibrosisMaddrey's DFAlcoholic hepatitis severityGlasgow-BlatchfordUpper GI bleed risk stratificationGAHSGlasgow alcoholic hepatitis scoreMontreal IBDIBD classification — CD & UCMayo ScoreUlcerative colitis activityBISAP ScoreBedside index for severity of pancreatitisCLIF-SOFAOrgan failure scoring in cirrhosisAlcohol ContentStandard drinks & alcohol grams calculatorAARC-ACLFAcute-on-chronic liver failure gradePELD / CR ScorePediatric end-stage liver diseaseHarvey-BradshawCrohn's disease activity indexCTSICT severity index — pancreatitisRockall ScoreGI bleed rebleeding & mortality riskCAGEAlcohol use disorder screening (4 questions)MELD 3.0Updated MELD — sex-inclusive formulaAUDIT ScoreAlcohol use disorders identification testVOCAL-Penn ScorePost-operative mortality risk in cirrhosis surgery

Liver & Cirrhosis

17
ALBI GradeAlbumin-bilirubin liver function grade in HCCUKELD ScoreUK model for end-stage liver diseaseMELD-XIMELD excluding INR — for anticoagulated patientsWest Haven CriteriaHepatic encephalopathy gradingMilan CriteriaLiver transplant eligibility in hepatocellular carcinomaLI-RADS v2018 (CT/MRI)Liver observation category from size, APHE and major featuresBCLC StagingHepatocellular carcinoma stage and treatment allocationSimplified AIH CriteriaSimplified criteria for autoimmune hepatitisRevised Original AIH ScoreIAIHG 1999 comprehensive autoimmune hepatitis scoreSAAGSerum-ascites albumin gradient — cause of ascitesR FactorHepatocellular vs cholestatic pattern in liver injuryCLIF-C ACLFMortality prediction in acute-on-chronic liver failureKing's College CriteriaTransplant criteria in acute liver failureGALAD ScoreHCC detection from gender, age, AFP-L3, AFP and DCPMetroticket 2.0AFP-adjusted up-to-seven for HCC transplant eligibilityRUCAMCausality in drug- and herb-induced liver injuryBaveno VII CriteriacACLD, CSPH and sparing screening endoscopy

Fibrosis & MASLD

8
NAFLD Fibrosis ScoreAdvanced fibrosis probability in MASLD/NAFLDBARD ScoreBMI, AST/ALT ratio, diabetes — MASLD fibrosisFatty Liver IndexPredicts hepatic steatosis from routine labsFibrotic NASH Index (FNI)At-risk NASH probability from AST, HbA1c and HDLNAFLD Activity Score (NAS)Histologic activity grade — steatosis, inflammation, ballooningMEFIB IndexMRE + FIB-4 rule for significant fibrosis (≥F2) in MASLDFAST ScoreFibroScan-AST — at-risk NASH from LSM, CAP and ASTSAFE ScoreSteatosis-Associated Fibrosis Estimator for MASLD in primary care

Pancreas & Biliary

8
Ranson's CriteriaAcute pancreatitis severity at 48 hoursGlasgow-Imrie CriteriaAcute pancreatitis severity — the PANCREAS criteriaHAPSHarmless acute pancreatitis scoreTokyo Guidelines — CholangitisTG18 diagnosis and severity grade for acute cholangitisTokyo Guidelines — CholecystitisTG18 diagnosis and severity grade for acute cholecystitisBiliary Pain (Rome IV)Rome IV — defining biliary-type pain before interventionFunctional Pancreatic SODRome IV — pancreatic sphincter of Oddi disorderRevised Atlanta ClassificationAcute pancreatitis severity — mild, moderately severe, severe

IBD

9
Truelove & Witts CriteriaAcute severe ulcerative colitis — admission decisionUCEISUlcerative colitis endoscopic index of severitySCCAISimple clinical colitis activity index — symptoms onlyCDAICrohn's disease activity index — the trial standardSES-CDEndoscopic severity in Crohn's diseasePUCAIPaediatric ulcerative colitis activity indexTravis (Oxford) CriteriaDay 3 colectomy risk in acute severe ulcerative colitisHo IndexDay 3 steroid failure risk in acute severe ulcerative colitisRutgeerts ScorePostoperative Crohn's recurrence at ileocolonoscopy

