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Logo of nihpaAbout Author manuscriptsSubmit a manuscriptHHS Public Access; Author Manuscript; Accepted for publication in peer reviewed journal;
 
Gastroenterology. Author manuscript; available in PMC 2011 March 1.
Published in final edited form as:
PMCID: PMC2945228
NIHMSID: NIHMS189211

Clinical Challenges and Images in GI: Glowing In The Dark: Not Always A Bad Thing

Question

A 55 year old male long distance runner of many years underwent evaluation for an unusual movement disorder of the right lower extremity. During the evaluation, a magnetic resonance angiogram of the abdomen, pelvis and lower extremities was performed to rule out intimal thickening and kinking ofpelvic arteries that could have contributed to some of his symptoms. An incidental finding of a 1.7cm lesion on the right lobe of the liver was identified (Figure 1).

Figure 1
T2-weighted image from a MRA of the abdomen. Arrow points to the 1.7cm lesion in the right liver lobe that was incidentally noted.

While undergoing hepatic evaluation, the patient denied any abdominal or associated symptomatology. Aside from his primary complaints, he did not have any significant medical history, and his only medication included daily aspirin intake. His physical exam and laboratory examination were unremarkable.

For better characterization of the unidentified mass, the patient underwent a triphasic computed tomography scan, which demonstrated a lesion that was hypodense on pre-contrast, hypervascular in the arterial phase, and isodense on delayed post-contrast images (Figure 2). As a definitive diagnosis had not been reached, he then underwent a 99mTc-sulfur-colloid liver-spleen scan, which clinched the diagnosis (Figure 3; Rotating image).

Figure 2Figure 2Figure 2
Triphasic CT of the abdomen. The mass is demonstrated to be hypodense on pre-contrast (2a), hypervascular in the arterial phase (2b), and isodense on delayed post-contrast (2c).
Figure 3
99mTc-sulfur-colloid liver-spleen scan. Arrow points to region of increased sulfur-colloid uptake.
Rotating Image
99mTc-sulfur-colloid liver-spleen scan demonstrating mass in the right lobe of the liver

What is the diagnosis?

Answer

The diagnosis of focal nodular hyperplasia (FNH) was made based on the findings of the 99mTc-sulfur-colloid liver-spleen scan, which showed increased sulfur-colloid uptake in the region of the mass, occurring in the first 40 seconds of the study. FNH, the second most common benign tumor of the liver following hemangioma, consists of a proliferation of normal hepatocytes and Kupffer cells.1, 2 It has an incidence of 5–8% in the adult population, with a 1:8 male to female ratio, and has been hypothesized to occur as a result of localized hepatocyte response to an underlying congenital or acquired defect of the arterial blood supply, leading to focal hyperperfusion of the hepatic parenchyma.1, 2

The differential diagnosis of a liver mass is vast, and hepatic adenomas (HA) are often confused with FNH. It is important to correctly differentiate between the two as HA's must often be resected, whereas FNH's are typically observed.2 Although radiologic approach consisting of CT or ultrasound, MRI, and scintigraphy has been advocated in differentiating FNH from HA, scintigraphy has been considered highly specific for FNH.2, 3 In a study by Herman et al, scintigraphy was found to have a sensitivity of 38.4% and specificity of 100%, and when this modality suggested the diagnosis, no future investigation was indicated.2 The typical finding in scintigraphy in FNH is normal or increased uptake, as the Kupffer cells that are present accumulate the sulfur-colloid that is used.2, 3 Note should be made that hypervascular malignant masses in the liver, such as hepatoma or neuroendocrine tumors, might have similar CT features to those presented here, however these would show as a “cold” area on scintigraphy.

In the presented patient the diagnosis was suspected following the CT scan and then confirmed with scintigraphy, thus saving the patient from unnecessary further procedures.

Acknowledgements

The authors thank Drs. Ahmed Gharib, MD, and James C. Reynolds, MD for their input into the case, as well as Priyantha Herath, MD PhD for the consultation and permission to publish.

Financial Support: This submission was supported by the Intramural Research Programs of the NIDDK, NIH.

Footnotes

Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

None of the authors has any financial interest or conflict of interest related to this submission.

References

1. Marin D, Brancatelli G, Federle MP, Lagalla R, Catalano C, Passariello R, Midiri M, Vilgrain V. Focal nodular hyperplasia: typical and atypical MRI findings with emphasis on the use of contrast media. Clin Radiol. 2008;63:577–85. [PubMed]
2. Herman P, Pugliese V, Machado MA, Montagnini AL, Salem MZ, Bacchella T, D'Albuquerque LA, Saad WA, Machado MC, Pinotti HW. Hepatic adenoma and focal nodular hyperplasia: differential diagnosis and treatment. World J Surg. 2000;24:372–6. [PubMed]
3. Shamsi K, De Schepper A, Degryse H, Deckers F. Focal nodular hyperplasia of the liver: radiologic findings. Abdom Imaging. 1993;18:32–8. [PubMed]