Pituitary disorders are diseases of the master endocrine gland at the base of the brain that either oversecrete or undersecrete one or more hormones, or compress adjacent structures by mass effect. Pituitary adenomas are common — incidental detection on MRI reaches roughly 10% of adults, while clinically significant disease affects about 1 in 1,000 people.
Pituitary disorders (ICD-10: E22, E23, E24) comprise diseases of the anterior and posterior pituitary gland that disrupt the regulated secretion of pituitary hormones — growth hormone, prolactin, adrenocorticotropic hormone (ACTH), thyroid-stimulating hormone (TSH), luteinizing hormone (LH), follicle-stimulating hormone (FSH), and antidiuretic hormone (ADH or vasopressin). The disorders span six broad clinical entities: pituitary adenomas (benign neoplasms classified by hormone secreted and by size — microadenomas <10 mm, macroadenomas ≥10 mm), hypopituitarism (deficiency of one or more anterior pituitary hormones), diabetes insipidus (ADH deficiency from posterior pituitary or hypothalamic damage), pituitary apoplexy (acute hemorrhage or infarction of the gland), syndrome of inappropriate ADH secretion (SIADH), and empty sella syndrome. Functional adenomas overproduce specific hormones: prolactinoma (50-60% of clinical adenomas), growth hormone-secreting adenoma causing acromegaly, ACTH-secreting adenoma causing Cushing disease, and rare TSH-secreting adenoma. Non-functional adenomas produce no clinical hormone excess but cause symptoms through mass effect on optic chiasm, cranial nerves, or surrounding pituitary tissue.
The key symptoms of Pituitary Disorders are: Persistent headache, often retroorbital or bitemporal, that does not respond to typical analgesics and may worsen with rising intracranial pressure., Visual disturbance — most classically bitemporal hemianopia (loss of the outer half of each visual field) from optic chiasm compression by a macroadenoma., Menstrual irregularity, amenorrhea, infertility, or galactorrhea (milk production unrelated to childbirth) in women with prolactinoma or any cause of hyperprolactinemia., Loss of libido, erectile dysfunction, infertility, or reduced muscle mass in men, reflecting hyperprolactinemia or secondary hypogonadism., Growth of hands, feet, and facial features (jaw, nose, supraorbital ridge) over years in untreated acromegaly, often with rings or shoes no longer fitting., Central weight gain with thin extremities, round red face, easy bruising, purple abdominal striae, hypertension, and proximal muscle weakness in Cushing disease., Excessive thirst (polydipsia) and dilute urination over 3 liters daily in central diabetes insipidus, often disrupting sleep..
Diagnosis of pituitary disorders combines clinical recognition, biochemical confirmation, and pituitary MRI. The workup begins by identifying which axis is affected. For suspected hyperprolactinemia, fasting serum prolactin above 200 ng/mL strongly suggests prolactinoma; modest elevations (25-100 ng/mL) require rule-out of pregnancy, hypothyroidism, renal failure, and dopamine-antagonist medications. For acromegaly, the Endocrine Society 2014 guideline recommends serum IGF-1 measurement first; a clearly elevated IGF-1 plus failure of growth hormone to suppress below 1 ng/mL during a 75-gram oral glucose tolerance test is diagnostic. For Cushing syndrome, screening uses 24-hour urinary free cortisol, late-night salivary cortisol, or low-dose dexamethasone suppression — two abnormal results from different tests confirm the diagnosis. ACTH measurement then distinguishes ACTH-dependent (pituitary or ectopic source) from ACTH-independent (adrenal) Cushing. Inferior petrosal sinus sampling localizes a pituitary source when MRI is non-revealing. For hypopituitarism, basal hormone testing (cortisol, free T4, TSH, prolactin, IGF-1, LH, FSH, sex hormones, plasma osmolality) is followed by stimulation tests (insulin tolerance test, glucagon stimulation, or short Synacthen) as needed. Diabetes insipidus is diagnosed with water-deprivation testing or copeptin measurement. Pituitary MRI with dedicated thin-slice gadolinium-enhanced protocol is the imaging gold standard, detecting microadenomas down to 3-5 mm. Formal visual field testing (Humphrey perimetry) is mandatory whenever a macroadenoma is identified. In suspected pituitary apoplexy, urgent MRI (or CT if MRI unavailable) plus immediate stress-dose hydrocortisone are the first steps.
Prognosis varies sharply by tumor type and treatment access. Prolactinomas have excellent prognosis: cabergoline normalizes prolactin in 80-90%, fertility is preserved, and long-term mortality is unchanged from the general population. Acromegaly treated to biochemical remission has near-normal life expectancy; untreated acromegaly carries doubled cardiovascular mortality. Cushing disease in remission has approximately normal survival; persistent active Cushing carries 4-5 fold mortality from cardiovascular and infectious complications. Non-functional macroadenomas have favorable prognosis when treated promptly for visual or chiasmal compression; visual recovery is partial in 80-90% of patients operated within months of symptom onset. Hypopituitarism, with optimal replacement, allows essentially normal life expectancy and quality of life, though long-term cardiovascular and skeletal risks remain modestly elevated. Pituitary apoplexy survival exceeds 90% with prompt steroid replacement and decompression when indicated. The decisive prognostic factors are early diagnosis, biochemical remission, and lifelong adherence to replacement and surveillance.
Pituitary disorders require coordinated care at a pituitary center of excellence because diagnosis spans seven hormone axes and imaging, treatment combines surgery, medication, and radiotherapy with significant volume-outcome relationships, and incidental pituitary lesions often need observation rather than intervention. Endocrinologists, transsphenoidal neurosurgeons, neuro-ophthalmologists, neuroradiologists, and radiation oncologists should review complex cases jointly.
Find specialists →Transsphenoidal surgery typically requires 2-3 days in hospital and 4-6 weeks for full activity. Visual fields begin to improve within days of decompression and continue to recover for 12 months. Biochemical remission is confirmed by hormone testing at 6 weeks. Cabergoline-treated prolactinomas show prolactin normalization in weeks and tumor shrinkage over 3-6 months. Radiotherapy effects unfold over 2-5 years for biochemical remission. Hypopituitarism replacement requires titration over 4-8 weeks to optimal symptom control. Diabetes insipidus responds within hours to desmopressin.
Most patients with treated pituitary disorders can exercise normally. Glucocorticoid-replacement patients should increase doses on heavy training or competition days. Acromegaly patients with cardiomyopathy or sleep apnea need clearance before high-intensity training. Patients with macroadenoma compressing the optic chiasm should avoid Valsalva-heavy resistance training preoperatively.
Look for an endocrinologist subspecialized in pituitary disease, partnered with a neurosurgeon performing at least 50 transsphenoidal pituitary operations annually (volume strongly correlates with remission rates), institutional access to stereotactic radiosurgery, on-site neuro-ophthalmology, and active multidisciplinary pituitary tumor boards. Pituitary centers of excellence are formally accredited in several countries.
Medically reviewed by AIHealz Medical Editorial Board · May 13, 2026
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