Neoplasms in the region of the pituitary fossa

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Neoplasms in the region of the pituitary fossa

Neoplasms in the region of the pituitary fossa may arise in the pituitary gland itself, the sphenoid bone that surrounds the fossa, or the suprasellar region (Figs 44.1, 44.2). Structures in the suprasellar region and adjacent to the pituitary fossa include the hypothalamus, optic chiasm, nasal sinuses, and cavernous sinuses and their contents.

44.1 Anatomic relationships of the pituitary gland.

44.2 Schematic illustration of the types and sources of neoplasm that can affect the pituitary gland.

Common neoplasms in this region are:

pituitary adenomas

meningiomas.

Uncommon neoplasms in this region are:

craniopharyngiomas

germinomas

metastatic carcinomas

astrocytomas.

Other neoplasms are rare.

LOCALIZATION IN THE DIFFERENTIAL DIAGNOSIS OF PITUITARY REGION LESIONS

Review of imaging or imaging reports is helpful in generating a differential diagnosis.

Pituitary adenomas are usually centered on the sella but can have suprasellar, clival, or cavernous sinus components.

Cystic suprasellar masses are most often craniopharyngiomas or Rathke cleft cysts. Occasionally, pituitary adenomas are cystic. Rarely, adenomas may contain Rathke cleft cysts.

A diffusely expanded pituitary gland should also prompt consideration of lymphocytic hypophysitis, other inflammatory processes, lymphoma, and pituitary hyperplasia.

The differential diagnosis of a suprasellar mass in a young person should include germ cell tumors and craniopharyngioma, in addition to pituitary adenoma.

A destructive clival lesion is most often a chordoma or chondrosarcoma, but can rarely be a pituitary adenoma.

Carcinomas from the salivary glands or sinonasal cavities may infiltrate up through the skull base to involve the pituitary region.

When a potential ‘adenoma’ is hormone-negative and synaptophysin-positive, correlation with imaging can be helpful, localizing tumor to sella or cribriform plate, but cribriform plate involvement requires exclusion of olfactory neuroblastoma.

Optic chiasm masses suggest pilocytic astrocytoma or meningioma.

The pituitary gland weighs about 600 mg and consists mainly of the adenohypophysis (anterior lobe) and the neurohypophysis (posterior lobe) (Figs 44.3–44.6); the pars intermedia is poorly developed in man.

44.3 Hormonal cell type is mediated by transcription factors and estrogen receptors.
ERa, estrogen receptor alpha; FSH, follicle stimulating hormone; GATA-2, GATA binding protein 2; GH, growth hormone; (GH repressor), postulated growth hormone repressor; LH, luteinizing hormone; NeuroD1, neurogenic differentiation 1; Pit-1, pituitary transcription factor 1; SF1, steroidogenic factor 1; TEF, thyroid embryonic factor; TPit, pituitary restricted transcription factor; TSH, thyroid stimulating hormone.

44.4 Normal adenohypophysis.
Nests of round or polyhedral cells, and an intervening network of vascular sinusoids are evident.

44.5 Normal adenohypophysis.
Cell nests are surrounded by reticulin.

44.6 Normal neurohypophysis.
This consists of non-myelinated hypothalamohypophysial nerve fibers and a meshwork of capillaries adjacent to which the fibers terminate. Also present are specialized astrocytes (pituicytes).

Adenomas are the commonest neoplasms in the pituitary gland and are derived from cells in the adenohypophysis. Neoplasms of neurohypophyseal origin are very rare.

PITUITARY ADENOMAS

Pituitary adenomas are derived from secretory cells in the adenohypophysis. Some adenomas secrete peptides in an unregulated manner and may therefore produce abnormal endocrine effects in addition to causing mass effects in the region of the pituitary fossa (Fig. 44.7).

44.7 Pituitary adenoma.
Large, hemorrhagic pituitary adenoma producing distortion of surrounding structures.

PITUITARY PEPTIDES

Secretory cells in the adenohypophysis synthesize six major peptide hormones:

Somatotrophs synthesize growth hormone (GH).

Lactotrophs (mammotrophs) synthesize prolactin (PRL).

Corticotrophs synthesize corticotropin (ACTH).

Thyrotrophs synthesize thyrotropin (TSH).

Gonadotrophs synthesize follicle stimulating hormone (FSH) and luteinizing hormone (LH).

TSH, FSH, and LH are glycoproteins composed of a common α-subunit and different β-subunits. The cross-reactivity sometimes seen with antibodies to these peptides is due to the considerable homology between the β-subunits.

