Endocrinology & Neurosurgery & Family Medicine
Gigantism and acromegaly
Gigantism is a syndrome caused by excessive secretion of growth hormone (GH) that occurs before the epiphyseal growth plates have fused, leading to excessive height growth. When GH hypersecretion occurs after the fusion of the growth plates—that is, in adults—the condition is called acromegaly, characterized by enlargement of the extremities (hands, feet, jaw) and progressive visceral changes. These two conditions represent the two clinical manifestations of the same pathophysiological process: chronic GH hypersecretion, responsible for a sustained elevation of IGF-1 (insulin-like growth factor 1—somatomedin C), the primary mediator of GH’s anabolic and growth effects. In more than 95% of cases, the cause is a somatotrophic (benign) pituitary adenoma—a microadenoma (<10 mm) or a macroadenoma (>10 mm). Pediatric forms of gigantism are particularly rare (estimated incidence of 5–10 cases per million children) and may be associated with genetic conditions (multiple endocrine neoplasia type 1—MEN1, Carney syndrome, XLAG syndrome—X-linked acrogigantism associated with duplications of the GPR101 gene). Without treatment, gigantism leads to a significantly increased adult height (often >2.0–2.5 m) as well as serious metabolic and cardiovascular complications, significantly reducing life expectancy. Acromegaly, which is more common (prevalence 40–70 per million), is often diagnosed late (average delay of 7–10 years between initial symptoms and diagnosis) due to the insidious progression of morphological changes.
Etiologies, clinical presentation, and biological diagnosis
- Etiologies and genetic forms of gigantism and acromegaly: Sporadic somatotropic pituitary adenoma (>95% of cases): microadenoma (<10 mm—more common in acromegaly) or macroadenoma (>10 mm—more common in pediatric gigantism) — autonomous GH secretion by tumor somatotrope cells — GNAS somatic mutation (Gs alpha protein — constitutive activation of adenylate cyclase): present in 40% of sporadic somatotropic adenomas (Gs-alpha+ adenomas) — smaller tumors + better response to somatostatin analogs; genetic forms and associated syndromes (10–15% of GH-secreting adenomas): MEN1 (multiple endocrine neoplasia type 1 — MENIN mutation — 11q13): pituitary adenomas (GH + prolactin + corticotropes) + parathyroid adenomas + pancreatic endocrine tumors (insulinomas + gastrinomas) → routine screening for MEN1 in all young patients with GH-secreting pituitary adenomas; Carney syndrome (PRKAR1A mutation — 17q24): GH-secreting pituitary adenomas + cardiac myxomas + cutaneous lentiginosis + pigmented adrenal nodules (PPNAD); XLAG syndrome (X-linked acrogigantism): duplication of the GPR101 gene on the X chromosome (Xq26.3) → pediatric gigantism with very early onset (before 2–4 years of age) + mixed GH/prolactin pituitary macroadenoma → adult height often >2 m; AIP (aryl hydrocarbon receptor interacting protein — 11q13): germline mutations in AIP in 20% of familial somatotropin-secreting adenomas (FIPA — familial isolated pituitary adenoma) — invasive adenomas with early onset — poor response to somatostatin analogs; Rare causes of ectopic hypersecretion of GH or GHRH: carcinoid tumors (lung + pancreas) secreting GHRH (growth hormone-releasing hormone) → pituitary stimulation → somatotrope cell hyperplasia → very rare (<1% of acromegaly cases)
- Clinical Presentation of Gigantism (Child) and Acromegaly (Adult): Gigantism (excessive GH secretion before cartilage fusion): accelerated height growth (growth velocity >3 standard deviations for age) + progressive tall stature (often >97th percentile from childhood onward + potential adult height >2.0 m if untreated) + enlargement of hands and feet + progressive coarse facial features (bulging forehead + prognathism) + macroglossia + deep voice + hyperhidrosis + headaches + signs of pituitary tumor compression if macroadenoma (bitemporal hemianopia + oculomotor paralysis) + puberty: delayed or precocious puberty depending on the mass effect on the pituitary gland + fatigue + early joint pain; acromegaly (GH hypersecretion after cartilage fusion — adult): hand signs (ring sign—increased ring size + rings needing to be resized) + increased shoe size + macroglossia + prognathism + dental diastema (gapped teeth) + bulging forehead (frontal bumps) + coarsening of facial features + hyperhidrosis + carpal tunnel syndrome (compression of the median nerve — present