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Research draft

acromegaly

vr.tr.acromegaly · XCT.STA

Enable an agent to recognise suspected acromegaly, record evidence of growth-hormone excess and its consequences, and support clinician-reviewed investigation, treatment and follow-up.

Thing Registry Cross-cutting context

Research draft, second pass

A second pass drafted this model: the structure a model of this thing needs, and what is known about it in the world. The line under this one says how the second half was obtained - researched against sources, or recalled without web access, in which case nothing here was read anywhere and every claim is a lead to verify. Unreviewed either way.

recalled by Codex without web access - no source was read

Researched by: Codex

Purpose and description

Enable an agent to recognise suspected acromegaly, record evidence of growth-hormone excess and its consequences, and support clinician-reviewed investigation, treatment and follow-up.

Acromegaly is a chronic endocrine disorder caused by sustained growth hormone excess, usually from a pituitary somatotroph adenoma, with increased insulin-like growth factor 1 activity producing characteristic acral, facial, soft-tissue and systemic changes after epiphyseal closure.

It can be Assemble progressive physical changes and associated symptoms into a traceable reason for endocrine assessment; Compare serial hormone results while flagging reference-range changes, confounders and discordance; Link biochemical disease to source investigations without inferring causation from imaging alone; Identify documented visual or neurological warning signs for urgent clinical review; Track treatment response alongside tumour findings, complications and patient priorities; Surface overdue assessments and unresolved evidence for clinician review.

Distinguishing features

Distinguish acromegaly from isolated tall stature by recording acral and soft-tissue overgrowth, biochemical evidence and timing relative to growth-plate closure. [NIDDK](https://www.niddk.nih.gov/health-information/endocrine-diseases/acromegaly)

Distinguish a suggestive appearance from established disease using age-adjusted IGF-1 interpreted with clinical findings; appearance alone does not establish the diagnosis. [Diagnostic consensus](https://pmc.ncbi.nlm.nih.gov/articles/PMC10837217/)

Distinguish a causal pituitary lesion from an incidental mass by requiring evidence of GH excess; imaging alone is insufficient. [Endocrine Society guideline](https://www.endocrine.org/clinical-practice-guidelines/acromegaly)

Distinguish current biochemical activity from persistent physical changes by recording hormone results and residual manifestations separately. [Diagnostic and remission consensus](https://pmc.ncbi.nlm.nih.gov/articles/PMC10837217/)

Scope

+ Progressive acral, facial and soft-tissue changes that prompt assessment for acromegaly

+ Biochemical evidence of GH and IGF-1 excess, including assay context and discordant results

+ The relationship between acromegaly and its pituitary or exceptional nonpituitary source

+ Acromegaly-associated complications and functional burden

+ Treatment response, biochemical control, remission and recurrence

- Pituitary gigantism as a separate growth disorder, while recording overlap when GH excess spans growth-plate closure

- Full classification and management of pituitary tumours independent of acromegaly

- Pseudoacromegaly and other causes of acromegaloid appearance as independent conditions

- Standalone models of diabetes, sleep apnoea, cardiovascular disease and arthropathy

- Drug prescribing protocols, surgical technique and radiotherapy delivery

Characteristics

Diagnostic standing
suspected | biochemically supported | clinician-confirmed | unresolved | excluded Prevents a screening signal or registry label from being treated as a confirmed diagnosis.
IGF-1 relative to reference range
Laboratory concentration and units, age-specific reference interval, and ratio to upper limit of normal Makes the biochemical result interpretable across ages, dates and laboratories.
GH measurement context
µg/L or equivalent ng/mL; random, serial or glucose-suppression nadir; assay and sampling time A GH value needs its sampling and assay context before it can support an interpretation.
Phenotypic progression
absent | uncertain | progressive | stable | improving, with dated observations Separates longstanding appearance from documented change.
Timing relative to growth-plate closure
before closure | after closure | spanning closure | unknown Locates the boundary and possible overlap with pituitary gigantism.
Source of hormone excess
Link to suspected or established pituitary or nonpituitary source, with supporting evidence Connects the endocrine syndrome to source-directed assessment.
Pituitary lesion extent
Dimensions in mm, dated anatomical extension and relationship to the optic apparatus Supports assessment of local effects independently of hormone concentrations.
Acromegaly-associated burden
Links to complications, functional limitations and patient-reported effects, with attribution confidence Captures consequences without assuming every coexisting condition is caused by acromegaly.
Treatment exposure
Dated links to surgery, medication or radiotherapy records Provides the context needed to interpret subsequent disease activity.
Longitudinal disease status
untreated active | persistent active | controlled on treatment | remission off medication | suspected recurrence | indeterminate Distinguishes treatment-dependent control from remission using explicitly recorded criteria.