The neurohypophysis is continuous with the infundibular stalk and the median eminence. Its two major peptide hormones are synthesized in the supraoptic and paraventricular nuclei of the hypothalamus and are:

Oxytocin.

Vasopressin.

MACROSCOPIC APPEARANCES

Pituitary adenomas are soft and have a beige or cream color. Discussion between the neurosurgeon and pathologist at the time of operation sometimes raises the possibility of an alternative diagnosis (e.g. a tough mass is more likely to be a meningioma).

By convention, macroadenomas and microadenomas have diameters above and below 10 mm, respectively. Most microadenomas diagnosed in life are ACTH-cell adenomas and PRL-cell adenomas presenting early with endocrine effects. Histopathologic assessment of surgically treated microadenomas requires a thorough examination of all submitted tissue.

GENETICS OF SPORADIC PITUITARY TUMORS

Nearly all pituitary adenomas are monoclonal.

Downregulation of tumor suppressor genes, such as RB1, CDKN2A, CDKN1A, and other cyclin-dependent kinase inhibitors, is often due to epigenetic changes such as promoter hypermethylation or histone modification. Somatic mutations of these genes are uncommon in most adenomas.

Oncogenes including GNAS, CREB1, and PTTG1 are associated with adenomas. The most consistent finding is GNAS mutation, which occurs in up to 40% of sporadic GH or somatotroph adenomas (Fig. 44.8).

The pituitary tumor transforming gene (PTTG1) is overexpressed in most adenomas. A postulated mechanism is promoter hypomethylation, as somatic mutations are generally not identified.

Oncogene-induced senescence (largely irreversible cell cycle arrest) is hypothesized to explain the relative indolence of pituitary adenomas. Animal studies suggest that PTTG1 overexpression when combined with DNA damage may lead to p21-mediated tumor cell senescence in GH adenomas.

Mutations of TP53, RB1, and NME1 as well as amplification of HRAS and MYC are observed in aggressive tumors. HRAS mutations have been documented in pituitary carcinoma.

MICROSCOPIC APPEARANCES

PITUITARY ADENOMAS

The commonest neoplasms in the region of the pituitary fossa, and represent 10–15% of intracranial neoplasms.

Have an incidence ranging from 1–15/100 000 in different series.

Most common in the third to sixth decades.

Show a female:male ratio of approximately 2:1 in younger patients.

May be an incidental finding in approximately 10% of elderly people according to some necropsy series (40% of these neoplasms are prolactinomas).

May present with the effects of increased peptide production (i.e. acromegaly or gigantism due to excess GH, Cushing syndrome due to excess ACTH, amenorrhea, galactorrhea, or impotence due to excess PRL, hyperthyroidism due to excess TSH).

May present with mass effects (i.e. headache, compression of the optic chiasm, (other) cranial nerve palsies, compression of the othalamus, hypopituitarism, pituitary infarction). Pituitary peptide deficiencies preceding complete hypopituitarism tend to occur in sequence (i.e. GH → FSH/LH → TSH → ACTH).

Can compress the pituitary stalk and thereby compromise transport of PRL inhibitory factor (dopamine) to the adenohypophysis, resulting in an elevated PRL level (‘stalk effect’), but PRL concentrations seldom exceed 200 mg/L in these circumstances.

May present acutely with mass effects when they undergo infarction or hemorrhage.

Non-neoplastic causes of infarction (pituitary apoplexy)

Postpartum hemorrhage (Sheehan syndrome).

Raised intracranial pressure.

Prolactinomas

Commonly present in young women as microadenomas because amenorrhea is an early hormonal effect.

Tend to be larger and have a higher incidence of dural invasion in men and older women.

Result in increased serum PRL concentrations, which correlate with the size of the adenoma.

Usually present with acromegaly if the tumor is a PRL and GH mixed cell adenoma or mammosomatotroph adenoma.

ACTH-cell adenomas

Result in serum ACTH and cortisol concentrations that correlate poorly with their size.

Occasionally clinically silent despite labeling with antibodies to ACTH.

