Drug Monograph

Exemestane

Aromasin
Steroidal Aromatase Inactivator (Irreversible) · Oral
Pharmacokinetic Profile
Half-Life
~24 hours
Metabolism
Hepatic; CYP3A4 (oxidation) + aldoketoreductases
Protein Binding
90% (albumin, α1-acid glycoprotein)
Bioavailability
~42% absorbed; food increases AUC by 59%
Volume of Distribution
Extensively distributed into tissues
Clinical Information
Drug Class
Third-generation steroidal aromatase inactivator
Available Doses
25 mg tablet
Route
Oral (must take after a meal)
Renal Adjustment
Not required (AUC ↑ but tolerated)
Hepatic Adjustment
Not required (AUC ~3× higher in moderate-severe)
Pregnancy
Contraindicated — may cause fetal harm
Lactation
Do not breastfeed; wait 1 month after last dose
Schedule / Legal Status
Prescription only (not scheduled)
Generic Available
Yes
Rx

Indications

IndicationApproved PopulationTherapy TypeStatus
ER-positive early breast cancer — adjuvant (sequential after tamoxifen)Postmenopausal women who have completed 2–3 years of tamoxifenMonotherapy; switch to complete 5 years total endocrine therapyFDA Approved
Advanced breast cancer — post-tamoxifen progressionPostmenopausal women with disease progression on tamoxifenMonotherapyFDA Approved

Exemestane occupies a distinct position among aromatase inhibitors as the only steroidal, irreversible aromatase inactivator in clinical use. In the landmark Intergroup Exemestane Study (IES), switching from tamoxifen to exemestane after 2–3 years significantly improved disease-free survival compared with completing 5 years of tamoxifen (HR 0.76, p=0.0001 at 55.7 months), with benefits translating into a modest overall survival improvement at long-term follow-up. For advanced disease progressing on tamoxifen, exemestane offers an effective second-line endocrine option with favourable tolerability compared with megestrol acetate.

Off-Label Uses

Breast cancer risk reduction in high-risk postmenopausal women (Evidence: High). In the MAP.3 trial (N Engl J Med 2011), exemestane 25 mg daily for 5 years reduced invasive breast cancer by 65% compared with placebo (HR 0.35, 95% CI 0.18–0.70; p=0.002) at a median follow-up of 35 months. No increase in serious adverse events, fractures, or cardiovascular events was observed.

ER-positive early breast cancer in premenopausal women with ovarian suppression (Evidence: High). The TEXT/SOFT combined analysis demonstrated that exemestane plus ovarian suppression significantly improved disease-free survival vs tamoxifen plus ovarian suppression (HR 0.72, p<0.001). This use is guideline-supported by ASCO and NCCN.

Dose

Dosing

Clinical ScenarioStarting DoseMaintenance DoseMaximum DoseNotes
ER+ early breast cancer — sequential switch after 2–3 years tamoxifen25 mg once daily25 mg once daily25 mg/dayContinue to complete a total of 5 years adjuvant endocrine therapy
Must be taken after a meal for optimal absorption
Advanced breast cancer — after tamoxifen progression25 mg once daily25 mg once daily25 mg/dayContinue until disease progression
Food increases bioavailability by ~59%
Breast cancer risk reduction — high-risk postmenopausal women (off-label)25 mg once daily25 mg once daily25 mg/day5-year course per MAP.3 protocol
Not FDA-approved for prevention
ER+ breast cancer in premenopausal women with ovarian suppression (off-label)25 mg once daily25 mg once daily25 mg/dayCombined with GnRH agonist, oophorectomy, or ovarian irradiation for 5 years
Per TEXT/SOFT protocol; guideline-supported
Concomitant strong CYP3A4 inducer (rifampicin, phenytoin, carbamazepine)50 mg once daily50 mg once daily50 mg/dayDose increase required; CYP3A4 induction reduces exemestane AUC by ~54%
FDA PI Section 2.2

Special Populations

PopulationStarting DoseMaintenance DoseMaximum DoseNotes
Renal impairment (including severe, CrCl <35 mL/min)25 mg once daily25 mg once daily25 mg/dayAUC ~3× higher but no dose adjustment required; well tolerated at repeated doses up to 200 mg/day (FDA PI)
Hepatic impairment (moderate-severe; Child-Pugh B/C)25 mg once daily25 mg once daily25 mg/dayAUC ~3× higher but no dose adjustment required based on tolerability data (FDA PI)
Elderly25 mg once daily25 mg once daily25 mg/dayNo age-related PK differences observed (age range 43–68 in PK studies) (FDA PI)
Clinical Pearl: Must Be Taken After a Meal

