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Magnetic Resonance Imaging · Molecular Imaging · Musculoskeletal Radiology Hepatobiliary-specific contrast agents are one of several classes of contrast Contrast agent–enhanced MR imaging of the liver and biliary tree is routinely Hepatobiliary-specific agents show promise in increasing the.
Table of contents
- Image Gallery
- MR contrast agents
- MR contrast agents
- Liver-specific agents for contrast-enhanced MRI: role in oncological imaging
Hemangiomas generally present typical imaging findings and are easily diagnosed by computed tomography or MRI with extracellular gadolinium contrast agent. However, the differentiation between FNH and adenoma is not always easy at conventional MRI, because both conditions may appear as nonspecific hypervascular lesions, generating anguish for the patient and challenging the physician, in addition to the cost and patient's anxiety with repeated examinations.
FNH is a benign lesion that does not require any intervention, while adenoma presents risk for malignization, necrosis and bleeding which might require emergency surgery. Hepatobiliary contrast allow for the differentiation between FNH and adenoma in most cases, even in those of small lesions. The typical FNH presents with septa and lobulated or microlobulated borders, with intermediate signal intensity on T1- and T2-weighted sequences, low lesion-organ contrast and homogeneous arterial contrast uptake, with decay in the subsequent phases, becoming isointense to the adjacent liver parenchyma.
The presence of central scar markedly hyperintense on T2-weighted and hypointense on T1-weighted sequences, with no contrast uptake in the arterial phase and late contrast uptake is typical. However, in some cases, especially those of small lesions without central scar , one cannot differentiate between FNH and adenoma due to overlapping imaging findings 1 , 4. FNH presents greater density of functioning hepatocytes than a healthy liver parenchyma, in association with abnormal bile ducts which do not communicate with greater bile ducts, with consequential slower biliary excretion as compared with the surrounding liver.
Therefore, FNH presents contrast uptake greater or equal to the adjacent liver parenchyma in the hepatobiliary phase 4 Figures 1 and 2. However, the presence of intralesional fat was detected on out-of-phase T1-weighted sequence. The presence of intralesional fat is not usually found in FNH and suggests the diagnosis of adenoma — adenomatosis, in the present case —, with a very different prognosis and approach. On the other hand, the lesions showed homogeneous hepatobiliary contrast uptake, hence the highest likelihood of the diagnosis of multiple FNHs.
Homogeneous hepatobiliary contrast uptake indicates the diagnosis of FNH. Adenomas are well defined, homogeneous or heterogeneous lesions. The largest ones tend to present signal heterogeneity, with mild to moderate hypersignal on T2-weighted, hyposignal on T1-weighted sequences, homogeneous or heterogeneous arterial contrast-enhancement, late washout, and possible development of capsule Adenomas are composed of hepatocytes containing glycogen and lipids surrounded by a capsule. Although containing functioning hepatocytes, there is a lack of biliary ducts resulting in deficiency in bilirubin and hepatobiliary contrast excretion.
Additionally, adenomas present smaller expression of membrane transporters such as OATP1 1 , 2. Thus, in the hepatobiliary phase, most adenomas are hypointense in relation to the surrounding parenchyma Figure 3.
Rarely, there is hepatobiliary contrast uptake by adenomas and, in cases where it occurs, such an uptake tends to be preferentially peripheral in the hepatobiliary phase 1 , 2 , 4. The smallest lesion arrowheads presents subtle hypersignal on T2-weighted and marked signal loss on out-of-phase T1-weighted sequence caused by the presence of intralesional fat. No hepatobiliary contrast uptake is observed.
The presence of intralesional fat and the absence of hepatobiliary contrast uptake indicate a probable diagnosis of adenoma. The largest lesion arrows presents high signal intensity on T2-weighted, hyposignal on t1-weighted sequence, and nodular, peripheral and discontinuous uptake in the arterial-phase, and no hepatobiliary contrast uptake that is a typical hemangioma behavior. Hemangiomas do not contain functioning hepatocytes so uptake of this contrast medium is not observed.
Also, in the delayed-phase, the fill-in pattern is not observed, which might occur with the utilization of hepatobiliary contrast agent. Hemangiomas normally have a typical presentation at MRI with extracellular contrast and are not an indication for investigation with hepatobiliary contrast. At conventional MRI, hemangiomas present marked hypersignal on T2-weighted, hyposignal on T1-weighted sequences, discontinuous, nodular, peripheral contrast enhancement in the arterial phase, tending to centripetal fill-in by the contrast agent in the subsequent phases 13 , However, considering that hemangiomas are common lesions, they will be frequently present on images acquired with hepatobiliary contrast for several reasons.
Hemangiomas present the same imaging findings at dynamic studies with hepatobiliary contrast; however, in the delayed phase, as the hepatobiliary contrast medium is leaving the interstitium and entering into the functioning hepatocytes, the hemangioma fill-in might or might not occur in this phase, differing from its usual behavior with the use of extracellular gadolinium Hemangiomas are formed by a clump of blood vessels and do not contain hepatocytes, therefore they do not present contrast enhancement during the hepatobiliary phase and appear hypointense in this phase 1 , 2 , 9 , 15 Figure 4.
