Goitre: causes, diagnosis and treatment | Clinique Omicron<\/title>\n<meta name=\"description\" content=\"Goiter is an enlargement of the thyroid gland. Simple, multinodular, toxic or Hashimoto's goiter: ultrasound diagnosis and management in Quebec.\">\n<meta name=\"keywords\" content=\"goitre traitement, goitre thyro\u00efde causes, goitre multinodulaire, goitre toxique, goitre Hashimoto, goitre simple, goitre sympt\u00f4mes, \u00e9chographie thyro\u00efde Qu\u00e9bec\">\n<link rel=\"preconnect\" href=\"https:\/\/fonts.googleapis.com\">\n<link href=\"https:\/\/fonts.googleapis.com\/css2?family=Cinzel:wght@600&family=Poppins:wght@400;500;600;700&display=swap\" rel=\"stylesheet\">\n<style>\n.co-wrap * { font-family: 'Poppins', sans-serif; box-sizing: border-box; }\n.co-wrap { max-width: 1100px; margin: 0 auto; padding: 30px 0 60px; }\n.co-label { font-family: 'Cinzel', serif; font-size: 14px; font-weight: bold; letter-spacing: 1px; text-transform: uppercase; color: #4D6577; margin-bottom: 14px; display: block; }\n.co-wrap h1 { font-size: 32px; font-weight: 500; color: #323C52; margin: 0 0 22px; line-height: 1.2; }\n.co-intro { font-size: 16px; line-height: 1.75; color: #4D6577; margin-bottom: 36px; padding-bottom: 32px; border-bottom: 1px solid rgba(77,101,119,.2); }\n.co-wrap h2 { font-size: 20px; font-weight: 600; color: #323C52; margin: 32px 0 12px; }\n.co-wrap p { font-size: 15px; color: #4D6577; line-height: 1.7; margin-bottom: 14px; }\n.co-list { list-style: none; padding: 0; margin: 12px 0 24px; }\n.co-list li { font-size: 15px; color: #4D6577; padding: 10px 14px 10px 38px; margin-bottom: 8px; border-radius: 6px; position: relative; background: rgba(77,101,119,.06); border-left: 3px solid #4D6577; }\n.co-list li::before { content: \"\u2713\"; position: absolute; left: 12px; font-weight: 700; color: #4D6577; }\n.co-table { width: 100%; border-collapse: collapse; margin: 14px 0 22px; font-size: 14px; border-radius: 8px; overflow: hidden; table-layout: fixed; }\n.co-table thead tr { background: #323C52; color: #fff; }\n.co-table thead th { padding: 11px 16px; text-align: left; font-weight: 600; font-size: 13px; }\n.co-table tbody tr:nth-child(even) { background: rgba(77,101,119,.06); }\n.co-table tbody tr:nth-child(odd) { background: #fff; }\n.co-table td { padding: 10px 16px; color: #4D6577; border-bottom: 1px solid rgba(77,101,119,.12); font-size: 14px; vertical-align: top; }\n.co-table td:first-child { font-weight: 600; color: #323C52; }\n.co-infobox { display: flex; gap: 12px; background: rgba(77,101,119,.06); border-radius: 8px; border-left: 4px solid #4D6577; padding: 14px 18px; margin: 18px 0 28px; font-size: 14px; color: #4D6577; line-height: 1.65; }\n.co-infobox .ico { font-size: 18px; flex-shrink: 0; }\n.co-urgence { background: #fff8f8; border-left: 5px solid #c0392b; border-radius: 6px; padding: 20px 26px; margin: 24px 0 32px; }\n.co-urgence .co-urgence-titre { font-size: 13px; font-weight: 700; color: #c0392b; letter-spacing: 1.5px; text-transform: uppercase; margin-bottom: 10px; }\n.co-urgence p { color: #5a2020; font-size: 14px; margin: 0 0 10px; line-height: 1.7; }\n.co-urgence p:last-child { margin-bottom: 0; }\n.co-disclaimer { font-size: 13px; color: #8a9aaa; font-style: italic; border-top: 1px solid rgba(77,101,119,.15); padding-top: 24px; margin-top: 40px; line-height: 1.6; }\n<\/style>\n<\/head>\n<body>\n<div class=\"co-wrap\">\n <span class=\"co-label\">Endocrinology & Family Medicine & Endocrine Surgery<\/span>\n <h1>Goiter<\/h1>\n\n <div class=\"co-intro\">\n A goiter is any enlargement of the thyroid gland beyond normal values, regardless of cause or associated thyroid function. Normal adult thyroid volume is 6-20 mL in women and 8-25 mL in men, measured by ultrasound. Classically, a distinction is made between simple (or euthyroid, diffuse or nodular, without thyroid dysfunction), multinodular goiter (with or without hyperthyroidism), inflammatory goiter (Hashimoto's thyroiditis, De Quervain's thyroiditis) and diffuse toxic goiter (Graves' disease). Iodine deficiency, the world's leading cause of goiter, has been virtually eliminated in Canada thanks to the mandatory iodization of table salt since 1949. In Quebec, goiters are therefore mainly autoimmune (Hashimoto's), benign nodular or linked to thyroid dysfunction. Assessment is based on TSH, thyroid antibodies and thyroid ultrasound - classically complemented by ultrasound-guided fine-needle cytopuncture (FNC) for any suspicious nodule. Treatment varies according to etiology, size, thyroid function and the presence of compressive symptoms.\n <\/div>\n\n <h2>Pathophysiology, classification and etiologies<\/h2>\n <ul class=\"co-list\">\n <li><strong>Mechanisms of goiter development :<\/strong> the thyroid increases in volume by three main, often interrelated mechanisms: diffuse hyperplasia: prolonged stimulation of thyreocytes by TSH (iodine deficiency + goitrogens + resistance to thyroid hormones) \u2192 increase in the number and size of follicles \u2192 diffuse goiter + focal hypertrophy (nodulogenesis) : clonal expansion of groups of thyreocytes with somatic mutations conferring an advantage in growth or functional autonomy (TSH receptor mutations - TSHR + Gs\u03b1 mutations + BRAF\/RAS alterations in case of malignant transformation) \u2192 benign nodules (adenomas) or malignant nodules (carcinomas) + inflammatory or fibrous infiltration : Hashimoto's thyroiditis (lymphoid infiltrate + progressive fibrosis) + De Quervain's thyroiditis (granulomatous inflammation) + Riedel's thyroiditis (extensive fibrosis - rare); role of iodine in goitrogenesis: iodine is the essential substrate for thyroid hormone synthesis (T3 + T4) \u2192 iodine deficiency \u2192 drop in free T4 \u2192 reflex increase in TSH (hypothalamic-pituitary axis) \u2192 stimulation of thyroidocyte growth \u2192 initially diffuse euthyroid goiter \u2192 multinodularity with age \u2192 recommended iodine intake (WHO): 150 \u00b5g\/d in adults + 250 \u00b5g\/d during pregnancy and breastfeeding \u2192 dietary sources: iodized salt + dairy products + eggs + sea fish + seaweed + dietary goitrogens: substances interfering with thyroid hormone synthesis \u2192 cabbage + broccoli + cauliflower (isothiocyanates) + manioc + soy (isoflavones) \u2192 negligible effect at usual dietary intakes except pre-existing iodine deficiency<\/li>\n <li><strong>Etiological classification of goitres :<\/strong> simple diffuse (euthyroid) goiter: absence of nodules + normal thyroid function + absence of significant antibodies \u2192 causes : iodine deficiency (rare in Canada - isolated rural areas + immigrant populations) + puberty + pregnancy (increased iodine requirements) + goitrogenic drugs (lithium + amiodarone + carbimazole + propylthiouracil - inhibits thyroid hormone synthesis) + genetic factors (familial - familial simple goiter); multinodular goiter (GMN): presence of multiple thyroid nodules of various sizes and structures + most frequent in clinical practice in middle-aged and elderly adults + two forms: euthyroid (non-toxic) GMN: normal thyroid function + benign nodules + ultrasound monitoring + toxic GMN (GMNT): one or more secretory autonomous nodules (toxic adenomas) \u2192 hyperthyroidism \u2192 collapsed TSH + elevated T3\/T4 \u2192 thyroid scintigraphy: \u00abhot\u00bb nodules (hypercaptans) + the rest of the thyroid is suppressed \u2192 treatment: radioactive iodine (\u00b9\u00b3\u00b9I) or surgery; Hashimoto's thyroiditis: autoimmune chronic lymphocytic thyroiditis \u2192 anti-TPO (anti-thyroperoxidase) + anti-thyroglobulin (anti-Tg) antibodies \u2192 lymphoid infiltration + fibrosis \u2192 firm + irregular goiter + progressive hypothyroidism \u2192 most common cause of autoimmune hypothyroidism and goiter in Quebec + prevalence: 5-10 % of adult female population \u2192 treatment: levothyroxine if hypothyroidism; Graves' disease: toxic diffuse goiter \u2192 TSH receptor stimulating antibodies (TSI or TRAb) \u2192 constitutive thyroid stimulation \u2192 hyperthyroidism + vascular diffuse goiter + triad: goiter + ophthalmopathy (exophthalmos) + dermopathy (pretibial myxedema - rare) \u2192 TRAb positive \u2192 treatment: synthetic antithyroid drugs + radioactive iodine + surgery; cervical goiter with endothoracic extension (plunging): goiter descending behind the sternum into the anterior mediastinum \u2192 often bulky multinodular goiter \u2192 tracheal compression + superior cava syndrome if bulky + cervicothoracic CT scan obligatory \u2192 often surgical indication.