Unlike anastrozole and letrozole, exemestane absorption is significantly affected by food. A high-fat meal increases the AUC by 59% and Cmax by 39% compared with fasting. The FDA label specifies administration after a meal for all indications. Patients should be counselled to take their tablet consistently after breakfast or another substantial meal to ensure reliable drug exposure. This is the most important practical prescribing distinction from the non-steroidal aromatase inhibitors.

PK

Pharmacology

Mechanism of Action

Exemestane is structurally related to the natural aromatase substrate androstenedione. It functions as a false substrate that is processed by the aromatase enzyme (CYP19A1) to a reactive intermediate which binds covalently and irreversibly to the active site, permanently inactivating the enzyme. This mechanism is termed “suicide inhibition” and distinguishes exemestane from the non-steroidal, reversible inhibitors anastrozole and letrozole. Because inhibition is irreversible, new aromatase protein must be synthesized before estrogen production can resume, resulting in prolonged estradiol suppression even after drug clearance. At the 25 mg daily dose, exemestane achieves 85–95% suppression of plasma estrogens and reduces whole-body aromatization by approximately 98%. Importantly, exemestane has no meaningful effect on adrenal corticosteroid or aldosterone synthesis, so no steroid replacement is required. A notable pharmacological feature is that the 17-dihydrometabolite of exemestane binds the androgen receptor with approximately 100 times the affinity of the parent compound, conferring mild androgenic activity that may partially protect against bone loss.

ADME Profile

ParameterValueClinical Implication
Absorption~42% absorbed; Tmax ~1.2 h (cancer patients), ~2.9 h (healthy); high-fat meal increases AUC by 59%Must be taken after a meal; faster absorption in patients with breast cancer than in healthy volunteers
Distribution90% plasma protein bound (albumin, α1-acid glycoprotein); extensively distributed; negligible blood cell distributionHigh protein binding; distribution independent of concentration
MetabolismExtensive hepatic; CYP3A4 (oxidation of position 6 methylene) + aldoketoreductases (17-keto reduction); <10% circulates unchanged; metabolites inactive or less potentDoes not inhibit major CYP isoenzymes; susceptible to CYP3A4 inducers (dose increase to 50 mg required)
Eliminationt½ ~24 h; 42% urine, 42% feces; <1% excreted unchanged in urineShorter half-life than non-steroidal AIs but irreversible binding compensates; once-daily dosing sufficient
SE

Side Effects

Side effect data below are primarily from the IES study (adjuvant setting, N=2,252 exemestane vs N=2,280 tamoxifen) unless otherwise stated. All rates represent incidence during treatment or within one month of treatment completion.