A potential confusion factor is the fact that some hemangiomas may present subtle central contrast uptake during the early hepatobiliary phase because of the tendency to persistent centripetal enhancement at dynamic study, like in those with extracellular gadolinium 1. The caudate lobe lesion arrowheads presents subtle hypersignal on T2-weighted sequence and signal loss on T1-weighted out-of-phase sequence caused by the presence of intralesional fat. Such a lesion shows intense and homogeneous contrast uptake in the arterial-phase, with decay in the portal and delayed phases, presenting greater hepatobiliary contrast uptake than the adjacent parenchyma, suggesting FNH as the first diagnostic hypothesis.
Considering that the presence of intralesional fat in NFH is rare, the patient will be maintained under imaging follow-up.opfitcompzacel.tk/map16.php
MR contrast agents
The lesions in segments VII and VIII arrows are similar, with marked hypersignal on T2-weighted, hyposignal on T1-weighted sequence, and nodular, peripheral and discontinuous uptake in the arterial phase, a characteristic of hemangiomas. In cirrhosis, the hepatobiliary contrast uptake by the nodules depends on their differentiation stage and on the presence of functioning hepatocytes. Low-grade regenerative and dysplastic nodules present preferentially portal vascularization, contain functioning hepatocytes and, like the surrounding parenchyma, show hepatobiliary contrast uptake. High-degree dysplastic nodules lose the portal vascularization and start gaining abnormal arterial vascularization.
Thus, high-grade dysplastic nodules tend to be hypovascular in the arterial and portal phases, but may also become hypervascular in the arterial phase in cases where the abnormal arterial vascularization is more developed. High-grade dysplastic nodules contain functioning hepatocytes and also demonstrate hepatobiliary contrast uptake in the same way as the surrounding parenchyma Figure 5. Hepatobiliary contrast uptake by HCC also depends on its differentiation stage.
Well-differentiated HCCs contain functioning hepatocytes and might show hepatobiliary contrast uptake. On the other hand, poorly-differentiated or undifferentiated hepatocarcinomas do not contain functioning hepatocytes and do not show hepatobiliary contrast uptake, remaining hypointense in relation to the surrounding parenchyma 2 , 10 , 17 - 19 Figure 6. Small nodules are observed adjacent to the gallbladder, with hyposignal on T2-weighted sequence, without expression on the other sequences and on the conventional dynamic study, but with hepatobiliary contrast uptake, leading to the diagnosis of regenerative nodules.
Well-differentiated HCCs show hepatobiliary contrast uptake, requiring imaging follow-up. Two liver nodules are seen in the segment VIII arrows as well as a larger nodule, in the segment VI arrowheads , all of them contrast-enhanced in the arterial-phase, washout in the delayed-phase, and without uptake in the hepatobiliary-phase, characterizing HCCs. Poorly differentiated or undifferentiated HCCs do not contain functioning hepatocytes so hepatobiliary contrast uptake is not observed.
MR contrast agents
The different enhancement patterns depend on the histological grade of the HCCs and may be explained by the membrane transporters expression. Hepatobiliary contrast uptake by HCCs depends on the tumor differentiation stage and on the amount of functioning hepatocytes 2 , 4. The diagnostic performance of MRI in the detection of HCCs of all sizes increases with the utilization of hepatobiliary contrast agents 1 , The incidence of side effects is low by comparison with the CT contrast agents. Serious side effects such as anaphylaxis are rare 0.
A recent concern is the development of nephrogenic systemic fibrosis NSF. This condition was first diagnosed in Other symptoms include skin thickening, which restricts joint mobility and can lead to contractures and immobility. The visceral organs may also be involved, including the lungs, liver, muscles and myocardium. As of February 1, , there have been biopsy-proven cases of NSF published in the peer-reviewed literature with the following associations: In that case, clinicians should administer only once during an imaging session, and monitor for signs and symptoms of NSF if GBCA is administered to patients with acute kidney injury, or chronic or severe kidney disease.
An estimate of kidney function should be performed through laboratory testing for patients at risk of having reduced kidney function. These reported cases of NSF were related to advanced renal dysfunction and appeared to develop over a period of several days or months. Among patients with end-stage renal disease, the incidence of NSF in those who received Gd-chelate contrast agent ranged from 2.
This is one of the mechanisms thought to provoke an inflammatory response resulting in NSF. These are usually present in normal liver tissue. Side effects are dose dependent. These include facial flushing, dyspnea, rash and lumbar pain.