Also called

canine acromegaly

Where this came from

wikidata · CC0 1.0

Drafted structure

Bundle to layer to finding to question, as the second pass will find it: 6 bundles · 11 layers · 19 findings · 35 questions.

Recognition and disease boundaries Establish whether the observed pattern warrants assessment for acromegaly and which neighbouring conditions remain plausible.

Gradual change can be missed, while a suggestive appearance can be overinterpreted.

Acral and facial progression

Record changes over time rather than relying on a single impression.

Documented overgrowth pattern

Record changes in hand, foot, facial and oral features with their dates and evidence. These are recognised manifestations of acromegaly. [NIDDK](https://www.niddk.nih.gov/health-information/endocrine-diseases/acromegaly)

  1. Which changes in ring fit, shoe size, facial appearance or dental spacing have developed, and over what interval? measurement
  2. Which observations come from examination, dated photographs, dental records or patient recollection? provenance

Growth timing and alternatives

Locate the syndrome relative to skeletal maturity and competing explanations.

Acromegaly versus neighbouring phenotypes

Record skeletal-growth timing and alternative explanations without using body size or appearance as a substitute for endocrine evidence.

  1. Did suspected GH excess begin before, after or across growth-plate closure, and what evidence supports that timing? boundary
  2. If biochemical excess is unconfirmed, which alternative explanations for the acromegaloid appearance require assessment? boundary
Biochemical establishment Represent the evidence and interpretation supporting or challenging the diagnosis.

Laboratory values cannot establish disease independently of reference ranges, clinical context and applicable criteria.

IGF-1 interpretation

Preserve the reference context and diagnostic rule used for each interpretation.

Age-adjusted IGF-1 evidence

The 2024 consensus supports diagnosis with characteristic clinical signs and IGF-1 above 1.3 times the age-adjusted upper limit of normal; equivocal results require contextual reassessment. Record the criterion applied. [Diagnostic consensus](https://pmc.ncbi.nlm.nih.gov/articles/PMC10837217/)

  1. What were the IGF-1 concentration, age-adjusted reference interval, upper-limit ratio, assay and collection date? measurement
  2. Which clinical findings and named diagnostic criteria support the interpretation? definition
  3. Which physiological, medical or treatment factors could affect this result? boundary

GH and discordant results

Record supplementary testing and uncertainty when clinical and biochemical evidence diverge.

Contextual GH assessment

Equivocal cases may benefit from repeated IGF-1 and oral glucose testing; record assay-specific interpretation rather than embedding a universal GH cutoff. [Diagnostic consensus](https://pmc.ncbi.nlm.nih.gov/articles/PMC10837217/)

  1. If glucose suppression testing was performed, what protocol, GH nadir, assay and interpretive threshold were used? measurement
  2. Do IGF-1, GH and clinical findings agree, and which discrepancy remains unresolved? boundary
  3. What repeat testing or specialist assessment has been agreed to resolve uncertainty? action
Hormone source and local effects Connect the endocrine syndrome to its source and distinguish secretion from anatomical consequences.

Hormone excess and lesion-related injury are separate dimensions requiring different evidence.

Source localisation

Record localisation findings and the strength of causal attribution.

Source attribution

Most acromegaly arises from a GH-producing pituitary tumour; uncommon nonpituitary sources require separate evidence. Record the basis for attribution. [NIDDK](https://www.niddk.nih.gov/health-information/endocrine-diseases/acromegaly)

  1. What does pituitary imaging show, including lesion dimensions and anatomical extension? measurement
  2. What biochemical, imaging or pathological evidence connects the proposed source to GH excess? provenance
  3. If pituitary imaging is negative or discordant, what source investigation has the specialist proposed? action

Compression and pituitary function

Capture local effects that hormone concentrations alone cannot describe.