GI Bleeding

7
EVendo ScorePredicts oesophageal varices needing treatmentForrest ClassificationPeptic ulcer bleeding — rebleeding risk at endoscopyAIMS65 ScoreUpper GI bleed mortality — five bedside criteriaOakland ScoreSafe-discharge risk for acute lower GI bleedingABC ScoreAge, blood tests, comorbidities — GI bleed mortalitySarin ClassificationEndoscopic classification of gastric varicesEGUS (Gastric Ulcer)Malignancy risk in a gastric ulcer, and who needs repeat endoscopy

Alcohol

2
ABIC ScoreAge, bilirubin, INR, creatinine — alcoholic hepatitisLille ModelSteroid response at day 7 in alcoholic hepatitis

Upper GI

4
Chicago Classification v4.0Oesophageal motility pattern from high-resolution manometryLA Classification (Oesophagitis)Los Angeles grade A–D for erosive oesophagitisPrague C & M CriteriaCircumferential and maximal extent of Barrett's oesophagusEREFS (Eosinophilic Oesophagitis)Endoscopic reference score — oedema, rings, exudates, furrows, stricture

Colorectal

3
Boston Bowel Prep ScaleColonoscopy preparation adequacy by segmentStool Osmotic GapOsmotic vs secretory diarrhoea from stool electrolytesATLAS Score (C. difficile)Predicted response to therapy in Clostridioides difficile infection

Functional GI

37
Bristol Stool ScaleStool form types 1–7 and colonic transitRome IV Criteria for IBSIrritable bowel syndrome diagnosis and subtypeFunctional ConstipationRome IV — two of six items, IBS excludedOpioid-Induced ConstipationRome IV — constipation tied to opioid therapyFunctional DiarrhoeaRome IV — loose stools without predominant painFunctional Bloating / DistensionRome IV — bloating without other bowel disorder criteriaUnspecified Functional Bowel DisorderRome IV — bowel symptoms fitting no other categoryCentrally Mediated Abdominal Pain (CAPS)Rome IV — continuous pain unrelated to gut eventsNarcotic Bowel SyndromeRome IV — opioid-induced hyperalgesia of the gutFaecal Incontinence (Rome IV)Rome IV — the criteria, and why nobody is askedFunctional Anorectal PainLevator ani, unspecified pain and proctalgia fugaxFunctional Defecation DisordersRome IV — dyssynergia and inadequate propulsionInfant RegurgitationRome IV — the happy spitter, and the alarm features that rule it outInfant ColicRome IV — recurrent unexplained crying in a well infant under 5 monthsInfant DyscheziaRome IV — straining before a soft stool, and why not to intervenePaediatric Functional ConstipationRome IV — two of six over one month, with overflow soiling as a criterionToddler's DiarrhoeaRome IV functional diarrhoea of childhood — painless, thriving childPaediatric Cyclic Vomiting SyndromeRome IV — both age bands, with different criteria for eachPaediatric Rumination SyndromeRome IV — infant and child/adolescent criteriaFunctional Nausea & Vomiting (Children)Rome IV — two separate disorders that can be met togetherAerophagiaRome IV — distension that increases through the dayPaediatric Functional DyspepsiaRome IV — four times a month, with PDS and EPS subtypingPaediatric Irritable Bowel SyndromeRome IV — plus the constipation clause clinicians missAbdominal MigraineRome IV — stereotypical incapacitating episodes weeks apartFunctional Abdominal Pain — NOSRome IV — the residual category, reached after the other threeNonretentive Faecal IncontinenceRome IV — soiling without retention, where laxatives make it worseFunctional DyspepsiaRome IV — with PDS and EPS subtypingRumination SyndromeRome IV — effortless regurgitation without retchingCyclic Vomiting SyndromeRome IV — stereotypical episodic vomitingCannabinoid HyperemesisRome IV — CVS pattern relieved by cannabis cessationChronic Nausea & VomitingRome IV — chronic nausea and vomiting syndromeBelching DisordersRome IV — supragastric vs gastric belchingFunctional HeartburnRome IV — heartburn with normal acid exposureReflux HypersensitivityRome IV — normal acid exposure, positive symptom associationFunctional Chest PainRome IV — non-cardiac, non-reflux chest painGlobusRome IV — painless lump-in-throat sensationFunctional DysphagiaRome IV — dysphagia with normal endoscopy and manometry
  1. Calculators
  2. /
  3. APRI
Fibrosis & MASLDMost used

APRI

AST to platelet ratio — liver fibrosis

Your laboratory's reference ceiling. It varies between labs and between sexes, and using the wrong one shifts every result.

