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Liver Mass in a Patient With Chronic Hepatitis B Infection

Stout, Jessica MD1; Ireland, James D. MD2; George, Nayana MD1; Rude, Mary Katherine MD1; Thandassery, Ragesh B. MD1

doi: 10.14309/crj.0000000000000175
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1Division of Gastroenterology, Department of Medicine, Central Arkansas Veterans Health Care System, Little Rock, AR

2Diagnostic and Therapeutic Imaging Services, Central Arkansas Veterans Health Care System, Little Rock, AR

Correspondence: Ragesh B. Thandassery, MD, Department of Medicine, 111 LR Central Arkansas Veterans Healthcare System, 4300 W 7th St, Little Rock, AR 72205 (doc.ragesh@gmail.com).

Received January 16, 2019

Accepted June 14, 2019

Online date: October 23, 2019

This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal.

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CASE REPORT

A 59-year-old man was brought in for evaluation and management of incidentally detected chronic hepatitis B virus (HBV) infection. He was being prepared for surgery to treat his carpal tunnel syndrome and was found to have mediastinal, cervical, and axillary lymphadenopathy. A fine-needle aspiration of the right axillary lymph node revealed marginal zone lymphoma. He had no symptoms related to lymphoma. His complete hemogram and lactate dehydrogenase levels were normal. He did not show any symptoms of chronic liver disease. He had left-sided nephrectomy and splenectomy in 1979 following trauma and cholecystectomy in 1995. His liver function tests and alfa-fetoprotein levels were normal.

HBV profile revealed HBeAb-negative chronic hepatitis with low HBV DNA levels. Abdominal ultrasound revealed an echogenic lesion measuring 3.7 cm in the left lobe of liver. He underwent magnetic resonance imaging (MRI), which showed a 3.6 × 6.1 × 2.8-cm bilobed subcapsular lesion in the left lobe of the liver (Figure 1). Multiple tiny lesions with the same enhancement pattern as the liver lesion were seen along the posterior abdominal wall (Figure 1). We obtained an autologous technetium-99m-tagged red blood cell scan with single-photon emission computed tomography imaging to confirm or exclude ectopic splenic tissue. It revealed a focus of increased uptake in the left lobe of the liver suggestive of intrahepatic splenosis (IHS) (Figure 2).

Figure 1

Figure 1

Figure 2

Figure 2

Splenosis represents fragment implants in sites other than the splenic bed. They develop into small spleens, which have typical functions like the spleen.1 Heterotopic implantation is seen in up to 67% of cases following splenic rupture.1 They are different from an accessory spleen, which derives blood supply from the splenic artery. Splenosis is usually asymptomatic, but can cause recurrent abdominal pain, adhesive intestinal obstruction, infarction, hematoma, hydroureteronephrosis, or, rarely, gastrointestinal bleed.2 A definitive diagnosis requires a high index of suspicion. Asymptomatic splenosis does not require any treatment. IHS is a very rare presentation. It is hypothesized that portal vein embolization of erythrocyte progenitor cells and hypoxic stimulation of these progenitor cells inside the liver lead to development of IHS.3 Chronic hepatitis is a driver for tissue hypoxia and growth of splenic deposits.3,4 There are only about 20 cases of IHS reported, and half of them have underlying chronic hepatitis B or C indicating the role of tissue hypoxia in stimulating growth of splenic deposits.4 Because of increased enhancement during arterial phase on MRI and computed tomography, IHS is often misdiagnosed as hepatocellular carcinoma, neuroendocrine liver metastases, or hepatocellular adenoma.4 Diagnostic modality of choice is noninvasive nuclear scintigraphy with Tc-99m sulfur colloid scan or Tc-99m heat-damaged erythrocytes or indium-111–labeled platelets, which are more sensitive and specific for splenic uptake.5 In patients with chronic hepatitis and intrahepatic lesions, particularly in the left lobe and subcapsular location, IHS should always be excluded.

Repeat MRI after 3 months revealed stable liver lesion. He is under clinical follow-up for marginal zone lymphoma. If chemotherapy is initiated, he will require antiviral prophylaxis for HBV, with tenofovir or entecavir, to be continued for 6 months until completion of chemotherapy.

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DISCLOSURES

Author contributions: All authors contributed equally to this manuscript.

Financial disclosure: None to report.

Informed consent could not be obtained for this case report. All identifying information has been removed.

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REFERENCES

1. Schenkein DP, Ahmed E. Case 29-1995—A 65-year-old man with mediastinal Hodgkin's disease and a pelvic mass. N Engl J Med. 1995;333(12):784–91.
2. Ksiadzyna D. A case report of abdominal splenosis—A practical mini-review for a gastroenterologist. J Gastrointestin Liver Dis. 2011;20(3):321–32.
3. Kwok CM, Chen YT, Lin HT, Su CH, Liu YS, Chiu YC. Portal vein entrance of splenic erythrocytic progenitor cells and local hypoxia of liver, two events cause intrahepatic splenosis. Med Hypotheses. 2006;67:1330–2.
4. Sato N, Abe T, Suzuki N, et al. Intrahepatic splenosis in a chronic hepatitis C patient with no history of splenic trauma mimicking hepatocellular carcinoma. Am J Case Rep. 2014;15:416–20.
5. Short NJ, Hayes TG, Bhargava P. Intra-abdominal splenosis mimicking metastatic cancer. Am J Med Sci. 2011;341(3):246–9.
© 2019 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of The American College of Gastroenterology.