Adrenal medulla cancer means a harmful (malignant) tumor that starts in the inner part of the adrenal gland, called the medulla. This inner zone is made of special nerve-like cells (chromaffin cells). These cells normally make stress hormones called catecholamines (adrenaline/epinephrine, noradrenaline/norepinephrine, and dopamine). When they turn cancerous, they can grow fast, invade nearby tissues, and spread (metastasize) to lymph nodes, bone, liver, or lungs. Many tumors still release large amounts of stress hormones, which cause sudden attacks of headache, heavy sweating, pounding heart, and very high blood pressure. In adults, the typical adrenal medulla cancer is a malignant pheochromocytoma. In children, a different adrenal medulla cancer, called neuroblastoma, is more common.
Adrenal medulla cancer starts in the inner part of the adrenal gland, a small organ that sits above each kidney. This inner part makes stress hormones called catecholamines (adrenaline and noradrenaline). When cancer grows there, the tumor can release too much of these hormones. That can cause sudden high blood pressure, fast heartbeat, headaches, sweating, paleness, shakiness, and anxiety-like attacks. Doctors also call this disease “malignant pheochromocytoma” when it spreads or shows aggressive behavior. Sometimes the tumor begins from similar nerve-related cells outside the adrenal gland; those are called malignant paragangliomas. This cancer is rare. Some people inherit gene changes (for example, in SDHB or other genes) that raise risk. Treatment aims to safely block the hormones, remove or shrink the tumor, control spread, and protect the heart and blood vessels.
Other names
Doctors use several related names. Malignant pheochromocytoma means a cancer that starts from chromaffin cells inside the adrenal medulla and has spread or shows clear invasive behavior. Adrenal medullary carcinoma is a broader phrase that also points to a malignant tumor of the medulla. Chromaffin cell carcinoma describes the same idea using the cell type. In children, adrenal neuroblastoma is a separate adrenal medulla cancer that comes from immature nerve cells and behaves very differently. You may also see sympathoadrenal cancer, referring to the sympathetic nervous system origin. When the same type of tumor starts outside the adrenal gland, it is called a paraganglioma; if that paraganglioma is malignant, some people loosely say “extra-adrenal pheochromocytoma,” but strictly speaking that is outside the adrenal.
Types
Malignant pheochromocytoma (adult type). A cancerous adrenal medulla tumor that invades nearby tissues and/or spreads to distant organs. It often makes catecholamines, so symptoms are driven by hormone surges.
Localized malignant pheochromocytoma. The main tumor appears limited to the adrenal, but pathology shows aggressive features or there are small local deposits; spread may appear later.
Metastatic malignant pheochromocytoma. Cancer has spread to lymph nodes or distant organs such as bone, liver, or lungs.
Hereditary malignant pheochromocytoma. The cancer happens in people with an inherited gene change (such as RET, VHL, NF1, or SDHB). These cases often occur at a younger age and can be multiple or recurrent.
Sporadic malignant pheochromocytoma. No known inherited mutation; the tumor arises by chance.
Biochemically functional malignant pheochromocytoma. The tumor releases measurable catecholamines or their breakdown products (metanephrines), causing classic attacks.
Biochemically “silent” malignant pheochromocytoma. Hormone tests are low or normal. Symptoms may be mild or due to tumor mass or spread, which can delay diagnosis.
Composite malignant pheochromocytoma. A rare tumor that contains pheochromocytoma plus another neural crest tumor part (for example, ganglioneuroma or neuroblastoma) in the same mass.
Adrenal neuroblastoma (pediatric). A different adrenal medulla cancer seen mainly in young children. It comes from very early nerve cells (neuroblasts), behaves and is staged differently, and has its own treatment path.
Therapy-related or radiation-associated adrenal medulla cancers (very rare). Tumors that arise after prior treatment or radiation to the area; evidence is limited, but the mechanism is possible.
Causes and risk factors
Note: For most patients, we cannot point to a single cause. Cancer usually forms from many small DNA changes over time. Below are the key risk factors and known genetic pathways.
SDHB gene mutation (hereditary). A change in the SDHB gene (part of the mitochondrial complex) strongly raises the risk of pheochromocytoma/paraganglioma and is linked to a higher chance of malignancy and spread.
RET gene mutation (MEN2). In Multiple Endocrine Neoplasia type 2, a RET mutation can cause pheochromocytomas. While many are benign, some may behave aggressively.
