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C a s e  

1.19 

Figure 1.19.1  Figure 1.19.2  Figure 1.19.3 

A B C

Figure 1.19.4 

Figure 1.19.5 

Hi sto ry: 30-year-old woman with a long-standing his- (Figure 1.19.4A) and delayed (Figure 1.19.4B) phase 3D SPGR
tory of palpitations and lightheadedness; she recently was images demonstrate gradual hypoenhancement of the mass
hospitalized for severe hypertension with hypertensive relative to background liver. A 90-minute delayed hepatobili-
retinopathy ary phase image (Figure 1.19.4C) shows only minimal hyper-
intensity in the center of the lesion. Fused image from PET
I m ag in g F in din gs : Coronal SSFSE (Figure  1.19.1), CT (Figure  1.19.5) demonstrates intense radiotracer activity
axial fat-suppressed FSE T2-weighted (Figure  1.19.2), and corresponding to the mass.
diffusion-weighted (b=600 s/mm2) (Figure  1.19.3) images
demonstrate a hyperintense mass in the posterior right hepatic D i ag n o sis : Primary hepatic paraganglioma
lobe with very high central signal intensity. No associated
signal dropout could be seen on IP and OP T1-weighted C om m e n t: There are only a handful of case reports
SPGR images (images not shown). Note the signal loss ante- describing primary hepatic paragangliomas; these lesions
riorly, which is likely secondary to 3-T shading artifact (see are, of course, most commonly found in the adrenals, where
Case 17.6). Axial postgadolinium (Multihance) portal venous they are known as pheochromocytomas. Approximately 10% of

c h a p t e r 1. L i ve r :   F o c a l   M a s s e s   •   37
pheochromocytomas are extra-adrenal in location, and 75% The lesion is more hyperintense on the T2-weighted image
of these occur in the organ of Zuckerkandl, the retroperito- than the typical FNH, but it does appear to have a central scar.
neal chromaffin body adjacent to the abdominal sympathetic However, the hepatobiliary phase image removes FNH from
plexus extending from above the inferior mesenteric artery the differential diagnosis because there is no contrast reten-
origin through the aortic bifurcation, with most remaining tion. Although the lesion had no signal dropout from IP to
lesions found in the neck, chest, and bladder. OP images to suggest the presence of fat, there is no convinc-
Patients generally present with signs related to their exces- ing evidence on MRI to exclude adenoma from the differential
sive catecholamine production, including paroxysmal hyper- diagnosis.
tension, flushing, tachycardia, headaches, diaphoresis, and chest PET CT was performed after the MRI and following
pain, although they may also be completely asymptomatic. documentation of elevated serum catecholamine levels, since
Paragangliomas are responsible for a very small percentage of it was considered very unlikely that the hepatic mass repre-
hypertension (0.1%-0.5%), and the diagnosis, when clinically sented the primary tumor. The endocrinologists thought it
suspected, can be made by screening plasma metanephrine (99% represented either a metastasis or a benign red herring, but
sensitivity) or urinary vanillylmandelic acid (95% sensitivity). PET CT also failed to detect any additional lesions. The
The appearance of this lesion is certainly not diagnostic patient underwent subsegmental resection of the mass, with
of hepatic paraganglioma. The 2 major differential diagnostic pathology demonstrating a paraganglioma without evidence
considerations in a patient of this age are FNH and adenoma. of malignancy.

38  •   M ayo C l i n i c B o dy M R I C a s e   R e vi ew

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