Hormonal Tumor

A hormonal tumor is a growth that makes and releases extra hormones. Hormones are chemical messengers. They are made by glands like the pituitary, thyroid, parathyroids, adrenals, pancreas, ovaries, and testes. When a tumor forms in these glands, it may “over-produce” one or more hormones. This leads to signs and symptoms in many body systems. Some hormonal tumors are benign (not cancer). Some are malignant (cancer). Some are functional (they make too much hormone). Others are non-functional (they do not make extra hormone but can still grow and press on nearby tissues). Hormonal tumors can be sporadic (happen by chance) or inherited (caused by gene changes that run in families). Early recognition is important because hormone excess can be treated, and removing or controlling the tumor can prevent serious harm.

A hormonal tumor is any growth that makes extra hormones and releases them into the blood, causing symptoms in distant parts of the body. Doctors also call these “functioning” or “hormone-secreting” tumors. They can arise from endocrine glands (like the pituitary, thyroid, parathyroids, adrenals, ovaries, testes) or from neuroendocrine cells throughout the body (for example in the gut or pancreas). Because the tumor’s cells keep producing hormones without normal control, patients may have symptoms from both the tumor mass (pressure, pain) and the hormone excess (for example flushing, diarrhea, high blood pressure, or abnormal growth). Hormone-making tumors include many types: pituitary adenomas (making prolactin, growth hormone, ACTH), thyroid cancers (including medullary thyroid cancer), parathyroid tumors, adrenal tumors (cortisol-, aldosterone- or catecholamine-secreting), and gastrointestinal-pancreatic neuroendocrine tumors (NETs). Cancer.gov+3Cancer.gov+3Cancer.gov+3

---

Other names

People and books may use different names for the same idea:

• Endocrine tumor — a tumor of a hormone-making gland.

• Hormone-secreting tumor or functional tumor — a tumor that releases extra hormone.

• Neuroendocrine tumor (NET) — a tumor from neuroendocrine cells; many NETs release hormones (for example, insulinoma, gastrinoma, carcinoid).

• Adenoma — a benign gland tumor; some adenomas are functional (for example, prolactinoma).

• Carcinoma — a malignant gland tumor (for example, adrenocortical carcinoma, medullary thyroid carcinoma).

• Pheochromocytoma and paraganglioma — adrenal and extra-adrenal catecholamine-secreting tumors.

• Pituitary adenoma, thyroid cancer, parathyroid adenoma, adrenocortical tumor, pancreatic NET, ovarian/testicular sex-cord stromal tumor — organ-specific names that can be hormone-secreting.

---

Types

You can classify hormonal tumors in a few simple ways.

By gland or origin

• Pituitary tumors (for example, prolactinoma, growth hormone adenoma, ACTH-secreting adenoma).

• Thyroid tumors (papillary, follicular, medullary thyroid carcinoma; some release calcitonin).

• Parathyroid adenoma or hyperplasia (causes high parathyroid hormone and high calcium).

• Adrenal tumors

  • Adrenocortical adenoma/carcinoma (cortisol, aldosterone, androgens).

  • Pheochromocytoma (adrenal medulla; catecholamines).

• Pancreatic neuroendocrine tumors (pNETs) (insulinoma, gastrinoma, glucagonoma, VIPoma, somatostatinoma).

• Carcinoid (NET) of lung, stomach, small bowel, or colon (may release serotonin and cause flushing and diarrhea).

• Gonadal tumors (ovarian granulosa cell tumor, thecoma, Sertoli-Leydig cell tumor, Leydig cell tumor; may release estrogen or androgens).

• Ectopic hormone–producing cancers (for example, small-cell lung cancer making ACTH).

By behavior

• Benign vs malignant.

• Functional (secreting) vs non-functional (non-secreting).

By inheritance

• Sporadic (no family link) vs hereditary (part of a syndrome such as MEN1, MEN2, VHL, NF1, TSC, or SDH-related paraganglioma).

You can group hormonal tumors by where they start and by which hormone they make:

1. Pituitary tumors
   These may make prolactin (prolactinoma), growth hormone (acromegaly), ACTH (Cushing disease), TSH, or rarely other hormones. Symptoms match the hormone made, plus headaches or vision problems if the tumor is large. NIDDK+1

2. Thyroid tumors
   Most thyroid nodules do not make excess hormone, but some “toxic” nodules do. Medullary thyroid cancer arises from C-cells and makes calcitonin (a peptide hormone). Evaluation follows thyroid society guidance to sort out risk. American Thyroid Association+1

3. Parathyroid tumors
   Usually benign adenomas that make too much parathyroid hormone (PTH), raising calcium. Diagnosis is high calcium with inappropriately high PTH. NIDDK+1

4. Adrenal tumors
   These may make cortisol (Cushing syndrome), aldosterone (primary aldosteronism), or catecholamines (pheochromocytoma/paraganglioma). Each hormone has specific screening tests. Endocrine+2Endocrine+2

5. Pancreatic and gastrointestinal NETs
   These include insulinoma (insulin), gastrinoma (gastrin), glucagonoma (glucagon), VIPoma (vasoactive intestinal peptide), and others. Insulinoma diagnosis rests on “Whipple’s triad” of low glucose, symptoms, and relief with sugar. PubMed Central

6. Other NETs
   Lung and small-bowel NETs may cause carcinoid syndrome (flushing, diarrhea) by releasing serotonin and other peptides. Specialized imaging often helps find them. Cancer.gov

Causes

Each short paragraph names one cause or risk and explains it simply.

