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Case Reports
. 2022 Jun 29;14(6):e26438.
doi: 10.7759/cureus.26438. eCollection 2022 Jun.

Brain and Adrenal Metastasis From Unknown Primary Tumor: A Case Report

Affiliations
Case Reports

Brain and Adrenal Metastasis From Unknown Primary Tumor: A Case Report

Ryo Katsumata et al. Cureus. .

Abstract

The clinical management of brain metastasis (BM) and adrenal metastasis (AM) of cancer of unknown primary (CUP) can be challenging. A 73-year-old man presented to the hospital with sudden-onset hemiplegia. His laboratory data were normal, except for elevated levels of carcinoembryonic antigen (CEA) (33.8 ng/mL). Contrast-enhanced magnetic resonance imaging revealed a 2-cm mass with ring enhancement in the right parietal lobe and extensive vasogenic edema around the tumor. The lesion was diagnosed as BM; however, we could not detect the primary origin by fluorodeoxyglucose (FDG) positron emission tomography-computed tomography (PET-CT). Stereotactic radiotherapy was then administered, resulting in reduced tumor size and relief of symptoms. Follow-up after one year revealed an elevated CEA level (148.6 ng/mL) and remarkable fluorodeoxyglucose (FDG) uptake in the right adrenal gland, with an area of enhancement of 20 mm, on FDG-positron emission tomography computed tomography, with normal findings in other distant organs. He underwent adrenalectomy, and the adrenal tumor was diagnosed as a poorly differentiated adenocarcinoma likely of lung origin based on the histopathologic and immunohistochemistry findings of cytokeratin (CK) 7 (+), CK 20 (-), thyroid transcription factor-1 (TTF-1) (+), inhibin (-), napsin A (+), prostate-specific antigen (PSA) (-), caudal type homeobox 2 (CDX-2) (-), synaptophysin (-), and p40 (-). Metastatic tumors of unknown primary origin remain latent. Aggressive treatment of these lesions can be beneficial for symptom relief, diagnosis, and prolongation of survival.

Keywords: adrenal metastasis of unknown primary; brain metastasis of unknown primary; cancer of unknown primary; carcinoembryonic antigen; stereotactic radiotherapy.

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Conflict of interest statement

The authors have declared that no competing interests exist.

Figures

Figure 1
Figure 1. Magnetic resonance image of brain.
(A) Contrast-enhanced magnetic resonance image revealing a 2-cm mass with ring enhancement in the right parietal lobe in the post-contrast T1-weighted condition (orange arrow). (B) Extensive vasogenic edema (green arrows) was confirmed by fluid-attenuated inversion recovery. (C) Reduced tumor with ring enhancement (orange arrow) and (D) reduced vasogenic edema (green arrows) after radiotherapy.
Figure 2
Figure 2. FDG positron emission tomography computed tomography at the time when brain tumor was detected.
(A and B) The images show unremarkable FDG uptake in distant organs from the brain. FDG: fluorodeoxyglucose
Figure 3
Figure 3. FDG positron emission tomography computed tomography after one-year surveillance period.
(A and B) The images show remarkable FDG uptake in the right adrenal gland with an enlargement area of 20 mm (white arrows). FDG: fluorodeoxyglucose
Figure 4
Figure 4. Pathological findings of the resected sample of adrenal gland.
Pathological examination of sample (A) demonstrates smooth white cut surface (B) and poorly differentiated solid carcinoma (C). (D) Hematoxylin and eosin staining of the tumor sample. Immunohistochemistry staining revealed (E) CK 7 (+), (F) CK 20 (-), (G) inhibin (-), (H) napsin A (+), and (I) TTF-1 (+). CK: cytokeratin; TTF-1: thyroid transcription factor-1
Figure 5
Figure 5. Clinical course of serum CEA level.
Clinical course of serum CEA level and therapeutic event demonstrated elevation of serum CEA level during follow-up period and prompt normalization after adrenalectomy. CEA: carcinoembryonic antigen

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