Fig.16.4. Tc-99m sestamibi imaging in a patient with hyperparathyroidism. The white arrow indicates the location of a mediastinal parathyroid gland located in the right thymic lobe.

sestamibi scanning, MRI with contrast enhancement or ultrasound is our next noninvasive study.

In situations where review of previous surgical and pathologic data combined with imaging studies have not yielded convincing localization information, or in situations where these data are discordant, we proceed to angiography and highly selective venous catheterization for PTH measurements (Fig. 16.5). This procedure is costly, invasive, time-consuming, and exposes the patient to a significant radiation dose. Accordingly, we select this procedure only after exhausting other localization methods. Occasionally, we have encountered confusing data when intact PTH levels are returned from our laboratory, often several days after venous sampling. We have recently begun using the rapid-PTH assay to quantify PTH levels during the catheterization procedure. This technique provides almost immediate hormone data during the procedure, and allows us to dynamically guide the angiographer to additional sampling if a subtle, but nondiagnostic, gradient is observed (authors, manuscript in preparation.).

Figure 16.6 provides a diagrammatic approach to preoperative localization studies in these patients.

Operative Approach in Patients with Persistent or Recurrent Hypercalcemia

After localization studies have identified the location of the tumor, careful operative planning is essential. Since the majority of patients will have a missed adenoma, we recommend a focused approach, in contrast to our standard practice of bilateral neck exploration for first-time operations. This approach minimizes the dissection required, and thus risk of injury to the recurrent laryngeal nerves. Prior to beginning each operative procedure, we prepare for cryopreservation of any resected parathyroid tissue, insuring the availability of reagents and equipment required for the procedure. In all reoperative parathyroid surgery, we consider the possibility that the parathyroid gland that we plan to resect may be the patient's only residual functioning parathyroid tissue.

The patient is positioned supine with support beneath their shoulders and neck extended. The chest is prepped and draped together with the neck, in preparation for possible partial or complete median sternotomy. If localization studies guide us to the lateral neck, we prefer to reopen the previous Kocher collar incision, through the level of the platysma muscle. Next, the lateral neck, on the side of interest, is entered in the space lateral to the strap muscles, and anterior to the sternocleido-mastoid muscle. This provides excellent exposure to the lateral neck. In the vast majority of cases, this route is free of adhesions, and facilitates recurrent laryngeal nerve identification and protection. The thyroid gland is approached laterally and posteriorly.

If the suspect parathyroid gland appears in the anterior mediastinum, we reopen the Kocher incision and mobilize the left and right horns of the thymus separately. The thymic lobes can be elevated into the operative field with gentle traction, and can be delivered intact. Frequently, a large vein diving below the clavicle and sternum along the thyrothymic ligament is a sentinel to an adenoma within the thymus.

Selective Venous Sampling
Fig.16.5. Highly selective venous sampling of the left thymic vein demonstrating a PTH level greater than 1,400 pg/ml. All other samples demonstrated PTH levels ranging from 100-150 pg/ml proving a specific gradient. Multiple surgical clips are from a previous failed exploration.

After locating and removing the parathyroid adenoma, we immediately halve the gland, and cryopreserve one portion. Cryopreservation requires reagents, technical expertise, and a liquid nitrogen storage facility. The cryopreserved tissue can subsequently be auto-transplanted into the nondominant forearm, with successful takes reported to occur in 85% of patients.5

Intraoperative Rapid PTH Assay

The recent development of a rapid assay for measurement of intact PTH has had a significant impact upon reoperative parathyroid surgery.6,7 The characteristics of the assay provide for complete sample analysis and reporting in less than fifteen minutes. This assay has become a standard component of all of our reoperative cases. A large-bore peripheral I.V. inserted into the antecubital vein provides reliable access for serial venous samples obtained during surgery. Two baseline samples are obtained at the start of the operation. Following excision of the suspect parathyroid gland, additional samples are obtained ten and fifteen minutes after removal. A greater than 50% decrease in PTH below baseline levels is considered a positive result.6,7

Fig.16.6. Preoperative localization studies in patients with persistent or recurrent hypercalcemia.

Postoperatively, we assess the patient for symptoms and signs of hypocalcemia. A serum ionized calcium level is obtained the following morning. The majority of patients are discharged the morning after surgery. They are carefully instructed to recontact us if they develop any symptoms or manifestations of hypocalcemia. Figure 16.7 provides a diagrammatic approach to operative exploration in these patients.