APRI is expressed relative to your own laboratory's AST upper limit of normal, so check that figure rather than assuming 40 U/L.

When to use
Use it as a simple non-invasive estimate of fibrosis when you have an AST and a platelet count and want a second opinion alongside FIB-4 — agreement between the two is more reassuring than either alone. It is most validated in chronic hepatitis C, where it was derived, and has been applied to hepatitis B, HIV co-infection and metabolic liver disease with more variable results. It is not a substitute for elastography where that is available, and the World Health Organization has recommended it specifically as a fibrosis assessment tool in settings where elastography and biopsy are not.
Why use it
Because it needs less than any other index: two numbers, one of which is on every full blood count. That matters in two situations. First, in resource-limited settings where transient elastography does not exist, APRI and FIB-4 are the only staging tools available at all, which is why WHO guidance names APRI for hepatitis B assessment. Second, as a cross-check — APRI and FIB-4 share only AST and platelets, so when they agree the conclusion rests on more than one arrangement of the same data, and when they disagree that is itself informative and usually means one of the inputs has a non-hepatic explanation.
Formula, evidence and interpretation

About the AST to Platelet Ratio Index (APRI)

APRI estimates liver fibrosis from just two values — AST expressed as a multiple of your laboratory's upper limit of normal, and platelet count. Below 0.5, significant fibrosis is unlikely; above 1.5, it is likely; between them the result is indeterminate. A separate, higher threshold of about 2.0 is used for cirrhosis. In the original chronic hepatitis C cohort the AUROC was 0.80 for significant fibrosis and 0.92 for cirrhosis in the training set, and 0.88 and 0.94 respectively in validation.

On this page

  • Formula
  • Interpreting the result
  • Inputs
  • What it returns
  • How it is calculated
  • Facts & figures
  • Evidence
  • How it compares
  • Pearls & pitfalls
  • Critical actions
  • Why it exists
  • About the creator
  • Limitations
  • If you are the patient
  • FAQ
  • Related calculators
  • References

Formula

APRI = [ (AST ÷ AST upper limit of normal) ÷ platelets (×10⁹/L) ] × 100
AST
U/L, as measured.
AST upper limit of normal
Your laboratory's reference ceiling in U/L. Laboratory-specific, and sex-specific in many labs.
platelets
×10⁹/L, identical to ×1,000/µL — no conversion between those two.
  • The × 100 is a scaling convention so the result lands in a convenient numeric range; it has no clinical meaning.
  • Because AST is expressed relative to a local reference range, the same patient can get slightly different APRI values at two hospitals. This is inherent to the score, not an error.
  • There are no floors or caps — every value enters as measured.

Interpreting the result

Read the low and high bands as rule-out and rule-in, and the middle as an instruction to do something else. Two different threshold sets are in circulation, and the distinction matters: roughly 0.5 and 1.5 are used for significant fibrosis, while about 2.0 is used when the question is cirrhosis specifically. Because APRI shares two of its inputs with FIB-4, it is best read alongside it — concordant results are considerably more useful than either in isolation, and discordant results usually mean a non-hepatic cause is distorting the AST or the platelet count.