VHL gene mutation (Von Hippel-Lindau disease). VHL syndrome can lead to adrenal tumors. VHL changes affect how cells sense oxygen and can drive tumor growth.
NF1 gene mutation (Neurofibromatosis type 1). NF1 affects cell-growth signaling. People with NF1 have higher risk for catecholamine-producing tumors, including adrenal medulla tumors.
SDHD/SDHC gene mutations. Like SDHB, these genes are in the succinate dehydrogenase family. Mutations can create a metabolic “on” signal that supports tumor growth.
MAX gene mutation. MAX controls parts of the MYC pathway (a growth switch inside cells). Faults here can promote adrenal medulla tumors, sometimes bilateral.
TMEM127 gene mutation. This gene helps regulate mTOR signaling (cell growth and metabolism). Changes can cause adrenal medulla tumors, including rare malignant cases.
FH gene mutation (fumarate hydratase). Abnormal Krebs cycle enzymes (like FH) can cause “pseudohypoxia,” a state that makes tumor growth signals stay active.
EPAS1/HIF2A mutation. This alters the cell’s oxygen-sensing machinery, pushing cells to grow and form blood vessels, supporting tumor survival and spread.
Family history of pheochromocytoma/paraganglioma. Even without a named syndrome, strong family history suggests a genetic risk factor.
Younger age at first adrenal tumor. Tumors in teens or young adults are more likely to be hereditary, which can raise lifetime risk of recurrence or a second tumor.
Prior extra-adrenal paraganglioma. People who already had a related tumor outside the adrenal can later develop an adrenal tumor, with a higher chance of aggressive behavior if SDHB-related.
Chronic “pseudohypoxia” pathways. Tumor cells hijack signals that normally respond to low oxygen. These signals (HIF pathways) stay on and drive growth.
Abnormal cell-cycle control (Ki-67, p53 pathways). When the brakes on cell division fail, cells can divide too fast and pick up more mutations.
Mitochondrial metabolic shifts. Build-up of succinate or fumarate acts like a “growth message” and silences tumor-suppressor signals through epigenetic effects.
Epigenetic changes (DNA methylation). Chemical tags on DNA can switch genes on/off abnormally, pushing chromaffin cells toward cancer.
Radiation exposure (rare contributor). High radiation to the abdomen could, in theory, raise risk, but clear evidence in adrenal medulla cancer is limited.
Men2-related high catecholamine environment. Constant hormone signaling might help selected tumor clones grow, though this is not a proven direct cause of malignancy.
Immune microenvironment failure. Tumors can learn to hide from immune cells, allowing survival and eventual spread.
Unknown sporadic mutations. Many cancers arise without a known gene syndrome. Random DNA errors over time in chromaffin cells can start the process.
Symptoms
High blood pressure that spikes. Sudden, severe rises in blood pressure can happen in attacks or stay high all the time.
Pounding heartbeat (palpitations). You may feel your heart race or thump hard in your chest, even while resting.
Heavy sweating. Drenching sweats often come with the blood pressure spikes and headaches.
Severe headaches. These can be throbbing and sudden, often during hormone surges.
Pale or flushed skin. Blood vessels tighten or open quickly, changing skin color.
Tremor or shaking. Adrenaline makes muscles twitch and hands shake.
Anxiety or a sense of doom. Hormones trigger “fight or flight,” so you may feel intense fear without a clear reason.
Chest pain or tightness. The heart works hard under high blood pressure and fast rate, causing pain.
Shortness of breath. Rapid heart rate and high blood pressure strain the lungs and heart.
Nausea, vomiting, or belly pain. The gut is sensitive to stress hormones and can cramp.
Weight loss and poor appetite. Long-term hormone excess speeds metabolism and reduces hunger.
Heat intolerance. You may feel too hot and sweat easily.
Blurred vision or visual spots. Very high blood pressure can disturb vision during attacks.
Weakness or fatigue. The body is “on high alert” too often and becomes exhausted.
Symptoms from spread (metastases). Bone pain, fractures, liver area pain, or cough and breathlessness can appear if the cancer spreads.
Diagnostic tests
A) Physical exam
Resting blood pressure and pulse check. The doctor measures your blood pressure and heart rate several times. Very high readings or a pattern of spikes suggest a hormone-releasing tumor.
General exam of skin, eyes, and thyroid. The doctor looks for pale/flushed skin, eye findings from long-term high blood pressure, and thyroid nodules (important in MEN2 families). These clues guide genetic and tumor work-up.
