2 Endocrine disorders hypothalamus and pituitary axis.pdf

CNS pathology

1. Endocrine Disorders:
The Hypothalamus and Pituitary glands

Lloyd Bowora
Chemical Pathology Unit
Dept. of Laboratory Diagnostic and Investigative Sciences
University of Zimbabwe

2. Session 1 Outline:
1.
2.
3.
4.
5.
Introduction
Major concepts in investigations of
endocrine disorders
Hypothalamic factors
Pituitary hormones
Clinical Applications

3. 1. INTRODUCTION
•
•
•
–
–
The hypothalamus
Located on the ventral surface of the
brain around the third ventricle.
Responsible for controlling pituitary
hormones secretion.
Secretes peptide hormones aka
hypothalamic releasing factors, either :
Into short private portal system to directly
impinge anterior pituitary gland
Directly into general circulation (vasopressi
n , oxytocin)

4. 2. MAJOR CONCEPTS
I.
II.
III.
IV.
Testing for pituitary dysfunction employs all
of the following concepts:
Stress
Feedback
Cyclic fluctuations
Development

5. i. STRESS
•Can alter pituitary secretion and can be
used to test for abnormality.

Insulin hypoglycaemic stress

CRF ACTH
CORTISOL
GHRH GH

6. ii. FEED BACK
CNS


HYPOTHALAMUS -

+ PITUITARY GLAND -


ENDOCRINE GLAND
POSITIVE
FEEDBAC
K
(rare
cases)
NEGATIVE
FEEDBACK
(By products of end
-organ endocrine
glands)

7. iii. CYCLIC FLUCTUATIONS
CNS


HYPOTHALAMUS -

PITUITARY GLAND -


ADRENAL
NEGATIVE
FEEDBACK
(By products of end
-organ endocrine
glands)
Cyclic fluctuations in pituitary secretion
are mediated via central nervous system
(CNS) regulation of hypothalamic factors.
ACTH
CORTISOL

8. iv. DEVELOPMENT
CNS


HYPOTHALAMUS -

+ PITUITARY GLAND -


GONADS
NEGATIVE
FEEDBACK
(sensitivity
diminishes during
puberty)
System remains in equilibrium (constancy)
via negative feedback mechanisms.
LH, FSH
GONADAL STEROID
GnRH

9. HYPOTHALAMIC REGULATORY
FACTORS
GHRH = Growth Hormone Releasing Hormone
SS = Somatostatin
TRH = TSH- releasing hormone (3aa)
CRF = Corticotrophin releasing factor (41aa)
GnRH = Gonadotropin releasing hormone
(10 aa)
DA = dopamine (1 aa)

The natural peptides and analogues have been
synthesized= small, cheap to make , diagnostically
and theraputically useful!

10. MAIN PITUITARY HORMONES:
GH = Growth Hormone (+ve GHRH , -ve SS)
FSH = Folicle stimulating hormone (+ve GnRH)
LH = Luteinizing Hormone (+ve GnRH)
PRL = prolacting (mainly –ve by Dopamine, +ve
high levels of TRH)
TSH = Thyroid stimulating hormone (+ve TRH)
ACTH =adreno-cortico-tropic hormone (+ve
CRF)
MSH = melanocyte stimulating hormone
ADH = antidiuretic hormone (vasopressin)
OT = oxytocin

12. Pituitary Hormones
•
•
Classifiable by structure and common
ancestry into three groups of peptide
hormones.
Within each group is some overlap in
activity eg HCG has only 0.1% thyroid
stimulating activity of TSH, women with a
hydatiform mole can produce enormous
quantities of HCG (>100000 x the non-
pregnant state ) so as to give thyroid
stimulation.

13. Group 1
•
–
–
–
Single chain polypeptides of 20 000 Mw
(20 kDa)
GH
PRL
hPL (has both GH and PRL activity and
antagonises insulin)

14. Group 2
•
•
•
•
•
Glycoproteins of 30kDa,
Alpha and beta chain non-covalently
bound
α-chain is identical in all the hormones
β-chain confers specificity
TSH, LH, FSH, HCG

15. Group3
•
•
•
A series of smaller peptides derived from
a single large precursor POMC.
POMC is cleaved specifically to produce a
family of biologically active peptides, the
most important is ACTH.
More extensive processing of POMC
happens in other cell types yielding MSH
and endorphins
ENDORPHINSACTHMSH

16. Applications
•
–
–
–
GnRH
Secreted under physiological conditions as
pulses with a frequency of 1 hour hence
pulsate adminstration to treat infertility due to
hypogonadotropic hypogonadism in both sexes and
delayed puberty.
Continuous High dose to down regulate FSH, LH in
PCOS, endometritis, uterine fibroids , ovarian , beast
Ca, precocious puberty in children , Pca in men.
GnRH with low dose steroid hormone is a promising
contraceptive in men and women , may reduce
incidence of breast Ca and Ovarian Cancer common
in women with large numbers of cycles .