1. Random DNA changes (somatic mutations)
   Most hormonal tumors are sporadic. Over time, cells gather DNA errors that let them grow without control and make extra hormone. PubMed Central

2. Inherited syndromes: MEN1
   The MEN1 gene (menin) normally slows cell growth. A harmful MEN1 change removes this brake. Tumors then form in parathyroid, pancreas, and pituitary glands. MedlinePlus+1

3. Inherited syndromes: MEN2 (RET)
   A RET gene change switches growth signals “on.” This drives medullary thyroid cancer and pheochromocytoma and can affect parathyroids. MedlinePlus+1

4. Inherited syndromes: MEN4 (CDKN1B)
   A change in CDKN1B weakens a cell-cycle brake (p27), raising tumor risk in endocrine and some non-endocrine tissues. MedlinePlus

5. Other genetic tumor syndromes
   VHL, NF1, and SDHx gene changes increase pheochromocytoma/paraganglioma risk by disrupting cell energy sensors and growth pathways. OUP Academic

6. Chronic iodine lack (thyroid)
   Long-term low iodine can lead to nodules; some nodules can make excess thyroid hormone (“toxic” nodules). Guidance emphasizes risk-based evaluation. American Thyroid Association

7. Past neck radiation (thyroid)
   Radiation exposure raises thyroid nodule and cancer risk later in life; careful ultrasound-based risk tools guide follow-up. American Thyroid Association

8. Long-standing hormone stimulation
   When a gland is pushed to work over time, rare cells with growth advantages may expand and become a functional tumor. This is a general principle observed across endocrine tissues. NCBI

9. Aging
   DNA repair weakens with age. With time, risk of sporadic endocrine tumors rises, including parathyroid adenomas and pituitary adenomas. NCBI

10. Sex-hormone environment
    Some tumors grow faster when estrogen or testosterone rises (for example, large prolactinomas can enlarge during pregnancy due to higher estrogen). Mayo Clinic

11. Metabolic stress
    Obesity, insulin resistance, and chronic inflammation may create a growth-friendly environment for some tumors, though links vary by tumor type. (General NET/oncology principles.) PubMed Central

12. Immune suppression
    A weak immune system may miss early tumor cells, allowing growth, though this risk differs across hormonal tumors. (General oncology principle in endocrine context.) PubMed Central

13. Environmental carcinogens
    Some chemicals and toxins damage DNA over years. Endocrine tissues are not exempt, but exact risks depend on exposure and tumor type. PubMed Central

14. Family history without a known gene
    Families can show clustering of endocrine tumors even when testing does not find a specific mutation, implying yet-unknown inherited risks. Cancer.gov

15. Chronic low vitamin D (parathyroid)
    Low vitamin D causes secondary hyperparathyroidism; over long periods, susceptible people may develop a true adenoma that keeps PTH high. NCBI

16. Prior adrenal growths
    Adrenal nodules are common; some later start making hormone (cortisol or aldosterone). Screening identifies who needs treatment. Endocrine

17. Germline SDHx mutations (PPGL)
    Changes in succinate dehydrogenase genes alter cell metabolism and stabilize growth signals, promoting catecholamine-secreting tumors. OUP Academic

18. Gastric acid-related stimulation (gastrinoma)
    In MEN1, repeated gastrin drive and cell changes favor gastrinoma formation in the pancreas/duodenum. MedlinePlus

19. Unknown (idiopathic)
    For many patients, no clear cause is found. The tumor likely reflects several small risks coming together. PubMed Central

20. Rare exposures or conditions
    Some rare drugs, toxins, or medical conditions can alter hormone-cell growth control and play a role in unusual cases. PubMed Central

Symptoms

Symptoms come from too much hormone and from the mass itself pressing on nearby tissue. The exact mix depends on the tumor.

1. Unexplained weight change
   Cushing syndrome (too much cortisol) causes central weight gain; excess thyroid hormone causes weight loss with appetite. First-line Cushing screening uses urine or saliva cortisol or a low-dose dexamethasone test. Endocrine+1

2. High blood pressure, headaches, pounding heart
   Pheochromocytoma releases catecholamines. The best initial tests are plasma free or urinary fractionated metanephrines. PubMed+1

3. Muscle weakness and purple stretch marks
   Cortisol excess breaks down muscle and thins skin, causing weakness and wide, purple striae. Screening follows Endocrine Society guidance. Endocrine

4. Spells of flushing and watery diarrhea
   Some NETs release serotonin or VIP, causing flushing and diarrhea. Specialized imaging helps locate the tumors. Cancer.gov

5. Sweating, tremor, fast heartbeat
   Too much thyroid hormone stimulates the heart and nerves. Thyroid society guidance supports risk-based evaluation of nodules. American Thyroid Association

6. Milk discharge from breasts and low sex drive
   Prolactinomas cause galactorrhea and reduced fertility or libido; NIDDK lists common sex-specific symptoms. NIDDK

7. Headaches and vision changes
   Large pituitary tumors can press on the optic chiasm, causing vision loss. Evaluation includes hormone tests and pituitary MRI. Endocrine