Reoperative parathyroid surgery is best avoided by performing a meticulous initial operation. Patients who present with persistent or recurrent hyperparathyroidism require a systematic, step-wise approach to confirm this diagnosis, localize the culprit gland, and extirpate the abnormal parathyroid tissue while avoiding injury to the recurrent laryngeal nerves.

It seems clear that patients benefit most from initial parathyroid exploration at the hands of experienced surgeons. Over 95% of patients who have exploration by an experienced surgeon are successfully treated at their first operation, while operation by inexperienced surgeons can decrease the success rate to 70%. When patients present with recurrent or persistent hypercalcemia due to elevated PTH levels, their

Fig.16.7. Operative approach for patients with persistent or recurrent hyperparathyroidism.

care is best undertaken by surgeons at institutions capable of providing a full range of noninvasive and invasive imaging studies.8


1. Parathyroid reoperations. In: Lo CY, van Heerden JA, eds. Textbook of Endocrine Surgery. 1997. Clark & Duh eds. 1997. A comprehensive review of perioperative assessment and planning.

2. Jaskowiak N, Norton JA, Alexander HR et al. A prospective trial evaluating a standard approach to reoperation for missed parathyroid adenoma. Ann Surg 1996; 224(3):308-320. A complete review of the NIH/NCIseries on parathyroid reoperations.

3. Libutti SK, Bartlett DL, Jaskowiak NT et al. The role of thyroid resection during reoperation for persistent or recurrent hyperparathyroidism. Surgery 1997; 122(6):1183-1187. Imaging and application of thyroid lobectomy for missed adenoma in patients with negative re-exploration.

4. Neumann DR, Esselstyn CB Jr, Kim EY et al. Preliminary experience with doublephase SPECT using Tc-99m sestamibi in patients with hyperparathyroidism. Clin Nucl Med 1997; 22(4):217-221. Review of refinements in nucleotide tracer imaging for parathyroid localization.

5. Norton JA. Reoperation for missed parathyroid adenoma. Adv Surg 1997; 31:273-297. Review of operative management.

G. Irvin GI, Dembrow V, Prodhomme D. Clinical usefulness of an intraoperative "quick" parathyroid hormone assay. Surgery 1993; 114:1G19-1G23. Describes the technique and usefulness of intraoperative parathyroid hormone analysis.

7. Clary BM, Garner SC, Leight GS Jr. Intraoperative parathyroid hormone monitoring during parathyroidectomy for secondary hyperparathyroidism. Surgery 1997; 122(G):1G34-1G38. Application of rapid-PTH assays in parathyroid surgery.

8. Sosa JA, Powe NR, Levine MA et al. Cost implications of Different Surgical Management Strategies for Primary Hyperparathyroidism. Surgery 1998; 124(G): 1G28-35; discussion 1998; 1G35-G. Reviews the dollar costs of failed surgery for primary hyperparathyroidism.

Richard A. Prinz History

Discovery of the human adrenal is credited to Eustachius who published the first accurate anatomic drawings depicting their presence and relationship to the kidneys, inferior vena cava and aorta. The function of these glands remained unknown for the next three centuries. In 1805, Cruvier described the anatomic division of the gland into an outer cortex and an inner medulla. The physiologic importance of the adrenals started to become apparent in 1855 when Addison described clinicalopathologic features of patients he studied at autopsy who had destruction of both adrenal glands. The clinical syndrome of adrenal insufficiency continues to bear the eponym Addison's disease. The following year Brown Sequard demonstrated that the adrenal glands were essential for life by performing adrenalectomy in experimental animals.

In 1886, Frankel first described a tumor which was subsequently called by the pathologist Pick in 1912 pheochromocytoma because of the dark color it turned when exposed to chromaffin salts. The presence of a substance in the adrenal medulla that raised blood pressure was described by the London physiologists Oliver and Scharpey-Schafer who named it adrenaline in 1893. Two years later Abel isolated epi-nephrine at Johns Hopkins. The structure of adrenocortical steroids was elucidated in the 1930s and this allowed Kendall and coworkers to synthesize cortisone.


