Reproductive Endocrinology & Gynecology & Family Medicine
Anti-Müllerian Hormone (AMH)
Anti-Müllerian hormone (AMH), also known as Müllerian Inhibiting Substance (MIS), is a dimeric glycoprotein of the TGF-β (Transforming Growth Factor-beta) superfamily, secreted in women by the granulosa cells of small (2-8 mm) pre-antral and antral ovarian follicles. Today, it is the most reliable marker of ovarian reserve - i.e. residual follicular stock - reflecting both the quantity and, to some extent, the quality of this stock. Unlike FSH and estradiol, AMH is remarkably stable over the menstrual cycle, can be measured at any time during the cycle, and shows little inter-cycle variation. AMH declines progressively with age, from a peak reached between 20 and 25, and becomes undetectable at menopause - the ovaries no longer containing secretory follicles. Its main clinical indications are assessment of ovarian reserve prior to medically assisted procreation (MAP), screening for premature ovarian failure (PCOI), diagnostic guidance in PCOS (very high values), monitoring gonadotoxicity of chemotherapy and ovarian surgery, and fertility preservation. In men, AMH is produced by Sertoli cells until puberty, and its measurement is useful in the assessment of sexual differentiation anomalies and non-palpable testes.
Biology, dosage, and reference values by age
- Physiology of AMH — secretion, regulation, and biological role: in women: secreted by granulosa cells of pre-antral (primary + secondary stage) and small antral follicles (2-8 mm) → not secreted or only slightly secreted by dominant follicles >10 mm (follicular selection → extinction of AMH expression in the dominant follicle) → physiological role of AMH in folliculogenesis: slows primordial follicle recruitment (inhibitory effect on quiescent pool exit) → slows follicle sensitivity to FSH → acts as a regulatory «brake» on the rate of follicular stock depletion → AMH-knockout mice (Durlinger 1999 - Journal of Clinical Investigation): premature depletion of follicular stock → early menopause → confirms the braking role of AMH on primordial stock; correlation AMH - antral follicle count (AFC): AFC (assessed by transvaginal ultrasound D2-J3): number of 2-10 mm follicles visible on echo → correlates strongly with AMH (r = 0.7-0.8 - Broekmans 2006 - Human Reproduction Update) → CFA and AMH are the two best markers of ovarian reserve + complementary → CFA: real-time evaluator (inter-cycle variability + operator-dependent) + AMH: more stable biochemical reflection → AMH gradually replaces FSH on D3 in assessing ovarian reserve → FSH D3: indirect marker + less sensitive + late in reserve decline → AMH is abnormal before FSH changes; hormonal regulation of AMH: quasi-independent of gonadotropins (FSH + LH) in the vast majority of the cycle → unlike FSH and estradiol → AMH stable whatever the day of the cycle (Hehenkamp 2006 - Fertility and Sterility) → slight peri-ovulatory variation (transient drop around D13-J14) → slight seasonal variation (higher in autumn - Lundin 2020 - Human Reproduction) → under combined oral contraception (COC): AMH reduced by 30-50 % → AMH rises again after COC discontinuation → interpretation under COC: possible underestimation of reserve → ideally dose after COC discontinuation × 3 months → but in clinical practice: normal AMH under COC is reassuring → AMH lowered under COC → repeat after discontinuation + in men: secretion by Sertoli cells → high from birth to puberty → decreases sharply at puberty (testosterone inhibits secretion) → male AMH measured in the workup of sexual ambiguities + cryptorchidism + anochidism + pediatric hypogonadism