8. Bone pain, kidney stones, and tiredness
   Parathyroid adenomas raise calcium, which can cause stones and bone loss. Diagnosis is high calcium with inappropriately high PTH. NIDDK

9. Repeated low blood sugar (shakiness, confusion)
   Insulinomas cause “Whipple’s triad”: low plasma glucose, symptoms, and relief with glucose. PubMed Central

10. Stomach ulcers and heartburn
    Gastrinomas increase acid, leading to ulcers and reflux. Workup focuses on fasting gastrin and imaging. PubMed Central

11. Change in body size (hands, feet, jaw)
    Growth hormone–secreting pituitary tumors cause acromegaly. IGF-1 is the first-line blood test. OUP Academic+1

12. Weakness, cramps, and tingling
    High or low calcium from parathyroid disease can cause neuromuscular symptoms; calcium and PTH testing confirms the cause. NIDDK

13. Anxiety or panic-like episodes
    Pheochromocytoma surges can feel like panic attacks; metanephrine testing is preferred. PubMed

14. Skin flushing with wheezing
    Carcinoid syndrome can cause flushing with bronchospasm due to vasoactive peptides. NET overviews describe these patterns. Cancer.gov

15. No symptoms at all
    Many hormonal tumors are found on routine labs or scans. Careful testing decides who needs treatment. NIDDK

Diagnostic tests

Your team chooses tests based on your symptoms and which hormone is likely high. Below are common, evidence-based tools.

A) Physical examination (bedside observation)

1. Vital signs and blood pressure
   Doctors check heart rate, blood pressure (including very high readings or big swings), and temperature. Severe or variable hypertension may suggest pheochromocytoma, which then calls for metanephrine testing. PubMed

2. Body shape and skin inspection
   Central obesity, thin skin, easy bruising, and purple striae point to cortisol excess and prompt Cushing screening (urine or saliva cortisol or low-dose dexamethasone test). Endocrine

3. Thyroid and neck exam
   Doctors look and feel for thyroid enlargement or nodules and check for neck tenderness or bruits. Suspicious nodules are worked up per ATA guidance with labs, imaging, and, if needed, fine-needle biopsy. American Thyroid Association

4. Neurologic and vision check
   Visual field loss and cranial nerve findings suggest a pituitary mass; MRI and hormone panels follow. Endocrine

5. Signs of dehydration or flushing
   Flushing and volume loss (from watery diarrhea) suggest hormone-secreting NETs like VIPoma or carcinoid; NET guidance supports targeted labs and imaging. Cancer.gov

B) “Manual” bedside tests (simple maneuvers)

6. Orthostatic blood pressure
   Measuring BP and pulse lying and standing can reveal catecholamine-driven instability or cortisol-related volume changes, guiding lab screening. PubMed

7. Trousseau and Chvostek signs
   Bedside calcium-related signs (carpopedal spasm or facial twitch) can point toward parathyroid problems and need for calcium and PTH testing. NIDDK

8. Bedside visual field confrontation
   A quick check for side (temporal) vision loss screens for chiasm compression by a pituitary macroadenoma; confirms need for formal imaging. Endocrine

9. Focused thyroid palpation
   Feeling for discrete nodules or tenderness helps triage who needs ultrasound and further thyroid work-up. American Thyroid Association

10. Abdominal exam
    General palpation and bowel sounds can show tenderness or masses that prompt abdominal imaging for adrenal or pancreatic NETs. PubMed Central

C) Laboratory and pathological tests

11. Low-dose dexamethasone suppression test (DST)
    You take dexamethasone at night; morning cortisol should fall. If it does not, Cushing syndrome is suspected. This is an Endocrine Society–endorsed first-line test. Endocrine+1

12. Late-night salivary cortisol
    Cortisol should be lowest at night. A high value is a sensitive screen for Cushing syndrome. Endocrine

13. 24-hour urine free cortisol (UFC)
    Measures total cortisol made in a day. High levels suggest Cushing syndrome. Endocrine

14. Aldosterone-renin ratio (ARR)
    Morning aldosterone and renin are measured together. A high ARR screens for primary aldosteronism; updated guidance supports broad screening in hypertension. Endocrine+1

15. Plasma free or urinary fractionated metanephrines
    Best initial test for pheochromocytoma/paraganglioma (PPGL), because metanephrines are steady breakdown products of catecholamines. PubMed+1

16. IGF-1 and GH testing for acromegaly
    IGF-1 is the first screen; if high or borderline, GH suppression during an oral glucose test confirms the diagnosis. OUP Academic+1

17. Calcium and PTH for hyperparathyroidism
    Diagnosis is high calcium with inappropriately high PTH. Doctors also check vitamin D and kidney function. NIDDK+1

18. Insulin, C-peptide, and supervised fasting (insulinoma)
    In hypoglycemia spells, inappropriately high insulin and C-peptide confirm insulin-driven low sugar. Whipple’s triad describes the classic pattern. PubMed Central

19. Gastrin (± secretin stimulation)
    Markedly high fasting gastrin suggests gastrinoma; some centers use a secretin test to confirm. PubMed Central

20. Pathology with immunostains (after biopsy or surgery)
    When tissue is sampled, special stains (e.g., chromogranin A, synaptophysin) and hormone stains confirm tumor type and help plan care. PubMed Central