Within the capsule of each adrenal are two anatomically and functionally distinct endocrine glands. The adrenal cortex arises from mesoderm while the medulla arises from neuroectoderm. During the 4-6 weeks of gestation cells destined to become the adrenal cortex develop from the mesoderm between the root of the dorsal meso-gastrium and the urogenital ridge. These developing cells are then penetrated by nerve fibers through which medullary cells will migrate. By the eighth week, the gland has differentiated into two distinct zones: a thin outer zone that will become the cortex in the adult and a large centrally located fetal zone. The fetal zone produces steroids during gestation but involutes during the first two weeks after birth and is completely gone by one year of age. During the second and third month of gestation, the weight of the adrenals increases from 5-80 mg and the glands are much larger than the adjacent kidneys. After the twentieth week of gestation, cortical growth and development is dependent on pituitary gland stimulation. Anencephalic fetuses are born with an atrophic adrenal fetal zone. After birth the three zones of the adult adrenal cortex develop as the fetal zone involutes. Nests of cells under the mesodermal capsule are the rudiment of the zona glomerulosa. The fascicular and reticular zones of the adult cortex arise from the glomerulosa after birth and are fully differentiated by about age 12.

During fetal development, primitive adrenocortical cells can migrate widely. Accessory or ectopic adrenal tissue can be found in the broad ligament, near the celiac access, adjacent to the ovarian or testicular veins and around the kidney or uterus. On rare occasions adrenocortical tissue has been found in other parts of the abdomen, thorax and central nervous system. These rests of ectopic adrenal tissue are important because they can cause persistent or recurrent hypercortisolism in patients with high levels of ACTH production.

The adrenal medulla and sympathetic nervous system develop together from the neuroectoderm. During the fourth week of gestation, the neural plate develops and then infolds to form the neural tube. A part of the neuroectoderm adjacent to the tube separates and remains between the neural tube and the ectoderm as the neural crest. In the second month of embryonic life cells from the neural crest migrate ventrally from the apex of the neural tube to the dorsal aorta. These cells aggregate and differentiate into neural blasts that form sympathetic neurons or pheochromoblasts that will form chromaffin cells. Some primitive adrenal medullary cells remain closely associated with the developing sympathetic nervous system and give rise to extra adrenal chromaffin cells and chromaffin bodies. Extra adrenal chromaffin cells regress and degenerate postnatally while those in the adrenal medulla complete their maturation. Some extra adrenal cells may persist anywhere along the embryonic path of neural crest cell migration. The persistence of extra adrenal chromaffin cells accounts for the occurrence of extra adrenal pheochro-mocytomas later in life.


The adrenal glands are bilateral retroperitoneal organs located on the superior medial aspect of the upper pole of each kidney. Each gland weighs from 3-6 gm and measures approximately 5 cm in length, 3 cm in width and 1 cm in thickness. The glands have a darker golden orange color compared to the surrounding perirenal fat.

The right adrenal is triangular or pyramidal in shape with its base resting on the kidney inferiorly. Medially, it abuts the lateral posterior aspect of the inferior vena cava while posteriorly it rests on the right crus of the diaphragm. The left adrenal is flatter and more crescent shaped. It extends more inferiorly along the medial aspect of the upper pole of the left kidney. It is found between the aorta medially, the pancreas and spleen anterior superiorly, the left renal artery inferiorly and the crus of the left diaphragm posteriorly.

The adrenals are highly vascular tissues and are supplied by multiple small branches of the inferior phrenic artery, the renal artery and the aorta. These numerous small arterioles anastomose over the surface of the gland before entering the perimeter of the capsule. The microvasculature within each gland integrates the function of the cortex and the medulla. The medulla has a dual blood supply. Some vessels pass directly through the cortex but the majority of medullary blood flow takes an indirect route entering first through the cortical plexus and then forming cortical sinusoids which empty into the medullary sinusoids. Blood coming through this indirect route is rich in cortisol when it reaches the medulla. This cortisol rich venous affluent stimulates the synthesis and enzymatic activity of phenylethanolamine-N-methyltransferase (PNMT) which converts norepinephrine to epinephrine. Extra adrenal chromaffin tissues lack this regulatory enzyme and therefore secrete norepinephrine predominantly. Nitric oxide is an important factor regulating local blood flow to the various zones of the cortex and medulla.

The rich venous plexus in each gland usually drains through a single adrenal vein. The right adrenal vein is typically short and drains directly into the inferior vena cava at the upper medial aspect of the gland. Because of its short course, the right adrenal vein can be difficult to catheterize when performing venous sampling studies for hormone analysis and difficult to ligate during adrenalectomy which makes the risk of life threatening caval hemorrhage much greater. On the left side, the adrenal vein is longer and drains into the left renal vein.