Abdominal exam and weight check. The doctor gently presses your belly to look for tenderness or masses and tracks weight loss, which can be a sign of hormone excess or cancer spread.
B) Manual tests
Orthostatic (lying-to-standing) blood pressure and heart rate. The clinician measures your vitals lying down and again after standing. Big drops or surges show autonomic imbalance from catecholamine excess.
Valsalva maneuver response (selected cases). You blow against resistance for a few seconds while vitals are monitored. An abnormal pattern can hint at disrupted autonomic control from excess catecholamines. It is supportive, not diagnostic on its own.
C) Lab and pathological tests
Plasma free metanephrines. This is the most sensitive blood test. It measures metanephrines, the stable breakdown products of catecholamines. High levels strongly suggest a catecholamine-secreting tumor.
24-hour urine fractionated metanephrines and catecholamines. You collect urine for a full day. This confirms and quantifies hormone production over time, smoothing out brief spikes.
Plasma catecholamines (selected). Direct adrenaline/noradrenaline levels can be checked but are more “spiky” and less stable than metanephrines, so interpretation is careful.
Urine creatinine and volume check. This confirms the urine collection is complete and valid, so results can be trusted.
Chromogranin A (CGA). This blood marker can be elevated in many neuroendocrine tumors, including adrenal medulla tumors. It supports the diagnosis but is not specific.
Clonidine suppression test (when results are borderline). After a medication called clonidine, normal nerve release of noradrenaline falls, but tumor-made catecholamines do not suppress well. Poor suppression suggests tumor production.
Genetic testing panel. A blood test looks for inherited changes in genes like RET, VHL, NF1, SDHB, SDHD, SDHC, MAX, TMEM127, FH, and EPAS1. Results guide screening, treatment choices, and family counseling.
Tumor pathology with immunohistochemistry. If the tumor is removed or biopsied, the pathologist confirms it is a chromaffin-cell cancer (positive for chromogranin and synaptophysin). Loss of SDHB staining suggests an SDH-mutated tumor.
Proliferation and grading (Ki-67, GAPP/PASS features). The pathologist measures how fast cells are dividing (Ki-67). Certain scores and features help estimate the risk of aggressive behavior and spread.
D) Electrodiagnostic and cardiovascular monitoring
12-lead electrocardiogram (ECG). Records heart rhythm and signs of strain from high blood pressure and catecholamine surges. It can show arrhythmias or ischemic changes.
24-hour Holter monitor. A wearable device tracks your heart rhythm over a day (or longer). It can catch fast runs, pauses, or irregular beats during symptom spells.
Echocardiogram (heart ultrasound). Looks for thickened heart muscle, reduced pumping function, or stress-induced cardiomyopathy caused by long-term hormone excess.
E) Imaging tests
Adrenal protocol CT or MRI. These scans show the adrenal mass, its size, shape, and relation to nearby structures. MRI often shows a very bright “light-bulb” signal on T2 images for catecholamine tumors.
MIBG scintigraphy (¹²³I-MIBG). A small amount of a norepinephrine-like tracer is injected. Tumor cells that take up the tracer “light up” on the scan. Useful for finding hidden or metastatic disease and for therapy planning.
PET/CT with specialized tracers (for staging). ⁶⁸Ga-DOTATATE PET/CT can detect somatostatin-receptor-positive disease. ¹⁸F-FDG PET/CT is helpful for more aggressive, SDHB-related, or fast-growing tumors. ¹⁸F-DOPA PET is another option in some centers. These scans map disease throughout the body.
Non-Pharmacological Treatments
Important: Exercise, breathing work, and any bodywork must be cleared by your oncology and anesthesia team first, because hormone surges can cause dangerous blood pressure spikes. Most plans start after alpha-blockade is in place and vital signs are stable.
Physiotherapy-focused interventions
Pre-surgery breathing training
Description (≈150 words): You learn diaphragmatic breathing and “smell the rose, blow the candle” pacing to calm the sympathetic system. Sessions teach slow nasal inhale, long mouth exhale, and brief breath holds only if blood pressure is stable. The therapist rehearses coughing and huff techniques to clear lungs after anesthesia without straining. You also practice incentive spirometry to expand lungs.
Purpose: Reduce post-op lung issues and sympathetic spikes.
Mechanism: Vagus-nerve-favoring breathing reduces adrenaline effects and supports oxygenation.