<\/li>\n <li><strong>Clinical presentation and compressive signs:<\/strong> asymptomatic goiter (most frequent): fortuitous discovery on clinical examination or during cervical imaging (ultrasound + CT + MRI) \u2192 TSH often normal \u2192 monitoring + symptomatic goiter: local functional symptoms: dysphagia (oesophageal compression) + dyspnoea (tracheal compression - inspiratory stridor) + hoarseness (compression of the recurrent laryngeal nerve \u2192 cordial paralysis \u2192 ENT opinion + laryngoscopy) + \u00abball\u00bb sensation in the throat + chronic postural cough + cervical discomfort + Pemberton sign: elevation of arms above head \u2192 cervical venous congestion + facial erythema + vertigo \u2192 compressive endothoracic goiter \u2192 urgent thoracic CT scan + associated systemic symptoms: hyperthyroidism if toxic goiter (palpitations + emaciation + tremors + diarrhea + heat intolerance + tachycardia) + hypothyroidism if Hashimoto's (asthenia + weight gain + frilosity + constipation + bradycardia) + acute neck pain : De Quervain's thyroiditis (viral - granulomatous inflammation) \u2192 pain radiating to jaw and ears + fever + very high SV (>100 mm\/h) + transient thyrotoxicosis \u2192 endocrinology opinion + signs suggestive of malignancy in a nodular goiter: rapidly growing nodule + hard cervical adenosathies + persistent hoarseness + stony consistency of nodule + history of cervical irradiation + familial MEN2 syndrome + ultrasound-guided CAF if suspicious<\/li>\n <\/ul>\n\n <h2>Diagnosis, clinical forms and management<\/h2>\n <table class=\"co-table\">\n <colgroup><col style=\"width:200px;\"><col style=\"width:42%;\"><col><\/colgroup>\n <thead>\n <tr><th>Clinical situation<\/th><th>Diagnosis and assessment<\/th><th>Treatment and follow-up<\/th><\/tr>\n <\/thead>\n <tbody>\n <tr>\n <td>Initial goiter assessment<br><small style=\"font-weight:400;color:#7a8fa0;\">TSH - antibodies - ultrasound - TI-RADS classification<\/small><\/td>\n <td>The initial workup of a newly diagnosed goiter follows a structured algorithm combining thyroid biology and imaging; 1st-line biological workup: ultrasensitive TSH (TSHus): reference test for assessing thyroid function - normal TSH: 0.4-4.0 mIU\/L \u2192 collapsed TSH (4.5 mIU\/L) \u2192 hypothyroid goiter \u2192 assay free T4 + anti-TPO antibodies + anti-Tg antibodies \u2192 normal TSH : euthyroid goiter \u2192 measure anti-TPO antibodies (Hashimoto's screening) + thyroid-specific antibodies: anti-TPO (anti-thyroperoxidase): marker of thyroid autoimmunity \u2192 positive in Hashimoto's (95 % of cases) + Graves' disease (70 %) + postpartum thyroiditis + TRAb (TSH receptor antibodies): specific for Graves' disease \u2192 sensitivity 95 % + specificity 99 % \u2192 positive TRAb + low TSH = Graves' disease almost certain \u2192 monitoring during antithyroid treatment (guides decision to stop) \u2192 serum calcitonin: to be measured if thyroid nodule suspected \u2192 marker of medullary thyroid carcinoma (MTC) \u2192 basal calcitonin >100 pg\/mL \u2192 MTC almost certain \u2192 genetic work-up (RET proto-oncogene) + pentagastrin stimulation test if calcitonin 10-100 pg\/mL (limited availability in Canada) + thyroglobulin (Tg): not useful in initial diagnosis \u2192 follow-up marker for differentiated thyroid cancer after total thyroidectomy; thyroid ultrasound: reference morphological examination \u2192 perform systematically in the presence of any palpated goiter \u2192 measure thyroid volume (ellipsoid formula: L \u00d7 W \u00d7 H \u00d7 0.524 for each lobe) \u2192 characterization of nodules: size + echogenicity + contours + presence of microcalcifications + Doppler vascularization + cervical adenopathies \u2192 ACR TI-RADS classification (Thyroid Imaging Reporting and Data System - Tessler 2017): score 1-5 according to ultrasound features + recommendations for CAF according to score and size: TI-RADS 1-2: benign \u2192 no CAF + TI-RADS 3: slightly suspicious \u2192 CAF if \u22652.5 cm + TI-RADS 4: moderately suspicious \u2192 CAF if \u22651.5 cm + TI-RADS 5: highly suspicious \u2192 CAF if \u22651.0 cm<\/td>\n <td>2nd-line examinations according to clinical orientation: thyroid scintigraphy (\u2079\u2079\u1d50Tc-pertechnetate or \u00b9\u00b2\u00b3I): indicated if TSH low or collapsed + nodular goiter \u2192 identifies \u00abhot\u00bb nodules (autonomous - hypercaptant) + \u00abcold\u00bb nodules (hypocaptant - higher risk of malignancy if cold) \u2192 allows diagnosis of GMNT (toxic multinodular goiter) + Graves' disease (diffuse intense homogeneous uptake) \u2192 NB: not indicated if TSH normal (cold nodule in this context \u2192 same risk of malignancy as any nodule \u2192 evaluate by TI-RADS + CAF); Cervico-thoracic CT with injection: indicated if: endothoracic plunging goiter + dyspnoea or dysphagia + positive Pemberton sign \u2192 precise mapping of extension + tracheal compression (measurement of tracheal diameter - stenosis if <9 mm) + vascular compression + surgical planning \u2192 caution: iodine from the contrast medium can precipitate hyperthyroidism in a GMNT (Jod-Basedow phenomenon) \u2192 inform the endocrinologist + discuss premedication + cervico-thoracic MRI: non-irradiating alternative - useful for mediastinal extension and surgical planning \u2192 no interference with future radioactive iodine; ultrasound-guided fine-needle cytopunction (FNC): outpatient procedure + optional local anesthesia \u2192 cell sampling of suspicious nodule \u2192 Bethesda classification (thyroid cytopathology reporting system - 2023): Bethesda I: non-diagnostic \u2192 repeat + Bethesda II: benign (70-80 % of CAFs) \u2192 surveillance + Bethesda III: atypia of undetermined significance (AUS\/FLUS) \u2192 molecular (ThyroSeq + Afirma) or surgery + Bethesda IV: follicular neoplasm \u2192 surgery (lobectomy) + Bethesda V: suspected malignancy \u2192 surgery + Bethesda VI: malignant \u2192 total thyroidectomy + extension workup.<\/td>\n <\/tr>\n <tr>\n <td>Multinodular euthyroid goiter<br><small style=\"font-weight:400;color:#7a8fa0;\">Surveillance - TI-RADS - CAF - surgical criteria<\/small><\/td>\n <td>Euthyroid multinodular goiter is the most common form of goiter in adults over 50 in Quebec - it is most often benign and requires surveillance only; epidemiology: ultrasound prevalence of thyroid nodules: 20-76 % depending on age and sex (more frequent in women and with age) \u2192 palpable: 5-7 % of the adult population + risk of malignancy of a thyroid nodule: 5-15 % (all sizes combined) \u2192 nodules <1 cm have a risk of malignancy 20 % or new suspicious feature \u2192 repeat CAF; criteria for surgery in euthyroid GMN: compressive symptoms (dysphagia + dyspnea + hoarseness) + large goiter (>80-100 mL) + endothoracic extension + suspicion of malignancy (CAF Bethesda IV-VI) + patient preference after full information + cosmetic (very large cervical goiter) \u2192 surgical indication discussed in multidisciplinary team (endocrinologist + endocrine surgeon); goiter surgery: total thyroidectomy (if large bilateral goiter) or lobectomy (if unilateral goiter or isolated nodule) \u2192 risks: transient or permanent hypoparathyroidism (hypocalcemia) + recurrent laryngeal nerve paralysis (hoarseness) + bleeding \u2192 high-volume surgical center \u2192 permanent complication rate: <2 % in expert centers \u2192 post-operative hypothyroidism: almost constant after total thyroidectomy \u2192 lifetime levothyroxine<\/td>\n <td>Radiofrequency ablation (RFA) of benign nodules: non-surgical