- Assay methods, standardization, and inter-laboratory variability: immunometric methods available: manual ELISA (Enzyme-Linked ImmunoSorbent Assay): AMH Gen I (Beckman Coulter) + AMH Gen II (Beckman Coulter, currently the most widely used) → results in pmol/L or ng/mL (conversion: 1 ng/mL = 7.14 pmol/L) → automated immunoassays: Elecsys AMH Plus (Roche Diagnostics) → ARCHITECT AMH (Abbott) → Access AMH (Beckman) → enable improved standardization + international standardization: WHO International Standard for AMH in place since 2014 → but residual inter-laboratory variability of 20-30 % depending on studies (Nelson 2015 - Journal of Clinical Endocrinology and Metabolism) → practical implication: compare a patient's AMH values only if assays are performed in the same laboratory with the same method + if change of laboratory → interpret trend (stable + decrease + increase) rather than absolute value → sampling: serum tube (red or yellow cap) → no time constraint or cycle day → stable at room temperature 24h → stable 4°C 48h → freezing possible → several thawings acceptable → no fasting required; reference values by age - female (pooled data - ESHRE 2023 + Nelson 2015 JCEM + Dewailly 2014 Human Reproduction Update): peak AMH: 20-25 years → median 3.0-5.0 ng/mL (21-36 pmol/L) → normal values by age range (median ± percentile 5-95): 20-24 years: 3.0-7.0 ng/mL + 25-29 years: 2.5-6.0 ng/mL + 30-34 years: 1.5-4.5 ng/mL + 35-39 years: 1.0-3.5 ng/mL + 40-44 years: 0.5-2.5 ng/mL + 45-49 years: 0.1-1.5 ng/mL + post-menopause: 1.2 ng/mL (depending on age) + Diminished Ovarian Reserve (DOR): <1.2 ng/mL or <8.6 pmol/L + severely diminished reserve: <0.5 ng/mL + probable premature ovarian insufficiency (POI): <0.2-0.5 ng/mL in a woman 3.5 ng/mL (some centers >5 ng/mL) → PCOS diagnostic criterion according to new ESHRE 2023 recommendations (Teede 2023)
- AMH and modifying factors — causes of low or high AMH: causes of lowered AMH (diminished reserve): age (main physiological cause) → ovarian endometriosis (endometriomas): endometriomas destroy adjacent ovarian parenchyma → direct reduction in follicular pool → lowered AMH proportional to size and number of endometriomas (Uncu 2013 - Human Reproduction) → ovarian surgery: ovarian cystectomy + endometrioma resection → always at risk of sacrificing healthy ovarian tissue → AMH drops significantly after bilateral ovarian surgery (Raffi 2012 - Journal of Clinical Endocrinology and Metabolism) → indicator of quality of surgery → discuss cystectomy vs puncture-aspiration if desire for pregnancy + gonadotoxic chemotherapy: alkylating agents (cyclophosphamide ++ - most gonadotoxic) + platinum salts + pelvic + craniospinal radiotherapy → AMH drops rapidly after chemotherapy → pre-chemotherapy value = reference for assessing recovery → post-chemotherapy monitoring: AMH at 6 months + 1 year + 2 years → active smoking (Freour 2008 - Human Reproduction): AMH lowered by 20-30 % in smokers + obesity + high BMI: AMH slightly reduced (but the effect is modest) + autoimmunity: autoimmune ovarian insufficiency (APCA + antiadrenal antibodies in autoimmune polyendocrinopathy - APS-1 and APS-2) + classic galactosemia → early POI + Turner (45,X) + FMR1 mutations (Fragile X premutation): IOP in 20 % of carriers + FSHR + BMP15 + GDF9 mutations → IOP + radiotherapy → ovarian doses >2 Gy → IOP risk; causes of high AMH: PCOS: follicular hyperactivity → very high AMH (2-5× normal for age) → marker of antral follicular mass ++ → AMH ≥3.5-5 ng/mL in a 30-35 year old woman → strongly suggestive of PCOS + ovarian granulosa tumors: AMH can be very high → follow-up tumor marker (Gustafson 1992 - Gynecologic Oncology) → pre- and post-surgery AMH dosage + follow-up → recurrence: AMH rises before clinical recurrence → useful as marker of recurrence + iatrogenic ovarian hyperplasia (excessive ovarian stimulation) → risk of ovarian hyperstimulation syndrome (OHSS) if AMH >3.5 ng/mL → adapted stimulation protocol
Clinical indications, interpretation, and management
| Indication / Context | Interpretation and course of action | Clinical Data and Follow-up |
|---|---|---|
| Fertility Assessment and Assisted Reproductive Technology (ART) — Ovarian Reserve Evaluation FIV - stimulation protocol - POSEIDON - ovarian response - SHO |
