Which imaging modalities often requires the use of intravenous iodinated contrast media for studies of the abdomen?

Computed Tomography of the Equine Upper Respiratory Tract

Martin J Philipp, in Equine Respiratory Medicine and Surgery, 2007

Contrast media

Intravenous contrast media can be used to provide direct visualization of perfused tissues. Perfused tissue shows up as hyperdense areas in contrast to non-perfused tissues, which remain the same density. This technique is valuable if the clinician wishes to know if an imaged area is perfused or not, for example to differentiate a fluid-filled cystic mass from a soft-tissue neoplasm with vascularization extending throughout the mass (Fig. 19.2). After performing the initial (native) CT scan, the same sequence is repeated following administration of contrast medium. Essentially the same contrast media can be used in CT imaging as in conventional radiography and the risks and precautions are the same. For intravenous administration of contrast media for CT studies, tri-iodinated, water-soluble compounds are used. They are administered as an intravenous bolus at a dose of 370 mg iodine/kg body weight. They are distributed by the vascular system and later excreted by the urinary system. Perivascular leakage should be avoided, as most ionic preparations are locally irritant. Renal vascular effects and renal damage induced by contrast media are well studied in humans and dogs (Porter 1993). Maintaining the patient's hydration status can minimize these adverse renal effects. Although extremely rare, severe side effects such as cardiac arrest and anaphylaxis have been described following administration of tri-iodinated, water-soluble compounds. Contrast agents with low osmolarity may have fewer adverse effects. Additionally, in equine imaging, cost is the main limitation in the use of intravenous contrast media.

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Carcinoma of the Thyroid Gland

In Oncologic Imaging, 2007

CT Tips

CT covers the primary tumor within seconds with multidetector CT scanners.

Iodinated intravenous contrast medium can interferewith iodine uptake by thyroid cells and may delay postoperative adjuvant radioactive iodine therapy of differentiated thyroid cancer. A CT scan without contrast agent provides adequate information in this scenario, but subtle findings (e.g., small recurrent nodule in thyroid bed or small lymph node) may be missed.

Contrast-enhanced CT can be used for assessment of local extent of disease if treatment with radioactive iodine is not anticipated. Aggressive differentiated carcinoma and poorly differentiated or anaplastic thyroid cancers do not concentrate radioactive iodine, and CT with contrast is an acceptable modality in these cancers.

CT is useful for early detection of extracapsular nodal spread that is generally not seen on MRI. Focal metastasis/necrosis within normal-sized lymph nodes can be detected on contrast-enhanced CT earlier than on MRI.

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Magnetic Resonance Imaging

Joana Chaby L.S. Coelho, Jennifer Kinns, in Equine Surgery (Fourth Edition), 2012

The Head

MRI is the gold standard modality to image the brain in humans and animals. The use of intravenous contrast media is indicated when imaging the equine brain. The contrast material used with MRI is a gadolinium derivate. Doses of 0.02 mmol/kg in adult horses and 0.1 mmol/kg in foals of gadolinium-diethylenetriamine penta-acetic acid (gadolinium-DTPA) have been reported for imaging the brain.10,50 However, an optimal dose of intravenous gadolinium contrast in horses has not been established. T1 images are used for evaluating contrast enhancement. Many congenital, toxic, inflammatory or infectious (including equine protozoal encephalopathy), and neoplastic processes affecting the brain can be identified with MRI.10,51-53

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Interventional Cardiology

Ellen Rawlinson, Natalie Forshaw, in A Practice of Anesthesia for Infants and Children (Sixth Edition), 2019