D) Electrodiagnostic tests

21. Electrocardiogram (ECG)
    Checks for rhythm changes from high thyroid hormone, low potassium in aldosteronism, or catecholamine surges. Findings guide urgent management and further hormone testing. Endocrine

22. Holter or ambulatory blood pressure monitoring
    Detects swings in heart rhythm or blood pressure that support a catecholamine-secreting tumor and prompt metanephrine testing. PubMed

23. EMG/nerve conduction studies (selected cases)
    In long-standing endocrine disease (e.g., diabetes with insulinoma unmasking, severe thyroid disease), these can document neuropathy or myopathy when symptoms are unclear. PubMed Central

E) Imaging tests

24. High-resolution pituitary MRI
    Best test to find pituitary adenomas after hormone testing suggests a pituitary source (e.g., prolactin, GH, ACTH). Endocrine

25. Thyroid ultrasound
    First-line imaging for thyroid nodules with risk stratification; guides fine-needle aspiration decisions. American Thyroid Association

26. Adrenal CT or MRI
    Identifies adrenal nodules and helps decide if a mass is likely benign. Imaging is part of PPGL and aldosteronism work-ups after biochemical confirmation. PubMed

27. MIBG scintigraphy (for PPGL)
    Uses a radiotracer that enters catecholamine-producing cells; helpful for multifocal or metastatic pheochromocytoma. PubMed

28. Ga-68 DOTATATE PET/CT (for NETs)
    Very sensitive for many NETs because these tumors carry somatostatin receptors; helps locate small or hidden tumors. PubMed Central

29. Endoscopic ultrasound (EUS) for pancreatic NETs
    A specialized ultrasound probe on an endoscope can find tiny insulinomas or gastrinomas that scans miss and allows fine-needle biopsy. PubMed Central

30. Sestamibi scan or 4D-CT (parathyroid localization)
    After biochemical diagnosis of primary hyperparathyroidism, imaging helps surgeons find the overactive gland before minimally invasive surgery. Mayo Clinic

Non-pharmacological treatments

1) Surgical removal of the tumor (when feasible).
Purpose: Cure or debulk the tumor and stop hormone excess. Mechanism: Physically removes hormone-producing cells; reduces mass effect (e.g., vision problems). Approach depends on location—transsphenoidal surgery for pituitary, thyroidectomy for thyroid cancer, parathyroidectomy for primary hyperparathyroidism, adrenalectomy for hormone-making adrenal tumors, and organ-specific resections for NETs. Decisions follow guideline pathways and imaging results. Cancer.gov+2NCCN+2

2) Active surveillance (watchful waiting) for very small, low-risk tumors.
Purpose: Avoid overtreatment when risks outweigh benefits. Mechanism: Regular labs and imaging monitor growth and hormone activity; treatment starts only if the tumor grows or symptoms appear. This is common for some small, asymptomatic NETs or micro-prolactinomas/thyroid nodules under strict criteria. PubMed

3) Stereotactic radiosurgery / focused radiation.
Purpose: Control residual or unresectable tumors (especially pituitary) and reduce hormone excess. Mechanism: Precisely targeted beams damage tumor DNA and its blood supply while sparing surrounding brain or tissues, gradually lowering hormone levels and controlling growth. Cancer.gov

4) External-beam radiation therapy (EBRT).
Purpose: Local control or palliation when surgery is not possible. Mechanism: Fractionated radiation causes tumor cell death; used for pituitary remnants, bone metastases from NETs/thyroid cancer, or unresectable disease. Cancer.gov

5) Thermal ablation (RFA/MWA) and liver-directed therapies (embolization/TACE) for NET metastases.
Purpose: Reduce hormone burden and shrink tumors in the liver to control symptoms. Mechanism: Heat destroys tumor nodules (ablation); embolization starves tumors of arterial blood, sometimes delivering chemo locally (TACE). Wikipedia

6) Nutrition counseling by an oncology dietitian.
Purpose: Maintain weight and strength, reduce diarrhea/flushing triggers, and correct deficiencies (e.g., B12, fat-soluble vitamins after bowel surgery). Mechanism: Structured meal plan (plant-forward, adequate protein, fluids), symptomatic trigger avoidance (e.g., high-amine foods in carcinoid syndrome), and supplement guidance. American Cancer Society+2NETRF+2

7) Physical activity (as tolerated).
Purpose: Improve energy, mood, and metabolic health; preserve muscle during treatment. Mechanism: Gradual aerobic and resistance exercise counters fatigue and treatment-related deconditioning; plans are individualized with medical clearance. American Cancer Society

8) Stress-reduction and sleep hygiene.
Purpose: Decrease sympathetic surges (helpful in pheochromocytoma) and improve overall well-being. Mechanism: Breathing, mindfulness, and regular sleep dampen catecholamine spikes and reduce perceived symptom severity. Mayo Clinic

9) Temperature and trigger control for flushing.
Purpose: Reduce flushing and diarrhea in serotonin-secreting NETs. Mechanism: Avoid alcohol, very spicy foods, large meals, and extreme heat when these worsen symptoms. Keep a symptom/food diary. Carcinoid Cancer Awareness Network+1

