Diagnosis and Management of Pituitary Tumors

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450 SAEGERTermDiffuse hyperplasiaNodular hyperplasiaDispersed hyperplasiaAbsolute hyperplasiaRelative hyperplasiaPrimary hyperplasiaSecondary hyperplasiaTable 1Types of HyperplasiaDefinitionDiffusely increased number of onepituitary cell typeSmall nodule composed nearlyexclusively of one pituitary celltype; alveolar basic structure maybe distortedSeveral nodules of one cell typeIncreased number of one cell typewithout decrease of other cell typesIncreased number of one cell type andsimultaneous decrease of other celltypesDevelopment without regulatorydisturbanceDevelopment from regulatoryhyperstimulationcytokeratin filaments are present in the paranuclear region, wherelysosomal vacuoles are also demonstrable, the so-called enigmaticbodies (15). Crooke’s cells with typical hyaline changes and paranuclearvacuoles are developed only in those patients who arehypercortisolemic (16). Therefore, some conclusions can be drawnfrom the presence of Crooke’s cells. If they can be found, ahypercortisolism must exist. If they are lacking, a significanthypercortisolism can be excluded (17). Most ACTH cell hyperplasiafound in surgical or postmortem specimens do not correlate toany dysfunction, but in cases with arterial hypertension, theyappear to be more frequent (18). Adjacent to clinically nonactiveACTH cell adenomas, they developed in about 10% of cases, butalso in other adenoma types, ACTH cell hyperplasia can be foundin up to 15% of cases (Table 2). In the para-adenomous pituitarywith active ACTH adenomas in Cushing’s disease, they have beenfound in up to 50% of cases (10) (Figure 4). Since transformationsof those hyperplasia into adenomas are demonstrable in a numberof cases (19,20), we can conclude that ACTH cell hyperplasia inCushing’s disease may be an early stage of an ACTH cell adenoma.That does not mean that adenomas usually arise as a downstreamconsequence of excess trophic influences from thehypothalamus. They may also arise as a result of an intrinsicpituitary defect (16). Patients with CRH-producing tumors candevelop endocrine active hyperplasia inducing Cushing’s disease(21,22). These tumors can be located in various organs (23,24).They stimulate the ACTH cell system chronically and inducehyperplasia. Corticotropin-releasing hormone- (CRH) producinggangliocytomas in the sellar region are very rare (25,26). ACTHcell hyperplasia can transform into ACTH cell adenomas inrare cases as reported previously (2). ACTH cell hyperplasia as thecause of pituitary Cushing’s disease is very rare (27–30) and canbe diagnosed only in those cases in which an ACTH cell adenomacannot be demonstrated. Since those adenomas can be extremelysmall, its demonstration may be very difficult, time-consuming,and expensive. An apparently unique case, an ACTH cell hyperplasiawith Cushing’s disease adjacent to a Crooke’s cell adenoma,was previously described (31). Since the latter presumably cannotbe the source of hyperfunction, the hyperplasia had to have beenhyperfunctional.In cases with primarily untreated Addison’s disease, the ACTHcells develop diffuse and nodular hyperplasia, and increase in sizeforming so-called Crooke-Russel’s cells, which show decreasednumbers of enigmatic bodies and of secretory granules and enlargedeuchromatic nuclei. Such ACTH cell hyperplasia may transforminto tumorlets, and also into ACTH cell microadenomas (32).In the intermedia zone of autopsy pituitaries ACTH cell hyperplasiaoccur in 29% of men and in 14% of women (33). Thecorticotrophs of the neurohypophysis, the so-called basophil invasion,are increased in number in 13% of postmortem pituitaries(17). In most cases, they are coincidental with adenohypophysealhyperplasia of the corticotrophs. Two-thirds of these patients sufferedfrom arterial