Page 22 - Delaware Medical Journal - October 2017
P. 22
Two Cases of Adrenal Insufficiency
Caused by Isolated Bilateral Adrenal
Metastasis from Breast Cancer
Trisha Pascall-Lopez, DO; Michael J. Guarino, MD; David D. Biggs, MD; Randi LaPoint, MD; James Hays, MD
Breast cancer is a leading cause of death in women across the world. Invasive ductal carcinoma is responsible for metastasis to various organs. Isolated metastasis without disseminated disease can occur. Rarely, however, does invasive ductal carcinoma (IDC) metastasize to the adrenal glands without disseminated disease. Metastasis of any carcinoma to the adrenal glands does not typically cause adrenal insufficiency. This case study aims to demonstrate, although rare, adrenal insufficiency can occur from invasive ductal carcinoma of the breast metastasizing to the adrenal glands. Shown here are two cases of long-term survival with isolated bilateral adrenal metastasis treated without adrenalectomy.
Introduction
Breast cancer is currently the most frequently diagnosed cancer and leading cause of cancer death in women across
the world. Invasive ductal carcinoma (IDC) is the most common type of breast cancer and metastasis is usually to the lungs, liver, bones, and brain, but rarely
to the adrenal glands.1 Very few cases of IDC metastasize to the adrenal glands without disseminated metastases have been reported. Additionally, adrenal metastasis as most of the adrenal cortex has to be damaged before hypofunction can occur. In a study looking at 464 patients with adrenal metastasis over a 2 There are approximately six cases described in the literature of IDC with solitary adrenal metastasis.3 Here we report the only two from IDC of the breast metastasizing to bilateral adrenal glands after a prolonged disease free interval; and survival without adrenalectomy.
CASE REPORT
Patient #1: A 70-year-old female for tobacco abuse, tonsillectomy, appendectomy, hypothyroidism, and history of ductal invasive carcinoma
of the right breast presented to her oncologist for annual follow up in September 2016 without complaints.
She was found to have diffuse hyperpigmentation and weight loss. In 2001 she had been diagnosed with stage IIIA (pT2, pN2a, pM0) right breast IDC, 4 cm in size. Immunohistochemical evaluation showed estrogen receptor (ER) positive, progesterone (PR) positive, human epidermal receptor-2 (HER-2) negative. Seven of 31 removed axillary nodes were positive. The patient mastectomy and axillary lymph node dissection; adjuvant Doxorubicin + years of Tamoxifen then transitioned to Anastrozole, which was not tolerated, then subsequently completed four and a
half years of Letrozole. She was followed for 15 years after initial diagnosis and was without clinical evidence of cancer.
In September 2016, during a routine
hyperpigmentation (as shown in Figure 1 and 2) as well as a 20-pound weight Basic metabolic panel was unremarkable, complete blood count revealed a hemoglobin of 11.7 (previously normal), thyroid stimulating hormone was normal, free thyroxine was normal; cortisol level was low at 2.6 and adrenocorticotropic hormone (ACTH) was high at 983 October 2016 a computed tomography (CT) scan of the chest/abdomen/pelvis showed moderate thickening/nodularity of the medial and lateral limbs of both adrenal glands; with subsequent CT breast origin, which was ER positive,
PR positive, Her-2/neu equivocal by immunohistochemistry (Figure 3). She
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Del Med J | October 2017 | Vol. 89 | No. 10
Abstract