interventional technique \u2192 radiofrequency probe introduced into the nodule under ultrasound guidance \u2192 heat \u2192 coagulative necrosis of the nodule \u2192 volume reduction 50-80 % in 6-12 months \u2192 indications: symptomatic (compressive + cosmetic) benign nodule + Bethesda II confirmed + patient refusing or unable to undergo surgery \u2192 advantages: ambulatory + no induced hypothyroidism + preserves thyroid function + rapid recovery \u2192 availability in Quebec: university centers specializing in interventional endocrinology (CHUM + CHU de Qu\u00e9bec - check current availability) \u2192 efficacy data: Ha 2021 meta-analysis (Thyroid): mean volume reduction 76 % at 12 months \u2192 European Thyroid Association recommends RFA as an alternative to surgery for symptomatic benign nodules (ETA 2020) + ethanol ablation (PEI - Percutaneous Ethanol Injection): reserved for cystic or mixed nodules (fluid predominant) \u2192 puncture + cyst emptying + pure ethanol injection + success rate: 85-95 % for pure cysts; long-term follow-up of GMN: risk of progression to GMNT (toxic multinodular goiter) with age \u2192 annual TSH \u2192 if TSH low \u2192 scintigraphy \u2192 if warm nodules \u2192 hyperthyroidism treatment + risk of malignancy in GMN: low but not zero \u2192 any ultrasound or clinical change \u2192 repeat CAF + iodine recommendation: do not supplement iodine in established GMN (risk of Jod-Basedow if subclinical autonomous nodules) \u2192 sufficient normal dietary iodine<\/td>\n <\/tr>\n <tr>\n <td>Hashimoto's goiter (chronic lymphocytic thyroiditis)<br><small style=\"font-weight:400;color:#7a8fa0;\">Anti-TPO - hypothyroidism - levothyroxine - target TSH<\/small><\/td>\n <td>Hashimoto's thyroiditis is the most common cause of hypothyroidism and autoimmune goiter in Canada - its management is well codified; clinical presentation and diagnosis: moderate + firm + irregular goiter (\u00abbumpy\u00bb or \u00abrubbery\u00bb appearance) + sometimes tender + asymptomatic or symptoms of progressive hypothyroidism \u2192 biology: anti-TPO: elevated (>35 IU\/mL) in 95 % of cases \u2192 titer correlated with inflammatory activity + anti-Tg: elevated in 60-80 % + TSH: normal in the euthyroid stage \u2192 progressively elevated with hypothyroidism \u2192 free T4: lowers as hypothyroidism progresses \u2192 natural evolution: euthyroid phase (sometimes initial transient thyrotoxicosis - \u00abhashitoxicosis\u00bb \u2192 release of preformed hormones from destroyed thyreocytes \u2192 5-10 % of Hashimoto's \u2192 transient low TSH \u2192 elevated free T4 \u2192 disappears in 2-4 months \u2192 distinguish Graves' disease: TRAb negative + scintigraphy: uptake collapsed) \u2192 subclinical hypothyroidism (TSH 4.5-10 mIU\/L + normal free T4) \u2192 frank hypothyroidism (TSH >10 mIU\/L + low free T4); peculiarity of Hashimoto's thyroiditis + thyroid cancer: primary thyroid lymphoma (MALT type - Mucosa-Associated Lymphoid Tissue) \u2192 rare but well-documented complication \u2192 risk \u00d760-80 compared with general population \u2192 to be evoked if sudden increase in volume of a Hashimoto's goiter + cervical adenopathies \u2192 CAF + surgical biopsy if doubt \u2192 papillary thyroid carcinoma: slight increase in risk (\u00d71.5-3) in Hashimoto's thyroiditis \u2192 justifies ultrasound follow-up<\/td>\n <td>Treatment of Hashimoto's thyroiditis: treatment of hypothyroidism with levothyroxine (L-T4): indication: TSH >10 mUI\/L \u2192 quasi-systematic treatment + TSH 4.5-10 mUI\/L (subclinical hypothyroidism) \u2192 treatment discussed: consensus indications: symptoms of hypothyroidism + pregnancy or desire for pregnancy + positive anti-TPO (risk of progression to frank hypothyroidism) + ischemic heart disease (target TSH 1-2.5 mUI\/L) + child or adolescent \u2192 comfort treatment if asymptomatic : discussed + initial dosage of L-T4: young adult without comorbidity: 1.6 \u00b5g\/kg\/d full dose + elderly or cardiopathic adult: start at 12.5-25 \u00b5g\/d and increase in increments of 12.5-25 \u00b5g\/d every 4-6 weeks \u2192 avoid rapid increases (risk of angina or tachyarrhythmia) + target TSH: general adult population: 0.5-2.5 mUI\/L + pregnancy: TSH <2.5 mUI\/L in 1st trimester + 75 years: 1.0-4.0 mUI\/L (avoid over-substitution \u2192 arrhythmias + osteoporosis + dementia) \u2192 take on an empty stomach in the morning, 30-60 min before meal (or 4h after calcium + iron + PPI supplements which reduce absorption) + TSH monitoring at 6-8 weeks after each dose adjustment + anti-TPO monitoring: do not monitor regularly (does not guide treatment); goiter reduction on L-T4: L-T4 can reduce goiter volume by partially suppressing TSH \u2192 modest effect \u2192 do not aim for TSH <0.5 mIU\/L to reduce goiter (risk of atrial fibrillation + osteoporosis) \u2192 if compressive goiter persists on L-T4 \u2192 surgery or RFA<\/td>\n <\/tr>\n <tr>\n <td>Toxic goiter - Graves' disease and GMNT<br><small style=\"font-weight:400;color:#7a8fa0;\">TRAb - antithyroid drugs - radioactive iodine - surgery<\/small><\/td>\n <td>Toxic (hyperthyroid) goiters represent a spectrum ranging from Graves' disease to toxic multinodular goiter - their management is specific; Graves' disease: most frequent cause of hyperthyroidism in women aged 20-50 + pathophysiology: IgG antibodies to TSH receptor (TRAb) \u2192 constitutive stimulation of adenylcyclase \u2192 excessive production of T3 + T4 \u2192 TSH suppression \u2192 Graves' triad: diffuse vascular goiter (murmur on auscultation) + ophthalmopathy (exophthalmos \u00b1 chemosis \u00b1 diplopia) + dermopathy (pretibial myxedema - rare) + biology: collapsed TSH (60 years + pre-existing multinodular goiter + often progressive, moderate hyperthyroidism + collapsed TSH + elevated T4\/T3 + negative TRAb + scintigraphy: multiple hot nodules + suppressed inter-nodular tissue \u2192 often subclinical hyperthyroidism (isolated low TSH) for years before frank hyperthyroidism \u2192 Jod-Basedow phenomenon: exposure to iodine (contrast PCI + amiodarone) \u2192 thyrotoxic decompensation in a pre-existing GMNT \u2192 inform radiologists and emergency physicians before any examination with iodinated contrast in a patient with known GMN<\/td>\n <td>Treatment of toxic goiter - three options: synthetic antithyroid drugs (STDs): methimazole (Tapazole) 10-30 mg\/d PO (1st line in North America except 1st trimester pregnancy) + propylthiouracil (PTU) 100-150 mg \u00d7 3\/d (1st line in 1st trimester pregnancy - risk of methimazole embryopathy: choanal atresia + aplasia cutis) \u2192 mechanism: inhibition of thyroperoxidase (TPO) \u2192 blockade of T3\/T4 synthesis + PTU also inhibits peripheral T4\u2192T3 conversion \u2192 time to efficacy: 4-8 weeks + goal: normalization of free T4 then TSH \u2192 NFS monitoring (risk of agranulocytosis 0.3-0.5 % \u2192 patient warning: \u00abconsult ER if fever or oral ulcerations\u00bb) + liver workup (PTU: risk of fulminant hepatitis - rare but serious) \u2192 remission of Graves' disease: 30-50 % after 12-18 months of TSA \u2192 favorable remission criteria: small goiter + low TRAb at end of treatment + HLADR3 and HLA-B8 genetic variants associated with low remission; radioactive iodine (\u00b9\u00b3\u00b9I): definitive treatment - single-dose oral administration \u2192 selective irradiation of hypercaptant thyroid tissue \u2192 destruction of the thyroid \u2192 almost-certain long-term hypothyroidism \u2192 indications: relapsed Graves' disease or 1st line if no desire for pregnancy within 6 months + GMNT (very effective) + solitary toxic adenoma \u2192 relative ICs: pregnancy + breastfeeding + compressive bulky goiter + active moderate to severe Graves' ophthalmopathy (risk of worsening - pretreatment with corticoids) \u2192 available in Quebec in nuclear medicine (CHU + CISSS with nuclear medicine) + thyroid surgery: total (or near-total) thyroidectomy: preferred indication if: very large goiter + compressive symptoms + severe ophthalmopathy (rapid euthyroidism improves ophthalmopathy) + desire for pregnancy within 6 months + associated suspicious nodule \u2192 surgery in euthyroidism (prepare with ATS + \u03b2blockers + Lugol's 5 days before) \u2192 lifelong hypothyroidism after total thyroidectomy \u2192 L-T4 started D1 post-op.