ScoreBandWhat it meansAction
< 0.5Low probabilitySignificant fibrosis unlikelyRoutine monitoring; recheck alongside FIB-4 over time
0.5–1.5IndeterminateThe index does not discriminate in this rangeCombine with FIB-4 and proceed to elastography or biopsy where available
> 1.5High probabilitySignificant fibrosis likely; cirrhosis becomes likely above about 2.0Refer to hepatology; confirm with elastography or biopsy

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What the APRI needs (3 inputs)

AST (U/L)
Aspartate aminotransferase. The absolute value matters less than its ratio to your laboratory's ceiling, which is why the next field exists.
AST upper limit of normal (U/L)
Your own laboratory's reference ceiling for AST. This is not a constant — it differs between laboratories and between sexes, commonly falling between about 30 and 40 U/L. Using the wrong figure rescales every result, and it is the single most common way APRI is calculated incorrectly.
Platelet count (×10⁹/L)
In the denominator, standing in for portal hypertension. As with FIB-4, any non-hepatic cause of thrombocytopenia inflates the score.

Units. AST and its upper limit of normal must be in the same units, which in practice is U/L for both. Platelets in ×10⁹/L and ×1,000/µL are the same number, so no conversion is needed. The one value you must look up rather than assume is your own laboratory's AST reference ceiling, which is commonly between 30 and 40 U/L and often differs between men and women.

What it returns

APRI score
A continuous value. Conventionally reported to two or three decimal places, since the cut-offs are close together at the low end.
Risk band
Low, indeterminate or high probability of significant fibrosis. A separate higher threshold is used when the question is specifically cirrhosis rather than significant fibrosis.

How it is calculated

APRI is the simplest of the fibrosis indices and its logic is transparent: as fibrosis progresses, hepatocellular injury raises AST while developing portal hypertension lowers the platelet count, so a ratio of the two moves in one direction. Wai and colleagues fitted it in patients with chronic hepatitis C who had undergone biopsy, and expressed AST as a multiple of the upper limit of normal rather than in absolute units specifically so the index would transfer between laboratories with different assays. That design choice is also its main practical hazard, because it makes the result depend on a number the user has to look up and frequently guesses.

Facts & figures

Derivation performance in chronic hepatitis C (Wai 2003)
OutcomeTraining set (n = 192)Validation set (n = 78)
AUROC — significant fibrosis0.800.88
AUROC — cirrhosis0.920.94

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In the training cohort, using optimised cut-offs allowed significant fibrosis to be predicted accurately in 51% of patients and cirrhosis in 81%.

Thresholds by question asked
QuestionRule-out belowRule-in above
Significant fibrosis (METAVIR F2+)0.51.5
Cirrhosis (F4)1.02.0

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Quoted thresholds vary between publications and guidelines. State which pair you used.

Evidence

Derivation — chronic hepatitis C, biopsy-controlled

2003 · n = 270

Patients with chronic hepatitis C who had undergone liver biopsy, split into a training cohort of 192 and a validation cohort of 78. AST expressed as a multiple of the local upper limit of normal, divided by platelet count.

AUROC 0.80 for significant fibrosis and 0.92 for cirrhosis in the training set; 0.88 and 0.94 respectively in validation. With optimised cut-offs, significant fibrosis was predicted accurately in 51% and cirrhosis in 81% of the training cohort.

WHO adoption for hepatitis B in resource-limited settings

2015

APRI has been recommended in World Health Organization hepatitis B guidance as a means of assessing fibrosis where transient elastography and biopsy are unavailable, on the basis that two routine laboratory values are obtainable almost anywhere.

Accepted as adequate for identifying patients who need treatment in settings without access to better tests, rather than as equivalent to elastography.

Performance outside chronic hepatitis C

2023

Applied to chronic hepatitis B, HIV/HBV co-infection and metabolic liver disease, where reported accuracy is more variable than in the derivation setting, and where age-specific cut-offs have been proposed for chronic hepatitis B.

Comparative studies against transient elastography generally find APRI and FIB-4 similar to each other and both inferior to elastography.

How it compares

APRI vs FIB-4

FIB-4 is the usual first-line choice in guideline pathways because it needs no local reference range — but APRI is a worthwhile cross-check, and it was the better performer for cirrhosis specifically in its derivation cohort.

Both indices combine AST and platelets. FIB-4 adds age and ALT and is specified in most MASLD and primary-care pathways, partly because it can be computed retrospectively from any historic blood panel with no extra lookup. APRI requires your laboratory's AST upper limit of normal, which makes automated calculation across a health system harder and hand calculation more error-prone. In the Wai cohort APRI reached an AUROC of 0.92–0.94 for cirrhosis, better than FIB-4's 0.765 for advanced fibrosis — though the two figures answer different questions in different populations and should not be compared directly.