The histology of pituitary adenomas is varied (Table 44.1). Many adenomas consist of small, oval, or polyhedral cells. These may be arranged in monotonous sheets or show a variety of acinar, papillary, trabecular, or other patterns (Figs 44.9–44.11). The nuclei of neoplastic cells are generally round or oval and contain the stippled chromatin typical of neuroendocrine neoplasms. Tiny nucleoli may be evident. Cytologic pleomorphism and mitotic figures may be present, but do not necessarily signify aggressive biologic behavior (Fig. 44.12). Invasion of local structures (Fig. 44.13), particularly the dura, is not infrequent, even by adenomas with bland cytologic features.

Table 44.1

Syndromes with pituitary adenomas

44.8 Activating mutations and relaxed imprinting of the GNAS1 gene in somatotroph adenomas.

44.9 Pituitary adenoma.
A monotonous sheet of cells is typical.

44.10 Pituitary adenoma.
A vascular network is seen between cells, some of which have formed pseudorosettes.

44.11 Pituitary adenoma composed of two populations of cells.
The larger cells were immunoreactive for GH.

44.12 Pituitary adenoma. (a,b)
Cytologic pleomorphism and rare mitotic figures may be present and do not necessarily signify aggressive behavior.

44.13 Entrapped hypothalamic neurons at the invading edge of a suprasellar adenoma.
Adenomas containing neoplastic ganglion cells are recorded but are very rare.

Dystrophic calcification and eosinophilic (amyloid) bodies are strongly associated with prolactinomas (Fig. 44.14). Long-term treatment of prolactinomas with bromocriptine before surgical resection produces fibrosis.

44.14 Large masses of eosinophilic amyloid in a prolactinoma. (Courtesy of Dr J Geddes, Royal London Hospital, UK.)

Crooke’s hyaline change describes the development of a zone of glassy agranular cytoplasm around the nuclei of non-adenomatous corticotrophs in patients with elevated corticosteroid concentrations due to an ACTH-cell adenoma, a systemic ACTH-producing neoplasm, an adrenal neoplasm or exogenous corticosteroid administration (Fig. 44.15). This appearance results from a massive accumulation of keratin microfilaments.

44.15 Crooke’s hyaline change.
Basophilic cytoplasm in corticotrophs is displaced by amorphous material. Perinuclear material has displaced the magenta granules in the corticotrophs to the periphery of the cytoplasm (arrows).

A small proportion of null-cell adenomas comprises oncocytomas (Fig. 44.16). The (arbitrary) ultrastructural criterion for a diagnosis of oncocytoma is that more than 10% of the cell volume must be occupied by mitochondria. ACTH-cell adenomas occasionally show oncocytic change.

44.16 Pituitary oncocytoma.
The uniform cells in this adenoma exhibit cytoplasmic granularity and eosinophilia. (Courtesy of Dr S van Duinen, Academisch Ziekenhuis, Leiden.)

Immunohistochemistry to assess the production of peptide hormones (Figs 44.17–44.20, Table 44.2) is used with electron microscopy (Figs 44.21, 44.22) to classify pituitary adenomas. The various pituitary trichrome stains are useful for demonstrating normal adenohypophysis, but of limited value for distinguishing different types of adenoma. Immunolabeling of a hormone in adenoma cells does not necessarily signify that it is secreted in a physiologically active form. This is exemplified by the patchy and usually weak labeling of cells in some adenomas with FSH, LH, TSH or α subunit antibodies. Pituitary adenomas label with antibodies tosynaptophysin, chromogranin-A, and low molecular weight cytokeratins (Table 44.3).

Table 44.2

Pituitary adenomas classified by peptide production

^a A synthesis of figures from several sources

^b O n ultrastructural examination

Table 44.3

Immunohistochemical profiles of neoplasms in the region of the pituitary fossa

+, nearly always immunoreactive;

−, no immunoreactivity;

+/−, majority of cases immunoreactive;

−/+, minority of cases immunoreactive.

^a Focal immunoreactivity in secretory meningiomas.

^b Immunoreactive in some anaplastic large cell lymphomas and lymphomas that show plasma cell differentiation.

^c Some immunoreactive examples recognized.

^d Immunoreactive sustentacular cells are present in some olfactory neuroblastomas.

44.17 Pituitary adenoma.
Immunohistochemical demonstration of prolactin.

44.18 Pituitary adenoma.
Immunohistochemical demonstration of ACTH.

44.19 Mammosomatotroph adenoma.
Cells in a mammosomatotroph adenoma label with a GH antibody.

44.20 Mammosomatotroph adenoma.
Cells in the adenoma shown in Figure 44.16 label with a PRL antibody.

44.21 Densely granulated GH adenoma.
Numerous secretory granules of varying size are evident.

44.22 Sparsely granulated GH adenoma.
The fibrous body (arrows) is a consistent feature in this neoplasm, which contains few secretory granules.