in 40–50% of acromegaly cases) + arthropathies + headaches (30–50% — mechanism not exclusively related to tumor size) + visual field defects if macroadenoma with chiasmatic compression + snoring + obstructive sleep apnea syndrome (OSAS — macroglossia + pharyngeal soft tissue hypertrophy — present in 60–80% of cases) + hypertension + cardiomegaly + cardiomyopathy + diabetes or glucose intolerance (insulin resistance induced by excess GH) + reddish-brown skin discoloration (melanotrophy) + acanthosis nigricans if marked insulin resistance; diagnostic delay for acromegaly: 7–10 years on average (progressive morphological changes largely unnoticed by close associates) — often discovered during evaluation for hypertension + diabetes + OSA + polyarthropathy + bilateral carpal tunnel syndrome + or during brain imaging performed for another reason
- Biological diagnosis and pituitary imaging : IGF-1 measurement (IGF-1 — insulin-like growth factor 1 — somatomedin C): first-line test — elevated in cases of chronic GH excess — interpretation based on age and sex (normal values vary by age — physiological peak at puberty + gradual decline with age) — elevated IGF-1 for age and sex is the best screening test for acromegaly/gigantism — high PPV + normal IGF-1 virtually rules out the diagnosis except in cases of exclusively pulsatile secretion; GH suppression test using an oral glucose load (75 g OGTT — diagnostic gold standard): in a normal subject, the glucose load suppresses GH to <0.4 ng/mL (GH nadir) — in acromegaly/gigantism: absence of GH suppression (nadir >1 ng/mL according to older criteria + nadir >0.4 ng/mL according to the current 2014 Endocrine Society criteria) or, paradoxically, an elevation in GH following glucose (paradoxical response — present in 10–20% of acromegalic patients) — GH samples at T0 + T30 + T60 + T90 + T120 min after glucose ingestion; Random basal GH: of limited use alone (pulsatile secretion) — useful if very high (>20–30 ng/mL) to quickly guide the diagnosis; Pituitary MRI with gadolinium: gold-standard morphological examination — T1 + T2 + FLAIR sequences + dynamic sequence after gadolinium injection — microadenoma: delayed contrast uptake compared to normal pituitary tissue + T1-hypointense signal — macroadenoma: mass >10 mm + suprasellar extension + chiasmatic compression + cavernous sinus invasion (Knosp grades I–IV) — fundus examination + visual field via automated perimetry: mandatory if macroadenoma + suprasellar extension → bitemporal hemianopia if optic chiasm compression; comprehensive pituitary workup (assessment of associated hypopituitarism — common with macroadenomas): cortisol + ACTH + Synacthen test (adrenal insufficiency) + TSH + T4L (central hypothyroidism) + FSH + LH + testosterone or estradiol (hypogonadism) + prolactin (hyperprolactinemia due to stalk effect or GH/PRL co-secretion)
Treatment of Gigantism and Acromegaly
| Therapeutic modality | Technique, dosage, and mechanism | Results, complications, and follow-up |
|---|---|---|
| Transsphenoidal surgery 1st line — endoscopy — tumor resection |
Transsphenoidal surgery (TSS) is the first-line treatment for gigantism and acromegaly in the vast majority of cases—it offers the possibility of immediate cure if the resection is complete; Surgical technique: endoscopic endonasal approach (current standard technique in most centers—gradually replacing microsurgery under a microscope): access to the sphenoid sinus via the nasal fossae → opening of the anterior wall of the sella turcica → tumor resection under direct endoscopic visualization (4K high definition) + preoperative MRI-guided neuronavigation → closure of the sella (abdominal fat + biological glue + mucosal graft) — advantages vs. the microscopic approach: better visualization of blind spots + reduced complications (rhinorrhea + olfactory disturbances) + better control of lateral extensions; postoperative biochemical cure criteria (assessed at 3 months): GH nadir <0.4 ng/mL on the glucose tolerance test + age- and sex-normalized IGF-1 — cure rates according to tumor size: microadenoma: 70–85% % biochemical cure rate as first-line treatment — macroadenoma without cavernous sinus invasion (Knosp 0–2): 50–65% % — invasive macroadenoma (Knosp 3–4 — cavernous sinus invasion): 10–30% % (total resection virtually impossible if cavernous invasion → mandatory adjunctive medical therapy); preoperative preparation: preoperative somatostatin analogs (3–6 months): used if large