≥10% Very Common
Adverse EffectIncidenceClinical Note
Hot flushes21.2%Most common effect; similar to tamoxifen (19.9%); reflects estrogen deprivation
Fatigue16.1%Similar to tamoxifen (14.7%); usually mild to moderate
Arthralgia14.6%Significantly higher than tamoxifen (8.6%); characteristic AI class effect
Headache13.1%Higher than tamoxifen (10.8%); generally self-limiting
Insomnia12.4%Higher than tamoxifen (8.9%); often co-occurs with hot flushes and mood changes
Increased sweating11.8%Similar to tamoxifen (10.4%); vasomotor symptom cluster
1–10% Common
Adverse EffectIncidenceClinical Note
Hypertension9.8%Similar to tamoxifen (8.4%); monitor BP at each visit
Dizziness9.7%Slightly higher than tamoxifen (8.4%); advise caution with driving
Pain in limb9.0%Higher than tamoxifen (6.4%); part of musculoskeletal syndrome
Back pain8.6%Similar to tamoxifen (7.2%)
Nausea8.5%Similar to tamoxifen (8.7%); usually mild; taking after a meal may help
Depression6.2%Similar to tamoxifen (5.6%); screen regularly with validated tool
Osteoarthritis5.9%Higher than tamoxifen (4.5%); AI-related musculoskeletal effect
Visual disturbances5.0%Higher than tamoxifen (3.8%); ophthalmology referral if persistent
Osteoporosis4.6%Higher than tamoxifen (2.8%); DEXA monitoring essential
Diarrhea4.2%Higher than tamoxifen (2.2%); usually self-limiting
Clinical fractures4.2%Higher than tamoxifen (3.1%); ensure calcium/vitamin D supplementation
Paresthesia2.6%Higher than tamoxifen (0.9%); includes carpal tunnel syndrome (2.4% vs 0.2%)
Cardiac ischemic events1.6%Higher than tamoxifen (0.6%); includes MI, angina, myocardial ischemia
Thromboembolism0.9%Lower than tamoxifen (2.0%); a key safety advantage of exemestane
Serious Serious (Regardless of Frequency)
Adverse EffectEstimated FrequencyTypical OnsetRequired Action
Cardiac ischemic events (MI, angina)1.6%During treatmentCardiovascular risk assessment before initiation; 6 deaths from stroke and 5 from cardiac failure on exemestane arm in IES
Clinical fractures4.2%Throughout treatmentBaseline DEXA; calcium/vitamin D; consider bisphosphonate if T-score ≤ −2.0
Hepatitis (including cholestatic)Very rare (post-marketing)VariableMonitor LFTs if symptoms arise; discontinue if hepatitis confirmed
Hypersensitivity reactionsVery rare (post-marketing)Any timeDiscontinue permanently; contraindicated on rechallenge
Acute generalized exanthematous pustulosisVery rare (post-marketing)Days to weeksImmediate discontinuation; dermatology referral
Severe lymphocytopenia (CTC grade 3–4)~20% in advanced disease (89% had pre-existing lymphopenia)During treatmentMonitor CBC; no increase in viral or opportunistic infections observed; 40% recovered during treatment
Discontinuation Discontinuation Rates
IES Study (Adjuvant, Sequential)
6.3% vs 5.1% tamoxifen
Top reasons: Musculoskeletal symptoms, hot flushes, fatigue
Advanced Breast Cancer Program
3% overall; 2.7% within first 10 weeks
Context: Only 1 death possibly treatment-related (MI in 80-year-old with known CAD)
Reason for DiscontinuationIncidenceContext
Musculoskeletal symptomsLeading cause in adjuvant settingArthralgia, pain in limb, back pain; may respond to AI switch
Hot flushesCommon contributorSimilar discontinuation rate to tamoxifen arm
Study 027 (vs placebo)12.3% exemestane vs 4.1% placeboHigher rate reflects true drug-attributable AE burden without tamoxifen comparator effects
Managing Exemestane-Related Musculoskeletal Symptoms

Arthralgia and musculoskeletal pain are the most clinically significant tolerability concerns with all aromatase inhibitors, including exemestane. Exemestane has a theoretical advantage in bone health due to its mild androgenic metabolite, but clinical fracture rates (4.2%) remain higher than tamoxifen (3.1%). In patients intolerant of a non-steroidal AI (anastrozole or letrozole), switching to exemestane may be effective — approximately one-third of patients intolerant of one AI can tolerate another, and the steroidal vs non-steroidal distinction may be clinically relevant. Regular exercise, physiotherapy, and short-term NSAID use are reasonable supportive strategies.

Int

Drug Interactions

Exemestane is metabolised primarily by CYP3A4 and aldoketoreductases. Notably, exemestane does not inhibit any major CYP isoenzymes (CYP1A2, 2C9, 2D6, 2E1, 3A4) and therefore has very low potential to affect other drugs. However, exemestane is susceptible to CYP3A4 induction, which is the most clinically important interaction requiring a dose adjustment.