Renal Adverse Reactions and Prevention

The term contrast media nephrotoxicity (CMN) refers to an increase in serum creatinine concentration by more than 25% or 0.5 mg/dL within 3 days of receiving IV contrast media in the absence of another cause.59 The underlying mechanism of injury is unclear, although it is thought that contrast can reduce renal perfusion and is toxic to tubular cells. CMN occurs more frequently but not exclusively in children with preexisting renal damage; additional risk factors include dehydration, cardiac failure, and the subclinical renal insufficiency seen in cyanotic children. It has been suggested that infants and children who receive more than 5 mL/kg of nonionic contrast agent are at increased risk for CMN.60 Contrast for angiography does not increase the risk of postbypass acute kidney injury61 and most CMN appears to resolve without intervention. However, a recent study of 233 heterogeneous children receiving contrast for CT scanning found an association between CMN and unfavorable outcome, suggesting the process may not be as benign as previously hoped.62 Many interventions have been given prophylactically to prevent CMN; preliminary studies with N-acetylcysteine (NAC) have been promising but no interventions have been more effective than normal saline hydration.63 Currently, the only modifiable risk factors are hydration status and dose of contrast used. When possible, potentially nephrotoxic drugs should be stopped at least 24 hours before the procedure. Gadolinium-based contrast materials are considered nonnephrotoxic in the normal MRI dose of up to 0.3 mmol/kg. However, there is some evidence that the increased doses required for cardiac angiography may confer adverse renal effects.64 Most radiologic contrast media have significant osmotic diuretic effects. During procedures requiring large volumes and/or repeated doses of contrast media, a significant diuresis may occur, causing concealed fluid losses and potential hypovolemia. Additional IV fluid may be required to avoid dehydration. Occasionally, bladder distention and retention can also occur, which should be considered in a child with unexplained postoperative distress.

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Pleural Effusion

V. Courtney Broaddus MD, Richard W. Light MD, in Murray and Nadel's Textbook of Respiratory Medicine (Sixth Edition), 2016

Computed Tomography

Chest CT is currently the best way to visualize the pleural space.133 Chest CT has its greatest utility in distinguishing parenchymal and pleural abnormalities.135 With current protocols involving the rapid injection of intravenous contrast medium, the unaerated perfused lung parenchyma will enhance, whereas the pleural fluid will not.136 The use of CT to discriminate transudates from exudates by their attenuation (Hounsfield units) has not been found to be clinically useful due to a great deal of overlap.137

Chest CT is quite useful in distinguishing a parenchymal lung abscess located near the chest wall from an empyema with an air-fluid level. The most distinctive features are the margins of the abnormality. With empyema, the cavity walls are of uniform thickness both internally and externally (see eFigs. 80-2, 80-5) and the adjacent lung is usually compressed. The angle of contact with the chest wall may be obtuse (see eFig. 33-7B). In addition, most empyemas have a lenticular shape and demonstrate the “split pleura” sign (Fig. 79-5A see also eFigs. 80-2, 80-5).138 With lung abscess, the walls of the cavity are not of uniform thickness and the adjacent lung is not compressed (see eFigs. 33-4, 33-13B and C, 33-21D and EeFigs. 33-4eFigs. 33-13eFigs. 33-21). The angle of contact with the chest wall may be acute (Fig. 79-5B).

In diffuse pleural disease, chest CT is useful in distinguishing malignant from benign causes. Features associated with malignancy include circumferential pleural thickening, pleural nodules (see eFig. 53-5), parietal thickening greater than 1 cm, and mediastinal pleural involvement (see eFig. 53-4 and Video 79-1

).139 The distinction of metastatic disease from mesothelioma can be difficult, although hilar adenopathy is more common with metastatic disease.133

CT pulmonary angiography (CTPA) has become a first-line imaging test for the evaluation of PE140 (see Chapters 18 and Chapter 57). The evaluation of a patient with a pleural effusion for PE can begin with a Doppler ultrasound of the lower extremities. If the ultrasound identifies thrombus, the patient can then be treated for thromboembolic disease. If it is negative, the patient may still have a PE. In the past the standard approach was to proceed to lung ventilation-perfusion scanning. However, this has largely been replaced by CTPA. CTPA is highly sensitive and specific for pulmonary emboli in the proximal, segmental pulmonary arteries.140 In contrast to ventilation-perfusion lung scanning, CTPA can establish alternate diagnoses as well. Where CTPA is not available, lung scanning can be used, perhaps after efforts to improve accuracy by withdrawing as much pleural liquid as possible. A diagnostic scan (normal or high probability) can then be used either to exclude the diagnosis or initiate anticoagulation. If nondiagnostic (e.g., of low or intermediate probability), the scan should be followed by pulmonary angiography.

