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Oxaliplatin is a commonly used chemotherapy drug for tumors such as colorectal cancer. Oxaliplatin-based chemotherapy can cause liver parenchymal damage manifested by steatosis, sinusoidal obstruction syndrome, and nodular regenerative hyperplasia.
Recently, BMJ Case Reports reported that a patient with rectal adenocarcinoma had a significant increase in the volume of low-density lesions in the liver after receiving chemotherapy, and the tumor was suspected of recurrence and metastasis. However, after a multidisciplinary team discussion, it was found that things were not as they seemed, and the "transfer" seemed to be closely related to oxaliplatin.
The following is a detailed summary of the case and an explanation of the identification, diagnosis and treatment process. If similar cases are encountered in clinical practice, they should be carefully identified to avoid unnecessary changes in treatment regimens.
Details of the case
The patient, a 49-year-old male, was admitted to the hospital with rectal bleeding and was diagnosed with rectal adenocarcinoma.
PET-CT assessment staging showed thickening of the rectal and upper anal canal walls with increased radionuclide uptake, multiple mesenteric and submesenteric lymph node metastases. No liver, lung, or bone metastases. In addition, posterior peritoneal lymph node involvement may be seen, excluding metastases. Diagnosed with stage III.A (cT2N1M0) rectal cancer.
Patients received 3 cycles of neoadjuvant chemotherapy with a FOLFOX4 regimen, followed by concurrent chemoradiotherapy with capecitabine (click for package insert). Follow-up PET-CT showed that the metabolically active area of the rectum was relatively stable, and there was no significant enlargement of the mesentery and submesenteric lymph nodes.
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The patient underwent anterior resection and ileostomy. Histopathology showed pathologic complete response (ypT0N0). Chemotherapy was continued with the FOLFOX4 regimen for 3 cycles after surgery. Patients tolerate chemotherapy well.
At follow-up after 6 months, the patient was asymptomatic. PET-CT was performed to assess disease status. Scan showed de novo metabolically inactive hypodense lesions in segment VI of the liver (Figure 1). Carcinoembryonic antigen (CEA) and liver function tests are normal.
图1 PET-CT（来源DOI：10.1136/bcr-2019-232628）
CT-guided liver biopsy was performed, and pathology showed no evidence of malignancy. Follow-up continued, and after 6 months, PET-CT showed that the liver lesions were stable and there was no evidence of metabolic activity.
After 6 months of follow-up, PET-CT showed that the volume of low-density lesions in liver segment VI was significantly increased, and the metabolic activity was increased (SUV 8), which was suspected to be malignant (Fig. 2).
图2 PET-CT（来源DOI：10.1136/bcr-2019-232628）
CT-guided liver biopsy was performed, and histopathology showed sinusoidal dilation with noncaseating granulomatous inflammatory features (Fig. 3).
Fig.3 Pathology of liver lesions (source: DOI: 10.1136/bcr-2019-232628)
At this point, the patient remains asymptomatic. History is followed up, and the patient is not taking other drugs that can cause liver granulomas. Serum ACE was 73.8 U/L (normal range: 8~52 U/L). CT showed no signs of sarcoidosis such as hilar lymph nodes or lung lesions. negative test for Mycobacterium tuberculosis and fungi; Negative test for viral markers such as hepatitis B, hepatitis C, and human immunodeficiency virus. CEA levels are normal.
After 3 months, PET-CT was followed up, and the volume of the metabolically active area of the liver was further increased, and new hypermetabolic small lesions (SUV 3.9) were developed in the caudate lobe of the liver, and metastasis was suspected (Fig. 4).
图4 PET-CT（来源DOI：10.1136/bcr-2019-232628）
What do you think is the "recurrent metastasis" in this case? What's next?
Is this liver lesion to fault with oxaliplatin? How to distinguish and diagnose it clinically?
Scan the QR code below or click "Read the original article" at the end of the article to learn relevant differential diagnosis skills and understand the follow-up treatment plan!
Bibliography:
[1] Sarathy V, et al. FOLFOX and capecitabine-induced hepatic granuloma mimicking metastasis in a rectal cancer patient. BMJ Case Rep. 2020; 13(3):e232628. [2] Aedma SK, et al. Oxaliplatin-associated sarcoid-like reaction masquerading as recurrent colon cancer. BMJ Case Rep. 2020; 13(9):e229548. [3] Chopra A, et al. Drug-Induced Sarcoidosis-Like Reactions. Chest. 2018; 154(3):664-677.
[4] Choi JH, et al. Sarcoidosis associated with oxaliplatin-based chemotherapy for colorectal cancer. Case Rep Oncol Med. 2014:2014:203027. [5] Wildner D, et al. Granulomatous lung disease requiring mechanical ventilation induced by a single application of oxaliplatin-based chemotherapy for colorectal cancer: a case report. Case Rep Oncol Med. 2013:2013:683948.
[6] Baughman RP, et al. New treatment strategies for pulmonary sarcoidosis: antimetabolites, biological drugs, and other treatment approaches. Lancet Respir Med. 2015; 3(10):813-22.
Source of this article: Yijia Medical Class
Editor in charge: Sheep
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