10) Salt and fluid optimization before pheochromocytoma surgery (with alpha-blockade).
Purpose: Prevent dangerous blood-pressure drops after tumor removal. Mechanism: Expands blood volume before surgery per endocrine guidelines. (Medication is also used—see drug section.) Mayo Clinic

11) Genetic counseling and testing (if syndromic features).
Purpose: Identify hereditary risk, guide screening for patients and family, and plan earlier surgery (e.g., prophylactic thyroidectomy in MEN2). Mechanism: Detects RET/MEN1/VHL/SDHx variants and links to surveillance protocols. PubMed

12) Vaccinations and infection prevention (general).
Purpose: Reduce interruptions to cancer care from infections. Mechanism: Staying up to date on standard vaccines (per local guidance) and hand hygiene lowers infection risk during therapy. (General supportive measure.) American Cancer Society

13) Vision preservation strategies for pituitary macroadenomas.
Purpose: Protect eyesight while awaiting surgery. Mechanism: Urgent ophthalmology checks and prompt surgical referral if visual field loss progresses. Cancer.gov

14) Bone protection plan in hyperparathyroidism or cortisol excess.
Purpose: Prevent fractures from high PTH or cortisol. Mechanism: Correct vitamin D/calcium carefully and treat osteoporosis as indicated after controlling the hormone source. Office of Dietary Supplements

15) Iodine nutrition balance for thyroid health.
Purpose: Support normal thyroid function post-treatment and avoid extremes. Mechanism: Use iodized salt in typical amounts and avoid high-dose, unsupervised iodine pills. Office of Dietary Supplements

16) Management of treatment-related fat malabsorption on somatostatin analogs.
Purpose: Reduce steatorrhea and nutrient losses. Mechanism: Dietitian-guided lower-fat meals, pancreatic enzymes if needed, and fat-soluble vitamin monitoring. Carcinoid Cancer Awareness Network

17) Pelvic floor and continence support (if diarrhea is prominent).
Purpose: Improve control and quality of life. Mechanism: Timed toileting, soluble fiber adjustments, and physiotherapy where appropriate. American Cancer Society

18) Multidisciplinary tumor boards / centers of excellence.
Purpose: Optimize outcomes by coordinated care. Mechanism: Surgeons, endocrinologists, oncologists, radiologists, and pathologists plan individualized therapy. SciSpace

19) Psychosocial and financial counseling.
Purpose: Lower stress and improve adherence. Mechanism: Navigation, social work, and counseling address mental health and access barriers during long-term care. American Cancer Society

20) Palliative care integration when needed.
Purpose: Control symptoms and maintain dignity at any stage. Mechanism: Specialist input for pain, diarrhea, flushing, anxiety, sleep, and advanced care planning—alongside active cancer treatment. PubMed

---

Drug treatments

1) Octreotide (Sandostatin LAR Depot).
Class/Mechanism: Long-acting somatostatin analog that binds somatostatin receptors to suppress hormone release (e.g., serotonin) and slow some NET growth. Dose/Time: Commonly 20–30 mg intramuscularly every 4 weeks; adjusted by response. Purpose: Control flushing/diarrhea in carcinoid syndrome and other functional NETs. Side effects: Gallstones, steatorrhea, abdominal pain, glucose changes, injection-site discomfort. Always individualize with your clinician. FDA Access Data

2) Lanreotide (Somatuline Depot).
Class/Mechanism: Long-acting somatostatin analog; slows hormone secretion and NET growth. Dose/Time: 120 mg deep-subcutaneous every 4 weeks (typical). Purpose: Symptom control and tumor stabilization in gastroenteropancreatic NETs. Side effects: GI upset, gallstones, glucose changes, injection-site reactions. FDA Access Data

3) Pasireotide (Signifor / Signifor LAR).
Class/Mechanism: Somatostatin analog with broader receptor binding; reduces ACTH in Cushing’s disease and GH/IGF-1 in acromegaly (LAR). Dose/Time: Short-acting s.c. twice daily for Cushing’s or LAR monthly for acromegaly. Side effects: High blood sugar is common; also GI symptoms and gallstones—monitor glucose. FDA Access Data

4) Pegvisomant (Somavert).
Class/Mechanism: Growth hormone receptor antagonist; blocks GH action, lowering IGF-1 in acromegaly. Dose/Time: Daily subcutaneous injections with dose titration by IGF-1. Side effects: Elevated liver enzymes, injection reactions; monitor LFTs. FDA Access Data

5) Osilodrostat (Isturisa).
Class/Mechanism: 11β-hydroxylase inhibitor; reduces cortisol synthesis in Cushing’s disease when surgery is not curative/possible. Dose/Time: Oral, titrated; frequent cortisol/potassium checks. Side effects: Adrenal insufficiency if over-suppressed, low potassium, edema, QT prolongation. FDA Access Data

6) Mifepristone (Korlym).
Class/Mechanism: Glucocorticoid receptor antagonist; blocks cortisol’s effects (improves hyperglycemia in Cushing’s). Dose/Time: Oral daily; titrate by clinical response and glucose. Side effects: Endometrial thickening, low potassium, fatigue; pregnancy contraindicated. FDA Access Data

7) Everolimus (Afinitor).
Class/Mechanism: mTOR inhibitor; slows growth in advanced pancreatic, GI or lung NETs. Dose/Time: Oral once daily; avoid grapefruit. Side effects: Stomatitis, infections, high blood sugar/lipids, non-infectious pneumonitis. FDA Access Data