17. Applications
•
–
•
–
–
–
Somatostatin
Inhibits just about everything in the gut where
its found!!!
Gut motility, gastric , biliary and pancreatic juice
secretion and hormones including insulin ,
glucagon, gastrin.
Initially isolated as a protein that inhibited
growth hormone secretion.
Uses: in treating many disorders eg
acromegaly, pancreatitis, gastrinoma,
glucanomas, nesidiblastosis.
Side effects: gall stones, malabsorption

18. Applications
•
•
Growth Hormone Release hormone (GHRH)
Less expensive alternative to GH in
treating GH-deficient children where
defect lies in the hypothalamus.
Continuos exposure does not lead to
receptor desensitization as in the case of
GnRH. This simplifies theraputic
application.

19. Applications
•
–
–
CRF
41 amino acid peptide diagnostically
used to establish hypocortisolism of pituitary
origion as part of the combined pituitary test
Used to distinguish Cushings syndrome due to
pituitary adenoma (good ACTH respone) from
ectopic ACTH-producing tumor (no response)

20. PEPTIDES OF THE POSTERIOR
PITUITARY
•
•
•
•
•
•
Unlike the anterior of endodermal origion , the
posterior pituitary is composed of neuronal tissue
and is really part of the hypothalamus.
ADH (Vasopressin) and Oxytocin are 9 amino acid
cyclic peptides long like thos of hypothalamus
Main difference is quantity
Secreted directly into hypophyseal portal system
few millimeters to anterior pituitary.
Posterior pituitary lobe secretes directly into the
general circulation reaching targets at an adequate
concentration.
Analogues of ADH,Oxytocin have found use in
stimulation of uterine contraction pre and post
partum, milk ejection, diabetes insipidus.

21. DISCUSSION TIME

22. Session 2:Disorders of the pituitary
1.
2.
1.
2.
3.
4.
5.
3.
Presentation of endocrine disorders
Pituitary hormones
Growth hormone
Prolactin
Thyroid stimulating hormone
Gonadotrophins
Adrenocorticotrophic hormone
Testing anterior pituitary function

23. ENDOCRINE DISEASES
PRESENTATION:
•
1.
2.
3.
Endocrine disease present in three ways:
Hypofunction
Hyperfunction
Local effects

24. Hypofunction:

•
•
•
–
–
–
•

Hypofunction refers to decreased or inadequate production or
secretion of hormones by an endocrine gland, leading to
hormone deficiency.
Causes of hypofunction can include autoimmune destruction of
the gland, congenital defects, surgical removal, or damage to the
gland due to injury or disease.
Clinical manifestations of hypofunction depend on the specific
hormone involved and may include:
Reduced metabolic rate (e.g., weight gain, fatigue) in hypothyroidism.
Growth retardation and delayed sexual development in growth hormone
deficiency.
Hypoglycemia, weakness, and adrenal crisis in adrenal insufficiency
(Addison's disease).
Diagnosis involves assessing hormone levels, clinical symptoms,
and imaging studies to identify the underlying cause of
hypofunction.

25. Hyperfunction
•
•
•
–
–
–
•
Hyperfunction refers to excessive production or secretion of
hormones by an endocrine gland, leading to hormone excess.
Causes of hyperfunction can include tumors (benign or
malignant), hyperplasia, or dysregulation of hormone feedback
mechanisms.
Clinical manifestations of hyperfunction depend on the
specific hormone involved and may include:
Weight loss, tremors, and tachycardia in hyperthyroidism (e.g., Graves'
disease).
Cushingoid features (e.g., central obesity, moon face), hypertension, and
glucose intolerance in Cushing's syndrome.
Hypertension, muscle weakness, and hypokalemia in primary
hyperaldosteronism (Conn's syndrome).
Diagnosis involves assessing hormone levels, imaging studies,
and functional tests to identify the underlying cause of
hyperfunction.