hypertension (17). Irrespectively of hypertension,the degree of migration of ACTH cells increases with patientage and is more common in men than in women (34).TSH CELL HYPERPLASIA Thyroid-stimulating hormone(TSH) cell hyperplasia is mainly diffuse and less frequent nodularor dispersed. The TSH cells are mostly enlarged. The immunoreactivityfor TSH may be strongly indicative of a high storage ofTSH or may be weakly suggestive of a minimal storage of thehormone. TSH cell hyperplasia can be accompanied by prolactincell hyperplasia and lead to an increase in size and weight of thepituitary (35). Stimulated TSH cells are enlarged and characterizedby a vacuolated slightly PAS-positive cytoplasm, which mayalso harbor large strongly PAS-positive globules. They are calledthyroidectomy cells. In the electron microscope (15), the roughendoplasmic reticulum is strongly increased and dilated as beingresponsible for light microscopical vacuolation. The Golgi complexesare also enlarged. The secretory granules vary in size and number.Hyperplasia is induced by chronic hyperstimulation owing tohypothyroidism (36) or TSH-stimulating drugs and hormones (37).In long-standing primary hypothyroidism, diffuse and nodularTSH cell hyperplasia was found in 69 and 25% of pituitaries, in12% of glands in the intermediate stages between nodular hyperplasiaand the development of microadenoma, and in 8% thyrotropicadenomas demonstrable (36).GONADOTROPH CELL HYPERPLASIA The frequency ofhyperplasia of gonadotroph cells is controversial in the literature.Whereas Lloyd (38) did not find it in surgically resected pituitaries,our material reveals a slight, but significant diffuse hyperplasiaof FSH and /or LH cells in many patients with metastasizingcancers of the breast or prostate who were palliatively treated bytotal hypophysectomy (39). Hyperplastic gonadotroph cells aremostly also hyperstimulated showing a slight increase in size,densely arranged vacuoles, and variably diminished granules inthe cytoplasm. These cells have been called castration cells orgonadectomy cells. Electron microscopically (15,39), the vacuolesare formed by strongly dilated rough endoplasmic reticulum.The Golgi apparatus is enlarged, and the number of secretorygranules decreased.The cause of gonadotroph hyperplasia is a chronic hypogonadism,which may be primary or secondary from gonadectomy.Chronic therapy with gonadotropins stimulating drugs (37) mayalso lead to gonadotroph cell hyperplasia. Transition of gonadotrophcells hyperplasia into an adenoma has not been observed to date.INFLAMMATORY LESIONSPituitary inflammation is comprised of a number of inflammatoryprocesses that are totally different in their etiology, pathogenesis,and structure. All can enlarge the pituitary or form local
CHAPTER 24 / TUMOR-LIKE LESIONS OF THE SELLAR REGION 451Table 2Coincidental CoincidentalDiffuse Nodular Dispersed with adenoma with adenomaCell type hyperplasia hyperplasia hyperplasia Total of same cell type of other cell typeGH cell 1 1Prolactin cell 2 13 1 16 5 2ACTH cell 18 11 43 72 10 11TSH cell 2 2FSH/LH cell 1 1Null cell 2 2 1Oncocyte 1 3 1 5Total 24 29 46 99a Author’s unpublished data.Table 3Types of Hyperplasia in Surgical Specimens aWithout With adenoma With adenomaCell type adenoma of same cell type of other cell type With other tumorGH cell 2 1 0 0Prolactin cell 5 1 4 1 CraniopharyngiomaACTH cell 28 2 1 2 Carcinoids of bronchusTSH cell 0 0 0 0FSH/LH cell 46 0 0 0Total 81 4 5 3a Author’s unpublished data.Figure 24-1 Prolactin cell hyperplasia adjacent to a denselygranulated GH cell adenoma (above and left). Antiprolactin,hematoxylin, ×110.Figure 24-2 Prolactin cell hyperplasia adjacent to a sparsely granulatedGH cell adenoma: prolactin cells (P) with sparse secretorygranules and slightly increased rough endoplasmic reticulum. Uranyl–acetate–leadcitrate, ×6100.