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The rapid action also meant that dynamic T1 sequences could be performed, 15 however, development and production of Resovist ceased in The main application of the hepatobiliary HPB agents is in the imaging of the liver parenchyma and the biliary tree. Like Gd-chelate agents, these also work by shortening the T1-relaxation times paramagnetic effects. Gd-chelate agents is that after the blood pool phase, they accumulate within the hepatocytes and are later excreted in bile. One of the earliest HPB agents available was Mangafodipir trisodium. Maximum enhancement of the liver is usually observed after 20 min and lasts for 4 hours.
Eovist is the first HPB-Gd agent approved for liver imaging. The enhancement on the hepatocyte phase following the administration of Eovist is a function of the organic anion transporting polypeptide OATP in functioning liver cells. The advent of faster, high-resolution, thin-slice MRI has allowed excellent multiplanar reconstruction MPR for the evaluation of the biliary system. HPB agents have been used in CE assessment of the biliary tree, including visualization of post cholecystectomy biliary leaks, 20 documenting patency of biliary-enteric anastamoses, 21 and determining the proximity of lesions to the intrahepatic biliary ducts.
The technique also allows for thin-section coverage of the liver in a single breathhold. Fat saturation is commonly used because it helps improve the dynamic range in liver imaging and accentuates enhancement.
This technique alone detects most of the clinically relevant focal liver lesions. The 3 phases of dynamic post Gd liver imaging include a late arterial phase, portal venous phases and excretory phase. In general, for the first phase, a bolus tracking technique is recommended. The arterial phase should begin with acquisition of data in the center of k space imaging at 8 to 10 sec after contrast has reached the aorta at the level of the celiac axis.
At our institution, a 5 min delayed phase of imaging is also routinely added. In the setting of the HPB-Gd agents, a hepatocyte-specific delayed phase is obtained. This is performed at 20 min for Eovist 23 and at 45 min to 3 hours for MultiHance. The manganese-based agent is not used in a dynamic fashion and is predominantly a T1-shortening agent.
The imaging features will mimic HPB-Gd during the hepatocyte phase of enhancement. Ferumoxide is given as a slow infusion over 30 min, followed by an interval of 30 min for accumulation, and an imaging window of 1 to 4 hours. Common focal liver lesions are classified as benign vs. Benign lesions include cysts, hemangiomas, focal nodular hyperplasia FNH , and adenoma, while common malignant lesions include hepatocellular carcinoma HCC , as well as hyper- and hypovascular metastases. CE MRI is commonly used as a problem-solving tool for lesions that are indeterminate on other forms of imaging.
A summary of the MRI imaging features is provided in Tables 3 and 4. Cysts are fluid-filled cavities, and are typically hypointense on T1W imaging and hyperintense on T2W imaging, and do not enhance Figure 1.
The contrast-to-noise ratio CNR increases significantly with contrast administration. With HPB agents Figure 3 , the cysts appear as hypointense in all phases. With Gd-chelate agents, hemangiomas demonstrate early peripheral nodular enhancement and delayed centripetal filling-in on T1W imaging dynamic gradient recalled echo , paralleling that of CT imaging with iodinated contrast Figure 4. As with other benign lesions, there can be some loss of T2 signal.
FNH is composed of multiple spherical aggregates of hepatocytes and proliferation of disordered biliary structures that do not communicate with the biliary tree. Differential diagnoses include hepatic adenomas and fibrolamellar HCC. Some atypical FNHs present without arterial enhancement but show enhancement in the portal venous and equilibrium phases. The difference from extracellular agents is that they are also taken up by the hepatocytes, and therefore remain hyperintense to the liver on hepatocyte phase imaging Figure 6.
Lesion conspicuity is reported to be higher than with the RE agents on delayed imaging. Adenoma cells are larger than normal hepatocytes and contain large amounts of glycogen and lipid. During the hepatobiliary phase, they selectively increase the liver signal intensity and aid the in the detection of small tumours. It goes by the trade name MultiHance Bracco. Its delayed imaging time is between 90 to minutes. Compared to gadobenate, it has more intense liver parenchymal enhancement. The delayed imaging time is also more convenient minutes.
This property results in the increase in signal intensity of normal hepatic parenchyma. Thus, in the presence of a focal liver lesion, the increased signal of normal parenchyma gives a high lesion-to-liver contrast and hence provides improved detection, characterization and evaluation of liver lesions. It goes by the trade name Teslascan. Unlike the gadolinium agents, mangafodipir trisodium readily dissociates to yield free manganese ions.
This in vivo instability of the chelate rose concerns about potential toxicity. Free manganese, in chronic exposure, causes a parkinsonism-like syndrome due to accumulation in the brain.
Liver-specific agents for contrast-enhanced MRI: role in oncological imaging
It can also have a depressive action on heart function. Mn-based nanoparticles are under research for its use as high-performance contrast agents with reduced toxicity. These crystals are coated with dextran or any other biodegradable polysaccharide which prevents particle aggregation. This modifies their biological behaviour and makes the total size of the iron oxide particle substantially larger. Superparamagnetic iron oxide particles do not leak into the interstitium.