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Original Report |
1
Department of Radiology, University of Pennsylvania Medical School, First
Floor Silverstein, 3400 Spruce St., Philadelphia, PA 19104-4283.
2
Department of Radiology, Hackensack University Medical Center, 30 Prospect
St., Hackensack, NJ 07601.
Received May 30, 2000;
accepted after revision July 26, 2000.
Address correspondence to E. S. Siegelman.
Abstract
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CONCLUSION. Unusual patterns of hepatic steatosis can be seen on MR imaging. Such patterns result from localized high concentrations of insulin. A rim of hepatic steatosis surrounding insulinoma metastases and a subcapsular distribution of hepatic steatosis in patients with diabetes treated with peritoneal dialysis are two such patterns that can be revealed on chemical shift imaging.
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TopAbstractIntroductionDiscussionReferences |
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Pattern 1
A 27-year-old man with a history of distal pancreatectomy for insulinoma
presented with recurrent symptoms of hypoglycemia. His fasting serum glucose
level was 27 mg/dL (reference range, 70-110 mg/dL), and his serum insulin
level was 86 IU/mL (reference range, 5-25 IU/mL). Abdominal MR imaging was
performed at 1.5 T (Signa; General Electric Medical Systems, Milwaukee, WI) to
evaluate for recurrent tumor or metastatic disease. In-phase gradient-echo
images showed a 12-mm hypointense liver mass
(Fig. 1A). On the corresponding
opposed-phase image, a peripheral 3- to 7-mm rim of low signal intensity was
revealed, indicating peritumoral hepatic steatosis
(Fig. 1B). The mass revealed on
in-phase imaging, but not the rim of steatosis, showed early enhancement on
dynamic contrast-enhanced imaging (Fig.
1C).
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The patient underwent surgical reexploration with intraoperative sonography of the liver. A lesion in the dome of the right lobe of the liver, corresponding to the lesion revealed on MR imaging, showed a peripheral rim of increased echogenicity (Fig. 1D). This lesion was treated with radiofrequency ablation. Another superficial lesion in the anterior right lobe was excised, which revealed an islet cell metastasis with surrounding hepatic steatosis (Fig. 1E).
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Pattern 2
A 35-year-old woman with end-stage renal disease caused by diabetes
mellitus presented with epigastric pain and persistent nausea. Unenhanced
abdominal CT revealed an irregular peripheral rim of low attenuation in the
liver (Fig. 2A). Abdominal MR
imaging was performed for further characterization. In-phase gradient-echo
images showed an irregular, scalloped peripheral subcapsular rim of higher
signal intensity relative to adjacent hepatic parenchyma
(Fig. 2B), which revealed loss
of signal intensity on the corresponding opposed-phase image
(Fig. 2C), indicating the
presence of microscopic lipid and cellular water.
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TopAbstractIntroductionDiscussionReferences |
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Chemical shift MR imaging with in-phase and opposed-phase gradient-echo pulse sequences has been shown to be sensitive in revealing microscopic fatty change of the liver [4]. Loss of signal intensity of hepatic parenchyma between the in-phase and opposed-phase images indicates the presence of microscopic lipid.
The subcapsular pattern of hepatic steatosis shown in pattern 2 has been described in the pathology literature in patients undergoing peritoneal dialysis [6]. Wanless et al. [6] reported 10 cases with a discontinuous subcapsular rim of hepatic steatosis ranging from 0.05 to 2 mm in thickness. The deep margin of the steatosis was usually scalloped. This pattern was present only in patients whose dialysate contained insulin. The subcapsular steatosis tended to be more severe in patients with a longer duration of peritoneal dialysis, higher intraperitoneal insulin dose, greater obesity, or higher serum triglycerides.
In those patients with severe steatosis, the subcapsular hepatocytes are exposed to high concentrations of insulin and glucose from the hyperosmolar dialysate bathing the hepatic surface. Insulin and glucose diffuse through the hepatic capsule and are absorbed by the subcapsular hepatocytes [6].
Insulin has been shown to be important in the pathogenesis of hepatic steatosis [6, 7]. In the fasting state (low insulin), free fatty acids in the liver are preferentially oxidated to ketone bodies. In the fed state, high insulin levels inhibit oxidation of free fatty acids and promote the esterification of free fatty acids into triglycerides, which then accumulate in hepatocytes. Focal deposition of fat, mostly in the form of triglycerides, occurs when hepatic triglyceride synthesis exceeds secretion. Thus, the peripheral subcapsular pattern of hepatic steatosis could be explained by the higher insulin concentration in the periphery of the liver.
Similarly, this theory can explain the pattern of peritumoral hepatic steatosis seen in our patient with metastatic insulinoma. The focal rim of fatty infiltration surrounding the insulinoma metastasis is likely a result of local insulin production by the tumor. Higher local insulin levels can promote the synthesis and accumulation of lipid in hepatocytes adjacent to the metastasis. A wedge-shaped region of fatty infiltration has been described peripheral to an insulinoma metastasis on CT and is hypothesized to be related to decreased portal flow and focal metabolic changes [8]. This prior report supports the role of localized insulin in focal fatty infiltration. It is important to recognize that the metastasis is confined to the central portion without extension into the adjacent hepatic steatosis, so that the size of the metastasis is not overestimated.
The peritumoral and subcapsular segments of hepatic steatosis were isointense to hyperintense to normal liver on in-phase imaging. This finding has increased specificity for hepatocellular tissue and thus can exclude a diagnosis of metastatic insulinoma or peritoneal-based metastatic disease, respectively.
In conclusion, focal hepatic steatosis caused by the local effects of insulin can present in the patterns of a focal rim surrounding insulinoma metastases and a subcapsular distribution related to insulin-rich peritoneal dialysate. Chemical shift MR imaging can reveal and characterize these unusual patterns of fatty infiltration.
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