The lymphatic drainage of each gland is through two plexuses. One deep to the capsule and one in the medulla. These drain into the adjacent periaorta, subdia-phragmatic and renal lymph nodes. Relative to its size, the adrenal has a larger autonomic supply than any other organ and this supply consists almost exclusively of sympathetic fibers. The adrenal cortex has little direct innervation but does have a vasomotor supply with sympathetic axons innervating the subcapsular arteriolar plexus. The medulla is richly supplied by preganglionic sympathetic nerve fibers from the greater splanchnic nerve, celiac ganglion and other plexuses. Sympathetic stimulation causes catecholamine release as is seen by the decrease of plasma cat-echolamines in normal persons after receiving clonidine, a central alpha-2 agonist, or phentolamine, a ganglionic blocking agent. Unlike the normal medulla, pheo-chromocytomas are not innervated so their release of catecholamines is not controlled by neural stimulation. Therefore the clonidine and phentolamine suppression tests fail to inhibit plasma catecholamine levels in patients with pheochromocytomas.

Microscopic Anatomy

Each gland consists of a thick outer cortex and a thin inner medulla. The cortex makes up 80-90% of the volume of a normal gland while the medulla accounts for 10-20%. The external cortex is rich in lipids which gives the gland its characteristic dark yellowish orange color. The cortex has a firmer consistency than the reddish brown well vascularized medulla. Histologically, the adult adrenal cortex is divided into three zones: an outer zona glomerulosa, a middle zona fasciculata and an inner zona reticularis. The outer most layer or zona glomerulosa gets its name from the arrangement of columnar epithelial cells in clusters or anastomosing cords. The aldosterone (mineralocorticoid) secreting cells of the zona glomerulosa are small, have an intermediate number of lipid inclusions and constitute about 15% of the cortex. The zona fasciculata comprises approximately 75% of the cortex. Its cells have a large amount of cytoplasm relative to the nucleus, appear foamy secondary to many lipid inclusions and are arranged in a parallel array. Cells of the inner zona reticularis have compact cytoplasm, few lipid inclusions and are arranged in clusters. ACTH stimulation causes cells in the fasciculata and reticularis zones to enlarge due to increased lipid storage and mitochondrial and endoplasmic reticulum proliferation. The two inner zones of the cortex secrete adrenocortical steroids. The fasciculata secretes primarily cortisol while the reticularis secretes sex hormones including testosterone, estradiol and dihydroepiandrosterone.

The center of the adrenal gland, the medulla, is composed of rounded clusters or short cords of chromaffin cells that are surrounded by nerves and blood vessels. The cells from the medulla give a characteristic color reaction determined by their content of catecholamines. With dichromate salts, they give the brown "chromaffin" reaction and with silver salts they give the black "argentaffin" reaction. These cells have large numbers of catecholamine containing granules. In the normal human adrenal, epinephrine predominates in these granules because of the high activity of PNMT induced locally by high levels of glucocorticoids.

Adrenal Steroid Biochemistry and Physiology

The adrenal cortex secretes steroid hormones including cortisol, aldosterone, and sex steroids. Plasma cholesterol is the source substrate used for all steroid synthesis. Cholesterol is either extracted from plasma or manufactured locally within the adrenal cortex. The biosynthetic pathways of all adrenal steroid synthesis are shown in Figure 17.1. The pathways are compartmentalized in the cortical zones with the zona glomerulosa producing aldosterone, the zona fasciculata producing cortisol and the zona reticularis producing testosterone, estrone and estradiol. All adrenal steroids have either 19 or 21 total carbon atoms and share a common 17 carbon structure made up of three hexane rings and a single pentane ring. Congenital absence of enzymes involved in any of the pathways shunts pregnenolone derivatives through unaffected pathways and causes specific clinical syndromes.


Aldosterone, the major mineralocorticoid in man, is secreted from the zona glomerulosa. Approximately 40% of this hormone circulates bound to albumin, 20% to transcortin and the remainder is free. Its plasma half life is approximately 15 minutes. Aldosterone is degraded in the liver by enzymatic reduction and conjugation with glucuronic acid and then excreted by the kidney. Only minute amounts of free aldosterone are normally found in the urine. Aldosterone plays a key role in regulating extra cellular fluid volume and fluid and electrolyte balance. It stimulates sodium reabsorption and potassium and hydrogen ion secretion by the distal convoluted tubule of the kidney. It has similar effects in enhancing sodium retention by sweat glands, salivary glands and the gastrointestinal mucosa. By causing the kidney and other tissues to retain sodium aldosterone increases the extra cellular fluid volume.