<\/td>\n <\/tr>\n <tr>\n <td>Goiter and pregnancy<br><small style=\"font-weight:400;color:#7a8fa0;\">Iodine requirements - TSH in pregnancy - Fetal Graves' disease - post-partum<\/small><\/td>\n <td>Pregnancy induces significant changes in thyroid physiology that may aggravate a pre-existing goiter or reveal a new one; physiological thyroid changes in pregnancy: increased iodine requirement (150 \u2192 250 \u00b5g\/d) \u2192 relative deficiency in Quebec possible \u2192 slight increase in thyroid volume (10-15 %) \u2192 no true goiter if iodine intake is sufficient + increase in TBG (thyroxine-binding globulin) \u2192 increase in total T4 and total T3 \u2192 free T4 and free T3 remain normal (reference parameters in pregnancy) + hCG stimulates TSH receptor (homologous structure) \u2192 TSH physiologically low in 1st trimester (0,1-2.5 mIU\/L) \u2192 peak free T4 \u2192 sometimes picture of transient gestational thyrotoxicosis (TGT): intense nausea + vomiting (hyperemesis gravidarum) \u2192 negative TRAb + transiently low TSH \u2192 spontaneous resolution 2nd trimester \u2192 no ATS; reference values for TSH in pregnancy (ATA 2017): 1st trimester: 0.1-2.5 mUI\/L + 2nd trimester: 0.2-3.0 mUI\/L + 3rd trimester: 0.3-3.5 mUI\/L \u2192 laboratory-specific values if available \u2192 screening for hypothyroidism in pregnancy: TSH in early pregnancy if: thyroid history + symptoms + known positive anti-TPO + infertility + repeated miscarriage + living in an iodine-deficient area; Graves' disease and pregnancy: ATS necessary to protect fetus from thyrotoxicosis \u2192 PTU in 1st trimester (methimazole teratogenic in 1st trimester) \u2192 switch to methimazole in 2nd trimester (PTU risk of hepatitis) \u2192 lowest possible dose + TRAb crosses placenta \u2192 fetal or neonatal thyrotoxicosis if high titre (>3\u00d7 normal in late pregnancy) \u2192 fetal ultrasound monitoring (tachycardia + fetal goiter) + TRAb assay in 3rd trimester (ACOG 2020)<\/td>\n <td>Thyroid management in pregnancy and postpartum: pre-existing hypothyroidism and pregnancy: increase L-T4 dose by 20-30 % as soon as pregnancy is confirmed (needs increase in 1st trimester) \u2192 target TSH: 4.0 mUI\/L + anti-TPO positive or symptoms \u2192 target TSH <2.5 mUI\/L; postpartum thyroiditis: occurs within 12 months of delivery + prevalence: 5-10 % of women + risk factors: anti-TPO positive before pregnancy (risk \u00d730) \u2192 classic biphasic course: thyrotoxic phase (1-4 months postpartum - destructive - release of stored hormones - low TSH + high T4 + collapsed uptake scintigraphy) \u2192 hypothyroid phase (4-8 months postpartum) \u2192 recovery in 80 % of cases in 12 months \u2192 20 % \u2192 permanent hypothyroidism \u2192 treatment: thyrotoxic phase: \u03b2blockers if symptomatic (no ATS - destructive thyrotoxicosis - no excessive hormone synthesis) + hypothyroid phase: L-T4 if symptomatic or desire for pregnancy \u2192 gradual weaning at 12 months; iodine supplementation in pregnancy: 250 \u00b5g\/d recommended \u2192 iodized salt + prenatal supplements with iodine \u2192 caution: especially women with GMN \u2192 excess iodine can trigger hypothyroidism (Wolff-Chaikoff effect) or hyperthyroidism (Jod-Basedow) in multinodular goiters \u2192 supplement with caution + TSH monitoring<\/td>\n <\/tr>\n <\/tbody>\n <\/table>\n\n <div class=\"co-infobox\">\n <span class=\"ico\">\u2139\ufe0f<\/span>\n <span><strong>A \u00abcold\u00bb thyroid nodule on scintigraphy is not necessarily suspicious of malignancy if the TSH is normal:<\/strong> thyroid scintigraphy is only indicated if TSH is low or collapsed. When TSH is normal, almost all nodules are \u00abcold\u00bb on scintigraphy, making it impossible to distinguish benign from malignant nodules. In this context, ultrasound with TI-RADS classification and fine needle aspiration (FNA) guide management - not scintigraphy.<\/span>\n <\/div>\n\n <div class=\"co-urgence\">\n <div class=\"co-urgence-titre\">Situations requiring urgent medical assessment<\/div>\n <p><strong>Goiter + progressive dyspnea + inspiratory stridor + positive Pemberton sign (venous congestion on raising the arms)<\/strong> \u2192 compressive goiter with tracheal stenosis or superior cave syndrome \u2192 urgent cervico-thoracic CT scan + endocrine surgery opinion \u2192 urgent surgical indication if tracheal stenosis <9 mm.<\/p>\n <p><strong>Sudden and rapid increase in Hashimoto's goiter + hard cervical adenopathy + general condition deterioration<\/strong> \u2192 primary thyroid lymphoma (MALT type) to be excluded \u2192 urgent CAF \u00b1 surgical biopsy \u2192 oncology-haematology opinion.<\/p>\n <p><strong>Fever + tachycardia + agitation + confusion + vomiting in a known hyperthyroid patient<\/strong> \u2192 thyrotoxic crisis (thyroid storm - Burch-Wartofsky score) \u2192 life-threatening emergency \u2192 PTU 500-1,000 mg by nasogastric tube + Lugol's iodine (1h after PTU) + dexamethasone 2 mg \u00d7 4\/d + propranolol + intensive care \u2192 mortality 10-30 % even treated.<\/p>\n <p><strong>Firm or stony thyroid nodule + rapid growth in weeks + persistent hoarseness + ipsilateral cervical adenopathy + history of cervical irradiation or MEN2 syndrome<\/strong> \u2192 thyroid cancer to be ruled out urgently \u2192 CAF guided by ultrasound + serum calcitonin + endocrinology opinion + endocrine surgery.<\/p>\n <\/div>\n\n <h2>Consult at Clinique Omicron<\/h2>\n <p>Clinique Omicron's physicians carry out the initial evaluation of the goiter - thyroid biology workup (TSH, antibodies, calcitonin), prescription of thyroid ultrasound, TI-RADS interpretation and referral to cytopuncture or endocrinology depending on the results. Medical follow-up for benign stable goiters, Hashimoto's thyroiditis and levothyroxine substitutions can be provided at one of our points of service in Quebec, or via telemedicine. To book an appointment, visit <a href=\"https:\/\/cliniqueomicron.ca\">cliniqueomicron.ca<\/a>.<\/p>\n\n <p class=\"co-disclaimer\">The content of this page is provided for information purposes only and does not replace the advice of a physician or endocrinologist. Any newly diagnosed or evolving goiter should be evaluated by a healthcare professional to identify its nature and guide appropriate management.<\/p>\n<\/div>\n<\/body>\n<\/html>\t\t\t\t<\/div>\n\t\t\t\t<\/div>\n\t\t\t\t\t<\/div>\n\t\t\t\t<\/div>\n\t\t\t\t<\/div>","protected":false},"excerpt":{"rendered":"<p>Goitre : causes, diagnostic et traitement | Clinique Omicron Endocrinologie & M\u00e9decine de famille & Chirurgie endocrinienne Goitre Le goitre d\u00e9signe toute augmentation du volume de la glande thyro\u00efde au-del\u00e0 des valeurs normales, quelle qu’en soit la cause et quelle que soit la fonction thyro\u00efdienne associ\u00e9e. Le volume thyro\u00efdien normal chez l’adulte est de 6… <a href=\"https:\/\/cliniqueomicron.ca\/en\/goitre\/\" rel=\"bookmark\">Read More \"<span class=\"screen-reader-text\">Goitre: causes, diagnosis and treatment | Clinique Omicron<\/span><\/a><\/p>","protected":false},"author":1,"featured_media":0,"parent":0,"menu_order":0,"comment_status":"closed","ping_status":"closed","template":"","meta":{"om_disable_all_campaigns":false,"neve_meta_sidebar":"","neve_meta_container":"","neve_meta_enable_content_width":"off","neve_meta_content_width":100,"neve_meta_title_alignment":"","neve_meta_author_avatar":"","neve_post_elements_order":"","neve_meta_disable_header":"","neve_meta_disable_footer":"","neve_meta_disable_title":"","_themeisle_gutenberg_block_has_review":false,"_metasync_otto_title":"Goitre : causes, diagnostic et | Brossard | Clinique Omicron","_metasync_otto_description":"Le goitre est une augmentation du volume de la glande thyro\u00efde. 