The Pathology of Pituitary Adenomas. I have nothing to disclose 10/13/2016. Pituitary Disorders: Advances in Diagnosis and Management

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1 The Pathology of Pituitary Adenomas Pituitary Disorders: Advances in Diagnosis and Management October 22, 2016 I have nothing to disclose Melike Pekmezci, MD University of California San Francisco Neuropathology and Ophthalmic Pathology Normal Pituitary Normal Pituitary 1

2 Pituitary adenoma Ultrastructural (densely vs sparsely granulated) Ultrastructural (densely vs sparsely granulated) Immunohistochemical 2

3 Cytodifferentiation Pathways Corticotroph Somatotroph T pit Rathke Pouch Stem Cell Pit 1 Somatotroph Stem Cell Mammosoma totroph SF 1 Gonadotroph Thyrotroph Ultrastructural (densely vs sparsely granulated) Immunohistochemical Typical vs Atypical Lactotroph Modified from Asa L. Practical Pituitary Pathology. Arch Pathol Lab Med. 2008;132: Ultrastructural (densely vs sparsely granulated) Typical vs Atypical Clinicopathologic Gonadotropin Family (FSH / LH Adenomas) Gonadotroph adenoma Silent gonadotroph adenoma SF 1 3

4 ACTH Family Densely granulated corticotroph adenoma Silent corticotroph type I Sparsely granulated corticotroph adenoma Silent corticotroph type II Crooke cell adenoma Densely Granulated Corticotroph Adenoma ACTH Sparsely Granulated Corticotroph Adenoma ACTH Crooke Cell Adenoma Keratin 80% macroadenoma, 72% invasive 60% recurrence rate (24 % multiple recurrences) 12% died, 8% after recurring as carcinoma George DH, et al. Am J Surg Path. 2003;10(27):

5 Why subclassify? Crooke s cell adenomas Silent corticotroph adenomas are more likely to present with invasion (than null cell)* # More likely to have high mitotic rate* More likely to show recurrence/progression* Silent subtype I adenomas are more likely to recur and/or progress (compared to silent subtype II and null cell)* TSH *Jahangiri, et al. Neurosurgery. 2013;73(1):8 17 # Ioachimescu, et al. Neurosurgery. 2012;71(2): Somatotroph adenomas Densely granulated somatotroph adenoma Sparsely granulated somatotroph adenoma (with fibrous bodies) Silent somatotroph adenoma GH Densely vs Sparsely Granulated GH 5

6 Why subclassify? Patients with acromegaly: 30 40% DGSA 20 30% SGSA 30 40% also Prolactin Patients with SGSA are younger* # SGSA tumors are larger* # SGSA tumors are more invasive # SGSA lower remission rate after surgery* SGSA decreased response to somatostatin analogs* # Syro L, et al. Pituitary. 2016;Epub ahead of print. PMID * Kiseljak Vassiliades K, et al. Endocrine. 2015;49(1): # Cuevas Ramos D, et al. J Clin Endoc Metab. 2015;100(1): Somatostatin receptor 2A Brzana J, et al. Pituitary. 2013;16(4): Kiseljak Vassiliades. et al. Molecular and Cellular Endocrinology. 2015;417: Somatotroph adenomas 3 Lacrotroph adenomas Sparsely granulated lactotroph adenoma Densely granulated lactotroph adenoma Silent lactotroph adenoma 2 Somatotroph adenomas 3 Lacrotroph adenomas 4 Somatotroph and Lactotroph Mixed somatotroph lactotroph adenoma Mammosomatotroph adenoma Acidophil stem cell adenoma (Lactotroph adenoma with GH reactivity) 6

7 Mixed Somatotroph Lactotroph Two cell population GH Mammosomatotroph Single cell population Acidophil Stem Cell Adenoma Lactotroph Adenoma with GH Reactivity Prolactin GH Prolactin ISH GH IHC Prolactin ISH Why subclassify? Patients with acromegaly: 30 40% also produce prolactin 20 25% mixed GH PRL 5 8% mammosomatotroph 3 6% plurihormonal 0.8% acidophil stem cell adenoma (ASCA) Decreased response to SSA (66%) compared to DGSA # Lower remission rates after surgery for mixed GH PRL adenomas (50%) * mammosomatotroph adenomas (42.9%)* ASCA always invasive, mostly treatment resistant Syro L, et al. Pituitary. 2016;Epub ahead of print. PMID # Brzana J, et al. Pituitary. 2013;16(4): * Kreutzer, et al. J Clin Endoc Metab. 2001;86(9): Saeger W, et al. Eur J Endoc. 2007;156: Somatotroph adenomas 3 Lacrotroph adenomas 4 Somatotroph and Lactotroph 5 Plurihormonal adenomas Silent subtype 3 adenoma (Pit 1 positive plurihorminal adenoma) 7

8 Pit 1 Silent Positive Subtype Plurihormonal 3 Adenoma Adenoma Invasive # * High MIB1 * Low remission rate # * High recurrence rate Null Cell Adenoma Negative for hormone stains Negative for transcription factors # Erickson D, et al. Clin Endoc. 2009;71(1):92 9. * Richardson TE, et al. JNEN 2015;74(12): Mete O. Modern Pathol. 2016;29(2): Red: Poor prognosis Functioning Nonfunctioning ACTH secreting Densely granulated ACTH Silent corticotroph subtype I Sparsely granulated ACTH Silent corticotroph subtype II Crooke cell adenoma GH secreting Densely granulated GH Sparsely granulated GH Silent somatotroph PRL secreting Sparsely granulated PRL Densely granulated PRL Silent lactotroph GH and PRL secreting Mixed GH PRL Mammosomatotroph Acidophil stem cell TSH secreting Thyrotroph Silent thyrotroph FSH/LH secreting Gonadotroph Silent gonadotroph Plurihormonal Unusual Pit 1 positive plurihormonalsilent subtype 3 None & no transcription factors Null cell References WHO Endocrine 2004 Asa L. Practical Pituitary Pathology. Arch PathLabMed. 2008;132: Brzana J, et al. Pituitary. 2013;16(4): Chiloiro S, et al. Neuroendocrinology 2015;101: Cuevas Ramos D, et al. J Clin Endoc Metab. 2015;100(1): Erickson D, et al. Clin Endoc. 2009;71(1):92 9. George DH, et al. Am J Surg Path. 2003;10(27): Ioachimescu, et al. Neurosurgery. 2012;71(2): Jahangiri, et al. Neurosurgery. 2013;73(1):8 17. WHO Endocrine 2017 Kiseljak Vassiliades K, et al. Endocrine. 2015;49(1): Kreutzer, et al. J Clin Endoc Metab. 2001;86(9): Mete O. Modern Pathol. 2016;29(2): Miermeister CP, et al. Acta Neuropathol Commun. 2015:3 50. Richardson TE, et al. JNEN 2015;74(12): Saeger W, et al. Eur J Endoc. 2007;156: Syro L, et al. Pituitary. 2016;Epub ahead of print. PMID Trouillas J, et al. Acta Neuropathol. 2013;126:

9 THANK YOU.??? 9

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