In some reports, invasive adenomas and adenomas that recur have a higher growth fraction as assessed by Ki-67 antibodies.

A diagnosis of pituitary carcinoma requires evidence of metastasis; either discontinuous spread of neoplasm within the CNS or spread outside the CNS. Pituitary carcinomas can produce any pituitary peptide, however, while about three-quarters do so, an endocrinopathy is rare. Production of ACTH or prolactin is usual.

ULTRASTRUCTURAL EXAMINATION OF PITUITARY ADENOMAS

Ultrastructural examination is most useful for further classification of GH-cell and combined PRL-cell plus GH-cell adenomas.

Sparsely granulated GH-cell adenomas are often refractory to somatostatin tend to be larger and more difficult to remove, grow more rapidly, and occur in younger patients than densely granulated GH-cell adenomas.

Sparsely granulated GH-cell adenomas (Fig. 44.22) contain circumscribed collections of intermediate filaments and smooth endoplasmic reticulum (fibrous bodies).

Ultrastructural differences between prolactinomas do not signify differences in behavior.

Ultrastructural examination is required for a definitive diagnosis of acidophil stem cell adenoma, which has poorly developed rough endoplasmic reticulum, giant mitochondria, fibrous bodies, inconspicuous Golgi apparatus, and few secretory granules.

The silent subtype III adenoma has large polar cells, prominent nucleoli, spheridia (nuclear inclusions), abundant smooth endoplasmic reticulum, large Golgi complex, and secretory granules in cell processes.

The mammosomatotroph adenoma, which like the acidophil stem cell adenoma comprises cells that immunolabel for both GH and PRL and contain abundant secretory granules.

PITUITARY ADENOMAS

Pituitary adenomas must be distinguished from normal adenohypophysis, other neoplasms in the region of the pituitary fossa, and non-neoplastic masses in the region of the pituitary fossa.

Secretory cells in the adenohypophysis

Generally form a mixed population, though different cell types predominate in different regions (see Fig. 44.28).

Arranged in nests surrounded by a network of reticulin (see Fig. 44.5).

Adenomas

Lose the normal pattern of nested cells.

Lack a honeycomb pattern of reticulin.

Usually contain cells with a higher than normal nuclear:cytoplasmic ratio.

May contain rare mitotic figures.

Can often be distinguished by a uniform pattern of immunolabeling with antibodies to pituitary peptides.

Other neoplasms in the region of the pituitary fossa

These can generally be diagnosed by conventional histology.

Immunohistochemistry may be helpful, especially for small biopsies (see Table 44.3).

Metastases from primary neoplasms outside the CNS are found mainly in the neurohypophysis, but can present in the adenohypophysis where their identification may be difficult (Figs 44.23–44.25). It is important to distinguish carcinomas from native squamous cell nests (Fig. 44.26) that are present in approximately 30% of normal pituitaries in the pars tuberalis and hypophyseal stalk, do not disrupt the normal acinar reticulin pattern, are cytologically bland, without mitoses or pleomorphism, and often coexist with gonadotroph cells.

44.23 Metastatic breast carcinoma in the pituitary gland.

44.24 Intracytoplasmic mucin in the metastatic breast carcinoma featured in Figure 44.23.

44.25 Cells immunoreactive for EMA in the metastatic breast carcinoma featured in Figure 44.23.

44.26 Squamous cell nests in the pars tuberalis.
This is a normal finding.

DIAGNOSIS OF ATYPICAL ADENOMA

Atypical adenomas have increased potential for aggressive behavior, including invasion of bone, nerves, and blood vessels, and recurrence or metastasis.

If a tumor is metastatic, it is not considered an atypical adenoma and is designated pituitary carcinoma.

Atypical adenomas are defined by a Ki-67 index >3%, in conjunction with extensive p53 nuclear immunoreactivity.

A Ki-67 immunolabeling index >10% in the absence of increased p53 expression is a criterion accepted by some pathologists.

Pituitary carcinomas may also demonstrate increased Ki-67 and p53 immunolabeling, though not invariably.

The etiology of the increased p53 expression is incompletely explained as TP53 mutations are present in only a minority of cases.