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\n\t\t\t\t\t\n\n\n\n\nGoitre: causes, diagnosis and treatment | Clinique Omicron<\/title>\n<meta name=\"description\" content=\"Goiter is an enlargement of the thyroid gland. Simple, multinodular, toxic or Hashimoto's goiter: ultrasound diagnosis and management in Quebec.\">\n<meta name=\"keywords\" content=\"goitre traitement, goitre thyro\u00efde causes, goitre multinodulaire, goitre toxique, goitre Hashimoto, goitre simple, goitre sympt\u00f4mes, \u00e9chographie thyro\u00efde Qu\u00e9bec\">\n<link rel=\"preconnect\" href=\"https:\/\/fonts.googleapis.com\">\n<link href=\"https:\/\/fonts.googleapis.com\/css2?family=Cinzel:wght@600&family=Poppins:wght@400;500;600;700&display=swap\" rel=\"stylesheet\">\n<style>\n.co-wrap * { font-family: 'Poppins', sans-serif; box-sizing: border-box; }\n.co-wrap { max-width: 1100px; margin: 0 auto; padding: 30px 0 60px; }\n.co-label { font-family: 'Cinzel', serif; font-size: 14px; font-weight: bold; letter-spacing: 1px; text-transform: uppercase; color: #4D6577; margin-bottom: 14px; display: block; }\n.co-wrap h1 { font-size: 32px; font-weight: 500; color: #323C52; margin: 0 0 22px; line-height: 1.2; }\n.co-intro { font-size: 16px; line-height: 1.75; color: #4D6577; margin-bottom: 36px; padding-bottom: 32px; border-bottom: 1px solid rgba(77,101,119,.2); }\n.co-wrap h2 { font-size: 20px; font-weight: 600; color: #323C52; margin: 32px 0 12px; }\n.co-wrap p { font-size: 15px; color: #4D6577; line-height: 1.7; margin-bottom: 14px; }\n.co-list { list-style: none; padding: 0; margin: 12px 0 24px; }\n.co-list li { font-size: 15px; color: #4D6577; padding: 10px 14px 10px 38px; margin-bottom: 8px; border-radius: 6px; position: relative; background: rgba(77,101,119,.06); border-left: 3px solid #4D6577; }\n.co-list li::before { content: \"\u2713\"; position: absolute; left: 12px; font-weight: 700; color: #4D6577; }\n.co-table { width: 100%; border-collapse: collapse; margin: 14px 0 22px; font-size: 14px; border-radius: 8px; overflow: hidden; table-layout: fixed; }\n.co-table thead tr { background: #323C52; color: #fff; }\n.co-table thead th { padding: 11px 16px; text-align: left; font-weight: 600; font-size: 13px; }\n.co-table tbody tr:nth-child(even) { background: rgba(77,101,119,.06); }\n.co-table tbody tr:nth-child(odd) { background: #fff; }\n.co-table td { padding: 10px 16px; color: #4D6577; border-bottom: 1px solid rgba(77,101,119,.12); font-size: 14px; vertical-align: top; }\n.co-table td:first-child { font-weight: 600; color: #323C52; }\n.co-infobox { display: flex; gap: 12px; background: rgba(77,101,119,.06); border-radius: 8px; border-left: 4px solid #4D6577; padding: 14px 18px; margin: 18px 0 28px; font-size: 14px; color: #4D6577; line-height: 1.65; }\n.co-infobox .ico { font-size: 18px; flex-shrink: 0; }\n.co-urgence { background: #fff8f8; border-left: 5px solid #c0392b; border-radius: 6px; padding: 20px 26px; margin: 24px 0 32px; }\n.co-urgence .co-urgence-titre { font-size: 13px; font-weight: 700; color: #c0392b; letter-spacing: 1.5px; text-transform: uppercase; margin-bottom: 10px; }\n.co-urgence p { color: #5a2020; font-size: 14px; margin: 0 0 10px; line-height: 1.7; }\n.co-urgence p:last-child { margin-bottom: 0; }\n.co-disclaimer { font-size: 13px; color: #8a9aaa; font-style: italic; border-top: 1px solid rgba(77,101,119,.15); padding-top: 24px; margin-top: 40px; line-height: 1.6; }\n<\/style>\n<\/head>\n<body>\n<div class=\"co-wrap\">\n <span class=\"co-label\">Endocrinology & Family Medicine & Endocrine Surgery<\/span>\n <h1>Goiter<\/h1>\n\n <div class=\"co-intro\">\n A goiter is any enlargement of the thyroid gland beyond normal values, regardless of cause or associated thyroid function. Normal adult thyroid volume is 6-20 mL in women and 8-25 mL in men, measured by ultrasound. Classically, a distinction is made between simple (or euthyroid, diffuse or nodular, without thyroid dysfunction), multinodular goiter (with or without hyperthyroidism), inflammatory goiter (Hashimoto's thyroiditis, De Quervain's thyroiditis) and diffuse toxic goiter (Graves' disease). Iodine deficiency, the world's leading cause of goiter, has been virtually eliminated in Canada thanks to the mandatory iodization of table salt since 1949. In Quebec, goiters are therefore mainly autoimmune (Hashimoto's), benign nodular or linked to thyroid dysfunction. Assessment is based on TSH, thyroid antibodies and thyroid ultrasound - classically complemented by ultrasound-guided fine-needle cytopuncture (FNC) for any suspicious nodule. Treatment varies according to etiology, size, thyroid function and the presence of compressive symptoms.\n <\/div>\n\n <h2>Pathophysiology, classification and etiologies<\/h2>\n <ul class=\"co-list\">\n <li><strong>Mechanisms of goiter development :<\/strong> the thyroid increases in volume by three main, often interrelated mechanisms: diffuse hyperplasia: prolonged stimulation of thyreocytes by TSH (iodine deficiency + goitrogens + resistance to thyroid hormones) \u2192 increase in the number and size of follicles \u2192 diffuse goiter + focal hypertrophy (nodulogenesis) : clonal expansion of groups of thyreocytes with somatic mutations conferring an advantage in growth or functional autonomy (TSH receptor mutations - TSHR + Gs\u03b1 mutations + BRAF\/RAS alterations in case of malignant transformation) \u2192 benign nodules (adenomas) or malignant nodules (carcinomas) + inflammatory or fibrous infiltration : Hashimoto's thyroiditis (lymphoid infiltrate + progressive fibrosis) + De Quervain's thyroiditis (granulomatous inflammation) + Riedel's thyroiditis (extensive fibrosis - rare); role of iodine in goitrogenesis: iodine is the essential substrate for thyroid hormone synthesis (T3 + T4) \u2192 iodine deficiency \u2192 drop in free T4 \u2192 reflex increase in TSH (hypothalamic-pituitary axis) \u2192 stimulation of thyroidocyte growth \u2192 initially diffuse euthyroid goiter \u2192 multinodularity with age \u2192 recommended iodine intake (WHO): 150 \u00b5g\/d in adults + 250 \u00b5g\/d during pregnancy and breastfeeding \u2192 dietary sources: iodized salt + dairy products + eggs + sea fish + seaweed + dietary goitrogens: substances interfering with thyroid hormone synthesis \u2192 cabbage + broccoli + cauliflower (isothiocyanates) + manioc + soy (isoflavones) \u2192 negligible effect at usual dietary intakes except pre-existing iodine deficiency<\/li>\n <li><strong>Etiological classification of goitres :<\/strong> simple diffuse (euthyroid) goiter: absence of nodules + normal thyroid function + absence of significant antibodies \u2192 causes : iodine deficiency (rare in Canada - isolated rural areas + immigrant populations) + puberty + pregnancy (increased iodine requirements) + goitrogenic drugs (lithium + amiodarone + carbimazole + propylthiouracil - inhibits thyroid hormone synthesis) + genetic factors (familial - familial simple goiter); multinodular goiter (GMN): presence of multiple thyroid nodules of various sizes and structures + most frequent in clinical practice in middle-aged and elderly adults + two forms: euthyroid (non-toxic) GMN: normal thyroid function + benign nodules + ultrasound monitoring + toxic GMN (GMNT): one or more secretory autonomous nodules (toxic adenomas) \u2192 hyperthyroidism \u2192 collapsed TSH + elevated T3\/T4 \u2192 thyroid scintigraphy: \u00abhot\u00bb nodules (hypercaptans) + the rest of the thyroid is suppressed \u2192 treatment: radioactive iodine (\u00b9\u00b3\u00b9I) or surgery; Hashimoto's thyroiditis: autoimmune chronic lymphocytic thyroiditis \u2192 anti-TPO (anti-thyroperoxidase) + anti-thyroglobulin (anti-Tg) antibodies \u2192 lymphoid infiltration + fibrosis \u2192 firm + irregular goiter + progressive hypothyroidism \u2192 most common cause of autoimmune hypothyroidism and goiter in Quebec + prevalence: 5-10 % of adult female population \u2192 treatment: levothyroxine if hypothyroidism; Graves' disease: toxic diffuse goiter \u2192 TSH receptor stimulating antibodies (TSI or TRAb) \u2192 constitutive thyroid stimulation \u2192 hyperthyroidism + vascular diffuse goiter + triad: goiter + ophthalmopathy (exophthalmos) + dermopathy (pretibial myxedema - rare) \u2192 TRAb positive \u2192 treatment: synthetic antithyroid drugs + radioactive iodine + surgery; cervical goiter with endothoracic extension (plunging): goiter descending behind the sternum into the anterior mediastinum \u2192 often bulky multinodular goiter \u2192 tracheal compression + superior cava syndrome if bulky + cervicothoracic CT scan obligatory \u2192 often surgical indication.