Major Strong CYP3A4 Inducers (Rifampicin, Phenytoin, Carbamazepine, Phenobarbital, St. John’s Wort)
MechanismInduce CYP3A4-mediated oxidation of exemestane, accelerating its clearance
EffectRifampicin co-administration reduced exemestane Cmax by 41% and AUC by 54% in a formal PK study
ManagementIncrease exemestane dose to 50 mg once daily after a meal (FDA PI Section 2.2); no dose adjustment needed when inducer is stopped
FDA PI
Major Estrogen-Containing Products (HRT, combined OC)
MechanismExogenous estrogen directly opposes exemestane’s pharmacological action
EffectMay negate the antitumor efficacy of exemestane
ManagementDiscontinue all systemic estrogen before starting exemestane; avoid vaginal estrogens unless carefully assessed
FDA PI
Minor CYP3A4 Inhibitors (e.g., Ketoconazole)
MechanismInhibit CYP3A4-mediated oxidation of exemestane
EffectIn a formal PK study, ketoconazole had no significant effect on exemestane pharmacokinetics
ManagementNo dose adjustment required; alternative metabolic pathways (aldoketoreductases) buffer against CYP3A4 inhibition
FDA PI
Minor CYP Substrates (general)
MechanismExemestane does not inhibit CYP1A2, 2C9, 2D6, 2E1, or 3A4
EffectClinically significant interactions with CYP substrates considered unlikely
ManagementNo routine adjustments for concomitant CYP substrates
FDA PI
Mon

Monitoring

  • Bone Mineral Density (DEXA) Baseline, then every 1–2 years
    Routine
    The IES bone substudy showed lumbar spine BMD decreased by 3.14% and femoral neck by 4.15% over 24 months with exemestane (vs −0.18% and −0.33% with tamoxifen). Women with osteoporosis or at risk should have formal DEXA at treatment commencement. Co-prescribe calcium (1,000–1,200 mg/day) and vitamin D.
  • Vitamin D Level (25-OH) Before starting treatment
    Routine
    The FDA PI specifically recommends routine 25-hydroxy vitamin D assessment prior to aromatase inhibitor treatment due to the high prevalence of deficiency in women with early breast cancer. Supplement if deficient.
  • Lipid Panel Baseline, then annually
    Routine
    Study 027 showed HDL cholesterol decreased by 6–9% with exemestane and an 18% increase in homocysteine was observed (vs 12% with placebo). Monitor and manage per cardiovascular risk guidelines.
  • Cardiovascular Risk Baseline assessment
    Routine
    Cardiac ischemic events occurred in 1.6% of IES patients on exemestane vs 0.6% on tamoxifen. Assess cardiovascular risk factors before initiation; note that tamoxifen’s cardioprotective effects are lost when switching.
  • Musculoskeletal Symptoms Each clinic visit
    Routine
    Actively inquire about joint pain, stiffness, and functional impairment. Arthralgia was 14.6% with exemestane vs 8.6% with tamoxifen. Early management improves adherence.
  • Liver Function If symptoms arise
    Trigger-based
    Treatment-emergent bilirubin elevations occurred in 5.3% (vs 0.8% tamoxifen); alkaline phosphatase elevations in 15% (vs 2.6%). Post-marketing hepatitis reported. Check LFTs for jaundice, malaise, or right upper quadrant pain.
  • Blood Pressure Each clinic visit
    Routine
    Hypertension occurred in 9.8% of IES patients (vs 8.4% tamoxifen). Monitor and treat per guidelines.
  • Pregnancy Status Within 7 days of initiation
    Trigger-based
    Pregnancy test recommended within 7 days before starting (FDA PI Section 8.3). Effective contraception during treatment and for 1 month after the last dose.
CI

Contraindications & Cautions

Absolute Contraindications

  • Known hypersensitivity to exemestane or any excipient (FDA PI Section 4).
  • Pregnancy. Exemestane can cause fetal harm based on animal data and mechanism of action. Caused abortions and embryo-fetal toxicity in rats and rabbits (FDA PI Section 8.1).

Relative Contraindications (Specialist Input Recommended)

  • Pre-existing severe osteoporosis (T-score < −2.5 or prior fragility fractures). DEXA showed lumbar spine BMD decrease of 3.14% and femoral neck decrease of 4.15% over 24 months. If exemestane is still required, co-prescribe bisphosphonate with close DEXA follow-up.
  • Pre-existing cardiovascular disease. Cardiac ischemic events were 1.6% with exemestane vs 0.6% with tamoxifen in the IES. Document risk-benefit discussion.

