Transcraniad surgery for pituitary adenomas Evolution of pituitary surgery 010

Transcraniad surgery for pituitary adenomas Evolution of pituitary surgery 010

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The first actually recorded

 surgical intervention for a pituitary tumor can be traced back to Frank Thomas Paul (1851–1941) in the year 1893. However, Sir Victor Horsley (1857–1916) was probably the first surgeon, who operated on a pituitary adenoma dating back to the year 1889. It is known, that he used a bifrontal craniotomy. In order to reach the sella region he described a technique of ‘‘cerebral dislocation’’. However, he encountered a cystic lesion, that he described as not inoperable [20]. Because of this experience and Horsley‘s former laboratory work on sheeps, Frank Thomas Paul eventually consulted Sir Horsley about a case of a young woman with acromegaly.

 Horsley eventually 

recommended a subtemporal approach. Paul’s pioneering transcranial procedure ended with intractable brain swelling and the consecutive death of the patient eight hours later. Another pioneer of transcranial surgery considering pituitary tumors, Otto Theobald Tiliani in New York, started gathering experience with a bifrontal intradural approach on cadavers in 1903. Almost at the same time Fedor Victor Krause (1857–1937), a surgeon in Berlin, Germany, tried to remove a shot gun bullet from the area of the right optic foramen in a patient who had attempted suicide, by an extradural right frontal approach (Fig. 1). Encouraged by the good outcome of this patient, it was Fedor Krause, who performed the first recorded successful resection of a pituitary tumor utilizing an extradural transfrontal approach avoiding extensive retraction of the frontal lobe in 1905 [19].

The mortality rates of transcranial surgery regarding the pituitary region ranged between 50% and 80% in these days. Between 1904 and 1906 Sir Victor Horsley went on approaching pituitary lesions by transcranial procedures and finally operated a consecutive series of 10 patients with pituitary tumors utilizing both, subfrontal and subtemporal approaches with an improved mortality rate of about 20%.

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Mortality / Morbidity 009

 Mortality / Morbidity 009

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Mortality rate related to pituitary tumors is low. Advances in medical and surgical management of these lesions and the availability of hormonal replacement therapies have contributed to successful management.  Pituitary apoplexy can be a lethal complication.   Morbidity associated with macroadenomas may include permanent visual loss, ophthalmoplegia, and other neurological complications.  Tumor recurrence is also a possibility.  CNS metastases and, rarely, distant metastases occur with pituitary tumors.  Endocrine abnormalities are amenable to correction. However, damage in many organ systems as a result of long-standing uncorrected deficiencies may be irreversible⁽⁵⁰⁾.

Race

No racial predilection is known .

Sex

Symptomatic prolactinomas are found more frequently in women. Cushing disease also Is ,more frequent in women (female-to-male ratio 3:1).

Age

Most pituitary tumors occur in young adults , but they may be seen in abolescents and elderly persons . Acromegaly usually is seen in the fourth and fifth decades of life .

Clinical history

The presentation of a pituitary macroadenoma relates to its mass effect and pressure on surrounding structures.  Fifty to sixty percent present with visual symptoms due to compression of optic nerve structures. Nonspecific headache can be seen.  Lateral extension can result in compression of the cavernous sinuses and may cause ophthalmoplegia, diplopia, and/or ptosis. Talkad et al recently reported an isolated, painful, postganglionic Horner syndrome as the initial sign of lateral extension of a large prolactinoma⁽⁴⁵⁾. Extension into the sphenoid sinuses can cause spontaneous cerebrospinal fluid (CSF) rhinorrhea.  In addition to visual symptoms, endocrine dysfunction⁽⁴⁹⁾.

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Hormonal overproduction Clinical effects 008

Hormonal overproduction Clinical effects 008

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Prolactin

Hypogonadism, if hyperprolactinemia is sustained. Women Amenorrhea, galactorrhea, and infertility . Men-Decreased libido, impotence, and rarely galactorrhea⁽⁴⁶⁾

Growth hormone

·      Children and adolescents - May result in pituitary gigantism

·      Adults - Acromegaly

Changes in the size of the hand and feet, coarseness of the face, frontal bossing, and prognathism result. Further changes in the voice, and hirsutism, confirm the diagnosis.  Acromegaly frequently results in glucose intolerance, with 20% of patients progressing to diabetes mellitus.  Respiratory difficulty and sleep apnea are fairly common.  Cardiac complications result from acromegalic cardiomyopathy.  Although patients' have a bulky appearance, they are generally weak as a result of associated myopathy.  Carpal tunnel syndrome is seen frequently.  Lumbar canal stenosis can present with a syndrome resembling amyotrophic lateral sclerosis.  Acromegaly may be associated with colonic polyps, although an increased colon cancer incidence has not been shown definitively⁽⁴⁴⁾.

