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Adrenocortical Carcinoma Treatment (PDQ®)

Cellular Classification of Adrenocortical Carcinoma

Adrenocortical carcinoma can be classified into functioning and nonfunctioning tumors by clinical and biochemical assessment. Approximately 60% of adrenocortical carcinomas produce hormones.[1] The associated clinical syndromes include the following:

  • Hypercortisolism (Cushing syndrome).
  • Hirsutism/virilization.
  • Feminization.
  • Precocious puberty.
  • Hyperaldosteronism.

Biochemical assessment aims to detect increased levels of cortisol (24-hour urine, 1 mg dexamethasone suppression test, serum adrenocorticotropic hormone and cortisol), androgens (dehydroepiandrosterone sulfate, testosterone), estrogens (estradiol) and mineralocorticoids (renin, aldosterone).

Pathology can differentiate high-grade and low-grade tumors according to the mitotic activity of the tumor. The differentiation of benign and malignant adrenocortical tumors can be achieved by determination of the Weiss score, which scores several histopathological criteria, including the following:[2]

  • Nuclear grade.
  • Number of mitoses.
  • Presence of atypical mitosis.
  • Percentage of clear cells.
  • Diffuse architecture.
  • Necrosis.
  • Venous invasion.
  • Sinusoidal invasion.
  • Capsular invasion.

References

  1. Allolio B, Fassnacht M: Clinical presentation and initial diagnosis. In: Hammer GD, Else T, eds.: Adrenocortical Carcinoma: Basic Science and Clinical Concepts. New York, Springer, 2010, pp 31-47.
  2. Weiss LM, Medeiros LJ, Vickery AL Jr: Pathologic features of prognostic significance in adrenocortical carcinoma. Am J Surg Pathol 13 (3): 202-6, 1989. [PUBMED Abstract]
  • Updated: November 15, 2012