Open the FIB-4 calculator →

APRI vs Transient elastography (FibroScan)

Elastography is more accurate and is preferred wherever it exists; APRI's role is in settings where it does not, which is why WHO guidance names APRI rather than elastography for hepatitis B assessment in resource-limited care.

Liver stiffness measurement outperforms both APRI and FIB-4 in head-to-head comparisons. It requires equipment, a trained operator and a fasted patient, and is confounded by obesity and ascites. APRI needs an AST, a platelet count and a reference range — available essentially everywhere — which is a different kind of advantage and the reason it remains in international guidance.

Pearls & pitfalls

  • The AST upper limit of normal is not 40 U/L by default. It differs by laboratory and often by sex, commonly between 30 and 40, and using the wrong value rescales every result proportionally.
  • APRI and FIB-4 share AST and platelets, so they are not independent tests. Agreement is reassuring but not as strong as two genuinely independent methods agreeing.
  • Two threshold sets are in circulation — roughly 0.5/1.5 for significant fibrosis and 1.0/2.0 for cirrhosis. Quoting a band without saying which question you asked is ambiguous.
  • Non-hepatic thrombocytopenia inflates the score exactly as it does with FIB-4. Check the platelet count has a hepatic explanation.
  • Acute hepatitis, recent alcohol and muscle injury all raise AST without fibrosis, and the index cannot distinguish those causes.
  • Platelets in ×10⁹/L and ×1,000/µL are the same number. Converting between them introduces hundred-fold errors.
  • Accuracy for cirrhosis was better than for significant fibrosis in the derivation study, which is the opposite of the intuition that harder questions are answered worse.

Critical actions

  • Look up your own laboratory's AST upper limit of normal rather than assuming a value — this is the difference between a correct and a misleading result.
  • Calculate FIB-4 alongside it and act on the more concerning of the two, investigating any discordance.
  • Treat an indeterminate result as an instruction to escalate, not as a normal finding.
  • Exclude non-hepatic causes of a low platelet count or a raised AST before referring on a high score.
  • Do not use it during acute hepatitis or soon after heavy alcohol intake.
  • Where elastography is available, use APRI to triage rather than to conclude.

Why this score exists

The most deliberate decision in APRI's design is the one users most often undo. Wai and colleagues expressed AST as a multiple of the upper limit of normal, rather than in absolute U/L, so that the index would be comparable across laboratories running different assays with different reference ranges. That is why the calculator asks for a value most clinicians have to look up — and why entering a remembered 40 U/L when the local ceiling is 31 quietly rescales the result by about 30%. The score was also built in biopsy-controlled chronic hepatitis C, at a time when biopsy was routine and the aim was to reduce how often it was needed; it was never presented as a staging tool.

About the creator

  • Chun-Tao Wai

    First author, 2003 derivation study

    Derived APRI in chronic hepatitis C, combining AST with platelet count to estimate fibrosis without biopsy.

  • Anna S.-F. Lok

    Senior author

    Led the Michigan hepatology programme in which APRI was developed and validated.

Limitations

  • Derived in biopsy-controlled chronic hepatitis C; performance in metabolic liver disease and hepatitis B is more variable, and age-specific cut-offs have been proposed for chronic hepatitis B.
  • Depends on a laboratory-specific AST upper limit of normal, so results are not strictly comparable between services and are easy to compute wrongly.
  • Only two variables, so it carries less information than indices that include age or other markers.
  • Cannot stage fibrosis — it estimates the probability of crossing a threshold.
  • Distorted by any non-hepatic cause of raised AST or low platelets, with no way for the score to signal that.
  • Competing threshold sets for significant fibrosis and for cirrhosis create real ambiguity in how results are reported.