26. Local Effects:

•
•
–
–
–
•

Endocrine tumors or nodules can exert local effects by
compressing adjacent structures or secreting
biologically active substances that affect nearby
tissues.
Local effects of endocrine tumors depend on their
location and size and may include:
Compression of nearby organs leading to symptoms such as
difficulty swallowing or breathing.
Mass effects causing pain, discomfort, or visible swelling.
Production of biologically active substances (e.g., parathyroid
hormone in parathyroid adenomas) leading to local tissue
damage or systemic effects.
Diagnosis involves imaging studies (e.g., ultrasound,
CT scan, MRI) to visualize the tumor or nodule and
assess its impact on adjacent structures. Biopsy may
be necessary to confirm the nature of the lesion.

27. Pituitary hormones

•
•
•
•
•
Growth hormone
Prolactin
Thyroid stimulating hormone
Gonadotrophins
Adrenocorticotrophic hormone

28. Growth Hormone:
•
•
–
–
200 aa and essential for normal growth
It has two major actions:
Stimulate production of IGF-1 mainly by liver
but to some extent by all tissues (promote
growth and inhibit protein breakdown.)
Directly promote lipolysis and antagonise
insulin-mediated glucose uptake,which is
appropriate to the fasting state.

29. Growth hormone
CNS


HYPOTHALAMUS -
+SS
PITUITARY GLAND -


LIVER
NEGATIVE
FEEDBACK
GH – released in
bursts after
onset of sleep
IGF-1
GHRH
EMPTY
STOMAC
H
Ghrelin

30. Growth hormone
•
•
–
•
•
•
GH secretion occur in bursts , particularly after onset of sleep. Thus
blood GH levels vary widely during the course of 24 hrs and
stimulation tests are required to prove deficiency.
These include:
Adrenergic stumulant drug clinidine, insulin induced
hypoglycemia, fasting , or exercise
GH secretion is inhibited by rise in glucose levels ie failure to
suppress GH with glucose overload indicate pathological secretion.
Excessive GH secretion causes gigantism in children and
acromegaly in adults.
GH deficiency presents growth failure in children while in adults
effects are subtule eg decrease in musclemass and increased
adiposity.

31. PROLACTIN
•
–
•
•
•
Similar in size and sequence to GH with a
different function:
Initiate and sustain lactation
Secretion increase during pregnancy but
declines promptly after child birth unless
breastfeed occurs.
The major regulator of PRL is dopamine from
the hypothalamus which inhibits secretion.
Though TRH stimulates PRL release , it is not
physiologically important except to explain
high levels seen in hypothyroidism.

32. PROLACTIN
•
•
•
•
Prolactinoma can cause hyperprolactinemia
Any obstruction to blood flow from
hypothalamus “stalk-effect” may cause
hyperprlactemia.
Stress and dopamine antagonists used to
treat major pyschiatric disorders are other
causes of elevated PRL levels
PRL deficiency only manifests as failure to
lactate = Sheehan’s syndrome

33. Thyroid stimulating hormone (TSH)
•
•
•
•
•
(TSH) is a large glycoprotein hormone composed of an α and β
subunit. The α-subunit is common to all the glycoprotein
hormones (FSH, LH, hCG), while the β-subunit is unique to TSH.
Secretion of TSH is controlled by stimulation by the
hypothalamic tri-peptideTRH, while the action and secretion of
TRH is inhibited by thyroid hormone (classic negative
feedback).
Measuring TSH is a widely-used and valuable diagnostic test in
thyroid disease; low blood levels of TSH indicates excess
thyroid hormone (hyperthyroidism);
high TSH indicates primary hypothyroidism.
Failure of TSH secretion can cause a secondary
hypothyroidism, whereas hyperthyroidism due to a TSH-
secreting tumor is extremely rare

34. Gonadotrophins (FSH & LH)
are glycoprotein hormones, similar in size and structure to TSH.
They contain a common α-subunit with a unique β-subunit that
determines their specificity.
Synthesis and release of both peptides is stimulated by the
pulsatile secretion of hypothalamic gonadotropin-releasing
hormone (GnRH), and modulated by feedback inhibition of
gonadal steroids and inhibin, which allows for their independent
regulation.
In males, LH stimulates testosterone production by the Leydig
cells, which feedback inhibits the action of GnRH on LH
secretion.
FSH stimulates spermatogenesis, and production by the testis of
a peptide, inhibin, which feedback inhibits further FSH release.