Benefits: Easier recovery, less atelectasis, steadier heart rate and blood pressure.Gentle, monitored walking program
Description: Short, flat, supervised walks with an automatic stop rule if you feel headache, chest tightness, pounding heart, dizziness, or BP rises. Start with 3–5 minutes, add 1–2 minutes every few days if vitals stay safe.
Purpose: Maintain conditioning without provoking catecholamine surges.
Mechanism: Low-intensity aerobic work improves endothelial function and insulin sensitivity with minimal sympathetic drive.
Benefits: Better stamina, mood, and sleep; safer surgical fitness.Seated and supine range-of-motion (ROM)
Description: Shoulder, hip, knee, and ankle ROM performed lying or sitting to avoid BP swings from standing. No Valsalva.
Purpose: Preserve joint mobility and reduce stiffness.
Mechanism: Gentle movement lubricates joints and keeps muscle length.
Benefits: Less deconditioning; easier daily tasks.Isometric light holds (no straining)
Description: Very light, 3–5-second holds for arms and legs while breathing out, never “bearing down.”
Purpose: Maintain muscle tone safely.
Mechanism: Brief, submaximal recruitment without big BP spikes.
Benefits: Strength support while awaiting surgery or systemic therapy.Postural training and ergonomic coaching
Description: Neutral spine sitting, hip-hinge lifting, and log-rolling in bed to reduce sudden pressure changes.
Purpose: Avoid Valsalva maneuvers that raise BP.
Mechanism: Body mechanics minimize intrathoracic pressure spikes.
Benefits: Safer movement and less pain.Orthostatic intolerance training
Description: Gradual head-up tilt with compression stockings if advised, and slow transitions from lying to standing.
Purpose: Reduce dizziness from treatment-related BP drops after alpha-blockade.
Mechanism: Conditioning baroreflexes and venous return.
Benefits: Fewer near-faints; more confidence walking.Pelvic and rib mobility with soft tissue release
Description: Gentle therapist-guided stretches and soft tissue work only if BP stable and cleared.
Purpose: Ease tension and breathing mechanics.
Mechanism: Relaxation lowers sympathetic tone; improved chest wall motion.
Benefits: Less pain, deeper breathing.Incision protection & early post-op mobilization
Description: Splinting incision with pillow for cough/huff; early hallway walks when cleared.
Purpose: Prevent clots, pneumonia, and stiffness.
Mechanism: Mobilization improves circulation and lung expansion.
Benefits: Faster recovery, shorter stay.Foot/ankle pumps and calf activation
Description: Sets of ankle pumps every hour while awake.
Purpose: DVT prevention.
Mechanism: Muscle pump increases venous return.
Benefits: Lower clot risk.Balance and fall-prevention drills
Description: Seated to standing progressions, wide-to-narrow stance with a support rail.
Purpose: Counteract dizziness or medication-related hypotension.
Mechanism: Neuro-muscular training of proprioception.
Benefits: Fewer falls, safer independence.Gentle flexibility (hamstrings, hip flexors, pectorals)
Description: 20–30-second holds with easy breath; avoid painful end-range.
Purpose: Reduce stiffness and stress tension.
Mechanism: Stretch reduces muscle spindle reactivity.
Benefits: Comfort, posture, sleep.Inspiratory muscle training (after clearance)
Description: Handheld device used at low resistance.
Purpose: Strengthen breathing muscles for surgery and recovery.
Mechanism: Specific load to diaphragm and intercostals.
Benefits: Less dyspnea, better cough.Scar care and desensitization (healed incision only)
Description: Once healed, gentle circular massage and moisturizers.
Purpose: Improve glide and comfort.
Mechanism: Remodel collagen alignment and reduce nerve hypersensitivity.
Benefits: Softer scar, less pulling.Energy conservation & pacing
Description: Plan tasks, rest before symptoms, sit for chores.
Purpose: Prevent symptom flares.
Mechanism: Keeps stress hormones steady.
Benefits: More predictable energy.Targeted core activation without strain
Description: Low-load transversus abdominis and pelvic floor activation while exhaling.
Purpose: Support posture without BP spikes.
Mechanism: Neuromuscular recruitment at low pressure.
Benefits: Less back pain; safer mobility.
Mind-Body, Education, and Genetics-focused strategies
Diaphragmatic breathing & paced exhalation practice
Purpose: Calm the stress response.
Mechanism: Extends exhalation, boosting parasympathetic tone.
Benefits: Fewer adrenaline-like surges; better control of symptoms.Progressive muscle relaxation (PMR)
Purpose: Release muscle tension that mimics “adrenaline rush.”