macroadenoma + high anesthetic risk (severe OSA + cardiomyopathy) → reduction in tumor size (10–20 % on average) + improvement in cardiovascular comorbidities + improvement in OSA → no demonstrated benefit on surgical cure rates in meta-analyses → not routinely recommended preoperatively in all patients | Complications of transsphenoidal surgery: transient diabetes insipidus (10–15% of cases — ADH deficiency → massive polyuria + polydipsia → treatment with desmopressin — resolution within a few days to weeks — permanent in <1% of cases) + cerebrospinal rhinorrhea (CSF leak through the sphenoid sinus — 1–3% of cases — risk of meningitis → reoperation if persistent) + postoperative hypopituitarism (5–15% of cases — normal anteropituitary function intraoperatively → adrenal insufficiency + hypothyroidism + hypogonadism → complete pituitary workup 3 months postoperatively) + bacterial meningitis (rare — <1 % — IV antibiotic therapy) + intrasellar hemorrhage + vascular injury (internal carotid artery — exceptional) + visual disturbances (worsening or onset of hemianopia due to traction on the chiasm — rare if careful technique is used); immediate postoperative follow-up: pituitary MRI 72 hours post-op (assessment of resection) + 3 months post-op (post-operative baseline MRI — before resorption of the packing fat) + hormonal workup on Day 3 (morning cortisol) + at 3 months (complete pituitary workup + IGF-1 + GH-stimulated pituitary function test) + systematic corticosteroid replacement therapy (hydrocortisone) in the first postoperative days (prevention of acute adrenal insufficiency); persistence or recurrence after surgery: tumor recurrence: annual MRI × 5 years then every 2–3 years if stable — biochemical recurrence: IGF-1 and GH-OGH annually for 10 years → medical treatment (ASN) or radiosurgery if recurrence is documented |
| Somatostatin analogues (SSA) Octreotide — lanreotide — pasireotide |
Somatostatin analogs (SSAs) are the first-line medical treatment for acromegaly and gigantism—they bind to somatostatin receptors (SSTR—primarily SSTR2 and SSTR5) expressed by tumor somatotrope cells → inhibition of GH secretion + reduction in tumor volume in 30–50% of cases; octreotide LP (Sandostatin LAR—Novartis): extended-release formulation — 10–40 mg deep IM (buttock) every 4 weeks — starting dose: 20 mg/4 weeks → adjustment based on IGF-1 and GH — available in Canada + covered by RAMQ with exception criteria for acromegaly; lanreotide autogel (Somatuline Depot — Ipsen): pre-filled syringe in hydrogel formulation — 60–120 mg deep SC every 4 weeks (or every 6–8 weeks in well-controlled patients — dosing flexibility) — self-injection possible by the patient or home care nurse — non-inferiority to octreotide demonstrated — available in Canada + covered by RAMQ; pasireotide LAR (Signifor LAR — Recordati): second-generation analog — affinity for SSTR1 + SSTR2 + SSTR3 + SSTR5 (broader profile than octreotide and lanreotide, which primarily target SSTR2) → more effective on adenomas with little or no SSTR2 expression — 40–60 mg IM every 4 weeks — PAOLA trial (Lacroix 2018): biochemical control (normalized IGF-1 and GH) in 15–20% of cases resistant to octreotide/lanreotide — adverse effects: hyperglycemia ++ (present in 57–73% of patients — mechanism: inhibition of insulin secretion by pancreatic SSTR5) → close glycemic monitoring + metformin or other antidiabetics if diabetes is induced; side effects common to NSAIDs: gastrointestinal intolerance (nausea + cramps + diarrhea — transient at the start of treatment) + gallstones (25–30% of treated patients — mechanism: inhibition of gallbladder motility → biliary stasis) → annual gallbladder ultrasound | Efficacy of SSAs in acromegaly: biochemical control (normal IGF-1 + GH <1 ng/mL): 55–60% of patients on octreotide or lanreotide (Caron 2014 meta-analysis) — reduction in tumor volume: 10–20 % on average (reduction ≥20 % in 35–40 % of cases) — predictive factors for a good response to SSS: strong SSTR2 staining on immunohistochemistry (on surgical specimen) + GNAS+ (gs-alpha) mutation + microadenoma + lower baseline GH level; resistance to first-generation SSS (octreotide + lanreotide): 40–45% of patients — definition: Persistent IGF-1 >1.3 × ULN (upper limit of normal) after 3–6 months of treatment at maximum dose → options: dose escalation + switch to long-acting semaglutide (LAR) + addition of cabergoline + switch to pegvisomant; follow-up on SRS: IGF-1 + GH every 3 months (titration phase) → every 6 months (stable phase) + annual pituitary MRI (monitoring of residual tumor growth) + annual biliary ultrasound + fasting blood glucose + HbA1c (pasireotide); AS in pediatric acromegaly: limited data (small pediatric populations) — used post-surgery if residual tumor present + uncontrolled GH/IGF-1 — effects on growth velocity: reduction but not cessation of growth if growth plates are still open — combination with GnRH analogs (to delay bone maturation) discussed in certain pediatric protocols |