35. Gonadotrophins (FSH & LH)
The situation in women is a little more complex.FSH secreted
in the early part of the menstrual cycle stimulates growth of
the Graafian follicle that secretes oestrogen.
Oestrogenand inhibin feedback inhibit FSH release (thereby
avoiding multiple follicle development).
At about mid-cycle, the increasing oestrogen leads to
explosive release of LH by a positive feedback mechanism.
This LH surge triggers ovulation, and subsequent formation
of a corpus luteum, which secretion of oestrogen and
progesterone that both prepares the uterus for implantation
and suppresses further FSH and LH secretion.
Failing conception, the corpus luteum regresses due to
declining LH. Steroid hormone levels fall, which triggers both
endometrial shedding (menstruation) and derepression of
FSH secretion, which heralds onset of a new cycle.

36. Gonadotrophins (FSH & LH)
Before puberty, both FSH and LH are very low, and
unresponsive to GnRH.
With onset of puberty, gonadotrophin secretion increases,
FSH before LH. Increased level of gonadotropins are seen
in ovarian failure, whether premature or at onset of the
menopause (loss of negative feedback).
In men with azoospermia (failure of sperm production),
FSH is increased, while LH increases in response to a fall in
testosterone.
Gonadotropin-secreting tumors of the pituitary are rare,
whereas gonadal failure secondary to decreased
gonadotropin secretion is much commoner.
Hypogonadotropic hypogonadism can be isolated due to
hypothalamic dysfunction, or be a part of generalized
pituitary failure

37. Adrenocorticotrophic hormone
(ACTH)
•
•
•
•
•
•
•
•
•
is a single polypeptide of 39 amino acids that stimulates adrenal
glucocorticoid (but not minerallocorticoid) secretion.
It is derived from the much larger pro-opio-melanocortin (POMC), and its
release is positively regulated by corticotrophin releasing peptide (CRP) from
the hypothalamus. ACTH secretion exhibits diurnal variation, highest at
08h00, lowest at midnight.
Secretion is greatly increased by stress, and inhibited by cortisol in a classic
negative feedback manner.
Excessive secretion of ACTH occurs with some pituitary tumors (Cushing’s
disease) and in primary adrenal failure (Addison’s disease).
It is also occasionally produced ectopically by non-pituitary tumors (eg. small
cell lung
CA) in large amounts.
Since ACTH has a melanocyte stimulating action, hyperpigmentation is a
feature of high circulating ACTH levels, as occurs in Addison’s disease.
Decreased ACTH leading to secondary adrenal failure is usually part of
generalised pituitary insufficiency, though it can occur in isolation.

38. Testing anterior pituitary function
•
•
•
•
Pulsatility of secretion of many pituitary hormones makes
it inappropriate to rely on a single measurement for
diagnostic purposes. For example, an IGF-1 measurement
is a better reflection of growth hormone status than a
single GH level, which can fluctuate widely over a 24h
period.
It is often useful to measure the pituitary hormone in
conjunction with its target organ product; eg a TSH in the
normal range associated with a low serum thyroxine
signifies pituitary insufficiency causing secondary
hypothyroidism i.e. the TSH is inappropriately normal,
whereas it should be high.
Dynamic tests are useful tools for investigating pituitary
function.
Stimulatory tests are employed in cases of suspected
insufficiency, and suppression tests for hyperfunction.

39. Testing anterior pituitary function
•
•
•
•
In assessing anterior pituitary reserve, it is often useful to assess all hormones in a
single procedure, hence the use of the combined pituitary function (triple bolus) test.
A single intravenous injection of TRH, GnRH and insulin is given, then all 6 anterior
pituitary hormones are measured serially over about 90min. TRH should evoke a TSH
and PRL response, GnRH a FSH and LH response, and the hypoglycaemic stress a GH,
ACTH and PRL response.
For technical reasons, cortisol assay is often substituted for ACTH. During the test, it
is important to document adequate hypoglycaemia by blood glucose measurements,
since failure of an ACTH response might well be due to an inadequate stimulus.
On the other hand, blood glucose might fall dangerously low (particularly in a subject
with an impaired insulin Counterregulatory hormone capacity), hence the test should
be done under close supervision, with injectable glucose solution at hand. To avoid
the danger of hypoglycaemia, the new trend is to substitute GHRH and CRF for insulin.
A recent test currently popular in assessment of pituitary reserve is the metyrapone
stimulation test. Metyrapone blocks the final step in cortisol synthesis (11-
hydroxylase). In normal subjects, the resulting fall in blood cortisol relieves the
feedback inhibition on ACTH, which in turn stimulates the adrenal. Unable to make
cortisol, the adrenal secretes 11 deoxycortisol, the cortisol synthesis intermediate just
proximal to the block. Hypopituitary individuals exhibit a subnormal or absent 11
deoxycortisol response to metyrapone.