Local risk assessment

Record visual effects and other pituitary hormone deficits alongside lesion anatomy; pituitary tumours may affect nearby structures and normal pituitary tissue. [NIDDK](https://www.niddk.nih.gov/health-information/endocrine-diseases/acromegaly)

  1. Are visual-field abnormalities or other pituitary hormone deficits documented, and by which assessments? measurement
  2. Are new visual or neurological symptoms present that require urgent clinical assessment? action
Systemic and lived burden Record clinically relevant consequences and the person's priorities.

Hormone control alone does not describe accumulated damage or everyday disability.

Associated complications

Connect acromegaly to assessed comorbidities while preserving their independent records.

Complication assessment status

Track assessment of hypertension, diabetes, cardiovascular disease, sleep apnoea and osteoarthritis, as recommended in acromegaly care. [Endocrine Society guideline](https://www.endocrine.org/clinical-practice-guidelines/acromegaly)

  1. Which associated complications are confirmed, suspected, excluded or not yet assessed? measurement
  2. What supports attribution to acromegaly rather than simple coexistence? provenance
  3. Which complication assessments or follow-up actions are due under the person's care plan? action

Function and personal impact

Capture consequences that matter to the person and may persist after treatment.

Patient-prioritised burden

Record pain, mobility, sleep, appearance-related distress and participation limitations as reported, separately from biochemical status.

  1. Which symptoms or limitations most affect daily activities, relationships or work? measurement
  2. Which changes would the person consider meaningful improvement? action
Treatment response and surveillance Relate interventions to biochemical, anatomical and patient-reported outcomes over time.

A treated condition may remain active, require ongoing medication or leave consequences that need continuing care.

Intervention and response

Preserve treatment intent and separate response dimensions.

Treatment-linked outcomes

Link surgery, medication and radiotherapy to dated outcomes and adverse effects. These are established treatment modalities for acromegaly. [NIDDK](https://www.niddk.nih.gov/health-information/endocrine-diseases/acromegaly)

  1. Which interventions occurred, when, and with what documented therapeutic objective? provenance
  2. How did IGF-1, relevant GH measurements, lesion findings and symptoms change after each intervention? measurement
  3. Which adverse effects, access constraints or patient preferences require treatment review? action

Control, remission and recurrence

Make longitudinal status explicit and dependent on dated evidence.

Evidence-based follow-up state

Record remission or control criteria, treatment context and assessment timing; biochemical interpretation and follow-up depend on treatment modality. [Diagnostic and remission consensus](https://pmc.ncbi.nlm.nih.gov/articles/PMC10837217/)

  1. Which dated results and criteria support active disease, control on treatment, remission or suspected recurrence? definition
  2. Were measurements obtained at an appropriate interval and interpreted for the treatment being used? boundary
  3. What biochemical, imaging and complication surveillance is planned, and what findings would prompt earlier review? action
Evidence and external alignment What the world already says about this thing, gathered so the model can be checked against it.

A model that cannot be lined up against existing standards, identifiers and practice cannot be adopted by anyone who already uses them.

Reported evidence

Findings from the breadth pass, kept separate from the structural claims.

Check these first

Recalled without web access and unsourced; every item is a lead to verify.

  • This is recalled knowledge, not a source-verified account; guideline versions and current consensus criteria require checking.
  • Diagnostic and treatment-response thresholds must be checked against the relevant assay and current guidance.
  • The supplied domain code is retained as registry context; acromegaly is described here in its clinical disease sense.
  1. Which of these check these first hold for the sense of acromegaly this model covers, and on what evidence? provenance

Kinds and varieties

Recalled without web access and unsourced; every item is a lead to verify.

  • Pituitary tumour-associated acromegaly
  • Acromegaly caused by ectopic growth hormone-releasing hormone secretion
  • Acromegaly caused by ectopic growth hormone secretion, which is exceptionally rare
  1. Which of these kinds and varieties hold for the sense of acromegaly this model covers, and on what evidence? provenance

Identifiers and schemes

Recalled without web access and unsourced; every item is a lead to verify.