8) Sunitinib (Sutent).
Class/Mechanism: Multi-targeted TKI; approved for progressive pancreatic NETs. Dose/Time: Oral, usually 37.5–50 mg in cycles or continuous per label; avoid grapefruit. Side effects: Fatigue, hypertension, hand-foot syndrome, diarrhea, cytopenias. FDA Access Data

9) ^177Lu-Dotatate (Lutathera).
Class/Mechanism: Radioligand therapy targeting somatostatin receptors; delivers radiation into NET cells. Dose/Time: Given IV in 4 cycles, 8 weeks apart, with amino acid infusions for kidney protection. Side effects: Nausea during infusion, transient marrow suppression, rare kidney/liver effects—specialty centers only. FDA Access Data

10) Abiraterone acetate (Zytiga) for androgen-driven tumors (e.g., prostate).
Class/Mechanism: CYP17 inhibitor; blocks androgen synthesis. Dose/Time: Oral daily with prednisone; take on empty stomach. Side effects: Hypertension, low potassium, fluid retention, liver enzyme rise. FDA Access Data

11) Tamoxifen.
Class/Mechanism: Selective estrogen receptor modulator (SERM); blocks estrogen action in ER-positive tumors. Dose/Time: Oral daily. Side effects: Hot flashes, risk of blood clots, endometrial changes—benefit/risk reviewed with clinician. FDA Access Data

12) Anastrozole (Arimidex).
Class/Mechanism: Aromatase inhibitor; lowers estrogen production (postmenopausal ER+ tumors). Dose/Time: Oral daily. Side effects: Joint pain, bone loss—bone health plan needed. FDA Access Data

13) Letrozole (Femara).
Class/Mechanism: Aromatase inhibitor similar to anastrozole. Dose/Time: Oral daily. Side effects: Hot flashes, arthralgia, bone density loss—monitor. FDA Access Data

14) Leuprolide (Lupron Depot) for hormone suppression (e.g., prostate; sometimes gynecologic indications).
Class/Mechanism: GnRH agonist causing medical castration after initial flare. Dose/Time: Depot injections monthly/quarterly. Side effects: Hot flashes, bone loss, metabolic changes; watch for flare in first weeks. FDA Access Data

15) Degarelix (Firmagon) / Relugolix (Orgovyx).
Class/Mechanism: GnRH antagonist (degarelix, injectable) and oral antagonist (relugolix); rapidly lower testosterone without flare. Dose/Time: Degarelix monthly injections; Relugolix oral daily. Side effects: Hot flashes, injection reactions (degarelix), metabolic effects. FDA Access Data+1

16) Cabergoline (Dostinex) / Bromocriptine (Parlodel) for prolactinomas.
Class/Mechanism: Dopamine agonists that suppress prolactin secretion and shrink tumors. Dose/Time: Cabergoline weekly dosing; bromocriptine daily; titrate by prolactin/MRI. Side effects: Nausea, dizziness; rare valvulopathy—lowest effective dose. FDA Access Data+1

17) Cinacalcet (Sensipar) for parathyroid carcinoma or refractory primary hyperparathyroidism with hypercalcemia.
Class/Mechanism: Calcimimetic that increases the calcium-sensing receptor’s sensitivity, lowering PTH and calcium. Dose/Time: Oral; titrate to calcium response. Side effects: Nausea, low calcium—monitor closely. FDA Access Data

18) Vandetanib (Caprelsa) for metastatic medullary thyroid cancer.
Class/Mechanism: TKI against RET/VEGFR/EGFR. Dose/Time: Oral daily; requires QT monitoring. Side effects: QT prolongation, diarrhea, rash; careful ECG and electrolytes. FDA Access Data

19) Cabozantinib (Cometriq) for progressive metastatic medullary thyroid cancer.
Class/Mechanism: TKI (MET/VEGFR2 and others). Dose/Time: Oral daily Cometriq capsules; do not substitute with Cabometyx tablets. Side effects: Bleeding, hypertension, hand-foot syndrome, diarrhea; avoid grapefruit. FDA Access Data+1

20) Levothyroxine (Synthroid) for TSH suppression after thyroid cancer.
Class/Mechanism: Thyroid hormone (T4); at tailored doses it suppresses TSH to reduce stimulation of residual thyroid cancer cells. Dose/Time: Oral daily on an empty stomach; interactions with calcium/iron/soy. Side effects: Overtreatment can cause palpitations and bone loss; dosing individualized. FDA Access Data+1

⚠️ Important safety note about “immunity boosters,” “regenerative,” and “stem cell drugs”:
There are no FDA-approved stem cell drugs or generic “immunity boosters” to treat hormonal tumors. Unregulated stem-cell products can be dangerous. Evidence-based care uses approved medicines, surgery, radiation, and clinical trials. If you’re interested in experimental therapies, discuss registered clinical trials with your oncologist. PubMed