Use with Caution

  • Premenopausal women. Exemestane is not indicated for premenopausal breast cancer unless combined with ovarian suppression (FDA PI Section 5.5). Without adequate ovarian suppression, aromatase inhibition is insufficient and compensatory gonadotropin rise may paradoxically stimulate ovarian function.
  • Vitamin D deficiency. The FDA label specifically recommends assessment and supplementation before starting any aromatase inhibitor (Section 5.2).
  • Lactation. Exemestane was detected in rat milk at concentrations equivalent to plasma. Advise against breastfeeding during treatment and for 1 month after the last dose (FDA PI Section 8.2).
  • Concomitant strong CYP3A4 inducers. Dose increase to 50 mg daily required to maintain therapeutic exposure (FDA PI Section 2.2).
FDA Warning — Embryo-Fetal Toxicity Exemestane May Cause Fetal Harm

Based on findings from animal studies and its mechanism of action, exemestane can cause fetal harm when administered to a pregnant woman. In rats and rabbits, exemestane caused abortions, embryo-fetal toxicity, prolonged gestation, and abnormal or difficult labour. Pregnancy testing is recommended within 7 days prior to initiation. Advise females of reproductive potential to use effective contraception during treatment and for 1 month after the last dose (FDA PI Sections 5.6, 8.1, 8.3).

FDA Warning — Bone Mineral Density Reduction Reductions in BMD Over Time

Reductions in bone mineral density over time are observed with exemestane use. During adjuvant treatment, women with osteoporosis or at risk of osteoporosis should have bone densitometry at treatment commencement and be monitored appropriately. The IES bone substudy demonstrated clinically significant BMD decreases at the lumbar spine and femoral neck over 24 months (FDA PI Section 5.1).

Pt

Patient Counselling

Purpose of Therapy

Exemestane works by permanently blocking the enzyme that produces estrogen in postmenopausal women. This deprives hormone-sensitive breast cancer cells of the estrogen they need to grow. In the adjuvant setting, it is typically prescribed after 2–3 years of tamoxifen to complete a total of 5 years of hormonal therapy, an approach that has been shown to reduce cancer recurrence more effectively than continuing tamoxifen alone.

How to Take

Take one 25 mg tablet by mouth once daily, after a meal. The meal is essential because it significantly increases drug absorption. Taking the tablet with a meal boosts the amount of drug reaching the bloodstream by about 60% compared with taking it on an empty stomach. Choose a daily meal (ideally breakfast) and take the tablet consistently at the same time each day. If a dose is missed, take it as soon as remembered after a meal; if it is close to the next dose, skip the missed dose. Do not double up.

Taking Exemestane with Food
Tell patient Always take your tablet after eating a meal, not on an empty stomach. This is different from some other breast cancer hormone tablets. Food helps your body absorb the medication properly. A full breakfast, lunch, or dinner is ideal.
Call prescriber If you are unable to eat regular meals due to nausea or appetite loss and are unsure how to take your medication.
Hot Flushes & Sweating
Tell patient Hot flushes affect about 1 in 5 patients and are the most common side effect. They are a sign that the medication is lowering estrogen levels effectively. Layered clothing, keeping rooms cool, avoiding triggers (caffeine, alcohol, spicy food), and staying well hydrated may help manage them.
Call prescriber If hot flushes are so severe they interfere with sleep or daily activities despite non-pharmacologic measures. Treatment options exist.
Joint Pain & Stiffness
Tell patient Joint aches and stiffness occur in about 15% of patients and are caused by the lowering of estrogen. Regular gentle exercise (walking, stretching, swimming) can significantly reduce these symptoms. Over-the-counter pain relief may help. Many patients find that symptoms improve over time.
Call prescriber If joint pain is severe enough to limit movement or daily activities, or if swelling develops. An alternative medication may be considered.
Bone Health
Tell patient Exemestane can decrease bone density over time. Take calcium supplements (1,000–1,200 mg daily) and vitamin D as directed. Engage in regular weight-bearing exercise. Your doctor will arrange bone density scans to monitor bone health during treatment.
Call prescriber If you experience a fall, sudden back pain, or pain in the hip or wrist, as fracture risk is increased during treatment.
Pregnancy & Contraception
Tell patient Exemestane can harm an unborn baby. Use effective contraception during treatment and for at least 1 month after the last dose. Do not breastfeed during treatment or for 1 month after stopping.
Call prescriber Immediately if pregnancy is suspected or confirmed during treatment.
Drug Interactions
Tell patient Inform your doctor and pharmacist about all medications you take, including herbal supplements. St. John’s Wort, some anti-seizure medications (phenytoin, carbamazepine), and the antibiotic rifampicin can reduce the effectiveness of exemestane and may require a dose adjustment. Avoid any estrogen-containing products (hormone replacement therapy, certain vaginal preparations).
Call prescriber Before starting any new prescription, over-the-counter medication, or supplement while on exemestane.
Ref