| Pegvisomant and GH receptor antagonists Somavert — AIDS resistance |
Pegvisomant (Somavert — Pfizer) is a GH receptor antagonist — it binds to the GH receptor (GHR) without activating it → blocks GH signaling → reduces hepatic IGF-1 production → normalizes IGF-1 levels; unique mechanism of action (distinct from SASTs): pegvisomant does not act on the pituitary tumor itself — it blocks the peripheral effects of GH → IGF-1 decreases → serum GH may paradoxically increase under pegvisomant (absence of negative feedback from IGF-1 on the pituitary) → do not use GH as a monitoring marker during pegvisomant treatment (use IGF-1 exclusively); dosage: loading dose of 80 mg SC followed by 10–30 mg SC/day — dose adjusted based on IGF-1 (target: IGF-1 within the normal range for age and sex); Efficacy: normalization of IGF-1 in 97% of patients treated at optimal doses (ACROSTUDY studies — international registry) — pegvisomant is the most effective treatment for normalizing IGF-1 in acromegaly — indications: resistance or intolerance to first- and second-generation SSS + combination with SSS (combined SSS + pegvisomant treatment): allows for a reduction in the pegvisomant dose (cost + frequency of injections) + improves control in patients partially controlled on SSS alone — SSS + pegvisomant combination therapy: positive data (Franck-Raue 2017 meta-analysis + ACROSTUDY registry); Adverse effects of pegvisomant: injection site reactions + elevated transaminases (5–10 times the upper limit of normal [ULN] — monthly liver function tests for the first 6 months, then every 6 months — discontinue if AST >5× ULN) + possible tumor growth (MRI monitoring — the absence of negative IGF-1 feedback may lift tumor growth inhibition in some cases — mandatory annual MRI monitoring) + lipodystrophy at the injection site (rotation of injection sites recommended); coverage in Canada: pegvisomant covered by most private insurance plans (high cost: 15,000–30,000 CAD/year depending on the dose) + Pfizer Canada special access program if coverage is insufficient | Combination therapy with pegvisomant + ASS — clinical practice in Quebec: indications for the combination: acromegaly partially controlled with ASA alone (IGF-1 between 1.0 and 2.0 × ULN) — large residual macroadenoma requiring tumor control (ASA) + optimal biochemical control (pegvisomant) — cost of the combination is lower than full-dose pegvisomant alone (reduction in daily pegvisomant dose by 30–50 %); comparison of medical strategies in post-surgical residual acromegaly: octreotide/lanreotide alone: 55–60% biochemical control + long-acting pasireotide (LAR): 15–20% additional control in patients resistant to first-generation ASS + pegvisomant alone: 97 % of IGF-1 normalization + combination of ASS + pegvisomant: 90–95 % of IGF-1 control at reduced doses — individualized decision based on: side effect profile (diabetes → avoid pasireotide) + cost + adherence (daily pegvisomant injection vs. monthly ASS) + presence of residual tumor (ASS for tumor control); cabergoline (dopamine agonist — Dostinex): 3rd-line treatment for acromegaly — effective especially in cases of GH + prolactin co-secretion or D2R-expressing tumors — normalization of IGF-1 in 20–35% of patients (results from meta-analyses) — dosage: 0.5–3.5 mg/week PO — well tolerated + low cost — attractive option for mild to moderate acromegaly or in combination with SSNIs |
| Radiotherapy and stereotactic radiosurgery Gamma Knife — CyberKnife — adjuvant treatment |