<\/li>\n <li><strong>Clinical presentation and compressive signs:<\/strong> asymptomatic goiter (most frequent): fortuitous discovery on clinical examination or during cervical imaging (ultrasound + CT + MRI) \u2192 TSH often normal \u2192 monitoring + symptomatic goiter: local functional symptoms: dysphagia (oesophageal compression) + dyspnoea (tracheal compression - inspiratory stridor) + hoarseness (compression of the recurrent laryngeal nerve \u2192 cordial paralysis \u2192 ENT opinion + laryngoscopy) + \u00abball\u00bb sensation in the throat + chronic postural cough + cervical discomfort + Pemberton sign: elevation of arms above head \u2192 cervical venous congestion + facial erythema + vertigo \u2192 compressive endothoracic goiter \u2192 urgent thoracic CT scan + associated systemic symptoms: hyperthyroidism if toxic goiter (palpitations + emaciation + tremors + diarrhea + heat intolerance + tachycardia) + hypothyroidism if Hashimoto's (asthenia + weight gain + frilosity + constipation + bradycardia) + acute neck pain : De Quervain's thyroiditis (viral - granulomatous inflammation) \u2192 pain radiating to jaw and ears + fever + very high SV (>100 mm\/h) + transient thyrotoxicosis \u2192 endocrinology opinion + signs suggestive of malignancy in a nodular goiter: rapidly growing nodule + hard cervical adenosathies + persistent hoarseness + stony consistency of nodule + history of cervical irradiation + familial MEN2 syndrome + ultrasound-guided CAF if suspicious<\/li>\n <\/ul>\n\n <h2>Diagnosis, clinical forms and management<\/h2>\n <table class=\"co-table\">\n <colgroup><col style=\"width:200px;\"><col style=\"width:42%;\"><col><\/colgroup>\n <thead>\n <tr><th>Clinical situation<\/th><th>Diagnosis and assessment<\/th><th>Treatment and follow-up<\/th><\/tr>\n <\/thead>\n <tbody>\n <tr>\n <td>Initial goiter assessment<br><small style=\"font-weight:400;color:#7a8fa0;\">TSH - antibodies - ultrasound - TI-RADS classification<\/small><\/td>\n <td>The initial workup of a newly diagnosed goiter follows a structured algorithm combining thyroid biology and imaging; 1st-line biological workup: ultrasensitive TSH (TSHus): reference test for assessing thyroid function - normal TSH: 0.4-4.0 mIU\/L \u2192 collapsed TSH (4.5 mIU\/L) \u2192 hypothyroid goiter \u2192 assay free T4 + anti-TPO antibodies + anti-Tg antibodies \u2192 normal TSH : euthyroid goiter \u2192 measure anti-TPO antibodies (Hashimoto's screening) + thyroid-specific antibodies: anti-TPO (anti-thyroperoxidase): marker of thyroid autoimmunity \u2192 positive in Hashimoto's (95 % of cases) + Graves' disease (70 %) + postpartum thyroiditis + TRAb (TSH receptor antibodies): specific for Graves' disease \u2192 sensitivity 95 % + specificity 99 % \u2192 positive TRAb + low TSH = Graves' disease almost certain \u2192 monitoring during antithyroid treatment (guides decision to stop) \u2192 serum calcitonin: to be measured if thyroid nodule suspected \u2192 marker of medullary thyroid carcinoma (MTC) \u2192 basal calcitonin >100 pg\/mL \u2192 MTC almost certain \u2192 genetic work-up (RET proto-oncogene) + pentagastrin stimulation test if calcitonin 10-100 pg\/mL (limited availability in Canada) + thyroglobulin (Tg): not useful in initial diagnosis \u2192 follow-up marker for differentiated thyroid cancer after total thyroidectomy; thyroid ultrasound: reference morphological examination \u2192 perform systematically in the presence of any palpated goiter \u2192 measure thyroid volume (ellipsoid formula: L \u00d7 W \u00d7 H \u00d7 0.524 for each lobe) \u2192 characterization of nodules: size + echogenicity + contours + presence of microcalcifications + Doppler vascularization + cervical adenopathies \u2192 ACR TI-RADS classification (Thyroid Imaging Reporting and Data System - Tessler 2017): score 1-5 according to ultrasound features + recommendations for CAF according to score and size: TI-RADS 1-2: benign \u2192 no CAF + TI-RADS 3: slightly suspicious \u2192 CAF if \u22652.5 cm + TI-RADS 4: moderately suspicious \u2192 CAF if \u22651.5 cm + TI-RADS 5: highly suspicious \u2192 CAF if \u22651.0 cm<\/td>\n <td>2nd-line examinations according to clinical orientation: thyroid scintigraphy (\u2079\u2079\u1d50Tc-pertechnetate or \u00b9\u00b2\u00b3I): indicated if TSH low or collapsed + nodular goiter \u2192 identifies \u00abhot\u00bb nodules (autonomous - hypercaptant) + \u00abcold\u00bb nodules (hypocaptant - higher risk of malignancy if cold) \u2192 allows diagnosis of GMNT (toxic multinodular goiter) + Graves' disease (diffuse intense homogeneous uptake) \u2192 NB: not indicated if TSH normal (cold nodule in this context \u2192 same risk of malignancy as any nodule \u2192 evaluate by TI-RADS + CAF); Cervico-thoracic CT with injection: indicated if: endothoracic plunging goiter + dyspnoea or dysphagia + positive Pemberton sign \u2192 precise mapping of extension + tracheal compression (measurement of tracheal diameter - stenosis if <9 mm) + vascular compression + surgical planning \u2192 caution: iodine from the contrast medium can precipitate hyperthyroidism in a GMNT (Jod-Basedow phenomenon) \u2192 inform the endocrinologist + discuss premedication + cervico-thoracic MRI: non-irradiating alternative - useful for mediastinal extension and surgical planning \u2192 no interference with future radioactive iodine; ultrasound-guided fine-needle cytopunction (FNC): outpatient procedure + optional local anesthesia \u2192 cell sampling of suspicious nodule \u2192 Bethesda classification (thyroid cytopathology reporting system - 2023): Bethesda I: non-diagnostic \u2192 repeat + Bethesda II: benign (70-80 % of CAFs) \u2192 surveillance + Bethesda III: atypia of undetermined significance (AUS\/FLUS) \u2192 molecular (ThyroSeq + Afirma) or surgery + Bethesda IV: follicular neoplasm \u2192 surgery (lobectomy) + Bethesda V: suspected malignancy \u2192 surgery + Bethesda VI: malignant \u2192 total thyroidectomy + extension workup.<\/td>\n <\/tr>\n <tr>\n <td>Multinodular euthyroid goiter<br><small style=\"font-weight:400;color:#7a8fa0;\">Surveillance - TI-RADS - CAF - surgical criteria<\/small><\/td>\n <td>Euthyroid multinodular goiter is the most common form of goiter in adults over 50 in Quebec - it is most often benign and requires surveillance only; epidemiology: ultrasound prevalence of thyroid nodules: 20-76 % depending on age and sex (more frequent in women and with age) \u2192 palpable: 5-7 % of the adult population + risk of malignancy of a thyroid nodule: 5-15 % (all sizes combined) \u2192 nodules <1 cm have a risk of malignancy 20 % or new suspicious feature \u2192 repeat CAF; criteria for surgery in euthyroid GMN: compressive symptoms (dysphagia + dyspnea + hoarseness) + large goiter (>80-100 mL) + endothoracic extension + suspicion of malignancy (CAF Bethesda IV-VI) + patient preference after full information + cosmetic (very large cervical goiter) \u2192 surgical indication discussed in multidisciplinary team (endocrinologist + endocrine surgeon); goiter surgery: total thyroidectomy (if large bilateral goiter) or lobectomy (if unilateral goiter or isolated nodule) \u2192 risks: transient or permanent hypoparathyroidism (hypocalcemia) + recurrent laryngeal nerve paralysis (hoarseness) + bleeding \u2192 high-volume surgical center \u2192 permanent complication rate: <2 % in expert centers \u2192 post-operative hypothyroidism: almost constant after total thyroidectomy \u2192 lifetime levothyroxine<\/td>\n <td>Radiofrequency ablation (RFA) of benign nodules: non-surgical