Aldosterone secretion is regulated primarily by the renin-angiotensin system and plasma aldosterone levels. Plasma sodium atrial natriuretic peptide and ACTH have a less important role in its regulation. The renin angiotensin system is activated by secretion of renin from the juxtaglomerular cells of the kidney in response to a

Fig. 17.1. The pathways for synthesis of steroid hormones in the adrenal cortex are depicted.

decrease in renal blood flow, sympathetic nerve stimulation or a decrease in plasma sodium. Renin then enzymatically cleaves angiotensinogen to form angiotensin I. This in turn is cleaved by angiotensin converting enzyme (ACE) in the lung to form angiotensin II. Angiotensin II is a potent vasoconstrictor that binds to membrane receptors on the zona glomerulosa cell surface. This stimulates aldosterone biosynthesis and release from the adrenal through the receptor mediated activation of phospholipase C. Factors that decrease renal artery blood flow such as hemorrhage, dehydration, upright posture or renal artery stenosis stimulate the renin angiotensin system. Restoration of blood volume and pressure as well as high levels of aldosterone inhibit the release of renin and angiotensin. In other words there is a negative feedback loop with angiotensin II and aldosterone causing reabsorption of sodium and expanding the extracellular fluid volume. This increase in sodium and in extracellular fluid volume decreases the secretion of renin and formation of angiotensin II. There is a reciprocal relationship between serum potassium and aldosterone. An increase of serum potassium will increase aldosterone secretion proportionately whereas a fall in serum potassium will decrease aldosterone secretion. ACTH plays a comparatively minor role in aldosterone regulation and unlike the zona reticularus and fasciculata, the zona glomerularosa does not atrophy after hypophysectomy.


Glucocorticoids are essential for human life. The principle glucocorticoid in man is cortisol which is produced in the zona fasciculata. A normal adult secretes 10-30 mg of cortisol each day. Cortisol secretion has a diurnal pattern with peak serum levels occurring in the early morning and low levels occurring at night. Serum cortisol levels are continuously regulated by a feedback loop involving the hypothalamus and the pituitary (Fig. 17.2). Release of ACTH from the pituitary is the main mediator of cortisol secretion. Several hormones can stimulate pituitary release of ACTH but the most important is corticotropin releasing factor (CRH) which is secreted by the hypothalamus. Increases in serum cortisol inhibits hypothalamic secretion of CRH and pituitary secretion of ACTH while decreases in serum cortisol will stimulate the secretion of these two hormones. ACTH binds to receptors on the adrenal cell surface. This hormone receptor complex activates the adenylate cyclase-cyclic-AMP-protein kinase A system. This increases the conversion of cholesterol to pregnenolone. Chronic ACTH stimulation increases the number and activity of enzymes involved in cortisol synthesis and causes hypertrophy of the adrenocortical cells involved in this synthesis.

Circulating cortisol is cleared primarily by the liver and has a plasma half life of approximately 90 minutes. The liver converts cortisol to inactive metabolites which are conjugated and then excreted in the urine. These conjugated metabolites can be measured as 17-hydroxycorticosteroids. Normally only a small quantity of free cortisol can be found in the urine. Approximately 75% of plasma cortisol is bound to transcortin (corticosteroid binding globulin) while 15% is bound to albumin. Only 10-15% of cortisol is present as the free active hormone.

To exert their physiologic effects, steroid hormones bind to specific intracellular cytosolic receptors. The activated steroid receptor complex enters the cell nucleus where it binds to DNA. This activates transcription of target genes. Glucocorticoids have broad physiologic actions and cortisol plays important roles in intermediary metabolism, immune modulation, wound healing and regulation of intravascular volume (Table 17.1).

Adrenal Sex Steroids

The cells of the zona reticularus convert pregnenolone to 17-hydroxypregnenolone and subsequently to dehydroepiandrosterone and androstenedione. DHEA is the major sex steroid produced by the adrenal cortex. DHEA and androstenedione are weak androgens and are converted in peripheral tissues to testosterone and estrogens. Adrenal androgen release is stimulated by ACTH and is not affected by gona-dotropin stimulation. There is no diurnal variation of serum DHEA.

Normally the gonads are the principal source of sex steroids in males and females. Adrenal androgens promote development of male secondary sexual characteristics. Excessive production of adrenal sex steroids either prenatally or postna-tally results in disorders of sexual development such as masculinization and femini-zation.

Diurnal Secretions Epinephrine
Fig. 17.2. The hypothalamic-pituitary-adrenal negative feedback loop that regulates cortisol secretion by the adrenal cortex is shown.


