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Figure 25-1.

Pituitary gland. (Reproduced with permission from Longo DL, Fauci AS, Kasper, DL, et al. (eds). Harrison's Principles of Internal Medicine, 18th ed. New York: McGraw-Hill, 2012: Fig 339–1.)

  • Pathophysiology: underactive pituitary gland, 2/2 complete/partial loss of lobe function
  • Signs/symptoms: features of specific hormone deficiency: GH → fatigue; ↓ FSH/LH → ↓ libido, impotence, ↓ menstruation, ↓ pubic hair, Δ in sexual function, ↓ ACTH (different from Addison's disease—no ↓ K, salt cravings, or hyperpigmentation) if present with hypothyroidism treat adrenal insufficiency 1st to avoid adrenal crisis; ↓ TSH → similar to central hypothyroidism, usually no goiter; ↓ prolactin → ↓ lactation (uncommon); ↓ ADH (common in 2° disorder) → polyuria, polydipsia, ↑ Na
  • Diagnosis: pituitary MRI & hormone studies; rule out anorexia, chronic liver disease, myotonia dystrophica, & polyglandular autoimmune disease
  • Treatment: resolve underlying cause & replace deficient hormones; doses based on individual needs

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Clinical Pearl 25-1

GFLAT P → order that anterior pituitary hormones are depleted → GH, FSH/LH, ACTH, TSH, prolactin

Table 25-1 Causes of Primary & Secondary Panhypopituitarism

  • Pathophysiology: hypofunction of the anterior pituitary resulting in ↓ GH; GH regulated by growth hormone releasing hormone (GHRH stimulation) & somatostatin (inhibition)

Diagnosis & Evaluation

  • Signs/symptoms: adults—↑ LDL, ↑ central adiposity, ↓ exercise tolerance, ↓ bone mineral density, ↓ cardiac output, depressed mood, ↓ QOL; pediatrics—abnormally slow growth & short stature with normal proportions; >2.5 SD below mean height for age
  • Diagnosis: GH release pulsatile ∴ ↓ [GH] not diagnostic; use GH stimulation tests → failure to ↑ GH after stimulation suggests GH deficiency → insulin tolerance test (<3mcg/L); glucagon test (<3mcg/L); GHRH-arginine test (<9mcg/L; cut-off levels may vary by lab) obesity may cause false +

Treatment & Follow-Up

  • Treatment: GH → cannot mimic endogenous pulsatile secretion; suppressed postprandially; elevated postabsorptive → administer HS to avoid postprandial GH elevations → weight based (varies by product) or initial 0.2mg/d → low-dose replacement <3mcg/kg/d may have benefits on glucose metabolism & insulin resistance vs higher doses (Diabetologia 2010;53:1304); 3–6mo required to establish benefit; titrate Q2–4wk
  • Monitor: lipids Q6mo, glucose Q3mo, T4 may ↓, T3 remains stable → patients using exogenous thyroid hormone may need dose ↑; adverse effects: edema, arthralgias, pancreatitis, insulin resistance

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