INFLAMMATORY DISEASES THAT MAY PRESENT AS A MASS IN THE PITUITARY FOSSA

Lymphocytic hypophysitis (Fig. 44.27a)

44.27 Hypophysitis.
(a) In this example of lymphocytic hypophysitis, cells of the adenohypophysis are separated by an inflammatory infiltrate consisting mainly of lymphocytes. (b) In granulomatous hypophysitis, the formation of granulomata, including multinucleated giant cells, is evident.

Occurs almost exclusively in women.

Usually occurs in pregnancy or the postpartum period.

Often presents with pituitary insufficiency.

Characterized by a mixed infiltrate of inflammatory cells, mainly lymphocytes.

Granulomatous hypophysitis (Fig. 44.27b)

Can be idiopathic.

Not associated with the puerperium, but is associated with rupture of a Rathke’s cleft cyst, or rarely with an immunogenic disorder.

Characterized by granulomata, including multinucleated giant cells.

CNS sarcoidosis (see Chapter 16)

Often associated with systemic sarcoidosis.

Preferentially affects structures in the suprasellar region.

Produces non-caseating, granulomatous inflammation with multinucleated giant cells.

More widespread than granulomatous hypophysitis.

PITUITARY HYPERPLASIA

Pituitary hyperplasia (Table 44.4) may be nodular or diffuse. Nodular hyperplasia is characterized by enlarged cell nests and can be demonstrated in a reticulin preparation. Diffuse hyperplasia may not be obvious, requiring an appreciation of the uneven distribution of cells in the adenohypophysis (Fig. 44.28) and cell counts to make the diagnosis.

Table 44.4

Conditions associated with pituitary hyperplasia

In some cases the stimulus for hyperplasia remains obscure.

44.28 Distribution of peptide-containing cells in the adenohypophysis.

CRANIOPHARYNGIOMAS

Craniopharyngiomas are slowly-growing epithelial neoplasms in the suprasellar region, and there are two variants:

adamantinomatous

papillary.

These variants have both common and differentiating histopathologic features. Transitional forms exist, but attempts should be madeto distinguish the two main variants, which have different outcomes; papillary neoplasms tend to occur in an older age group, are more readily resected, and recur less often.

The histogenesis of craniopharyngiomas is not established. Adamantinomatous neoplasms closely resemble the adamantinoma of the jaw and the calcifying odontogenic cyst. Papillary neoplasms may be related to Rathke’s cleft cyst, which can show marked squamous metaplasia.

MACROSCOPIC APPEARANCES

An admixture of cystic and solid components is characteristic (Figs 44.29–44.31), and there is sometimes a smooth lobulated capsule. The solid tissue often contains foci of calcification and the cysts may contain a thick liquid that has been likened to machine oil. The papillary craniopharyngioma tends to be more circumscribed than the adamantinomatous type, and does not contain the calcification or oil-like cyst fluid of the adamantinomatous variant.

44.29 Craniopharyngioma.
This craniopharyngioma has solid and cystic components, and disrupts the diencephalon. Note the ‘machine oil’ nature of the cyst fluid.

44.30 Craniopharyngioma.
A craniopharyngioma (arrow) bulging from the tuber cinereum.

44.31 Histology of the craniopharyngioma shown in Figure 44.30 (arrow).

CRANIOPHARYNGIOMAS

Account for approximately 2% of all intracranial neoplasms and about 5% of childhood intracranial tumors.

Show a peak incidence in children aged 5–10 years, but also occur in adults.

Tend to be adamantinomatous when they occur in a child and adamantinomatous or papillary when they occur in an adult.

Present with symptoms and signs due to increased intracranial pressure, compression of the optic pathways (causing visual dysfunction), and compression of the hypothalamus or pituitary (leading to endocrine dysfunction).

Recur in 10–20% of patients.

MICROSCOPIC APPEARANCES

Features of the adamantinomatous craniopharyngioma (Figs 44.32–44.35) include:

44.32 Adamantinomatous craniopharyngioma.
Multiple cysts in an adamantinomatous craniopharyngioma.

44.33 Adamantinomatous craniopharyngioma.
A loose matrix (stellate reticulum) is due to intercellular fluid accumulation (arrows).

44.34 Adamantinomatous craniopharyngioma.
(a,b) Sheets and nodules of keratinized ‘ghost’ cells are evident.

44.35 Multinucleated giant cells surround cholesterol clefts in a craniopharyngioma.

groups of squamous cells, often surrounded by a peripheral palisade of columnar cells

intercellular accumulations of fluid that separate the cells in some parts of the neoplasm

cohesive clusters or sheets of keratinized anuclear ‘ghost’ cells

calcification, which may progress to metaplastic bone formation

cholesterol clefts, which are often related to necrotic debris within the cysts.