The adrenal medulla synthesizes and secretes a number of biologically active amines including dopamine, norepinephrine and epinephrine. These catecholamines are synthesized from tyrosine. The conversion of tyrosine to dihydroxyphenylalanine (DOPA) by the cytosolic enzyme tyrosinehydroxylase is the rate limiting step in catecholamine synthesis (Fig. 17.3) Phenylethanolamine-n-methyltranspherase (PNMT) which is required for the conversion of norepinephrine to epinephrine is localized exclusively in cells in the adrenal medulla and the organ of Zuckerkandl. This explains why epinephrine secreting tumors arise only in these two tissues with few exceptions. Catecholamines are stored in the adrenal medulla in granular vesicles in which epinephrine represents approximately 80%, norepinephrine 20% and dopamine a minute fraction of the content of these chromaffin granules. These granules are discharged into the circulation by exocytosis when these cells are

Table 17.1. Effects of glucocorticoids (cortisol)


Metabolism Carbohydrate

Protein Lipid

Circulation Immune System




TBlood glucose TRelease of glucagon TGlycogenolysis and gluconeogenesis TInsulin resistance ¿Glucose uptake

TProtein catabolism

TMobilization of free fatty acids TTruncal obesity

TCardiac output TIntravascular volume TBlood pressure ¿Cellul ar permeability

¿Lymphocyte activation ¿Monocyte and neutrophil migration ¿Mast cell lysosomal degranulation ¿Antibody formation ¿Resistance of infection

TMuscle weakness TOsteoporosis ¿Collagen synthesis ¿Fibroblast activity ¿Wound healing

TPsychosis TEuphoria

TCataracts TCorneal ulcers stimulated. The half life of plasma epinephrine and norepinephrine is very short (1-2 minutes). There are three pathways by which catecholamines are cleared from the circulation. These include uptake by sympathetic neurons, uptake and degradation by peripheral tissues and excretion in the urine. Catecholamines are metabolized in the liver and kidney by two enzymes, monoamine oxidase (MAO) and cat-echol-o-methyl transferase (COMT). The inactive metabolites that result from this enzyme degradation are vanillylmandelic acid (VMA), normetanephrine and metanephrine. These breakdown products are cleared by the kidney and can be measured in the urine either as free compounds or as conjugates of glucuronide or sulfate.

Catecholamines have wide ranging effects on almost all tissues and organs in the body. Catecholamines act by forming complexes with alpha or beta receptors on the

Fig. 17.3. Catecholamine synthesis.

cells of target tissues. Alpha receptors have the highest affinity for norepinephrine and less for epinephrine. Beta receptors are more responsive to epinephrine. Catecholamines have profound cardiovascular and metabolic effects and also influence the secretion of many hormones. The principal physiologic effect of alpha receptor stimulation is vasoconstriction. There are two types of beta receptors. The betarreceptor mediates inotropic and chronotropic stimulation of cardiac muscle. The beta2-receptor induces relaxation of smooth muscle in noncardiac tissues including blood vessels, bronchi, uterus and adipose tissue. Catecholamines increase cellular calorigenesis by increasing oxygen consumption and heat production. In the liver and heart they stimulate glycogenolysis which increases the availability of carbohydrate for tissue use. They induce lipolysis and increase release of fatty acids and glycerol from adipose tissue. Both norepinephrine and epinephrine inhibit insulin secretion.


1. Gröndal S, Hamberger B. Adrenal physiology. In: Clark OH, Duh Q-Y eds. Textbook of Endocrine Surgery. Philadelphia: WB Saunders 1997:461-465. The physi-ologyofboth the adrenal cortex and medulla andthe hormones they secrete are discussed in detail.

Hughes S, Lynn J. Surgical anatomy and surgery of the adrenal glands. In: Lynn J, Bloom SR eds. Surgical Endocrinology. Oxford: Butterworth-Heinemann Ltd 1993:458-467. The clinical aspects of adrenal anatomy are well delineated. Mihai R, Farndon JR. Surgical embryology and anatomy of the adrenal glands. In: Clark OH, Duh Q-Y eds. Textbook of Endocrine Surgery. Philadelphia: WB Saunders 1997:447-459. This is an in depth reviewofthe embryology and anatomyof the adrenal glands written from the point of view of an endocrine surgeon. Norton JA. Adrenal. In: Schwartz SI, Shires GT, Spencer FC, et al eds. Principles of Surgery. New York: McGraw-Hill 1999:1630-1659. The anatomy, physiology and clinical implications of the adrenal gland are well summarized.

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