Cushing disease

Weight gain, centripetal obesity, moon facies, violet striae, easy bruisability, proximal myopathy, and psychiatric changes. Other possible effects-Arterial hypertension, diabetes, cataracts, glaucoma, and osteoporosis⁽⁴⁷⁾

Incidence

In the United States: Pituitary tumors represent anywhere between 10% and all intracranial tumors. at pituitary tumors are found in approximately 10% of autopsies .

The incidence of acromegaly is approximately 3 per million. Acromegaly has no sex predilection 

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Classification of pituitary tumors 007

Classification of pituitary tumors 007

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Based on size, pituitary tumors can be divided into microadenomas (<1cm diameter) and macroadenomas (>1 cm diameter). They also can be classified on the basis of staining characteristics, as chromophobic and chromophilic tumors. The latter can be further subdivided using hematoxylin and eosin stains (ie, eosinophilic or basophilic).

However, this classification has proven to be of no clinical value and now has been replaced by a more functional classification that involves electronmicroscopy and immunohistochemistry. These techniques have identified hormones in many chromophobe adenomas, enabling pathologists to identify that they are produced by eosinophilic tumors. They also have demonstrated that many tumors produce more than one hormone. The mutated form p53, a tumor suppressor, also can be determined histologically. This mutated gene suggests a tumor with rapid growth.

The endocrinologic morbidity that is associated with pituitary tumors is dependent on the specific underproduction or overproduction of a hormone or hormones associated with the tumor⁽⁴⁴⁾.

Hormonal deficiencies Clinical effectsGrowth hormone deficiency

Adults - Increased rate of cardiovascular disease, obesity, reduced muscle strength and exercise capacity, and increased cholesterol Infants - Hypoglycemia Children - Decreased height and growth rate .

Gonadotrophin deficiency 

Men - Diminished libido and impotence; testes shrink in size, but spermatogenesis is generally preserved Women - Diminished libido and dyspareunia; breast atrophy in chronic deficiency Children - Delayed or frank absence of puberty Adolescent girls - Present similarly to adult women .Thyrotropin deficiency - Malaise, weight gain, lack of energy, cold intolerance, constipation  .

Corticotrophin deficiency

Unlike primary adrenal insufficiency, rnineralozortlcold function (which is dependent on the angiotensin-renin axis) is not affected; deficiency is limited to glucocorticoids and adrenal androgens . Initially, symptoms are nonspecific (eg, weight loss, lack of energy, malaise); severe aorenal insufficiency may present as a medical emergency .

Panhypopituitarism - Refers to deficiency of several anterior pituitary hormones. It may occur in a slowly progressive fashion.

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Pathophysiology of the Pituitary gland 006

Pathophysiology of the Pituitary gland 

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Pituitary tumors are

 common neoplasms, and recognition of their presentation is critical since a favorable therapeutic outcome is dependent on early identification of the lesion.

Multiple oncogene abnormalities may be involved in pituitary tumorigenesis. Glycoprotein abnormalities, gene mutations, p53 gene deletions, mutations, and rearrangements, and association of pituitary tumors with the syndrome of multiple endocrine neoplasia have been described and are involved in the development of adenomas in the pituitary gland.

 The pituitary

 tumor transforming gene-1 (PTTG-1) is a newly discovered oncogene that serves as a marker of malignancy grades in several endocrine malignancies; this gene is known to regulate the cellular mitosis process and forced expression of this gene induces tumor formation in mice. PTTG-1 is overexpressed in pituitary tumors.⁽⁴⁸⁾ most of these tumors are benign, but certain factors involved in the genesis of  the tumor may determine its rate of growth and aggressiveness. For instance, the presence of p53 gene correlates with more aggressive tumor behavior.

Clinical manifestations are due to the local effect of the mass and distant endocrine manifestations that can affect a variety of organ systems. These effects are due to lack or excess of a given stimulating hormone on the targe. Pituitary adenomas, with a few exceptions, are not under the control of hypothalamic releasing factors⁽⁴⁸⁾

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SECOND HORMONES OF THE POSTERIOR PITUITARY GLAND 005

SECOND HORMONES OF THE POSTERIOR PITUITARY GLAND

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The posterior pituitary is an extension of the hypothalamus and contains the axon terminals of magnocellular neurons located in the Supraoptic and paraventricular nuclei. These neurons generate and propagate action potentials, producing membrane depolarization and exocytosis of the contents of their secretory granules. The neuropeptides oduced by the magnocellular neurons, and consequently released from posterior pituitary, are oxytocin and arginine vasopressin

1.      Oxytocin :

The neuropeptide oxytocin is synthesized by magnocellular neurons in the supraoptic and paraventricular nuclei of the hypothalamus and is released from the posterior pituitary into the peripheral circulation. The release of oxytocin is stimulated during breast-feeding (lactation) 

and childbirth (parturition)⁽⁴²⁾.