Sources

Regulatory (PI / SmPC)
  1. AROMASIN (exemestane) Tablets. Full Prescribing Information. Pfizer Inc. Revised 05/2018. FDA Label Primary regulatory source for all dosing, pharmacokinetics, adverse reaction incidence rates, contraindications, and drug interaction data used in this monograph.
  2. Exemestane Tablets. DailyMed / National Library of Medicine (revised 02/2025). DailyMed Entry NLM-hosted prescribing information supporting cross-reference of current safety and PK data.
Key Clinical Trials
  1. Coombes RC, Hall E, Gibson LJ, et al. A randomized trial of exemestane after two to three years of tamoxifen therapy in postmenopausal women with primary breast cancer. N Engl J Med. 2004;350(11):1081–1092. DOI Landmark IES initial results demonstrating 32% risk reduction in disease-free survival events with sequential switch to exemestane.
  2. Coombes RC, Kilburn LS, Snowdon CF, et al. Survival and safety of exemestane versus tamoxifen after 2–3 years’ tamoxifen treatment (Intergroup Exemestane Study): a randomised controlled trial. Lancet. 2007;369(9561):559–570. DOI IES update at 55.7-month median follow-up confirming persistent disease-free survival benefit and emerging overall survival improvement.
  3. Bliss JM, Kilburn LS, Coleman RE, et al. Disease-related outcomes with long-term follow-up: an updated analysis of the Intergroup Exemestane Study. J Clin Oncol. 2012;30(7):709–717. DOI IES 91-month analysis confirming 18% DFS and 14% OS improvements; source for mature safety data.
  4. Goss PE, Ingle JN, Alés-Martínez JE, et al. Exemestane for breast-cancer prevention in postmenopausal women. N Engl J Med. 2011;364(25):2381–2391. DOI MAP.3 trial demonstrating 65% reduction in invasive breast cancer with exemestane vs placebo in high-risk postmenopausal women.
  5. Pagani O, Regan MM, Walley BA, et al. Adjuvant exemestane with ovarian suppression in premenopausal breast cancer. N Engl J Med. 2014;371(2):107–118. DOI Combined TEXT/SOFT analysis establishing exemestane plus ovarian suppression as superior to tamoxifen plus ovarian suppression in premenopausal women.
Guidelines
  1. Burstein HJ, Lacchetti C, Anderson H, et al. Adjuvant endocrine therapy for women with hormone receptor-positive breast cancer: ASCO clinical practice guideline focused update. J Clin Oncol. 2019;37(5):423–438. DOI ASCO guideline positioning aromatase inhibitors (including exemestane) as preferred initial or sequential adjuvant endocrine therapy.
  2. Visvanathan K, Fabian CJ, Bantug E, et al. Use of endocrine therapy for breast cancer risk reduction: ASCO clinical practice guideline update. J Clin Oncol. 2019;37(33):3152–3165. DOI ASCO guideline recommending exemestane as a chemoprevention option for high-risk postmenopausal women.
Mechanistic / Basic Science
  1. Di Salle E, Ornati G, Paridaens R, et al. Exemestane (FCE 24304), a new steroidal aromatase inhibitor. J Steroid Biochem Mol Biol. 1992;43(1–3):137–143. DOI Foundational characterisation of exemestane as an irreversible, mechanism-based aromatase inactivator.
Pharmacokinetics / Special Populations
  1. Goss PE, Ingle JN, Pritchard KI, et al. Exemestane versus anastrozole in postmenopausal women with early breast cancer: NCIC CTG MA.27 — a randomized controlled phase III trial. J Clin Oncol. 2013;31(11):1398–1404. DOI Head-to-head comparison demonstrating similar efficacy and safety between exemestane and anastrozole as upfront adjuvant therapy.
  2. Coleman RE, Banks LM, Girgis SI, et al. Reversal of skeletal effects of endocrine treatments in the Intergroup Exemestane Study. Breast Cancer Res Treat. 2010;124(1):153–161. DOI IES bone substudy demonstrating BMD changes with exemestane and reversal after treatment cessation.