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Kidneys and Ureters

Gabriela S. Seiler, in Textbook of Veterinary Diagnostic Radiology (Seventh Edition), 2018

Technique

Imaging protocols always include a precontrast image series to identify presence of mineralization in the renal parenchyma or collecting system, because mineralization cannot be differentiated from the hyperattenuating contrast medium. In most patients, intravenous contrast medium has to be administered (400 to 800 mg I/kg body weight) to outline renal parenchymal lesions and filling defects in the collecting system. Contraindications to using iodinated contrast media are the same as described in the Excretory Urography section. The renal parenchyma is enhanced immediately after contrast-medium administration. Optimal ureteral opacification occurs 3 minutes post injection.37 However, image series may have to be repeated several times to visualize the entire course of both ureters because of ureteral peristalsis. Ureteral opacification persists for about 1 hour.37 Positioning the patient in sternal recumbency with the bony pelvis elevated is helpful in outlining the ureterovesical junctions, because the contrast medium will accumulate in the bladder apex away from the neck, facilitating the distinction between the contrast-medium–filled ureters and the bladder neck (Fig. 41.7). Filling the bladder with carbon dioxide increases the contrast between the bladder and ureters further; however, the balloon of the Foley catheter may distort anatomy and impair visibility of the ureteral openings. Dual-phase renal angiography can be performed to assess the arterial and venous blood supply of the kidneys separately. This is used mainly for presurgical assessment of feline kidney donors.40,41

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Extended Resections for Lung Cancer

Valerie W. Rusch, Paul E. Van Schil, in IASLC Thoracic Oncology (Second Edition), 2018

Pretreatment Evaluation

The presence of a Pancoast syndrome is not always associated with NSCLC. Other diseases, including lymphoma, tuberculosis, and primary chest wall tumors, may be associated with an apical mass and chest wall involvement. Transthoracic needle biopsy should be performed to establish a diagnosis before treatment.

Pancoast tumors are, by definition, classified as stage IIB or higher and require an extent-of-disease evaluation before treatment is initiated, including contrast-enhanced CT of the chest and upper abdomen, whole-body PET, and MRI of the brain (Fig. 30.4A–B). Because Pancoast tumors with mediastinal node metastases (N2 or N3 disease) have a poor prognosis, mediastinal staging via either endobronchial ultrasound or mediastinoscopy should be considered.

MRI with use of intravenous contrast medium is the modality of choice for evaluating structures of the thoracic inlet, including the brachial plexus, subclavian vessels, spine, and neural foramina and is crucial for preoperative planning.36 The extent of nerve root involvement must be assessed. Resection of the T1 nerve root usually does not cause motor function deficit, but resection of the C8 nerve root or lower trunk of the brachial plexus leads to loss of hand and arm function. A careful neurologic examination is informative and supplements MRI findings.37 Pain extending along the ulnar aspect of the forearm and hand is consistent with T1 involvement. Weakness of the intrinsic muscles of the hand indicates involvement of the C8 nerve root or lower trunk of the brachial plexus. Resection of a Pancoast tumor should be planned jointly with a spine neurosurgeon to allow optimal patient selection and the best chance of complete resection.

Patients must be evaluated to determine whether they can tolerate combined-modality therapy. Performance status, renal function, and neurologic function must be adequate in order for the patient to receive platinum-based chemotherapy. Pulmonary function tests and, when necessary, cardiac stress tests are done to evaluate the ability of the patient to tolerate pulmonary resection.

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Computed tomography of the liver, biliary tract, and pancreas

Seth S. Katz, in Blumgart's Surgery of the Liver, Biliary Tract and Pancreas, 2-Volume Set (Sixth Edition), 2017

Technique and Protocols

CT imaging of the pancreas relies on the differential IV contrast enhancement between tumor tissue and normal pancreatic parenchyma. The use of IV contrast agent is mandatory for accurate diagnosis, and timing of the contrast injection and accurate delivery of the appropriate volume requires use of a dedicated CT power injector. As with liver imaging, several methods are available to determine the time of maximal arterial enhancement for each patient. These include fixed timing (subject to suboptimal imaging due to variation in cardiac function and hydration state), timing bolus (Kalra et al, 2004), and commercially available solutions in which scanning may be triggered automatically when a vascular structure reaches a predefined attenuation.