If you are the patient

APRI is a simple calculation from two things in a routine blood test: a liver enzyme called AST, and your platelet count. As liver scarring develops, AST tends to rise and platelets tend to fall, so the ratio between them gives an estimate of how likely significant scarring is. A low result makes significant scarring unlikely; a high result makes it likely and means you will be referred to a liver specialist; a middle result means the test could not tell and another test is needed. It is often calculated together with a similar score called FIB-4, and your team pays most attention when the two agree. One caveat worth knowing: a low platelet count from a cause unrelated to your liver — some medicines, or a blood condition — will push this score up without your liver being the problem, so your team will check for that before drawing conclusions.

Frequently asked questions

What is the APRI score?#

APRI is the AST to Platelet Ratio Index, a non-invasive estimate of liver fibrosis calculated as [(AST ÷ AST upper limit of normal) ÷ platelet count] × 100. Below 0.5 significant fibrosis is unlikely, above 1.5 it is likely, and about 2.0 is used as the threshold for cirrhosis.

How is the APRI score calculated?#

Divide the AST by your laboratory's upper limit of normal for AST, divide that result by the platelet count in ×10⁹/L, then multiply by 100. Expressing AST relative to the local reference range is deliberate, so the index transfers between laboratories with different assays.

What AST upper limit of normal should I use?#

Your own laboratory's, which is typically between 30 and 40 U/L and often differs by sex. It is not a fixed constant, and substituting a remembered value for the local one rescales the whole result — this is the commonest error in calculating APRI.

What APRI score indicates cirrhosis?#

Around 2.0 is the conventional rule-in threshold for cirrhosis, with about 1.0 used as the rule-out. These are higher than the 0.5 and 1.5 thresholds used for significant fibrosis, so it matters which question you are asking. In the derivation study APRI reached an AUROC of 0.92–0.94 for cirrhosis.

Is APRI or FIB-4 better?#

They perform similarly and are often used together. FIB-4 is specified more often in guideline pathways because it needs no local reference range and can be computed automatically from existing blood results. APRI is simpler and performed strongly for cirrhosis in its derivation cohort. Where the two disagree, look for a non-hepatic cause affecting AST or platelets.

How accurate is the APRI score?#

In the original chronic hepatitis C cohort the AUROC was 0.80 for significant fibrosis and 0.92 for cirrhosis in the training set, and 0.88 and 0.94 in validation. Accuracy is more variable outside chronic hepatitis C, and it is consistently less accurate than transient elastography.

Can APRI be used in hepatitis B?#

Yes, and World Health Organization guidance has recommended it for assessing fibrosis in hepatitis B where transient elastography and biopsy are not available. Reported performance in hepatitis B is more variable than in hepatitis C, and age-specific cut-offs have been proposed.

Why does a low platelet count raise the APRI score?#

Platelets are in the denominator, standing in for portal hypertension — as cirrhosis develops, splenic sequestration and reduced thrombopoietin lower the count. That is the intended signal, but any other cause of thrombocytopenia produces the same arithmetic effect without any liver fibrosis, which is why the cause of a low count should be established before acting on a high APRI.

Related calculators

  • MASLD–MASH NIT — Integrated non-invasive assessment of MASLD fibrosis and at-risk MASH — FIB-4, APRI, NFS, FAST, Agile 3+, Agile 4, ELF and ADAPT in one pass
  • FIB-4 Index — Liver fibrosis scoring index
  • NAFLD Fibrosis Score — Advanced fibrosis probability in MASLD/NAFLD
  • Child-Pugh Score — Assesses the prognosis of chronic liver disease, mainly cirrhosis

References

Original / primary reference

  1. Wai CT, Greenson JK, Fontana RJ, et al. A simple noninvasive index can predict both significant fibrosis and cirrhosis in patients with chronic hepatitis C. Hepatology. 2003;38(2):518-526.

Clinical practice guidelines

  1. WHO Guidelines for the Prevention, Care and Treatment of Persons with Chronic Hepatitis B Infection. World Health Organization, 2015.
  2. EASL Clinical Practice Guidelines on non-invasive tests for evaluation of liver disease severity and prognosis. J Hepatol. 2021;75(3):659-689.

Last updated July 29, 2026. Clinical knowledge base written and curated by GastroAGI Team from primary medical literature.

Written from primary literature and not yet independently clinically reviewed.

For use by qualified healthcare professionals. This calculator supports clinical judgement and does not replace it.