Androgen deprivation therapy prostate

Androgen Deprivation Therapy and Systemic Treatments reduce circulating testosterone to castrate levels, commonly defined as <50 ng/dL (1.7 nmol/L), and are used to control prostate cancer growth, relieve symptoms, and extend survival. Medical castration is achieved with luteinizing hormone–releasing hormone (LHRH) agonists or antagonists; surgical orchiectomy gives immediate castrate testosterone. For localized low-risk disease observation or local therapy may suffice, while ADT is standard for metastatic hormone-sensitive disease and often combined with radiation for high-risk localized cases. Common side effects include hot flashes, decreased libido, fatigue, and bone density loss, which often begin within weeks to months and accumulate over years. Decisions also account for age, comorbidities, and life expectancy.

Androgen suppression works by lowering testosterone to levels that no longer stimulate prostate tumor growth, interrupting androgen receptor signaling and reducing prostate-specific antigen (PSA) production. Guideline frameworks such as NCCN and AUA use PSA level, Gleason score, and metastatic status to decide when to start ADT prostate cancer treatment. Systemic therapy prostate cancer options include LHRH agonists/antagonists, surgical castration, androgen receptor pathway inhibitors (abiraterone, enzalutamide, apalutamide), and chemotherapy (docetaxel). Trials like CHAARTED and LATITUDE established survival benefits for adding docetaxel or abiraterone in metastatic hormone-sensitive disease. Monitoring uses serial PSA and testosterone measurements; an adequate PSA response typically follows castrate testosterone within 1–3 months. A PSA drop of about 50% within three months is commonly expected and confirms response to therapy.

A key nuance is that ADT prostate cancer is not universally required at diagnosis; timing depends on stage, PSA kinetics, and patient goals. For example, biochemical recurrence after prostatectomy with a slow PSA doubling time (for example, >12 months) often allows observation or delayed hormone therapy prostate cancer initiation, whereas a short doubling time (for example, <12 months), symptomatic metastases, or radiographic spread prompt systemic therapy. 'Castration-resistant' is commonly misunderstood: metastatic castration-resistant prostate cancer means tumor progression by PSA or imaging despite confirmed castrate testosterone (commonly <50 ng/dL). Treatment selection then shifts from testosterone-lowering alone to agents targeting the androgen receptor pathway or chemotherapy, and effects on quality of life and bone health must be weighed. Oligometastatic patients sometimes receive stereotactic metastasis-directed radiation, which can affect timing of systemic therapy.

Practical steps include confirming castrate testosterone after initiation (typically within 1–3 months), measuring PSA every 3–6 months while on treatment, and assessing baseline bone mineral density with repeat testing as indicated. Management of common side effects—hot flashes, sexual dysfunction, fatigue, metabolic changes—often combines lifestyle measures, referral to rehabilitation or sexual health services, and consideration of bone-protecting drugs (zoledronic acid or denosumab) for patients at fracture risk. Coordination with primary care for cardiovascular and metabolic monitoring is important. Baseline labs often include fasting lipids and glucose plus a DEXA scan before long-term androgen suppression. This page presents a structured, step-by-step framework.