Initial scan protocols for dedicated pancreas evaluation/CT angiography recommended four phases, but more modern practice uses three acquisitions, omitting early arterial imaging because pancreatic parenchyma and peripancreatic arterial anatomy are both well evaluated in the late arterial phase (Fletcher et al, 2003). The precontrast scan permits evaluation of pancreatic calcifications and allows localization of the gland and pertinent arteries in the z-axis for subsequent acquisition of contrast-enhanced phases. IV contrast medium is injected at a high flow rate of 4 to 6 mL/seconds. The late arterial or pancreatic parenchymal phase, acquired roughly 30 to 40 seconds after initiating contrast injection, is designed to maximize differences in contrast enhancement between pancreatic neoplasms and adjacent normal pancreatic tissue and is also useful in evaluating hypervascular liver metastases seen in patients with pancreatic endocrine neoplasms. Last, the routine portal venous phase acquired at approximately 70 to 90 seconds from the start of IV contrast injection provides the best evaluation of hepatic metastases from pancreatic ductal adenocarcinoma (Bashir & Gupta, 2012; Cantisani et al, 2003; Takeshita et al, 2002) and in some cases offers the best contrast to identify the primary pancreatic lesions themselves.

The dedicated pancreas protocol uses 750 to 1000 mL of oral water as a negative contrast agent administered before the examination, to aid distinction of enhanced vessels from the gastrointestinal tract (Lawler & Fishman, 2002; Soriano et al, 2004; Takeshita et al, 2002) and to facilitate identification of tumor invasion into adjacent bowel. Avoiding positive oral contrast also facilitates analysis on the 3D workstation. Images are typically reviewed at 2.5-mm collimation in all planes.

Routine evaluation for the follow-up of pancreatic cancer in a postoperative patient or for evaluation of response to medical therapy uses 500 to 1000 mL of oral water-soluble iodinated contrast solution or equivalent 2% barium sulfate suspension administered 45 minutes before scanning. This examination type requires an injection rate of only 2.5 mL/sec, so a small 20-gauge catheter may be used. Only the routine portal venous phase is acquired. Five-millimeter axial slices are typically reviewed, although thinner images may always be requested by the radiologist provided the raw image data are still extant.

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Liver Failure

Deirdre Kelly, in Pediatric Gastrointestinal and Liver Disease (Fourth Edition), 2011

Investigations

Biochemical Liver Function Tests

Biochemical liver function tests (Table 77-2) reflect the severity of hepatic dysfunction but rarely provide diagnostic information on individual diseases. The most useful tests of liver “function” are plasma albumin concentration and coagulation time. Low serum albumin indicates chronicity of liver disease, whereas abnormal coagulation indicates significant hepatic dysfunction, either acute or chronic. Fasting hypoglycemia in the absence of other causes (e.g., hypopituitarism or hyperinsulinism) indicates poor hepatic function and is a guide to prognosis in acute liver failure. Diagnostic tests are summarized in Table 77-3.

Radiology

Several radiologic techniques provide valuable information in the investigation and diagnosis of pediatric liver disease. Chest x-rays may show skeletal abnormalities, for example, butterfly vertebrae in Alagille’s syndrome or a dilated heart secondary to fluid overload in end-stage liver disease. Wrist and knee x-rays will demonstrate bone age and/or the development of osteopenia or rickets in chronic liver disease.

Ultrasound

Ultrasonic investigation of the abdomen provides information on the size and consistency of the liver, spleen, and portal and hepatic veins. Cirrhosis may be suggested if there is abnormal homogeneity of the liver architecture, and an irregular liver edge. Color-flow Doppler techniques permit rapid evaluation of vascular patency without the use of intravenous contrast material. It is particularly useful in pretransplant examinations to identify whether the portal vein, hepatic veins and artery, and splenic vessels are patent. Portal hypertension is suggested by the presence of ascites, splenomegaly, and splenic or gastric varices.