interventional technique \u2192 radiofrequency probe introduced into the nodule under ultrasound guidance \u2192 heat \u2192 coagulative necrosis of the nodule \u2192 volume reduction 50-80 % in 6-12 months \u2192 indications: symptomatic (compressive + cosmetic) benign nodule + Bethesda II confirmed + patient refusing or unable to undergo surgery \u2192 advantages: ambulatory + no induced hypothyroidism + preserves thyroid function + rapid recovery \u2192 availability in Quebec: university centers specializing in interventional endocrinology (CHUM + CHU de Qu\u00e9bec - check current availability) \u2192 efficacy data: Ha 2021 meta-analysis (Thyroid): mean volume reduction 76 % at 12 months \u2192 European Thyroid Association recommends RFA as an alternative to surgery for symptomatic benign nodules (ETA 2020) + ethanol ablation (PEI - Percutaneous Ethanol Injection): reserved for cystic or mixed nodules (fluid predominant) \u2192 puncture + cyst emptying + pure ethanol injection + success rate: 85-95 % for pure cysts; long-term follow-up of GMN: risk of progression to GMNT (toxic multinodular goiter) with age \u2192 annual TSH \u2192 if TSH low \u2192 scintigraphy \u2192 if warm nodules \u2192 hyperthyroidism treatment + risk of malignancy in GMN: low but not zero \u2192 any ultrasound or clinical change \u2192 repeat CAF + iodine recommendation: do not supplement iodine in established GMN (risk of Jod-Basedow if subclinical autonomous nodules) \u2192 sufficient normal dietary iodine<\/td>\n <\/tr>\n <tr>\n <td>Hashimoto's goiter (chronic lymphocytic thyroiditis)<br><small style=\"font-weight:400;color:#7a8fa0;\">Anti-TPO - hypothyroidism - levothyroxine - target TSH<\/small><\/td>\n <td>Hashimoto's thyroiditis is the most common cause of hypothyroidism and autoimmune goiter in Canada - its management is well codified; clinical presentation and diagnosis: moderate + firm + irregular goiter (\u00abbumpy\u00bb or \u00abrubbery\u00bb appearance) + sometimes tender + asymptomatic or symptoms of progressive hypothyroidism \u2192 biology: anti-TPO: elevated (>35 IU\/mL) in 95 % of cases \u2192 titer correlated with inflammatory activity + anti-Tg: elevated in 60-80 % + TSH: normal in the euthyroid stage \u2192 progressively elevated with hypothyroidism \u2192 free T4: lowers as hypothyroidism progresses \u2192 natural evolution: euthyroid phase (sometimes initial transient thyrotoxicosis - \u00abhashitoxicosis\u00bb \u2192 release of preformed hormones from destroyed thyreocytes \u2192 5-10 % of Hashimoto's \u2192 transient low TSH \u2192 elevated free T4 \u2192 disappears in 2-4 months \u2192 distinguish Graves' disease: TRAb negative + scintigraphy: uptake collapsed) \u2192 subclinical hypothyroidism (TSH 4.5-10 mIU\/L + normal free T4) \u2192 frank hypothyroidism (TSH >10 mIU\/L + low free T4); peculiarity of Hashimoto's thyroiditis + thyroid cancer: primary thyroid lymphoma (MALT type - Mucosa-Associated Lymphoid Tissue) \u2192 rare but well-documented complication \u2192 risk \u00d760-80 compared with general population \u2192 to be evoked if sudden increase in volume of a Hashimoto's goiter + cervical adenopathies \u2192 CAF + surgical biopsy if doubt \u2192 papillary thyroid carcinoma: slight increase in risk (\u00d71.5-3) in Hashimoto's thyroiditis \u2192 justifies ultrasound follow-up<\/td>\n <td>Treatment of Hashimoto's thyroiditis: treatment of hypothyroidism with levothyroxine (L-T4): indication: TSH >10 mUI\/L \u2192 quasi-systematic treatment + TSH 4.5-10 mUI\/L (subclinical hypothyroidism) \u2192 treatment discussed: consensus indications: symptoms of hypothyroidism + pregnancy or desire for pregnancy + positive anti-TPO (risk of progression to frank hypothyroidism) + ischemic heart disease (target TSH 1-2.5 mUI\/L) + child or adolescent \u2192 comfort treatment if asymptomatic : discussed + initial dosage of L-T4: young adult without comorbidity: 1.6 \u00b5g\/kg\/d full dose + elderly or cardiopathic adult: start at 12.5-25 \u00b5g\/d and increase in increments of 12.5-25 \u00b5g\/d every 4-6 weeks \u2192 avoid rapid increases (risk of angina or tachyarrhythmia) + target TSH: general adult population: 0.5-2.5 mUI\/L + pregnancy: TSH <2.5 mUI\/L in 1st trimester + 75 years: 1.0-4.0 mUI\/L (avoid over-substitution \u2192 arrhythmias + osteoporosis + dementia) \u2192 take on an empty stomach in the morning, 30-60 min before meal (or 4h after calcium + iron + PPI supplements which reduce absorption) + TSH monitoring at 6-8 weeks after each dose adjustment + anti-TPO monitoring: do not monitor regularly (does not guide treatment); goiter reduction on L-T4: L-T4 can reduce goiter volume by partially suppressing TSH \u2192 modest effect \u2192 do not aim for TSH <0.5 mIU\/L to reduce goiter (risk of atrial fibrillation + osteoporosis) \u2192 if compressive goiter persists on L-T4 \u2192 surgery or RFA<\/td>\n <\/tr>\n <tr>\n <td>Toxic goiter - Graves' disease and GMNT<br><small style=\"font-weight:400;color:#7a8fa0;\">TRAb - antithyroid drugs - radioactive iodine - surgery<\/small><\/td>\n <td>Toxic (hyperthyroid) goiters represent a spectrum ranging from Graves' disease to toxic multinodular goiter - their management is specific; Graves' disease: most frequent cause of hyperthyroidism in women aged 20-50 + pathophysiology: IgG antibodies to TSH receptor (TRAb) \u2192 constitutive stimulation of adenylcyclase \u2192 excessive production of T3 + T4 \u2192 TSH suppression \u2192 Graves' triad: diffuse vascular goiter (murmur on auscultation) + ophthalmopathy (exophthalmos \u00b1 chemosis \u00b1 diplopia) + dermopathy (pretibial myxedema - rare) + biology: collapsed TSH (60 years + pre-existing multinodular goiter + often progressive, moderate hyperthyroidism + collapsed TSH + elevated T4\/T3 + negative TRAb + scintigraphy: multiple hot nodules + suppressed inter-nodular tissue \u2192 often subclinical hyperthyroidism (isolated low TSH) for years before frank hyperthyroidism \u2192 Jod-Basedow phenomenon: exposure to iodine (contrast PCI + amiodarone) \u2192 thyrotoxic decompensation in a pre-existing GMNT \u2192 inform radiologists and emergency physicians before any examination with iodinated contrast in a patient with known GMN<\/td>\n <td>Treatment of toxic goiter - three options: synthetic antithyroid drugs (STDs): methimazole (Tapazole) 10-30 mg\/d PO (1st line in North America except 1st trimester pregnancy) + propylthiouracil (PTU) 100-150 mg \u00d7 3\/d (1st line in 1st trimester pregnancy - risk of methimazole embryopathy: choanal atresia + aplasia cutis) \u2192 mechanism: inhibition of thyroperoxidase (TPO) \u2192 blockade of T3\/T4 synthesis + PTU also inhibits peripheral T4\u2192T3 conversion \u2192 time to efficacy: 4-8 weeks + goal: normalization of free T4 then TSH \u2192 NFS monitoring (risk of agranulocytosis 0.3-0.5 % \u2192 patient warning: \u00abconsult ER if fever or oral ulcerations\u00bb) + liver workup (PTU: risk of fulminant hepatitis - rare but serious) \u2192 remission of Graves' disease: 30-50 % after 12-18 months of TSA \u2192 favorable remission criteria: small goiter + low TRAb at end of treatment + HLADR3 and HLA-B8 genetic variants associated with low remission; radioactive iodine (\u00b9\u00b3\u00b9I): definitive treatment - single-dose oral administration \u2192 selective irradiation of hypercaptant thyroid tissue \u2192 destruction of the thyroid \u2192 almost-certain long-term hypothyroidism \u2192 indications: relapsed Graves' disease or 1st line if no desire for pregnancy within 6 months + GMNT (very effective) + solitary toxic adenoma \u2192 relative ICs: pregnancy + breastfeeding + compressive bulky goiter + active moderate to severe Graves' ophthalmopathy (risk of worsening - pretreatment with corticoids) \u2192 available in Quebec in nuclear medicine (CHU + CISSS with nuclear medicine) + thyroid surgery: total (or near-total) thyroidectomy: preferred indication if: very large goiter + compressive symptoms + severe ophthalmopathy (rapid euthyroidism improves ophthalmopathy) + desire for pregnancy within 6 months + associated suspicious nodule \u2192 surgery in euthyroidism (prepare with ATS + \u03b2blockers + Lugol's 5 days before) \u2192 lifelong hypothyroidism after total thyroidectomy \u2192 L-T4 started D1 post-op.