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DIAGNOSIS AND MANAGEMENT OFPITUITAR
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To my beloved Hazel, whose love and
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PrefacePituitary tumors represent a
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ContributorsCHARLES F. ABBOUD, MD,
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Color PlatesColor Plates appear aft
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2 RANDALL, SCHEITHAUER, AND KOVACSF
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4 RANDALL, SCHEITHAUER, AND KOVACSr
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6 RANDALL, SCHEITHAUER, AND KOVACSw
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10 RANDALL, SCHEITHAUER, AND KOVACS
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12 RANDALL, SCHEITHAUER, AND KOVACS
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14 RHOTONFigure 2-1 Osseous relatio
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16 RHOTONFigure 2-3 Septa in the sp
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18 RHOTONFigure 2-5 Stepwise dissec
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20 RHOTONFigure 2-7 (continued on n
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22 RHOTONFigure 2-8 (continued on n
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24 RHOTONFigure 2-9 Relationships i
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26 RHOTONFigure 2-11 Six sagittal s
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28 RHOTONFigure 2-13 (continued on
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30 RHOTONFigure 2-15 Anterosuperior
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32 RHOTONFigure 2-17 (continued on
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34 RHOTONFigure 2-18 Right anterior
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36 RHOTONOPHTHALMIC ARTERY The opht
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38 RHOTONFigure 2-21 Anterior cereb
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40 RHOTONcrosses the optic chiasm t
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42 GOTH, MAKARA, AND GERENDAIFigure
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44 GOTH, MAKARA, AND GERENDAImedial
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46 GOTH, MAKARA, AND GERENDAIplatel
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48 GOTH, MAKARA, AND GERENDAIcomple
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50 GOTH, MAKARA, AND GERENDAImembra
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52 GOTH, MAKARA, AND GERENDAITable
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54 GOTH, MAKARA, AND GERENDAITable
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CHAPTER 4 / EPIDEMIOLOGY OF PITUITA
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Taiwan-South part, 1983-1992 23.2%
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72 SHIMON AND MELMEDTable 1G Protei
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74 SHIMON AND MELMEDnal allelic mut
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76 SHIMON AND MELMEDgrowth factor s
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78 SHIMON AND MELMED35. Lowy DR, Wi
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CHAPTER 6 / TUMORIGENESIS EXPERIMEN
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CHAPTER 7 / PITUITARY ADENOMAS AND
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CHAPTER 8 / MOLECULAR PATHOLOGY 155
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166 VANCETable 1Lesions of the Sell
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168 VANCEFigure 9-1 Twenty-four-hou
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170 VANCEclude that every neurosurg
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172 VANCEgaly, prolactinoma). Pitui
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174 STIVER AND SHARPEFigure 10-1 Co
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176 STIVER AND SHARPEFigure 10-5 Cr
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178 STIVER AND SHARPEFigure 10-8 Fi
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180 STIVER AND SHARPETable 1Inciden
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182 STIVER AND SHARPEFigure 10-11 (
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184 STIVER AND SHARPEFigure 10-13 F
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186 STIVER AND SHARPEFigure 10-15 F
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188 STIVER AND SHARPEFigure 10-17 W
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190 STIVER AND SHARPEpituitary apop
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192 STIVER AND SHARPEin extrafoveal
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194 STIVER AND SHARPEinto the empty
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196 STIVER AND SHARPE5. Hoyt WF. Co
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198 STIVER AND SHARPE104. Wertenbak
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200 STIVER AND SHARPE204. Nakane T,
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202 EMERY AND KUCHARCZYKFigure 11-1
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216 EMERY AND KUCHARCZYK3. Kulkarni
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CHAPTER 12 / PET IN SELLAR TUMORS 2
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CHAPTER 13 / PITUITARY SURGERY 2251
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CHAPTER 13 / PITUITARY SURGERY 227F
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CHAPTER 13 / PITUITARY SURGERY 235T
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CHAPTER 13 / PITUITARY SURGERY 237h
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CHAPTER 13 / PITUITARY SURGERY 2451
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CHAPTER 14 / MEDICAL THERAPY 24714M
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CHAPTER 14 / MEDICAL THERAPY 249Tab
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CHAPTER 14 / MEDICAL THERAPY 251One
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CHAPTER 14 / MEDICAL THERAPY 253Fig
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CHAPTER 14 / MEDICAL THERAPY 255and
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CHAPTER 14 / MEDICAL THERAPY 257abs
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CHAPTER 14 / MEDICAL THERAPY 259but
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CHAPTER 14 / MEDICAL THERAPY 26124.