Computed Tomography

Computed tomographic (CT) scanning of the liver is usually not required for the diagnosis of chronic liver failure but may be useful for the identification and biopsy of hepatic tumors or regenerative nodules. Intravenous contrast medium causes enhancement of vascular lesions and the walls of abscesses, and it may be helpful in differentiating tumors from other solid masses. CT scans of the brain are helpful for the detection of cerebral edema in acute liver failure.

Endoscopic Ultrasound

Endoscopic ultrasound (EUS) is a new imaging modality that visualizes the lower biliary tree. The technique uses mini probes (external diameter 2.6 mm), which are small enough to be passed via the operating channel of conventional pediatric duodenoscopes. EUS has also proved useful in the diagnosis of submucosal esophageal and gastric varices.11

Angiography

Visualization of the celiac access and hepatic and splenic blood vessels is obtained by femoral artery catheterization and injection of radiologic contrast. This technique has two parts: (1) the arterial phase, which provides information on the celiac axis, hepatic and splenic artery abnormalities, vascularization and anatomy of hepatic tumors, hepatic hemangiomas, and detection of hepatic artery thrombosis; and (ii) the venous phase, which provides information about the patency of the portal, splenic, and superior mesenteric veins and the presence of portal hypertension by identification of mesenteric, esophageal, or gastric varices.

Splenoportography

This technique, in which the splenic and portal veins are visualized by the injection of radiologic contrast into the spleen, has largely been replaced by hepatic angiography. It may be useful for measuring splenic pulse pressures in the evaluation of portal hypertension but carries a small risk of splenic rupture.

Magnetic Resonance Imaging

Magnetic resonance imaging (MRI) scanning has now replaced hepatic angiography as the best way to stage or diagnose hepatic tumors or regenerative nodules and identify their vascular supply. It may provide valuable information about liver or brain consistency and storage of heavy metals, for example iron in hemochromatosis, copper in Wilson’s disease, and cerebral edema in acute liver failure.12

Endoscopy

Upper gastrointestinal endoscopy (gastroscopy) using a flexible fiberoptic endoscope is the best way to diagnose esophageal and gastric varices secondary to portal hypertension. The technique is normally performed under sedation or general anesthetic. In children with hematemesis, gastroscopy not only provides rapid diagnosis but enables therapy with variceal banding or endoscopic sclerotherapy for bleeding varices or injection of bleeding ulcers with adrenaline or thrombin.

Neurophysiology

Electroencephalography is mostly used in the assessment of hepatic encephalopathy. It will identify abnormal rhythms secondary to encephalopathy due to either acute or chronic liver failure or drug toxicity such as posttransplant immunosuppression. It may also be of value in determining brain death: A flat electroencephalogram (EEG) in the absence of sedation is an indication for withdrawal of therapy. CT or MRI scans of the brain (see previous discussion) may identify cerebral edema, infarction, or hemorrhage.

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Bilirubin Metabolism and Its Disorders

Jayanta Roy-Chowdhury, Namita Roy-Chowdhury, in Zakim and Boyer's Hepatology (Sixth Edition), 2012

Dubin-Johnson Syndrome

In 1954, Dubin and Johnson373 and Sprinz and Nelson374 described a syndrome with chronic nonhemolytic jaundice characterized by accumulation of conjugated bilirubin in serum and grossly pigmented, but otherwise histologically normal, livers.

Clinical Findings

Except for mild icterus, physical examination results are within normal limits. Patients are usually asymptomatic, although an occasional patient complains of weakness and vague abdominal pain, and, rarely, hepatosplenomegaly is observed.375,376 Because serum total bile acid levels are normal,377 pruritus is absent. Hyperbilirubinemia is increased by intercurrent illness, oral contraceptives, and pregnancy.377 The diagnosis is often made after puberty, although some patients have been diagnosed during the neonatal period.376,378 Sometimes the disorder is noted for the first time when a woman becomes pregnant or receives oral contraceptives, which increase the hyperbilirubinemia to a clinically detectable level.377

