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Neurology India, Vol. 58, No. 3, May-June, 2010, pp. 341-342 Editorial Non-functional pituitary adenomas Geeta Chacko Section of Neuropathology, Departments of Neurological Sciences and Pathology, Christian Medical College, Vellore - 632 004, India Date of Acceptance: 31-Jan-2010 Code Number: ni10095 PMID: 20644259 In this issue of the journal, Rishi et al. present a series of non-functional pituitary adenomas, seen over a 1.5-year period in a single institution. Not surprisingly, the authors demonstrate that a significant proportion of clinically non-functional adenomas show immunohistochemical evidence of hormone production. Their findings are predominantly confirmatory of previously published data and add to the growing literature on the immunoprofile of non-functional adenomas. [1],[2],[3],[4],[5],[6] The authors' conclusion that diagnosing subtypes such as gonadotroph adenomas will help selecting such patients for adjunctive medical therapies and is thus of clinical relevance, should be viewed with caution, particularly since at the present time there is no targeted medical therapy for this group of tumors. In fact, the ultimate clinical relevance lies not in the detection of null cell adenomas and gonadotroph adenomas, both of which have low rates of invasion, but rather in the detection of some of the aggressive subtypes of clinically non-functional adenomas. These aggressive subtypes include: 1) Silent corticotroph adenomas, subtypes I and II. [3],[7],[8] These tumors are unaccompanied by elevations in ACTH or clinical evidence of Cushing's disease but display immunopositivity for ACTH. They are usually invasive macroadenomas and have a higher potential for apoplexy and recurrence; 2) Acidophil stem cell adenomas. [9] These tumors are usually clinically non-functional, but are often associated with hyperprolactinemia. Immunohistochemically, they demonstrate production of growth hormone and prolactin. These tumors often display oncocytic change and in addition to ultrastructural evidence of growth hormone and prolactin production, contain gigantic mitochondria not seen in any other subtype. The recognition of this neoplasm is important because the lesions are prone to progressive growth and invasive behavior; 3) Silent adenoma, subtype 3. [5] These tumors may show minor immunopositivity for any combination of pituitary hormones, but could also be immunonegative for all and hence are an important differential to consider with null cell adenomas. These tumors are clinically silent or non-functional and are usually seen in the second and third decades in females and at any age in males. Ultrastructural examination shows that these are highly differentiated with resemblance to glycoprotein hormone producing adenomas. A distinctive feature however is the presence of pleomorphic nuclei containing multiple spheridia. They are reported to be highly infiltrative with a rapid growth rate and a high recurrence rate. Although dopamine agonists are found to reduce serum prolactin levels in this tumor, the tumor has been observed to continue to grow despite therapy. [1],[10],[11] The current World Health Organization (WHO) classification of the pituitary adenomas, formulated in 2004, [1] takes into consideration clinical, biochemical, surgical findings, neuroimaging as well as the histology, immunohistochemistry and ultrastructural features. The present study reiterates the fact that immunohistochemical analysis of pituitary adenomas, once considered a dispensable tool because of cost constraints, needs to be an integral part of every neuropathology core facility. References
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