Mechanism: Tense-release cycles retrain the body’s alarm system.
Benefits: Lower heart rate and perceived stress.Mindfulness or brief meditation (5–10 minutes)
Purpose: Reduce reactivity to symptoms.
Mechanism: Nonjudgmental attention decreases amygdala firing.
Benefits: Less anxiety; better sleep and pain control.Biofeedback (if available)
Purpose: Give visual or audio feedback on pulse, breathing, or temperature.
Mechanism: Operant conditioning of calm physiologic states.
Benefits: Practical self-regulation during “spells.”Sleep hygiene coaching
Purpose: Restore regular sleep to support BP control and healing.
Mechanism: Consistent circadian cues reduce sympathetic tone.
Benefits: More energy; fewer headaches.Trigger-avoidance education
Purpose: Identify and avoid things that can provoke surges (heavy lifting, straining, intense exertion, high caffeine, some decongestants, stimulants).
Mechanism: Reduces catecholamine spikes.
Benefits: Fewer crises.Home BP/HR monitoring skills
Purpose: Catch patterns, guide medication timing.
Mechanism: Self-measurement plus symptom diary.
Benefits: Safer titration; earlier help.Nutrition counseling
Purpose: Plan steady meals; hydration; avoid high-amine “spike” foods if advised.
Mechanism: Smooths glucose and sympathetic swings.
Benefits: More stable BP and energy.Genetic counseling & family screening
Purpose: Address inherited risk (SDHB, VHL, RET, NF1, others).
Mechanism: Testing and scheduled surveillance.
Benefits: Early detection for you and relatives.Pre-op education & emergency plan
Purpose: Know when to call for help and how surgery is staged (alpha-blocker first).
Mechanism: Clear steps lower fear and mistakes.
Benefits: Safer path through treatment.
Drug Treatments
Phenoxybenzamine (non-selective alpha-blocker)
Class: Alpha-adrenergic antagonist.
Typical dose/time: Start 10 mg orally twice daily, increase every 2–3 days to effect (often 20–40 mg twice daily).
Purpose: First-line to control high BP and protect the heart before surgery.
Mechanism: Irreversible alpha blockade prevents adrenaline from tightening blood vessels.
Side effects: Low BP when standing, nasal stuffiness, fatigue, reflex fast heartbeat.Doxazosin or Prazosin (selective alpha-1 blockers)
Class: Alpha-1 antagonists.
Dose: Doxazosin 1–16 mg daily; prazosin 1–5 mg two or three times daily, titrated.
Purpose: Alternative or adjunct to phenoxybenzamine with fewer side effects for some.
Mechanism: Blocks alpha-1 receptors, relaxing arteries.
Side effects: Dizziness, fatigue, rare fainting on first dose.Propranolol (or Atenolol/Metoprolol) – add after alpha-blockade
Class: Beta-blocker.
Dose: Propranolol 10–40 mg three times daily; atenolol/metoprolol daily or bid as directed.
Purpose: Control tachycardia once alpha blockade is established.
Mechanism: Blocks beta receptors on the heart, slowing rate.
Side effects: Fatigue, cold hands, low heart rate, wheeze in asthma.Calcium channel blocker (Nicardipine/Amlodipine)
Class: Dihydropyridine CCB.
Dose: Amlodipine 5–10 mg daily; nicardipine IV is used peri-op by clinicians.
Purpose: Additional BP control or if alpha-blockers not tolerated.
Mechanism: Relaxes vascular smooth muscle via calcium channel inhibition.
Side effects: Ankle swelling, headache, flushing.Metyrosine
Class: Catecholamine synthesis inhibitor.
Dose: Start 250 mg every 6 hours; titrate to effect (max 4 g/day) as tolerated.
Purpose: Reduce hormone production in severe or metastatic cases or before surgery.
Mechanism: Inhibits tyrosine hydroxylase, the rate-limiting step in catecholamine synthesis.
Side effects: Sedation, depression, diarrhea, crystalluria (hydrate well).High-specific-activity I-131 iobenguane (MIBG) therapy
Class: Radiopharmaceutical.
Dose: Weight-based; given in specialized centers with thyroid blockade.
Purpose: Treat MIBG-avid metastatic tumors.
Mechanism: MIBG is taken up by tumor cells; I-131 delivers targeted radiation.
Side effects: Bone marrow suppression, nausea, fatigue; radiation precautions apply.Lutetium-177 DOTATATE (PRRT)
Class: Peptide receptor radionuclide therapy.
