Pathology Associates Of Lexington, P.A.
Pathology Associates Of Lexington, P.A.
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        Adrenal gland cancer vs. adenoma
      

As with thyroid gland masses, adrenal gland masses are often discovered incidentally during CT or MRI exams for other reasons. and are then termed adrenal incidentalomas . Most cortical tumors are straight-forwardly adenomas or carcinomas.

When to biopsy5? In a chinese study, the ratio of malignant to benign climbed to 1 in 8 (12.5%) at the 4CM size4. And, pre-biopsy features concerning for malignant behavior are irregular margins, image heterogeneity, contrast enhancement, intermediate T2 intensity, soft tissue density CT, and associated enlarged nodes4.

An adenoma is said to be thoroughly encapsulated2. When one is left in a sort of "indeterminate tumor" situation, it is possibly time for not only expert pathologist consultation but tertiary level clinical oncologist consultation: do we have more to gain by treating as a low grade cancer or by just following? Incidentally, when recording weight, there is "specimen weight" and there is "tumor weight" (a recent case was only 25% adenoma, 75% of total specimen weight being organizing intra-adenoma hemorrhage [LMC-05-575]). Cortical lesions under 50 grams are generally cured by excision; most carcinomas weigh 10 grams [about 3CM diameter] or more2. "Except for the cases situated at the two extremes, it may be more honest and accurate to designate the tumors as adrenocortical neoplasms followed by an estimate of the risk of the tumor recurring or metastasizing on the basis of all the evaluable parameters, the list of which is likely to increase further in the next few years2."

IHC is another line of evidence in cortical lesions. Renal cell carcinoma metastatic to the adrenal tends to be EMA positive, while adrenal cortical primaries tend to be EMA negative. We have a current (4/21/05) case...LMC-05-3324...of Conn's syndrome with the removed gland hyperplastic & with a dominant 1.0 cm nodule and lots of extra-glandular, peri-adrenal cellularity of cortical cells exactly similar to those in the gland (and the extra-glandular, peri-adrenal cellularity is vimentin positive & LMW-keratin negative)! Benign & malignant cortical tumors can be vimentin, keratin, and neurofilment positive; and adenoma and carcinoma are MELAN A positive3. Adenomata have a Ki-67 of 8% or less; cortical ca. has a Ki-67 over 8% & tending to be about 20%3.

Weiss is the Favored System:
system/criteria of Weiss (best2):
  1. Venous invasion (smooth muscle in wall)
  2. Mitotic rate > 5/50 HPF
  3. Atypical mitotic figures
  4. high Fuhrman nuclear grade
  5. Diffuse architecture (≥ 33% of tumor)
  6. Necrosis
  7. Eosinophilic tumor cell cytoplasm (≥ 75% of tumor cells)
  8. Sinusoidal invasion (no smooth muscle in wall)
  9. Capsular invasion
  10. these, above, are most highly correlated with recurrence or metastasis
system/criteria of Hough:

Numeric sum of the following (a group of 41 tumors): a mean of 2.91 when subsequent malignant behavior; a mean of 1.00 when indeterminate; a mean 0.17 when benign:

Criteria

Numeric value
Histologic Criteria  
  1. Diffuse growth pattern
 0.92
  1. Vascular invasion
 0.92
  1. Tumor cell necrosis
 0.69
  1. Broad fibrous bands
 1.00
  1. Capsular invasion
 0.37
  1. Mitotic index (1/10 HPF or more)
 0.60
  1. Pleomorphism (moderate/marked)
 0.39
Non-histologic Criteria  
  1. Tumor mass (≥ 100 g)
 0.60
  1. Urinary 17-ketosteroids (10 mg/g creatinine/24 hours)
 0.50
  1. Response to ACTH (17-hydroxysteroids increased two times after 50 µg ACTH IV)
 0.42
  1. Cushing's syndrome with virilism, virilism alone, or no clinical manifestations
 0.42
  1. Weight loss (10 lb/3 months)
 2.00
system/criteria of Van Slooten:

If numeric sum of the following is 8 or higher, correlates highly with subsequent malignant behavior (a group of 45 cases with 10 year follow up):
  1. Extensive regressive changes (necrosis, hemorrhage, fibrosis, calcification)
 5.7
  1. Loss of normal structure
 1.6
  1. Nuclear atypia (moderate/marked)
 2.1
  1. Nuclear hyperchromasia (moderate/marked)
 2.6
  1. Abnormal nucleoli
 4.1
  1. Mitotic activity (2/10 HPFs)
 9.0
  1. Vascular or capsular invasion
 3.3

References:

  1. Weidner, Noel, The Difficult Diagnosis in Surgical Pathology, 944 pages (in EBS's office); 1996.
  2. Rosai J, Rosai AND Ackerman's Surgical Pathology, 9th Ed., p. 1118-1142, 2004.
  3. Ronald A. DeLellis , MD, Pathologist-in-Chief @ Lifespan Academic Med. Ctr in Providence, Rhode Island. He has served on key committees, including the WHO Project on Classification of Endocrine Tumoprs. He was a speaker at The Second International Course in Applied Immunohistochemistry and Molecular Pathology (Santa Barbara, Calif. 1/28/08-2/1/08).
  4. comprehensive e-Medicine website overview HERE.
  5. American College of Radiology (2000) biopsy appropriateness criteria guidelines HERE.
  6. Mayo Clinic info HERE.
  7. UMCCC Endocrine Oncology Program is one of the only fully-integrated, interdisciplinary clinics (as of early 2010) for adrenal patients in the world HERE (& I'd guess Mayo).

      (posted 20 December 2003; latest addition 29 March 2010)
 
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