---

Dietary molecular supplements

1) Vitamin D (cholecalciferol).
Dose: Typical adults 600–800 IU/day (15–20 mcg); higher only if doctor-prescribed for deficiency. Function/Mechanism: Supports calcium balance and bone health, important in patients with prior hyperparathyroidism, cortisol excess, aromatase inhibitor therapy, or reduced mobility. Vitamin D increases intestinal calcium absorption and helps maintain bone mineralization. Notes: Avoid high, unsupervised doses—excess can cause hypercalcemia and kidney problems. Pair with dietary calcium as advised. Office of Dietary Supplements

2) Calcium (diet first; supplement only if needed).
Dose: Usually 1000–1200 mg/day from food + supplements combined; use lowest supplement dose to meet the gap. Function/Mechanism: Rebuilds bone stores after controlling hormone excess (e.g., post-parathyroidectomy or Cushing’s treatment). Notes: Too much calcium can cause constipation and kidney stones; space from levothyroxine tablets by at least 4 hours. FDA Access Data

3) Iodine (from iodized salt/food—not high-dose pills).
Dose: Adults generally ~150 mcg/day from diet; use iodized salt in normal culinary amounts. Function/Mechanism: Essential to make thyroid hormones; deficiency or excess both harm thyroid health. Notes: Avoid high-dose iodine supplements unless your doctor prescribes them for specific short-term indications. Office of Dietary Supplements

4) Selenium.
Dose: ~55 mcg/day from diet; supplements only if deficient. Function/Mechanism: Component of selenoproteins (e.g., deiodinases) that help activate/deactivate thyroid hormones and protect cells from oxidative stress. Notes: High doses can be toxic (hair/nail changes, GI upset). Diet sources are preferred. Office of Dietary Supplements

5) Omega-3 fatty acids (EPA/DHA).
Dose: Common supplemental range 1 g/day; tailor with clinician. Function/Mechanism: Anti-inflammatory fatty acids that may help general cardiovascular health during cancer therapy; can modestly improve triglycerides and may support appetite in some settings. Notes: Watch bleeding risk with TKIs if taking high doses. American Cancer Society

6) Vitamin B12 (if malabsorption or bowel surgery).
Dose: Individualized; oral or injections if levels are low. Function/Mechanism: Replaces deficiency and supports red blood cell and nerve function, which can be affected after small-bowel NET surgery or chronic diarrhea. Notes: Check levels before supplementing. American Cancer Society

7) Fat-soluble vitamins A, E, K (only if deficient).
Dose: Based on labs; avoid high doses. Function/Mechanism: Replace losses when steatorrhea occurs on somatostatin analogs or after bowel resection. Notes: Work with a dietitian/doctor to avoid toxicity. Carcinoid Cancer Awareness Network

8) Soluble fiber (psyllium/pectin).
Dose: Start low, titrate to effect. Function/Mechanism: Thickens stools and reduces diarrhea frequency in carcinoid syndrome; also supports microbiome health. Notes: Avoid very high insoluble fiber during active diarrhea. Alberta Health Services

9) Oral rehydration solutions (ORS).
Dose: As needed during diarrhea flares. Function/Mechanism: Balanced glucose–electrolyte solutions enhance water absorption in the gut and prevent dehydration. Notes: Useful adjunct to medical therapy; watch sugar load if diabetic. Sunnybrook Hospital

10) Protein supplements (whey/plant) if intake is low.
Dose: To meet daily protein goals (often 1.0–1.2 g/kg/day unless restricted). Function/Mechanism: Preserves lean body mass during treatment and recovery. Notes: Choose low-fat options if steatorrhea is an issue; dietitian guidance helps. American Cancer Society

Caution: Supplements do not treat tumors. Use them only to correct deficiencies or support nutrition, and always clear them with your oncology/endocrine team to avoid drug interactions. American Cancer Society

---

Surgeries (what is done & why)

1) Transsphenoidal pituitary surgery.
What/Why: Endoscopic removal of a pituitary adenoma through the nose to relieve pressure on the optic chiasm and stop hormone excess (e.g., ACTH, GH, prolactin if resistant to medicines). Cancer.gov

2) Thyroidectomy (± central neck dissection).
What/Why: Removes thyroid cancer such as medullary thyroid carcinoma; lymph nodes are sampled/removed to control spread and to normalize calcitonin if possible. PubMed

3) Parathyroidectomy.
What/Why: Curative removal of the overactive parathyroid gland(s) to stop excess PTH, lower calcium, and protect bones and kidneys. PubMed

4) Adrenalectomy (minimally invasive when appropriate).
What/Why: Takes out cortisol-, aldosterone-, or catecholamine-secreting adrenal tumors; for pheochromocytoma, pre-op alpha-blockade and volume expansion are essential. Mayo Clinic

5) NET resections and liver-directed surgery/ablation.
What/Why: Debulk hormone-secreting NETs, remove primary tumors, and treat liver metastases to reduce hormone load and improve quality of life. PubMed

---

Preventions

1. Genetic counseling/testing when family history suggests MEN/VHL/NF1/SDHx; follow syndrome-specific screening/surgery timing. PubMed

2. Don’t smoke; limit alcohol—supports overall cancer risk reduction and surgical fitness. American Cancer Society

3. Maintain healthy weight and activity—helps metabolic control when hormones are abnormal. American Cancer Society

4. Balanced iodine intake—use iodized salt in normal amounts; avoid high-dose iodine pills. Office of Dietary Supplements