Dose: Typically 7.4 GBq every 8 weeks for 4 cycles in centers.
Purpose: For somatostatin-receptor–positive disease.
Mechanism: Somatostatin analogue binds tumor; Lu-177 emits radiation to kill cells.
Side effects: Nausea, mild marrow suppression, rare kidney effects (amino acid protection used).Cyclophosphamide + Vincristine + Dacarbazine (CVD regimen)
Class: Cytotoxic chemotherapy.
Dose (typical cycle): Cyclophosphamide ~750 mg/m² day 1; vincristine ~1.4 mg/m² day 1; dacarbazine ~600–750 mg/m² days 1–2, every 21–28 days.
Purpose: Shrink metastatic or rapidly progressive tumors.
Mechanism: DNA damage and microtubule disruption stop cancer cell division.
Side effects: Nausea, hair loss, low blood counts, neuropathy (vincristine), infertility risk.Temozolomide
Class: Alkylating agent.
Dose: 150–200 mg/m² daily on days 1–5 of a 28-day cycle.
Purpose: Option for metastatic disease, especially with SDHB mutations.
Mechanism: Methylates DNA to trigger cancer cell death.
Side effects: Fatigue, nausea, lowered white blood cells/platelets.Sunitinib
Class: Multi-target tyrosine kinase inhibitor (TKI).
Dose: 37.5–50 mg daily (continuous or 4 weeks on/2 weeks off per protocol).
Purpose: Slow growth and cut blood supply to tumors.
Mechanism: Inhibits VEGFR, PDGFR, and others to block angiogenesis and signaling.
Side effects: Fatigue, hand-foot syndrome, high BP, mouth sores, thyroid dysfunction.Pazopanib or Cabozantinib (TKIs)
Class: Multi-target TKIs.
Dose: Pazopanib 800 mg daily; cabozantinib 60 mg daily (dose-adjust as needed).
Purpose: Alternatives when sunitinib not suitable or after progression.
Mechanism: Anti-angiogenic and signaling blockade.
Side effects: Diarrhea, hypertension, liver test changes, skin issues.Everolimus
Class: mTOR inhibitor.
Dose: 10 mg daily (adjust for tolerance).
Purpose: Selected patients with progressive disease.
Mechanism: Blocks mTOR pathway to slow cell growth.
Side effects: Stomatitis, high blood sugar/lipids, infections.Pembrolizumab (or Nivolumab ± Ipilimumab)
Class: Immune checkpoint inhibitors.
Dose: Pembrolizumab 200 mg IV every 3 weeks (or 400 mg q6w); other regimens per protocol.
Purpose: Considered in selected advanced cases or trials.
Mechanism: Releases immune “brakes” (PD-1/PD-L1, CTLA-4) so T-cells attack cancer.
Side effects: Immune-related inflammation (thyroid, colon, lung, skin).Short-acting IV agents for crisis (in hospital)
Class: Nitroprusside, phentolamine, esmolol (administered by specialists).
Dose: Continuous IV titration.
Purpose: Control dangerous intra-op or ICU spikes.
Mechanism: Rapid vasodilation or rate control.
Side effects: Low BP, cyanide toxicity risk (nitroprusside) with prolonged use.Pain and symptom control medicines
Class: Acetaminophen, cautious opioids, anti-nausea drugs; avoid decongestants/stimulants.
Dose: As needed and supervised.
Purpose: Comfort and function.
Mechanism: Central/peripheral symptom relief.
Side effects: Depend on drug; watch interactions and BP effects.
Medication safety notes: Alpha-blocker before beta-blocker; hydrate and add salt as directed pre-op to avoid low BP when standing; never start or stop these medicines without your team’s plan.
Dietary Molecular Supplements
Omega-3 fatty acids (EPA+DHA)
Dose: Common 1–2 g/day combined EPA+DHA with meals.
Function/Mechanism: Anti-inflammatory and may improve endothelial function and triglycerides.
Relevance: Supports heart health during long treatment.
Cautions: Can increase bleeding risk at higher doses or with anticoagulants.Vitamin D3
Dose: Typical 1,000–2,000 IU/day; test levels for personalized dosing.
Mechanism: Immune modulation and bone health.
Relevance: Prevents deficiency during limited sun/therapy.
Cautions: Avoid high doses without labs; watch calcium.Magnesium (glycinate or citrate)
Dose: 200–400 mg/day.
Mechanism: Smooth muscle relaxation, supports rhythm and sleep.