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CHAPTER 14 / MEDICAL THERAPY 263110
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270 MOOSE AND SHAWtherapy and compa
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272 MOOSE AND SHAWCUSHING’S SYNDR
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274 MOOSE AND SHAWFor patients with
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276 MOOSE AND SHAW19. Gomez F, Reye
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CHAPTER 16 / PROLACTINOMAS 27916Pro
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CHAPTER 16 / PROLACTINOMAS 281In th
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CHAPTER 16 / PROLACTINOMAS 283resol
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CHAPTER 16 / PROLACTINOMAS 285term
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CHAPTER 16 / PROLACTINOMAS 287Figur
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CHAPTER 16 / PROLACTINOMAS 289level
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CHAPTER 16 / PROLACTINOMAS 291Optio
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CHAPTER 16 / PROLACTINOMAS 29398. B
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CHAPTER 17 / ACROMEGALY 29517Somato
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CHAPTER 17 / ACROMEGALY 297Figure 1
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CHAPTER 17 / ACROMEGALY 299pedograp
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CHAPTER 17 / ACROMEGALY 301Table 1C
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CHAPTER 17 / ACROMEGALY 303In histo
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CHAPTER 17 / ACROMEGALY 305Table 2D
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CHAPTER 17 / ACROMEGALY 307must be
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CHAPTER 17 / ACROMEGALY 30973. Åst
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CHAPTER 17 / ACROMEGALY 311143. Van
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CHAPTER 17 / ACROMEGALY 313213b. Sh
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CHAPTER 17 / ACROMEGALY 315266. Shi
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318 LO, TYRRELL, AND WILSONTable 1C
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320 LO, TYRRELL, AND WILSONFigure 1
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322 LO, TYRRELL, AND WILSONFigure 1
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324 LO, TYRRELL, AND WILSONterm cur
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326 LO, TYRRELL, AND WILSON(118). O
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328 LO, TYRRELL, AND WILSONREFERENC
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330 LO, TYRRELL, AND WILSON70. Mill
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332 LO, TYRRELL, AND WILSON157. Nel
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334 BUCHFELDER AND FAHLBUSCHsized o
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336 BUCHFELDER AND FAHLBUSCHimmunoh
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338 BUCHFELDER AND FAHLBUSCHFigure
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340 BUCHFELDER AND FAHLBUSCHFigure
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342 BUCHFELDER AND FAHLBUSCH39. Gri
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344 YOUNGFigure 20-1 Serum prolacti
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346 YOUNGFigure 20-3 Images from a
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348 YOUNGFigure 20-5 Visual fields
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350 YOUNGFigure 20-7 Serial MRI fro
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CHAPTER 21 / PEDIATRIC PITUITARY TU
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370 PERNICONE AND SCHEITHAUERFigure
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384 PERNICONE AND SCHEITHAUER32. Th
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CHAPTER 23 / SELLAR TUMORS 38723Sel
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CHAPTER 23 / SELLAR TUMORS 389mode
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CHAPTER 23 / SELLAR TUMORS 391Figur
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Page 472 and 473: 456 SAEGERabnormality of the arachn
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Page 483 and 484: INDEXABC peroxidase method, 94Acrom
Page 485 and 486: INDEX 469Chordomas (cont.) Cranioph
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Page 489 and 490: INDEX 473Invasion (cont.)Lymphomas
Page 491 and 492: INDEX 475Osteogenic sarcomas, 416-4
Page 493 and 494: INDEX 477Pro-opiomelanocortin (POMC
Page 495: INDEX 479Visual outcomes (cont.) Vi
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Diagnosis and Management of Pituitary Tumors

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