Papillary craniopharyngiomas (Fig. 44.36) consist of groups of squamous cells, which may form keratin pearls. Cysts are infrequent and an adamantinomatous pattern is absent. There are no nodules of keratinized ‘ghost’ cells and calcification is rare.

44.36 Papillary craniopharyngioma.
This variant lacks an adamantinomatous architecture and foci of degenerating keratinocytes.

CRANIOPHARYNGIOMA

The craniopharyngioma must be distinguished from several cystic suprasellar lesions: epidermoid and dermoid cysts (Chapter 45), pilocytic astrocytoma (Chapter 35), and the Rathke cleft cyst.

Epidermoid and dermoid cysts

The epidermoid cyst is characterized by an epithelium containing prominent keratohyaline granules and an orderly maturation of squamous cells with formation of keratin flakes.

The dermoid cyst is very rare in the region of the pituitary fossa and contains dermal adnexal structures.

Pilocytic astrocytoma

Florid reactive astrocytosis and Rosenthal fibers in a biopsy taken adjacent to rather than within a craniopharyngioma may simulate a pilocytic astrocytoma.

Cholesterol clefts or giant cells suggest a craniopharyngioma.

Microcystic areas (contributing to a biphasic architecture), loosely arranged astrocytic cells, and degenerative, atypical nuclear features support the diagnosis of pilocytic astrocytoma.

Rathke cleft cyst

The radiologic and operative findings may help, because papillary craniopharyngiomas rarely contain large cysts.

The Rathke cleft cyst does not have the biphasic architecture, stellate reticulum or oil-like cyst fluid of an adamantinomatous craniopharyngioma.

The Rathke cleft cyst does not have the papillary architecture of the papillary craniopharyngioma, and is much more likely to have an epithelium with cilia or goblet cells.

The surrounding brain parenchyma is usually densely gliotic (Fig. 44.37) and may contain many Rosenthal fibers. Leakage of cyst contents may provoke an inflammatory reaction, which includes multinucleated giant cells (see Fig. 44.35).

44.37 Craniopharyngiomas elicit a gliotic reaction in surrounding brain tissue.
(a) The gliotic reaction resembles a pilocytic astrocytoma, one of the principal entities in the differential diagnosis of craniopharyngioma, and can include Rosenthal fibers (b).

RATHKE CLEFT CYST

Small cysts lined by cuboidal epithelium in the pars intermedia of the pituitary gland are remnants of Rathke’s pouch and can enlarge to produce a Rathke cleft cyst (Fig. 44.38). Small examples may be an incidental postmortem finding, but if the cysts are large enough they can produce endocrine or visual abnormalities.

44.38 Rathke cleft cyst.
(a) Remnants of Rathke’s pouch in the adenohypophysis. (b) Rathke cleft cyst is lined by a simple columnar epithelium, but in this example also shows focal squamous metaplasia. (c) The epithelium is usually ciliated.

MACROSCOPIC AND MICROSCOPIC APPEARANCES

Rathke cleft cysts usually have a thin wall and slightly cloudy mucinous contents. The cyst is lined by cuboidal or columnar epithelium, which may be ciliated (Fig. 44.38), and usually contains goblet cells. Peptide-containing cells may occasionally be found in the epithelium. The cuboidal/columnar epithelium sometimes incorporates a metaplastic stratified squamous epithelium. Microscopic cysts with a similar appearance are occasionally found in pituitary adenomas.

GRANULAR CELL NEOPLASM OF THE INFUNDIBULUM

Granular cells in the infundibulum or neurohypophysis are thought to be of glial origin. Symptomatic neoplasms of these cells are rare. Asymptomatic tiny groups of granular cells in this region, sometimes called choristomas or tumorlets, are more common.

MACROSCOPIC AND MICROSCOPIC APPEARANCES

A granular cell neoplasm of the infundibulum is a well-circumscribed, soft, homogeneous neoplasm that may straddle the diaphragma sellae.

Choristomas/tumorlets and granular cell neoplasms share cytologic features (Fig. 44.39). Their oval cells contain finely granular, eosinophilic, strongly PAS-positive cytoplasm. In larger neoplasms the cells may be arranged in fascicles. There is little nuclear pleomorphism and mitotic figures are not found. The cells are reactive for S-100 and CD68 with immunohistochemistry.