Relevance: May help cramps from TKIs and stress tension.
Cautions: Diarrhea (citrate), dose adjust in kidney disease.Coenzyme Q10
Dose: 100–200 mg/day with fat-containing meal.
Mechanism: Mitochondrial support; antioxidant.
Relevance: Fatigue support in some patients.
Cautions: Interacts with warfarin (INR changes).Probiotics (lactobacillus/bifidobacterium blends)
Dose: As labeled, often 10–20 billion CFU/day.
Mechanism: Gut barrier and immune tone support.
Relevance: May reduce antibiotic-related GI symptoms.
Cautions: Avoid if severely immunocompromised without approval.Soluble fiber (psyllium/β-glucan)
Dose: 5–10 g/day with water.
Mechanism: Smooths glucose and lipids; supports microbiome.
Relevance: Helps bowel regularity on pain meds.
Cautions: Separate from oral meds by 2+ hours.Curcumin (turmeric extract)
Dose: 500–1,000 mg/day standardized extract.
Mechanism: Anti-inflammatory signaling effects.
Relevance: Joint/soft tissue comfort.
Cautions: Drug interactions (e.g., anticoagulants), variable absorption.Green tea extract (EGCG) – food form preferred
Dose: Prefer brewed tea; avoid high-dose extracts unless cleared.
Mechanism: Antioxidant; metabolic effects.
Relevance: Gentle stimulant alternative to coffee in some.
Cautions: Can raise BP/HR in sensitive people; extracts may affect liver.Selenium (if deficient)
Dose: 50–100 mcg/day if low.
Mechanism: Antioxidant enzyme cofactor.
Relevance: Thyroid and immune enzyme support.
Cautions: Toxicity if excessive; test first.Electrolyte solutions (oral rehydration)
Dose: As needed on hot days or with diarrhea.
Mechanism: Replaces sodium/potassium/glucose for stable blood volume.
Relevance: Helps orthostatic symptoms during blockade.
Cautions: Tailor sodium with your clinician.
Key point: Supplements do not treat adrenal medulla cancer. They may support comfort or nutrition. Always check for interactions with alpha-/beta-blockers, TKIs, chemo, and radiopharmaceuticals.
Immunity booster / regenerative / stem-cell drugs
There are no approved stem-cell drugs or “immune boosters” that cure adrenal medulla cancer. Here is what clinicians may actually use or discuss:
Filgrastim or Pegfilgrastim (G-CSF)
Dose: Weight-based injections during chemo cycles.
Function/Mechanism: Stimulates bone marrow to raise neutrophils after chemotherapy.
Relevance: Lowers infection risk so treatment can stay on schedule.Erythropoiesis-stimulating agents (ESAs) – selected cases
Dose: Per protocol if severe symptomatic anemia and not rapidly correctable.
Mechanism: Stimulates red cell production.
Relevance: Improves energy in specific scenarios; risks and benefits carefully weighed.Vaccinations (influenza, pneumococcal, COVID-19)
Dose: Standard schedules, timed around therapy.
Mechanism: Prepares immune system against infections.
Relevance: Prevents setbacks during cancer care.Checkpoint inhibitors (Pembrolizumab / Nivolumab ± Ipilimumab)
Dose: IV on schedule per protocol.
Mechanism: Unleash T-cells to recognize cancer.
Relevance: Selected advanced cases or trials; not a general “booster.”Clinical trials of cellular or vaccine-based therapies
Function: Research approaches to direct the immune system at PPGL cells.
Relevance: Access via specialty centers; evidence still evolving.Nutritional and physical reconditioning
Function: Adequate protein, safe activity, sleep.
Mechanism: Supports innate and adaptive immunity.
Relevance: Practical, low-risk support for resilience.
Surgeries
Laparoscopic adrenalectomy
Procedure: Keyhole removal of the adrenal tumor under general anesthesia, with careful blood pressure control.
Why: Standard for localized tumors with suitable size and imaging features; faster recovery.Open adrenalectomy
Procedure: Larger incision to remove tumor en bloc.
Why: Very large tumors, invasion to nearby tissues, or need for wide margins.Cortical-sparing adrenalectomy (selected hereditary bilateral cases)
Procedure: Remove the medullary tumor while saving some adrenal cortex.
Why: Reduce lifelong steroid dependence when both adrenals are involved.Metastatic tumor debulking / metastasectomy
Procedure: Surgical removal of accessible metastases.