The two main target organs for oxytocin's physiologic effects are the lactating breast and the uterus during pregnancy. In the lactating breast, oxytocin stimulates milk ejection by producing contraction of the myoepithelial cells that line the alveoli and ducts in the mammary gland. In the pregnant uterus, oxytocin produces rhythmic contractions to help induce labor and to promote regression of the uterus following delivery. Oxytocin is used clinically during labor and delivery to promote uterine contractions and during the postpartum period to help decrease bleeding and return the uterus to its normal size (uterine involution) ⁽⁴²⁾.

2.      Arginine Vasopressin (AVP)

Arginine vasopressin, also known as antidiuretic hormone (ADH),  the other neuropeptide produced by magnocellular neurons of the hypothalamus and released from the posterior pituitary. The principal effect of AVP is to increase water reabsorption by enhancing permeability to water in the distal convoluted tubules and the medullary collecting ducts in the kidney. The result is the production of smaller volumes of concentrated urine. In addition, AVP increases vascular resistance. This function of AVP may be important during periods of severe lack of responsiveness to other vasoconstrictors, as may occur during severe blood loss (hemorrhagic shock) or systemic infection  (sepsis)⁽⁴³⁾.

The importance of AVP is better understood in terms of the total amount of urine that would be. excreted in its absence. For example, in a healthy individual an average of 180 L of glomerular filtrate is formed per day. Thus, without AVP-mediated reabsorption of 10% of filtered water in the distal collecting ducts, urine output would be close to 18 L/d. This is 10-fold higher than the volume of urine output (1.5-2 L/d) under  normal conditions⁽⁴³⁾. 

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Growth Hormone and Prolactin Family 004

Growth Hormone and Prolactin Family 004

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GR, a hormone with structural similarity to prolactin, is released from thes omatotrophs, an abundant (50%) cell type in the anterior pituitary. GR is released in pulsatile bursts, with the majority of secretion occurring hocturnally in association with slow-wave sleep. ⁽⁴⁰⁾

stimulated release of GH is inhibited by somatostatin, a peptide synthesized in most brain regions, predominantly in the periventricular nucleus, arcuate nucleus, and ventromedial nucleus of the hypothalamus. Somostatin is also produced in peripheral organs, including the endocrine pancreas, where it also plays a role in the inhibition of hormone release. Axons from somatostatin neurons run caudally through the hypothalamus to form a discrete pathway toward the midline that enters the median eminence.

GH induces physiologic effects on its target cells directly by activating the GH receptor and indirectly by stimulating the synthesis and secretion of IGF-I. IGF-I is a small peptide (about 7.5 kD) structurally related to proinsulin that mediates several of the anabolic and mitogenic effects of GH in peripheral tissues. GH stimulates longitudinal growth by increasing the formation of new bone and cartilage. The growth effects of GH are not critical during the gestational period, but begin gradually during the first and second years of life and peak at the time of puberty. Before the epiphyses in long bones have fused, GH stimulates chondrogenesis and widening of the cartilaginous epiphysial plates, followed by bone matrix deposition .⁽⁴⁰⁾

1.      Prolactin :

Prolactin is a polypeptide hormone synthesized and secreted by lactotrophs in the anterior pituitary gland. The lactotrophs account for approximately 15-20% of the cell population of the anterior pituitary gland. However, this percentage increases dramatically in response to elevated estrogen levels, particularly during pregnancy. Prolactin levels are higher in females than in males, and the role of prolactin in male physiology is not completely understood. Plasma concentrations of prolactin are highest during sleep and lowest during the 

waking hours in humans⁽⁴¹⁾.

The physiologic effects of prolactin are mediated by the prolactin receptors which are found in the mammary gland. The main physiologic effects of prolactin are stimulation of growth and development of the mammary gland, synthesis of milk, and maintenance of milk secretion. Prolactin stimulates glucose and amino acid uptake and synthesis of the milk proteins casein and -lactalbumin, the milk sugar lactose, and milk fats by the mammary epithelial cells. Prolactin modulates immune cell function through endocrine mechanisms. Finally, prolactin can act as a cytokine because it is released by cells of the immune system and regulates the lymphocyte responses by both paracrine and autocrine mechanisms.⁽⁴¹⁾

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