Adrenal Gland, Cortex - Hypertrophy







comment:
Adrenal cortical hypertrophy refers to an increased cell size without an appreciable increase in cell numbers. Hypertrophic cortical cells have increased amounts of cytoplasm, which may be pale to brightly eosinophilic ( Figure 1








Diffuse cortical hypertrophy ( Figure 5




Cortical hypertrophy (of the zona fasciculata) in rats and mice usually results from elevated levels of adrenocorticotropic hormone (ACTH), which in turn can be elevated due to various causes, such as primary hypothalamic or pituitary disease or decreased glucocorticoid feedback regulation caused by adrenal cortical toxic or degenerative lesions. Diffuse, bilateral, and often prominent hypertrophy in the zona fasciculata can also be a sequela to stress from various causes, a finding that is especially common in rats.
Hypertrophy (and hyperplasia) of zona glomerulosa cells can result from derangements of the renin-angiotensin system that result in elevated angiotensin II.
Whether focal or diffuse, cortical hypertrophy is generally not considered to be a preneoplastic change. However, cortical hypertrophy (increased cell size) and hyperplasia (increased cell numbers) can often be concurrent lesions in the same gland or even in the same focus. Thus, as a practical matter, determining which change is predominant in a given lesion and/or gland can be very difficult. Cortical hypertrophy can also be confused with the cortical cell enlargement that occurs in many cases of cytoplasmic vacuolization.
recommendation:
Adrenal cortical hypertrophy should be diagnosed and assigned a severity grade and appropriate distribution modifier (i.e., focal, diffuse). The modifier "bilateral" should be used when hypertrophy is present in both glands. An attempt should be made to distinguish cortical hypertrophy from hyperplasia, though the frequent superimposition of both changes in the same lesion can make this determination very challenging. In cases where both findings are concurrent in the same focus, only hyperplasia should be recorded, with the hypertrophy feature described in the pathology narrative. If there are a small number of atypical cells in the focus of hypertrophy, they should be described in the narrative. However, if the pathologist feels there is a large enough proportion of atypical cells, cellular atypia should be diagnosed (see Adrenal Gland, Cortex - Cellular Atypia).related links:
Adrenal Gland, Cortex - Cellular Atypiareferences:
Brix AE, Nyska A, Haseman JK, Sells DM, Jokinen MO, Walker NJ. 2005. Incidences of selected lesions in control female Harlan Sprague-Dawley rats from two-year studies performed by the National Toxicology Program. Toxicol Pathol 33:477-483. Abstract: https://www.ncbi.nlm.nih.gov/pubmed/16036865
Dunn TB. 1970. Normal and pathologic anatomy of the adrenal gland of the mouse, including neoplasms. J Natl Cancer Inst 44:1323-1389. Abstract: http://jnci.oxfordjournals.org/content/44/6/1323.abstract
Ferreira JC, Cruz CD, Neves D, Pignatelli D. 2007. Increased extracellular signal regulated kinases phosphorylation in the adrenal gland in response to chronic ACTH treatment. J Endocrinol 192:647-658. Abstract: https://www.ncbi.nlm.nih.gov/pubmed/17332532
Frith CH, Botts S, Jokinen MP, Eighmy JJ, Hailey JR, Morgan SJ, Chandra M. 2000. Non-proliferative lesions of the endocrine system in rats, E-1. In: Guides for Toxicologic Pathology. STP/ARP/AFIP, Washington, DC. Full Text: https://www.toxpath.org/docs/SSNDC/EndocrineNonprolifRat.pdf
Hamlin MH, Banas DA. 1990. Adrenal gland. In: Pathology of the Fischer Rat: Reference and Atlas (Boorman GA, Eustis SL, Elwell MR, Montgomery CA, MacKenzie WF, eds). Academic Press, San Diego, 501-518. Abstract: https://www.ncbi.nlm.nih.gov/nlmcatalog/9002563
Harvey PW, Sutcliffe C. 2010. Adrenocortical hypertrophy: Establishing cause and toxicological significance. J Appl Toxicol 30:617-626. Abstract: https://www.ncbi.nlm.nih.gov/pubmed/20687119
Mazzocchi G, Rebuffat P, Belloni AS, Robba C, Nussdorfer GG. 1980. An ultrastructural stereologic study of the effects of angiotensin II on the zona glomerulosa of the rat adrenal cortex. Acta Endocrinol 95:523-527. Abstract: https://www.ncbi.nlm.nih.gov/pubmed/7006292
McEwan PE, Lindop GB, Kenyon CJ. 1996. Control of cell proliferation in the rat adrenal gland in vivo by the renin-angiotensin system. Am J Physiol (Endocrinol Metab) 34:E192-E198. Abstract: https://www.ncbi.nlm.nih.gov/pubmed/8760097
National Toxicology Program. 2006. NTP TR-520. Toxicology and Carcinogenesis Studies of 3,3',4,4',5-Pentachlorobiphenyl (PCB 126) (CAS No. 57465-28-8) in Female Harlan Sprague-Dawley Rats (Gavage Studies). NTP, Research Triangle Park, NC. Abstract: https://ntp.niehs.nih.gov/go/9301
National Toxicology Program. 2013. NTP TR-578. Toxicology and Carcinogenesis Studies of Gingko biloba Extract in F344/N Rats and B6C3F1 Mice (Gavage Studies). NTP, Research Triangle Park, NC. Abstract: https://ntp.niehs.nih.gov/go/37193
Nyska A, Maronpot RR. 1990. Adrenal gland. In: Pathology of the Mouse: Reference and Atlas (Maronpot RR, Boorman GA, Gaul BW, eds). Cache River Press, Vienna, IL, 509-536. Abstract: http://www.cacheriverpress.com/books/pathmouse.htm
Ulrich-Lai YM, Figueiredo HF, Ostrander MM, Choi DC, Engeland WC, Herman JP. 2006. Chronic stress induces adrenal hyperplasia and hypertrophy in a subregion-specific manner. Am J Physiol (Endocrinol Metab) 291:E965-E973. Abstract: https://www.ncbi.nlm.nih.gov/pubmed/16772325
Web page last updated on: January 02, 2015