Role of AMH in fertility workup: AMH is the best predictor of ovarian response to gonadotropic stimulation (exogenous FSH) in IVF → predictor of quantity of oocytes recovered + not pregnancy rate per embryo (oocyte quality is determined by age, not solely by AMH) → Broer 2013 - Human Reproduction Update: meta-analysis → AMH: best predictor of poor ovarian response (AUC 0.82) and excessive response (SHO) → superior to FSH D3 + CFA slightly superior to AMH for excessive response in some meta-analyses → AMH + CFA association = better diagnostic accuracy; POSEIDON (Patient-Oriented Strategies Encompassing IndividualizeD Oocyte Number) classification - 2019 (Poseidon Group - Frontiers in Endocrinology): classification of patients with low ovarian response in IVF according to AMH and CFA: Group 1 (good prognosis - low unexpected response): age <35 years + AMH ≥1.2 ng/mL + CFA ≥5 → response <4 oocytes despite standard stimulation → Group 2 (good prognosis - low unexpected response): age ≥35 years + AMH ≥1.2 ng/mL + CFA ≥5 → same context → Group 3 (poor prognosis - low expected response): AMH <1.2 ng/mL + DWI <5 + age <35 → Group 4 (poor prognosis - low expected response): AMH <1.2 ng/mL + DWI 3.5 ng/mL + PCOS): risk of OHSS → GnRH antagonist protocol (short-term antagonist: cetrorelix + ganirelix) + low-dose FSH (75-112 IU/d) + GnRH agonist trigger (Lupron trigger) instead of hCG → reduces risk of OHSS + normal AMH (1.2-3.5 ng/mL): standard protocol → long agonist or antagonist → FSH 150-225 IU/d + decreased AMH (<1.2 ng/mL): antagonist protocol + high-dose FSH (225-450 IU/d) + Dublin score or Bologna criteria → consider oocyte donation if AMH 38 years; predictive value of AMH on pregnancy: AMH does NOT predict the pregnancy rate per embryo transferred → a patient with very low AMH can conceive if embryo quality is good → AMH predicts the quantity of oocytes available + the number of attempts required → important message to avoid fatalism in patients with DOR | Ovarian hyperstimulation syndrome (OHSS) - AMH-guided prevention: OHSS: iatrogenic complication of ovarian stimulation → increased vascular permeability → ascites + pleural effusions + hemoconcentration + thromboses → pathogenesis: massive VEGF secretion by stimulated granulosa → AMH >3.5 ng/mL = major risk factor for severe OHSS (Nardo 2009 - Human Reproduction) → PCOS = OHSS risk ++ → AMH-guided prevention strategies: antagonist protocol + reduced doses of FSH + coasting (reduction or cessation of FSH from E2 >15,000 pmol/L) + GnRH agonist triggering (instead of hCG) → LH/FSH receptor stimulation → peak ovulation + corpus luteum with less VEGF → 90 % severe OHSS reduction → freezing of all embryos (freeze-all) + delayed transfer → avoid risky luteal phase + inositol + cabergoline (dopaminergic agonist) : SHO prevention by VEGFR-2 reduction → dosage: 0.5 mg/d × 8 days → reference: Alvarez 2007 - Fertility and Sterility; oocyte donation - when to consider it: AMH <0.2-0.5 ng/mL + DWI 38-40 + response <3 oocytes over several IVF cycles → pregnancy rate with oocyte donation does not depend on recipient's AMH (depends on donor's AMH + uterine age) → ethical discussion + delay (waiting list in Quebec) + RAMQ reimbursement : IVF covered for women with diagnosed infertility + oocyte donation: not covered by RAMQ → cost 15,000-25,000 $ CAD (full protocol) |
| Premature Ovarian Insufficiency (POI) and Early Menopause AMH <0.5 ng/mL before age 40 — elevated FSH — amenorrhea — etiology — HRT |
Definition and diagnosis of PIO (ESHRE 2016 - Human Reproduction): amenorrhea or oligomenorrhea >4 months + FSH >25 IU/L on 2 assays 4-6 weeks apart + in a woman <40 years old → AMH: collapsed or undetectable (<0.1-0.2 ng/mL) in established POI → AMH lowered for age (<0.5 ng/mL) may precede POI by several years → early marker before FSH elevation + marker of transition to POI; etiological assessment of POI: genetic causes (20-25 % of POI): Turner syndrome (45,X or 45,X/46,XX mosaics) → karyotype + fragile X syndrome (FMR1 premutation: 55-200 CGG repeats) → FMR1 molecular testing + rare mutations: BMP15 + GDF9 + NOBOX + FIGLA + NR5A1 → NGS genetic panel available in specialized center + autoimmune causes (30-50 % of idiopathic POI): anti-adrenal antibodies (21-hydroxylase) → APS-1 + APS-2 → risk of associated adrenal insufficiency → cortisol dosage + Synacthen test + anti-thyroid antibodies → associated autoimmune hypothyroidism (30 % of autoimmune PIOs) + APCA (anti-gastric parietal cell antibodies) → Biermer anemia → CBC + B12 + anti-tissue antibodies: ANCA + FAN → lupus + history of chemotherapy or radiotherapy → iatrogenic + classic galactosemia → galactose-1-phosphate uridyl-transferase dosage + rare infiltrative diseases (ovarian tuberculosis + amyloidosis); consequences of untreated PIO: chronic hypoestrogenism → osteoporosis (accelerated bone loss - 3-5 %/year) → increased cardiovascular risk (early menopause → endothelium + lipids) + vasomotor disorders + vaginal dryness + urogenital atrophy → cognitive risk (menopause <40 years → dementia risk × 1.5 - Bove 2020 - Neurology) → major psychological impact: sudden infertility + fertility grief + anxiety + depression → imperative psychological support. | Treatment of POI - hormone replacement therapy (HRT): ESHRE 2016: HRT recommended up to age 50-51 (average age of natural menopause) for all women with POI → cardio-protective + osteoprotective + cognitive → lower thromboembolic risk than in treated late natural menopause → transdermal route (patch or gel) preferred → avoids hepatic first pass → less thromboembolic risk → transdermal estradiol 75-100 µg/24h (biweekly patch) + progestin if uterus present (micronized progesterone 200 mg/d × 12d/month or Duphaston 10 mg/d × 12d/month) → if desire for pregnancy associated with HRT : HRT and IVF with oocyte donation are not incompatible → HRT prepares the endometrium for embryo transfer → spontaneous pregnancy remains possible in POI (5-10 % of idiopathic POI - documented «partial cure» spontaneous conception) → contraception: if patient does not wish pregnancy → contraception even under HRT → PIO does not mean absolute sterility + monitoring: bone densitometry (DXA) at diagnosis + every 2-3 years + annual TSH + cortisol + ACTH if antiadrenal antibodies positive + psychological follow-up; fertility preservation before gonadotoxicity: indication: chemotherapy + planned pelvic radiotherapy in a woman of childbearing age → pre-treatment AMH: reference value + predictor of response to ovarian stimulation → oocyte or embryo freezing (IVF): reference method → emergency ovarian stimulation (short antagonist protocol) + oocyte puncture + vitrification + delay: 2-3 weeks → ovarian transposition (oophoropexy) if pelvic radiotherapy → moves ovaries away from irradiation field → partial efficacy + cryopreservation of ovarian tissue: option if delay <2 weeks or in prepubertal girls → under evaluation in Quebec (CHUM + CHU Sainte-Justine) |
| AMH and PCOS — diagnostic marker and monitoring AMH ≥3.5–5 ng/mL — ESHRE 2023 criteria — role in folliculogenesis — therapeutic implications |
Elevated AMH in PCOS - mechanism and diagnostic value: in PCOS: arrest of follicular development at early antral stage (2-8 mm) → accumulation of numerous small antral follicles → hypersecretion of AMH by these blocked follicles (× 2-3 normal for age) → elevated AMH = reflection of stagnant follicular mass + granulosa dysfunction in PCOS → AMH in diagnostic criteria for PCOS: Rotterdam 2003 criteria: 2/3 criteria (oligo-anovulation + hyperandrogenism + polycystic ovaries on echo) → AMH not formally included in Rotterdam 2003 → ESHRE 2023 (Teede 2023 - Human Reproduction): updated criteria → AMH ≥3.5 ng/mL (according to certain thresholds) may replace the ultrasound criterion of ovarian polycystic ovary in the absence of a high-resolution ultrasound scanner or in adolescents → avoids endovaginal ultrasound not accepted by some adolescents → threshold retained variable according to consensus: >3.5 ng/mL (ESHRE 2023 threshold) or >5.0 ng/mL (more specific threshold) → sensitivity 65-82 % + specificity 86-92 % for the diagnosis of PCOS (Eilertsen 2012 - Clinical Endocrinology); AMH very high in PCOS (≥8-10 ng/mL): evoke a granulosa tumor → inhibin B assay + ovarian imaging → AMH can be used as a follow-up marker for PCOS under treatment: weight loss + metformin + COC → modest reduction in AMH over the long term → but AMH remains elevated in PCOS even when treated → complete normalization of AMH in PCOS is not a therapeutic goal in itself; practical implications of elevated AMH in PCOS for MAP: high risk of OHSS → systematic antagonist protocol + low-dose FSH + Lupron trigger → IVF pregnancy rate: better in