5. Manage blood pressure and glucose—critical in catecholamine or cortisol excess. Mayo Clinic

6. Regular check-ups for known nodules or hereditary risk; follow imaging/lab schedules. PubMed

7. Bone health plan if at risk (vitamin D/calcium adequacy, weight-bearing exercise, fall prevention). Office of Dietary Supplements

8. Medication review—avoid drug/food interactions (e.g., grapefruit with some TKIs). FDA Access Data

9. Vaccinations per local guidance to reduce treatment interruptions. American Cancer Society

10. Early specialist referral (endocrinology/oncology) for symptoms of hormone excess. Cancer.gov

---

When to see a doctor

See a doctor now if you have: sudden severe headaches/vision changes; pounding headaches with sweats and palpitations; flushing with watery diarrhea; unexplained fractures or kidney stones; rapid weight gain with purple stretch marks; breast discharge without pregnancy; a fast-growing neck lump; or repeated high blood-pressure spikes. These can be warning signs of active hormone-secreting tumors that need urgent evaluation and targeted testing. Cancer.gov+2PubMed+2

---

What to eat and what to avoid

1. Overall pattern: A balanced, plant-forward diet with adequate protein and fluids supports strength through treatment. American Cancer Society

2. Carcinoid syndrome: Many patients feel better avoiding alcohol, very spicy foods, high-amine foods (aged cheeses, chocolate), and very high-fat meals that can worsen flushing/diarrhea; keep a personal trigger diary. Carcinoid Cancer Awareness Network+1

3. Steatorrhea on somatostatin analogs: Consider smaller, lower-fat meals and talk to your team about pancreatic enzymes and fat-soluble vitamins if needed. Carcinoid Cancer Awareness Network

4. Hydration: Use oral rehydration solutions during diarrhea flares. Sunnybrook Hospital

5. Bone health: Ensure adequate vitamin D and calcium (food first, supplements if needed). Office of Dietary Supplements

6. Thyroid medicine tip: Take levothyroxine on an empty stomach and separate from calcium/iron/soy by ≥4 hours. FDA Access Data

7. Pheochromocytoma pre-op plan: Follow clinician advice on salt and fluid with alpha-blockade. Mayo Clinic

8. Weight and heart health: Limit ultra-processed foods and added sugars; focus on vegetables, fruits, whole grains, legumes, nuts, and fish. American Cancer Society

9. Individualize: If you have no GI symptoms, you don’t need broad food bans—personalize with a dietitian. MD Anderson Cancer Center

10. Supplements: Avoid high-dose, non-prescribed supplements that claim to “shrink tumors”; discuss all products with your care team. American Cancer Society

---

Frequently asked questions

1) Are hormonal tumors cancer?
Some are benign (like many pituitary or parathyroid adenomas). Others are cancers (e.g., many NETs, medullary thyroid cancer). What matters most is the behavior (growth, spread) and hormone effects. Cancer.gov+1

2) Can a small tumor cause big symptoms?
Yes—tiny tumors can cause major symptoms if they release potent hormones (for example insulin, ACTH, or serotonin). PubMed

3) What’s the best first test if pheochromocytoma is suspected?
Plasma free or urine fractionated metanephrines. PubMed

4) How are pituitary hormonal tumors treated?
Often surgery (transsphenoidal), targeted medications (dopamine agonists, somatostatin analogs, GH-blocker), and sometimes radiation. Cancer.gov

5) Do somatostatin analogs shrink tumors?
They mainly control hormone symptoms and may slow growth; some patients see shrinkage, but goals are symptom control and stabilization. Dayton Physicians

6) What is PRRT (Lutathera)?
A radioligand therapy that carries radiation to somatostatin-receptor-positive NETs; used in specialized centers under strict safety protocols. FDA Access Data

7) Are there pills for Cushing’s disease?
Yes—osilodrostat lowers cortisol production; mifepristone blocks cortisol’s effects. Surgery remains first-line when feasible. FDA Access Data+1

8) Will I need long-term follow-up?
Yes. Many hormonal tumors can recur or change over time; follow-up scans and labs are standard. PubMed

9) Can diet cure a hormonal tumor?
No. Diet can help symptoms and strength, but it cannot remove or cure tumors. American Cancer Society

10) Is high-dose iodine helpful for thyroid tumors?
No—routine high-dose iodine is not recommended and can harm the thyroid; only use when your specialist prescribes it. Office of Dietary Supplements

11) What if I’m planning pregnancy?
Pre-pregnancy counseling is important; some medicines and imaging must be adjusted or deferred. Coordinate with endocrinology/OB. Cancer.gov

12) Are “immunity boosters” or stem-cell shots recommended?
No. There are no approved stem-cell drugs or generic “immunity boosters” for these tumors; avoid unproven therapies. PubMed

13) Do TKIs interact with foods?
Yes—grapefruit and some supplements can alter drug levels; follow label guidance. FDA Access Data

14) After thyroid cancer surgery, why take levothyroxine?
To replace normal hormone and—at tailored higher doses in many cases—to suppress TSH, reducing stimulation of any residual thyroid cancer cells. FDA Access Data

15) Where can I read patient-friendly, evidence-based care paths?
NCCN Guidelines for Patients (NETs) and NCI PDQ pages are excellent free resources. NCCN+1

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: November 10, 2025.

PDF Documents For This Disease Condition References