  • ICD-10 - E22.0 - The category covers acromegaly and pituitary gigantism; it does not distinguish them.
  1. Which of these identifiers and schemes hold for the sense of acromegaly this model covers, and on what evidence? provenance

Standards and regulation

Recalled without web access and unsourced; every item is a lead to verify.

  • Endocrine Society clinical practice guideline on acromegaly addresses diagnosis, treatment and follow-up.
  • Acromegaly Consensus Group consensus statements address biochemical diagnosis, disease control and management.
  1. Which of these standards and regulation hold for the sense of acromegaly this model covers, and on what evidence? provenance

Real-world use

Recalled without web access and unsourced; every item is a lead to verify.

  • Clinical recognition of progressive enlargement of hands and feet, facial changes and associated systemic disease.
  • Biochemical investigation of suspected growth hormone excess.
  • Pituitary imaging and assessment of tumour effects and pituitary function.
  • Selection and monitoring of surgery, medical therapy or radiotherapy.
  • Assessment and management of cardiovascular, metabolic, respiratory and musculoskeletal complications.
  1. Which of these real-world use hold for the sense of acromegaly this model covers, and on what evidence? provenance

Typical measurements

Recalled without web access and unsourced; every item is a lead to verify.

  • Serum insulin-like growth factor 1 concentration - Commonly above the age-adjusted reference interval in active disease; interpretation depends on the assay and clinical context. - ng/mL or nmol/L
  • Serum growth hormone concentration, including nadir during an oral glucose tolerance test - Failure of appropriate suppression can support diagnosis; thresholds depend on assay sensitivity and diagnostic context. - ng/mL or µg/L
  • Maximum pituitary tumour diameter - Microadenoma: less than 10 mm; macroadenoma: 10 mm or greater. - mm
  1. Which of these typical measurements hold for the sense of acromegaly this model covers, and on what evidence? provenance

Failure modes and hazards

Recalled without web access and unsourced; every item is a lead to verify.

  • Slow progression can delay recognition and allow partly irreversible skeletal and joint changes.
  • Hypertension, cardiomyopathy and other cardiovascular complications can increase morbidity and mortality.
  • Insulin resistance, diabetes mellitus and obstructive sleep apnoea are important associated conditions.
  • A pituitary tumour can cause visual impairment and deficiencies of other pituitary hormones.
  • Pulsatile growth hormone secretion, assay differences and conditions affecting insulin-like growth factor 1 can complicate biochemical interpretation.
  1. Which of these failure modes and hazards hold for the sense of acromegaly this model covers, and on what evidence? provenance

Regional variation

Recalled without web access and unsourced; every item is a lead to verify.

  • Access to hormone assays, pituitary imaging, specialist surgery and long-term medical treatment varies between health systems.
  1. Which of these regional variation hold for the sense of acromegaly this model covers, and on what evidence? provenance

Neighbouring kinds and how to tell them apart

Recalled without web access and unsourced; every item is a lead to verify.

  • Pituitary gigantism - Growth hormone excess begins before epiphyseal closure and causes excessive linear growth; acromegaly describes the characteristic changes after closure, although features can overlap.
  • Nonfunctioning pituitary adenoma - It may cause similar mass effects but does not produce the growth hormone excess responsible for acromegaly.
  • Pseudoacromegaly - Acromegaly-like physical features occur without the biochemical growth hormone and insulin-like growth factor 1 excess characteristic of acromegaly.
  1. Which of these neighbouring kinds and how to tell them apart hold for the sense of acromegaly this model covers, and on what evidence? provenance

What the second pass must settle

  • Which diagnostic and remission consensus, assay-specific thresholds and update policy should govern implementations of this model?
  • How should borderline IGF-1 elevation and persistent GH-IGF-1 discordance be represented across different treatments and physiological contexts?
  • How should cases with GH excess spanning growth-plate closure link acromegaly and gigantism without duplicating the underlying disease episode?
  • Which complication surveillance schedules, including colorectal assessment, apply by jurisdiction, prior findings and individual risk?
  • Does an existing Vercy world model already own this disease concept, requiring this registry entry to link to it instead of creating a separate publication?