Prolactin and Growth Hormones
Important pathologies: hyperprolactinemia (What causes it? How does it present? What types of tests
would you run to test for it?
What can cause hyperprolactinemia?
 Tumor of the Pituitary gland: Macroadenoma (larger than 3 cm) or microadenoma
(smaller than 3cm)
o Function Macroadenoma- Massive proliferation of the pituitary lactotrophs 
overproduction of prolactin
o Non-functional Macroadenoma- Massive tumor that does not produce prolactin
but can block the pituitary stalk and prevent dopamine from inhibiting prolactin
production (overproduction of prolactin) STALK EFFECT
 HYPO-thyroidism – LOW T3 and T4 will feedback to increase TRH, which in turn will
increase Prolactin
o So you may see a case of a patient that is experience weight gain, fatigue, but
also presenting with hyperprolactemia (Low GnRH, ameneria)
 Reduced elimination/clearance of Prolactin  (renal failure, hepatic insufficiency)
 Physiological stimulation of prolaction: Pregnancy, estrogen, suckling
 Medication: Neuropleptics/Antipsychotics, Opiates, H2 blockers
How does hyperprolactinemia present?
 Breast – enlargement, tenderness, or abnormal milk production
 Over Suppression of GnRH (normal suppression - makes sense you don’t want to
stimulate fertility when you are already taking care of a child/pregnant)
o But too much prolactin and abnormal suppression of GnRH can lead to..
-Menstrual Irregularities
-Infertility
-Decreased Libido
 If GnRH is decrease so will FSH, LH, and Estrogen will decrease
o Decreased Estrogen  Acne, hirsutism (hair on chin/jaw)
o Decreased Bone mineral density  Osteoporosis (Estrogen apparently
stimulates osteoblast, so prolactin decreases GnRH which eventually leads to
decreased estrogen and decreased osteoblast
What type of tests would you run to test for hyperprolactinemia?
 First and foremost, HISTORY and medical review, and physical exam
o Clinical suspicion rules everything
 Then actual lab stuff:
o 1) FIRSTLY VERY IMPORTANT TO GET A PREGNANCY TEST, if they are
experiencing lack of menses general low GnRH presentations
o 2) TSH, Free T4 (Urine and Saliva) and Creatinine (Kidney test to see if it is
properly eliminating prolactin)
o 3) Visual Fields (If MRI shows macroadenoma because it could push on optic
chiasm)
o

Side note: Hook Effect a laboratory flaw where if the Prolactin levels are too
high, all the antibodies and coating gets saturated and does not detect the
extra prolactin. So the main point is if you send out blood work for prolactin lvl,
and it comes back much lower than you thought. Ask for a redo with dilution
because you could falsely think the pt has a microadenoma when it is a
macroadenoma (much higher Prolactin) and make the patient undergo
unnecessary surgery (to treat microadenoma) when it could’ve been treat
medicinally (macroadenoma main treatment)
How do you treat hyperprolactemia?
o TREATING MACROADENOMA
o Dopamine-Agonist  increased the inhibiting effect of Prolactin secretion and it
even reduces the tumor size!! 😊
 Types of Dopamine AGONIST
 Bromocriptine
 Cabergoline
Too much Growth Hormone: (What causes it? How does it present? What types of tests would you
run to test for it?
o What causes increased GH release?
 Hypoglycemia
 Starvation/Hunger hormone – Ghrelin (GI lining)
 GHRH – Hypothalamus
 Sleep/Exercise/Stress
o What decreases GH?
 Postprandial hyperglycemia
 Increased FFA
 Somatostatin
 Obesity
o How dose abnormal levels of GH present clinically?
o Growth hormone related conditions will vary based on where you are in your
growth.
 Before Puberty – excess GH  Gigantism – excess linear growth
 After Puberty – excess GH  Acromegaly- abnormal growth of the hands,
feet, and face
o Pt with Acromegaly have risks for many other conditions such as
sleep apnea, cardiovascular disease
o Deficient GH
 Pan-Hypo-pituitarism
 Isolated GH deficiency
o
How do you test for abnormal GH?
o IGF-1 measurement?
 IGF-1 level changes throughout the day based on meals etc
o
o
 Measure multiple time
Oral Glucose Test (Gold standard)
 Remember hunger stimulates GH while fed state/glucose will increase
GH production so if you purposely give a GH inhibitor, but GH remains
high, something is wrong
How do you treat for excess GH?
 Medical:
o 1) Octreotide – Somatostatin analog
 Reduces size of tumor and GH levels
o 2) Pregvisomat (GH receptor antagonist)
 Prevents induction of IGF1 production
o 3) Bromocriptine or Cabergoline (Dopamine agonist)
 Reduces GH and IGF-1 levels

Surgery: Treatment of Choice – cure 40-60%
o Radiation as an adjunct to surgery: cure 70%
Too little Growth Hormone: (What causes it? How does it present? What types of tests would you run
to test for it?
 What can cause a deficient GH?
o Congenital
 Brain defect such as sepo-ooptic dysplasia
 Empty Sella syndrome
 Midline face defect
o Acquired GH deficiency
 Trauma
 CNS infection
 Tumor of hypothalamus/pituitary
 Infarct of the brain (Sheehan syndrome)
 Idiopathic
 Cranial Radiation


How does GH deficiency present?
o In Children: Short stature, low growth velocity for age and delayed puberty
o Adults: Low energy, decreased strength, difficulty losing weight, emotional
lability, anxiety, social isolation, decreased libido, and impaired sleep
How do you test if your patient has deficient GH?
o Basel IGF-1 (poor sensitivity- can’t rule in but good specificity can rule out if it
comes out negative)
o Stimulate GH production and see if you get increase it!
 Induce starvation-like environment/hypoglycemia (GIVE INSULIN)
 GHRH- arginine combination


Glucagon and other combination
How do you Treat deficient GH?
o Give recombinant GH but assess risk and benefit
 Children would benefit for obvious reasons, they have more growing to
do
 But adults it may not be necessary + it might add more risk (chance of
colon-breast cancer)
Diabetes:
Type one verses type two
Also why would you never want to give fluids BEFORE insulin to someone with extreme hyperglycemia
Why would you never want to give potassium
In patients with severe Hyperglycemia ALWAYS ALWAYS check the potassium  should be at least 3.3
(it’s probably pretty high due to the body’s nature response to excrete Na and H2O while reabsorbing
potassium)