Radiotherapy and stereotactic radiosurgery are third-line treatment options for acromegaly and gigantism — they are reserved for patients with post-surgical residual tumor that is not controlled by medical treatment, or who are not candidates for further surgery; Stereotactic radiosurgery (Gamma Knife — Leksell Gamma Knife + CyberKnife — Accuray): delivery of a high-dose focused radiation in a single session (Gamma Knife) or in multiple fractions (CyberKnife — stereotactic fractionation) — principle: ablative dose to the residual tumor + maximum protection of adjacent structures (optic chiasm — dose limit 8 Gy + cranial nerves of the cavernous sinus) — condition: minimum distance of 3–5 mm between the residual tumor and the optic chiasm (otherwise conventional fractionated radiotherapy) — efficacy: biochemical control (normalization of IGF-1) in 40–60% of cases at 5–10 years — time to response: 2–10 years (slow — requires bridging medical therapy during the waiting period); fractionated conformal radiotherapy (IMRT — intensity-modulated radiation therapy): administered in 25–30 fractions over 5–6 weeks (total dose 45–54 Gy) — indicated if tumor residue is near the chiasm or infiltrating surrounding structures → second-line treatment compared to stereotactic radiosurgery — efficacy: biochemical control 50–60% at 10 years (Minniti meta-analysis 2011); proton therapy: available at a few centers in Canada (TRIUMF Vancouver) → irradiation with protons (Bragg peak → precise dose delivery) → reduction in irradiated surrounding structures + data on acromegaly similar to stereotactic radiosurgery; main complication of pituitary radiation therapy: radiation-induced hypopituitarism: adrenal insufficiency + hypothyroidism + hypogonadism → onset: 2–15 years after irradiation → cumulative incidence: 50–80% at 10 years → annual hormonal monitoring for life following irradiation | Indications for stereotactic radiosurgery in acromegaly in Quebec: visible post-surgical tumor residue on MRI + not controlled by medical treatment (somatostatin analogs + pegvisomant) + chiasm-tumor distance ≥3 mm (otherwise fractionated radiotherapy) + patient refusing or unable to benefit from a second surgery + residual invasive cavernous sinus macroadenoma (Knosp 3-4) after surgery + unreimbursed or intolerable medical treatment; Quebec stereotactic radiosurgery centers: CHUM (CyberKnife + Gamma Knife) + Montreal General Hospital (CUSM — Gamma Knife) + CHUS Sherbrooke + Hôtel-Dieu de Québec (CHU de Québec); post-radiosurgery follow-up: IGF-1 + complete pituitary assessment every 6 months × 5 years + annual pituitary MRI × 5 years then every 2 years — medical treatments (somatostatin analogs + pegvisomant) must be maintained until biochemical evidence of post-radiosurgical cure (often 3-7 years after irradiation) → risk of rebound if premature cessation of somatostatin analogs; biochemical cure criteria after radiosurgery: normal IGF-1 for age and sex + GH nadir <0.4 ng/mL on OGTT (2 successive controls 6 months apart) → medical treatment withdrawal possible if these criteria are met + lifelong surveillance maintained (late recurrences documented up to 15-20 years post-irradiation) |
| Systemic complications and multidisciplinary follow-up Cardiovascular — Metabolic — Quality of Life |
Untreated or inadequately treated acromegaly and gigantism are associated with multiple systemic complications that significantly reduce life expectancy (mortality 2–3 times higher than in the general population in uncontrolled acromegaly) — their screening and management are an integral part of multidisciplinary follow-up; cardiovascular complications (leading cause of death in acromegaly): hypertension (30–40 mmHg — mechanism: sodium retention + activation of the renin-angiotensin-aldosterone system [RAAS] + functional hyperaldosteronism) → standard antihypertensive treatment → target BP <130/80 mmHg + cardiomegaly (acromegalic cardiomyopathy): thickening of the septum + posterior wall (concentric hypertrophy) → diastolic dysfunction → heart failure → TEE (transthoracic echocardiogram) at the start of follow-up + every 2–3 years + arrhythmias (atrial fibrillation + ventricular tachycardias) + annual ECG; metabolic complications: diabetes mellitus or glucose intolerance (30–50% of acromegalic patients — insulin resistance induced by GH antagonism on insulin sensitivity + inhibition of insulin secretion by pasireotide) → fasting blood glucose + HbA1c every 6 months + HOMA-IR → metformin ± insulin depending on severity; obstructive sleep apnea syndrome (OSAS): 60–80% of acromegaly patients — mechanism: macroglossia + pharyngeal soft tissue hypertrophy + craniofacial deformity → polysomnography if snoring + daytime sleepiness + CPAP if OSA confirmed → partial improvement with medical treatment (reduction in macroglossia); colorectal cancer: 2–3 times increased risk (frequent adenomatous polyposis