PCOS than in DOR (PCOS paradox - many oocytes + preserved quality depending on age) → but risk of oocyte unripening + risk of OHSS → fine balance | AMH and granulosa tumors - use as a tumor marker: granulosa cell tumor (GCT): rare ovarian tumor → represents 2-5 % of ovarian tumors → secretes AMH + inhibin B → AMH very high in GCTs (often >10-20 ng/mL) → Gustafson 1992 - Gynecologic Oncology: first description of AMH as a marker for GCTs → post-surgical follow-up: AMH measured at 4-6 weeks post-surgery (should drop to zero if complete resection) → quarterly monitoring the 1st year → then biannually × 5 years → AMH elevation on monitoring = recurrence likely → imaging workup (CT TAP or PET) → inhibin B: complementary marker of GCT → sometimes more sensitive than AMH in certain forms → combined use of AMH + inhibin B → better performance; AMH in men - pediatric indications: newborn and infant: AMH elevated (normal) → confirms presence of functional testicular tissue → useful in: bilateral cryptorchidism (non-palpable testes) → AMH normal = testicular tissue present → refer for exploratory surgery (orchidopexy) + true anochidism (absence of testicular tissue) → AMH undetectable → confirms absence of testicular tissue → bilateral anorchidism → testicular regression syndrome → complete androgen insensitivity syndrome (AIS - CAIS): high AMH (testicular tissue present + normal AMH secretion) + normal or high androgens + female phenotype → allows confirmation of inguinal testicular tissue to be removed (risk of gonadoblastoma) + male hypogonadotropic hypogonadism (HH): low AMH → confirms chronic FSH/LH deficiency affecting Sertoli cells → differentiates from anochidism if AMH detectable |
| AMH and fertility preservation — particular situations Egg freezing — endometriosis — ovarian surgery — cancer — FtM transition |
Fertility preservation by oocyte or embryo freezing - role of AMH: pre-stimulation AMH is the best predictor of the number of oocytes recovered at puncture → AMH >1.2 ng/mL → standard stimulation → expected number of mature oocytes : 8-15 → AMH 0.5-1.2 ng/mL → FSH dose increased → 4-8 oocytes expected → AMH <0.5 ng/mL → low reserve → maximum stimulation → risk of <4 oocytes → discuss realism of preservation → number of oocytes needed for a reasonable chance of pregnancy: Rienzi 2017 - Human Reproduction : 10-15 mature oocytes vitrified → cumulative birth rate ≈ 60-70 % in <35 years → oncological preservation: AMH pre-chemotherapy → reference value → AMH post-chemotherapy at 6 months + 1 year + 2 years → assesses gonadotoxicity and recovery → Anderson 2013 - Journal of Clinical Oncology: AMH as the best marker for post-chemotherapy ovarian follow-up → tobacco and AMH: Freour 2008 - Human Reproduction: AMH 20-30 % lower in smokers → advice: stop smoking before PMA; endometriosis and AMH - when to operate on an endometrioma? : surgical dilemma: surgery (cystectomy) reduces AMH → but the endometrioma itself reduces AMH and destroys adjacent ovarian parenchyma → Raffi 2012 - JCEM: bilateral cystectomy → AMH reduction of 50 % → personalized decision: if endometrioma 4 cm + significant symptoms + AMH still satisfactory → cautious surgery with maximum sparing of healthy ovarian tissue → laparoscopy with minimal hemostasis (minimal coagulation) → experienced surgeon → Somigliana 2012 - Human Reproduction: ESHRE recommendations on fertility preservation in endometriosis; AMH and gender transitions (FtM transgender people - female to male): long-term testosterone in FtM transgender people → reduction of AMH (partial gonadotoxicity of testosterone → Moravek 2020 - Fertility and Sterility) → reversible effect after discontinuation → before testosterone initiation: propose discussion of fertility preservation + baseline AMH → monitoring of AMH under testosterone → if desire for future pregnancy: oocyte or embryo freezing before testosterone + amenorrhea under testosterone: cycles may resume on discontinuation → AMH can guide decision on ovarian stimulation | AMH limitations and misinterpretations to avoid: AMH does NOT predict natural fertility (spontaneous pregnancy rate): prospective studies on women of childbearing