40. HYPOPITUITARISM
•
•
•
•
Clinical presentation varies, largely depending
on age. Growth failure is a common
presentation in children,
adults often present with sexual and/or
reproductive dysfunction.
Symptoms depend on which hormone(s) are
affected; GH and gonadotrophins (FSH and
LH) are usually the first to go, followed by
ACTH and TSH.
A table of the clinical features (from Marshall
‘Clinical Chemistry, 4th Ed)) is shown below

41. HYPOPITUITARISM

42. HYPOPITUITARISM
•
–
•
•
An isolated deficiency of a single hormone is usually
congenital and due to a deficiency of the relevant
hypothalamic releasing factor.
Kallman’s syndrome is an example that presents with primary
infertility and anosmia (loss of the sense of smell), and is due to
defective migration of GnRH-secreting and olfactory neurones to
their correct location during embryogenesis.
While the posterior pituitary is often spared in
hypopituitarism , presence of diabetes insipidis (DI)
should always be considered. Posterior pituitary
involvement is usually due to an invasive tumor or surgical
damage.
DI can be masked by a concurrent ACTH Deficiency. Since
cortisol is required to excrete a water load, dehydration
may only become a problem once glucocorticoid
replacement is started.

43. Causes of hypopituitarism include:

•
•
•
•
•
•
Tumors - eg non-functioning (chromophobe
adenoma, craniopharyngioma) or functioning
pituitary tumors,hypothalamic tumors,
Post traumatic - eg fracture base of skull
Post-infection - eg after bacterial or TB
meningitis
Vascular – eg necrosis following post partum
haemorrhage (Sheehan’s syndrome)
Infiltration – eg haemochromatosis,
sarcoidosis
Iatrogenic – eg post pituitary surgery, radiation

44. Treatment of hypopituitarism
•
–
generally entails replacing :
glucocorticoid and thyroxine, and either sex
steroids themselves if fertility is not desired,
or GnRH/gonadotrophins, if it is desired

45. Anorexia nervosa
•
•
a disorder of self-imposed starvation,
may mimic hypopituitarism (amenorrhoea,
weight loss), but loss of body hair does
not occur, and GH and cortisol levels are
increased as an appropriate response to
starvation, rather than decreased in
pituitary disease.

46. Growth Hormone deficiency

This an uncommon but important and treatable cause of
growth retardation.
A random GH level above 10ng/ml excludes the condition,
but since GH may be undetectable in serum of normal
children at a particular time, a low result is not diagnostic.
Certain stimulation tests can be done, using vigorous
exercise, clonidine (an adrenergic agonist), GHRH, or
insulin. Another option is to perform multiple GH
measurements during sleep via an indwelling catheter.
Sex steroids enhance the GH response.
Thus equivocal responses in pre-pubertal children may
need to be repeated after priming with testosterone or
oestrogens (in boys & girls, respectively).

47. •
•
•
Treatment is based on GH replacement –
originally obtained from human cadavers
(with the risk of Creutzveld-Jacob disease) –
but now made by recombinant DNA
technology. Since most cases of isolated GH
deficiency are actually due to lack of
hypothalamic GHRH, treatment with the latter
is becoming an option.
In GH deficient adults, GH is reported to
improve vigor and muscle mass, and
decrease fat accumulation. GH is used illicitly
by weightlifters for this purpose.