Why: Reduce hormone load, relieve symptoms, or prepare for other therapies.Image-guided ablation (RFA/MWA) or SBRT (stereotactic radiation)
Procedure: Needle-based heat ablation or focused radiation to specific lesions.
Why: Local control when surgery is not possible or to palliate pain.
Preventions and risk-reduction strategies
You cannot fully “prevent” this cancer, but genetic counseling and scheduled screening catch tumors earlier.
Know your gene status (e.g., SDHB, VHL, RET, NF1) if family history exists; follow the surveillance plan.
Control blood pressure and follow alpha-blocker instructions before any biopsy or surgery.
Avoid triggers that can spike catecholamines: heavy lifting, straining, intense exertion, stimulants, some decongestants.
Medication review before dental or minor procedures—local anesthetics with epinephrine may be risky.
Hydration and salt as your team prescribes pre-op to prevent fainting from alpha-blockers.
Regular follow-up imaging and labs after treatment to catch recurrence early.
Medical alert information about pheochromocytoma on your phone/wallet.
Stress-management routine (breathing, PMR, mindfulness) to keep sympathetic tone down.
Vaccinations and infection prevention to avoid treatment delays.
When to see doctors
Right away / emergency: Sudden severe headache, chest pain, shortness of breath, fainting, very high blood pressure, new neurologic symptoms, or relentless palpitations and sweating.
Prompt appointment: Recurrent “spells” of pounding heart, tremor, pallor, nausea, or abdominal/flank pain; new high blood pressure, or a known adrenal mass on imaging.
During treatment: Any severe dizziness, very low blood pressure when standing, fever ≥38.0°C, uncontrolled pain, persistent vomiting/diarrhea, signs of infection, or new medication side effects.
What to eat and what to avoid
Eat: Regular, balanced meals with lean protein, whole grains, vegetables, and fruit to keep glucose steady.
Eat: Adequate fluids; use electrolyte solutions on hot days if your team agrees.
Eat: Sufficient salt pre-op only if your doctor directs (common with alpha-blockade).
Eat: Foods rich in potassium and magnesium (leafy greens, beans, bananas) unless restricted.
Eat: Fiber (oats, legumes, psyllium) for gut health and lipid control.
Avoid: High-caffeine or energy drinks that can raise heart rate and BP.
Avoid: Sympathomimetic decongestants (e.g., pseudoephedrine) unless cleared.
Avoid: Large amounts of alcohol (can destabilize BP, interact with meds).
Avoid or limit: Tyramine-rich aged foods (very aged cheeses, cured meats) if your team advises trigger avoidance.
Avoid: Nicotine and recreational stimulants (amphetamines, cocaine)—dangerous with this condition.
Frequently Asked Questions
Is adrenal medulla cancer always dangerous?
Yes, because hormone surges can harm the heart and brain. With proper blockade and expert care, the risk drops a lot.Is it the same as an adrenal cortical cancer?
No. The cortex makes steroid hormones; the medulla makes adrenaline-type hormones. They are different diseases.What symptoms are most typical?
Episodes of severe headache, pounding heart, sweating, tremor, paleness, and sudden high blood pressure.Can I exercise?
Only with your team’s plan. Start after alpha-blockade and use gentle, supervised activity. Stop with any warning signs.Why do I need alpha-blockers before surgery?
They protect you from dangerous BP spikes when the tumor is touched during surgery.Why add a beta-blocker later?
To slow heart rate after the blood vessels are safely relaxed by alpha-blockers.Do all tumors spread?
No. Many are removed and cured. Some behave aggressively, especially with certain gene changes like SDHB.How will doctors find it?
Blood or urine tests for catecholamine breakdown products, plus imaging (CT/MRI) and special scans (MIBG or somatostatin PET).Can a biopsy be done?
Usually avoided before blockade because it can trigger a crisis. Diagnosis relies on labs and imaging first.What are targeted radiotherapies?
MIBG and PRRT deliver radiation directly to tumor cells that “take up” the tracer, sparing more normal tissues.Do I need both adrenals removed?
Only in specific cases. If both are involved, surgeons may try to spare some adrenal cortex to avoid lifelong steroid dependence.Will I need lifelong follow-up?
Yes. Recurrence can happen. Regular checks keep you safe.Are there diet cures?
No. Diet supports overall health but does not cure cancer. Avoid stimulants and follow your team’s plan.Can immunotherapy help?
Sometimes, in advanced cases. It is not for everyone; your oncologist will decide based on biology and prior treatments.
Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.
The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members
Last Updated: September 09, 2025.