<\/td>\n <\/tr>\n <tr>\n <td>Goiter and pregnancy<br><small style=\"font-weight:400;color:#7a8fa0;\">Iodine requirements - TSH in pregnancy - Fetal Graves' disease - post-partum<\/small><\/td>\n <td>Pregnancy induces significant changes in thyroid physiology that may aggravate a pre-existing goiter or reveal a new one; physiological thyroid changes in pregnancy: increased iodine requirement (150 \u2192 250 \u00b5g\/d) \u2192 relative deficiency in Quebec possible \u2192 slight increase in thyroid volume (10-15 %) \u2192 no true goiter if iodine intake is sufficient + increase in TBG (thyroxine-binding globulin) \u2192 increase in total T4 and total T3 \u2192 free T4 and free T3 remain normal (reference parameters in pregnancy) + hCG stimulates TSH receptor (homologous structure) \u2192 TSH physiologically low in 1st trimester (0,1-2.5 mIU\/L) \u2192 peak free T4 \u2192 sometimes picture of transient gestational thyrotoxicosis (TGT): intense nausea + vomiting (hyperemesis gravidarum) \u2192 negative TRAb + transiently low TSH \u2192 spontaneous resolution 2nd trimester \u2192 no ATS; reference values for TSH in pregnancy (ATA 2017): 1st trimester: 0.1-2.5 mUI\/L + 2nd trimester: 0.2-3.0 mUI\/L + 3rd trimester: 0.3-3.5 mUI\/L \u2192 laboratory-specific values if available \u2192 screening for hypothyroidism in pregnancy: TSH in early pregnancy if: thyroid history + symptoms + known positive anti-TPO + infertility + repeated miscarriage + living in an iodine-deficient area; Graves' disease and pregnancy: ATS necessary to protect fetus from thyrotoxicosis \u2192 PTU in 1st trimester (methimazole teratogenic in 1st trimester) \u2192 switch to methimazole in 2nd trimester (PTU risk of hepatitis) \u2192 lowest possible dose + TRAb crosses placenta \u2192 fetal or neonatal thyrotoxicosis if high titre (>3\u00d7 normal in late pregnancy) \u2192 fetal ultrasound monitoring (tachycardia + fetal goiter) + TRAb assay in 3rd trimester (ACOG 2020)<\/td>\n <td>Thyroid management in pregnancy and postpartum: pre-existing hypothyroidism and pregnancy: increase L-T4 dose by 20-30 % as soon as pregnancy is confirmed (needs increase in 1st trimester) \u2192 target TSH: 4.0 mUI\/L + anti-TPO positive or symptoms \u2192 target TSH <2.5 mUI\/L; postpartum thyroiditis: occurs within 12 months of delivery + prevalence: 5-10 % of women + risk factors: anti-TPO positive before pregnancy (risk \u00d730) \u2192 classic biphasic course: thyrotoxic phase (1-4 months postpartum - destructive - release of stored hormones - low TSH + high T4 + collapsed uptake scintigraphy) \u2192 hypothyroid phase (4-8 months postpartum) \u2192 recovery in 80 % of cases in 12 months \u2192 20 % \u2192 permanent hypothyroidism \u2192 treatment: thyrotoxic phase: \u03b2blockers if symptomatic (no ATS - destructive thyrotoxicosis - no excessive hormone synthesis) + hypothyroid phase: L-T4 if symptomatic or desire for pregnancy \u2192 gradual weaning at 12 months; iodine supplementation in pregnancy: 250 \u00b5g\/d recommended \u2192 iodized salt + prenatal supplements with iodine \u2192 caution: especially women with GMN \u2192 excess iodine can trigger hypothyroidism (Wolff-Chaikoff effect) or hyperthyroidism (Jod-Basedow) in multinodular goiters \u2192 supplement with caution + TSH monitoring<\/td>\n <\/tr>\n <\/tbody>\n <\/table>\n\n <div class=\"co-infobox\">\n <span class=\"ico\">\u2139\ufe0f<\/span>\n <span><strong>A \u00abcold\u00bb thyroid nodule on scintigraphy is not necessarily suspicious of malignancy if the TSH is normal:<\/strong> thyroid scintigraphy is only indicated if TSH is low or collapsed. When TSH is normal, almost all nodules are \u00abcold\u00bb on scintigraphy, making it impossible to distinguish benign from malignant nodules. In this context, ultrasound with TI-RADS classification and fine needle aspiration (FNA) guide management - not scintigraphy.<\/span>\n <\/div>\n\n <div class=\"co-urgence\">\n <div class=\"co-urgence-titre\">Situations requiring urgent medical assessment<\/div>\n <p><strong>Goiter + progressive dyspnea + inspiratory stridor + positive Pemberton sign (venous congestion on raising the arms)<\/strong> \u2192 compressive goiter with tracheal stenosis or superior cave syndrome \u2192 urgent cervico-thoracic CT scan + endocrine surgery opinion \u2192 urgent surgical indication if tracheal stenosis <9 mm.<\/p>\n <p><strong>Sudden and rapid increase in Hashimoto's goiter + hard cervical adenopathy + general condition deterioration<\/strong> \u2192 primary thyroid lymphoma (MALT type) to be excluded \u2192 urgent CAF \u00b1 surgical biopsy \u2192 oncology-haematology opinion.<\/p>\n <p><strong>Fever + tachycardia + agitation + confusion + vomiting in a known hyperthyroid patient<\/strong> \u2192 thyrotoxic crisis (thyroid storm - Burch-Wartofsky score) \u2192 life-threatening emergency \u2192 PTU 500-1,000 mg by nasogastric tube + Lugol's iodine (1h after PTU) + dexamethasone 2 mg \u00d7 4\/d + propranolol + intensive care \u2192 mortality 10-30 % even treated.<\/p>\n <p><strong>Firm or stony thyroid nodule + rapid growth in weeks + persistent hoarseness + ipsilateral cervical adenopathy + history of cervical irradiation or MEN2 syndrome<\/strong> \u2192 thyroid cancer to be ruled out urgently \u2192 CAF guided by ultrasound + serum calcitonin + endocrinology opinion + endocrine surgery.<\/p>\n <\/div>\n\n <h2>Consult at Clinique Omicron<\/h2>\n <p>Clinique Omicron's physicians carry out the initial evaluation of the goiter - thyroid biology workup (TSH, antibodies, calcitonin), prescription of thyroid ultrasound, TI-RADS interpretation and referral to cytopuncture or endocrinology depending on the results. Medical follow-up for benign stable goiters, Hashimoto's thyroiditis and levothyroxine substitutions can be provided at one of our points of service in Quebec, or via telemedicine. To book an appointment, visit <a href=\"https:\/\/cliniqueomicron.ca\">cliniqueomicron.ca<\/a>.<\/p>\n\n <p class=\"co-disclaimer\">The content of this page is provided for information purposes only and does not replace the advice of a physician or endocrinologist. Any newly diagnosed or evolving goiter should be evaluated by a healthcare professional to identify its nature and guide appropriate management.<\/p>\n<\/div>\n<\/body>\n<\/html>\t\t\t\t<\/div>\n\t\t\t\t<\/div>\n\t\t\t\t\t<\/div>\n\t\t\t\t<\/div>\n\t\t\t\t<\/div>","protected":false},"excerpt":{"rendered":"<p>Goitre : causes, diagnostic et traitement | Clinique Omicron Endocrinologie & M\u00e9decine de famille & Chirurgie endocrinienne Goitre Le goitre d\u00e9signe toute augmentation du volume de la glande thyro\u00efde au-del\u00e0 des valeurs normales, quelle qu’en soit la cause et quelle que soit la fonction thyro\u00efdienne associ\u00e9e. Le volume thyro\u00efdien normal chez l’adulte est de 6… <a href=\"https:\/\/cliniqueomicron.ca\/en\/goitre\/\" rel=\"bookmark\">Read More \"<span class=\"screen-reader-text\">Goitre: causes, diagnosis and treatment | Clinique Omicron<\/span><\/a><\/p>","protected":false},"author":1,"featured_media":0,"parent":0,"menu_order":0,"comment_status":"closed","ping_status":"closed","template":"","meta":{"om_disable_all_campaigns":false,"neve_meta_sidebar":"","neve_meta_container":"","neve_meta_enable_content_width":"off","neve_meta_content_width":100,"neve_meta_title_alignment":"","neve_meta_author_avatar":"","neve_post_elements_order":"","neve_meta_disable_header":"","neve_meta_disable_footer":"","neve_meta_disable_title":"","_themeisle_gutenberg_block_has_review":false,"_metasync_otto_title":"Goitre : causes, diagnostic et | Brossard | Clinique Omicron","_metasync_otto_description":"Le goitre est une augmentation du volume de la glande thyro\u00efde. 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