age with low AMH → time to conception similar to women with normal AMH if age is controlled (Steiner 2017 - JAMA) → low AMH in a 30-year-old woman seeking pregnancy naturally does not justify the absolute urgency of immediate IVF → but requires follow-up + advice not to delay pregnancy + AMH does NOT measure oocyte quality: normal AMH in a 42-year-old woman does not mean good oocyte quality → age remains the most important determinant of oocyte quality + aneuploidies + FCS → low AMH in an adolescent should be interpreted with caution: physiological variations + impact of COCs + intercurrent illnesses → repeat assay before concluding + monitoring AMH post ovarian surgery: measure at 3 months post-op (stabilization) → baseline post-surgery → monitor at 1 year + 2 years → if AMH continues to fall → surgery has sacrificed more than expected → discussion of early MAP; ethnic and genetic factors modifying AMH: African-American origin: AMH slightly lower than Caucasian women of the same age (Bleil 2014 - Fertility and Sterility) → interpretation of reference values with ethnic data if available + genetic polymorphisms of the AMH and AMHR2 gene → modify basal levels → ongoing research |
ℹ️
Low AMH doesn't predict natural infertility in a young woman: A major prospective study (Steiner 2017 — JAMA) of 750 women aged 30–44 demonstrated that low AMH was not associated with a prolonged time to conception or a reduced rate of natural pregnancy when age was controlled for. AMH predicts the quantity of oocytes available for ovarian stimulation (ART), not the likelihood of spontaneous pregnancy. A low AMH result should never, on its own, trigger an indication for IVF or generate a sense of despair in a young woman seeking pregnancy naturally.
Situations requiring immediate specialized medical evaluation
Low AMH (25 IU/L + amenorrhea in a woman <35 years old → Premature ovarian insufficiency → confirm with a second assay at 4–6 weeks + complete etiological workup (karyotype + FMR1 + anti-adrenal antibodies + TSH) → initiate hormone replacement therapy rapidly to prevent osteoporosis and cardiovascular risks → refer to reproductive endocrinology or specialized gynecology → psychological support.
Very high AMH (>8–10 ng/mL) in a woman whose clinical context does not correspond to typical PCOS (no oligomenorrhea + no hyperandrogenism) → Evoke a granulosa cell tumor → Inhibin B assay + urgent pelvic ultrasound → Pelvic CT or MRI if ovarian mass → Referral to gynecologic oncology.
Woman about to start gonadotoxic chemotherapy (alkylating agents, cyclophosphamide, platinum salts) without having completed her family-building plans → Fertility emergency → Immediate referral to an ART center → Emergency ovarian stimulation in 2-3 weeks → Oocyte or embryo cryopreservation before chemotherapy initiation → Pre-chemotherapy AMH measurement as a baseline.
Brutal drop in AMH post-ovarian surgery (bilateral cystectomy) >50 % of preoperative value in a woman with parental plans → Compromised ovarian reserve → Urgent referral to fertility treatment → Discuss IVF before any new ovarian surgery → Avoid any non-essential new ovarian intervention.
Consult at Clinique Omicron
Clinique Omicron physicians prescribe AMH testing as part of fertility assessments, amenorrhea evaluations, or suspected premature ovarian insufficiency, and interpret the results within their overall clinical context. Patients requiring assisted reproductive technology (ART), fertility preservation, or reproductive endocrinology care are referred to specialized partner centers. Consultations are available at several service points in Quebec as well as via telemedicine. To book an appointment, visit cliniqueomicron.ca.
The content of this page is provided for informational purposes only and does not substitute for the advice of a physician, gynecologist, or reproductive endocrinologist. The interpretation of AMH should always take into account age, clinical context, assay method, and laboratory used.
Omicron Clinic
Need to consult a doctor?
Treatment within 24-48 hours. In-clinic or telemedicine, anywhere in Quebec.
Insurance receipts. 7j/7. No family doctor required.