48. Laron dwarfism

•
•
•
•
•
A distinct form of childhood dwarfism is due to a
genetic defect in the GH receptor.
Since the growth promoting effects of GH operate via
IGF-1, these children clinically resemble those with GH
deficiency,
except that their blood GH levels are high, IGF-1 is low,
and they do not of course respond to GH therapy.
They are called ‘Laron’ dwarfs after the Israeli who first
described the condition 20 years ago.
Much commoner forms of functional GH deficiency
include emotionally-deprived children, who fail to grow
at the normal rate, and severely malnourished children,
eg kwashiorkor, where GH secretion is diminished,
probably by low circulating leptin (a logical response to
starvation)

49. Pituitary tumors
•
•
–
–
–
•
–
–
•
•
Pituitary tumors can be non-functional (eg. chromophobe adenomas,
craniopharyngiomas),
Or functional often produce an excess of a particular hormone.
PRL-secreting tumors (prolactinomas) are commonest,
followed by GH, ACTH, gonadotrophin
and, rarest of all, TSH producing tumors.

Apart from specific symptoms due to hypersecretion of a particular pituitary
hormone eg galactorrhoea, acromegaly), any tumour can give rise to:
Hypopituitarism, by encroaching on space occupied by normal pituitary cells
Local effects eg raised intracranial pressure (headache, vomiting, papilloedema),
visual field defects due to its proximity to the optic chiasma (typically bitemporal
hemianopia)

Acromegaly and gigantism is caused 95% of the time by a GH-secreting pituitary
tumor (the remainder are due to ectopic production of GH and GHRH by tumors
elsewhere).
Whether gigantism or acromegaly develops depends entirely on whether the tumor
arises before long bone epiphyses have fused.

50. •
•
Many of the tumors show mutations in the
Gs protein that links GHRH stimulation to
GH secretion in a gonadotrope.
These mutations abolish the GTPase
activity of the Gs protein, permanently
switching it on,thereby driving the
production of GH independent of receptor
activation by GHRH.

51. The clinical features of acromegaly

52. Confirmation of acromegaly
•
•
GH in a random serum sample is usually raised, but
since GH secretion in normal subjects is episodic,
one should confirm by a failure of GH to suppress
following a glucose tolerance test.
In acromegaly, glucose tolerance is frequently
impaired, and may even be frankly diabetic.

Other confirmatory evidence for tumor-derived GH
secretion is:
• Stimulation of GH by TRH, which does not normally affect
GH secretion
• Elevated levels of IGF-1, which give a more integrated view of
GH secretion, since it is not subject to such wide fluctuations.
IGF-1 levels are also useful for following response to
treatment.

53. Treatment of acromegaly
•
•
•
•
involves reducing GH levels, preventing or treating
other pituitary hormone deficiencies, and preventing
damage to nearby structures, like the optic nerve.
First line of treatment is surgical – transphenoidal
for small tumors, but by frontal craniotomy for large
tumors with suprasellar extension.
External radiation can be used, and many tumors
respond to medical treatment with somatostatin, or,
less frequently, dopamine.
Appropriate hormone replacement is instituted, and
patients are followed up regularly to check for tumor
regrowth and further loss of normal pituitary
function.

54. HYPERPROLACTEMIA
•
•
•
•
Elevated serum prolactin is a common disorder,
causing impotence in males, amenorrhoea in females,
and infertility and/or galactorrhoea in either sex.
PRL down-regulates the entire hypothalamic-pituitary-
gonadal axis by disrupting the normal pulsatile
secretion of GnRH (this occurs physiologically during
lactation).
High PRL can be due to a pituitary tumor that secretes
PRL directly (prolactinoma) or any pituitary lesion that
disrupts flow of portal blood carrying dopamine from
the hypothalamus (so-called ‘stalk’ effect ).
.

55. Increased PRL secretion may also
be due to:

• Anti-dopaminergic drugs (commonly used
to treat psychosis or hypertension)
• Primary hypothyroidism, where it is due to
stimulation by hypothalamic TRH
• Stress

56. HYPERPROLACTEMIA
•
•
•
Blood levels of PRL are generally highest in PRL-secreting
tumors, particularly among invasive macroadenomas, as
opposed to smaller (<1cm) microadenomas.
Regarding treatment, most prolactinomas are exquisitely
sensitive to dopamine agonists – eg bromocryptine, which
both lowers PRL levels and results in significant tumor
shrinkage. Microadenomas may require no further treatment,
though macroadenomas often ultimately still require surgical
removal.
ACTH secreting tumors will be discussed more fully in the
adrenal section. Just to note here that adrenalectomy as
treatment for the excessive cortisol secretion in such patients
carries the risk of accelerating tumor expansion and causing
hyperpigmentation (Nelson’s syndrome)This is due to removal
of the restraining influence of cortisol on tumor cell growth
and ACTH secretion

58. THE END
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