due to IGF-1 hypersecretion → colonocyte growth factor) → colonoscopy upon diagnosis + every 5 years if active acromegaly + every 10 years if controlled; Acromegalic arthropathies: thickened articular cartilage + ligament laxity + early osteoarthritis (knees + hips + spine) → physical therapy + NSAIDs + analgesics → joint replacement if severe, disabling osteoarthritis | Multidisciplinary care for acromegaly and gigantism in Quebec: multidisciplinary team: endocrinologist (coordination + medical treatment) + pituitary neurosurgeon (transsphenoidal surgery) + neuroradiologist (high-resolution pituitary MRI) + radiation oncologist (stereotactic radiosurgery) + ophthalmologist (visual field + fundus examination) + cardiologist (echocardiogram + cardiovascular monitoring) + pulmonologist/sleep specialist (OSAS + polysomnography) + gastroenterologist (colonoscopy) + rheumatologist (arthropathies) + ENT specialist (macroglossia + snoring) + maxillofacial surgeon (severe prognathism - orthognathic surgery if acromegaly is controlled) + psychologist (psychosocial impact + quality of life) + coordinating nurse; Quebec reference centers: Centre de neuroendocrinologie hypophysaire du CHUM (pituitary tumors) + CHU Sainte-Justine (pediatric gigantism) + CHUS Sherbrooke + CHU de Québec; patient associations: Acromégalie Québec + Acromegaly Community (international) + Cushing's Support and Research Foundation (for pituitary tumors); quality of life in acromegaly: even in biochemical remission, many patients report altered quality of life (chronic fatigue + joint pain + cognitive disorders + depression + morphological sequelae) → psychological support + physical rehabilitation + validated questionnaires (AcroQoL — Acromegaly Quality of Life Questionnaire) at diagnosis + annual follow-up → adaptation of the therapeutic plan based on functional impact. |
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Pediatric Gigantism — XLAG Syndrome and Early Diagnosis: XLAG (X-linked acrogigantism) syndrome, linked to a duplication of the GPR101 gene on the X chromosome, is the best-characterized genetic cause of very early-onset gigantism (before 2-4 years of age). These children present with explosive statural growth, macrocephaly and a mixed GH/prolactin pituitary macroadenoma that is often large at diagnosis. In any child presenting an abnormal statural acceleration with a growth rate exceeding +3 DS for age, an IGF-1 assay and pituitary MRI should be carried out without delay. Early diagnosis is crucial: every year of delay in diagnosis translates into several centimetres of irreversible excessive statural growth.
Situations requiring urgent medical assessment
Sudden visual deficit (hemianopsia) + intense headaches in a patient with known or suspected acromegaly → pituitary apoplexy (intratumoral hemorrhage) → emergency brain MRI + neurosurgery + IV corticosteroids (acute corticotropic insufficiency).
Child with statural growth velocity >+3 SD + acromegaly (large hands + feet) + headaches → gigantism on pituitary adenoma → IGF-1 urgent + pituitary MRI + pediatric endocrinology + neurosurgery opinion.
Postoperative transsphenoidal surgery: polyuria >3 L/24h + polydipsia + very dilute urine → postoperative central diabetes insipidus → desmopressin (DDAVP) SC or nasal + ionogram + urinary and plasma osmolality + endocrinology.
Known acromegaly + decompensated heart failure + severe OSA + uncontrolled HTN → severe cardiovascular complications of uncontrolled acromegaly → hospitalization + cardioprotection + optimization of anti-GH therapy + polysomnography + CPAP.
Consult at Clinique Omicron
Clinique Omicron physicians evaluate patients presenting with signs suggestive of gigantism or acromegaly (increased hand or foot size in adults, facial feature changes, prognathism, bilateral carpal tunnel syndrome, persistent headaches), order IGF-1 levels, and refer to the appropriate pituitary neuroendocrinology center. Follow-up for comorbidities (hypertension, diabetes, sleep apnea) in treated patients is managed in coordination with specialized teams at several service points in Quebec. To make an appointment, visit cliniqueomicron.ca.
The content of this page is for informational purposes only and does not replace the advice of an endocrinologist or neurosurgeon specializing in pituitary tumors. The management of gigantism and acromegaly requires an experienced multidisciplinary team.
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