Laboratory Tests

Complete blood count, prothrombin time, and serum levels of bile acids, transaminases, alkaline phosphatase, and albumin are normal.376,377 Serum bilirubin concentration is usually between 2 and 5 mg/dL but can be as high as 20 to 25 mg/dL. More than 50% of total serum bilirubin is direct-reacting. Serum bilirubin levels fluctuate and individual measurements may yield normal results. Because of the general abnormality of canalicular transport of non–bile acid organic anions, oral cholecystography, even using a “double dose” of contrast material, usually does not visualize the gallbladder. However, visualization may occur 4 hours after administration of intravenous contrast medium.379 The liver is grossly black and light microscopy reveals a dense pigment (Fig. 62-7), which on electron microscopy appears to be contained within lysosomes.380 Histochemical staining and physicochemical properties of the pigment suggest that the pigment is related to melanin.381 Following infusion of [3H]epinephrine into mutant Corriedale sheep (an animal model for Dubin-Johnson syndrome), the isotope is incorporated into the hepatic pigment,382 supporting the concept that the pigment is a melanin-like derivative. However, electron spin resonance spectroscopy shows that the pigment differs from authentic melanin.383 It may be composed of polymers of epinephrine metabolites.384,385 Interestingly, following liver disease, such as acute viral hepatitis, the pigment is cleared from the liver.386 Following recovery, the pigment reaccumulates slowly, starting from the centrizonal region.

Organic Anion Transport

The hepatic secretion of bilirubin glucuronides and the glutathione conjugate of BSP is disturbed in these patients.275,387 The hepatic secretion of negatively charged iopanoic acid is disturbed whereas the secretion of neutral iopamide is normal. The bile acid secretion is unaffected.387 Pharmacokinetic analysis of plasma disappearance of bilirubin, BSP, and ICG revealed normal hepatic storage but impaired secretion.275,387,388 Impaired canalicular secretion of non–bile acid organic anions represents the basic defect of this syndrome. After intravenous injection of BSP, plasma BSP concentration decreases at near-normal rate for 45 minutes. However, in 90% of patients, plasma BSP concentration increases after this time, such that the concentration at 90 minutes is greater than that at 45 minutes.363 This secondary rise results from reflux of glutathione-conjugated BSP from hepatocytes into the circulation. A similar secondary rise occurs after intravenous administration of bilirubin.387 The secondary rise of plasma BSP level has been observed in other hepatobiliary disorders,388 and is therefore not diagnostic of Dubin-Johnson syndrome.

The Genetic Background of Dubin-Johnson Syndrome

Dubin-Johnson syndrome is caused by mutations of the MRP2 gene causing a deficiency of canalicular MRP2 expression.180-182 More than a dozen genetic lesions, including nucleotide transition of a single-nucleotide deletion, resulting in amino acid substitutions, premature truncation, or exon skipping, have been reported to cause Dubin-Johnson syndrome.389 Some of the reported mutations may lead to impaired glycosylation of the MRP2 protein, impaired sorting to the canalicular membrane, and premature proteasome-dependent degradation.390 As in TR− rats and EHBR rats, the absence of MRP2 (mrp2 in rats) in the canalicular membrane causes severe impairment of canalicular secretion of bilirubin conjugates, the leukotriene LTC4, reduced and oxidized glutathione, and numerous glucuronide and glutathione conjugates.391 As a consequence, these patients and animals have a mild conjugated hyperbilirubinemia. Experiments with the animal models provided firm evidence for the existence of different pathways for the canalicular secretion of bilirubin conjugates and bile acids.392 In contrast to bile acids with a free 3-hydroxyl, 3-hydroxyl-conjugated bile acids are transported by mrp2, rather than bsep, as evidenced by impaired secretion of bile acid conjugates in TR− and EHBR rats.393 On feeding TR− rats a diet enriched with tryptophan, tyrosine, and phenylalanine, intravenous injection of metanephrine results in the accumulation of a black lysosomal pigment in hepatocytes, identical to that seen in patients with Dubin-Johnson syndrome.394 Despite the absence of MRP2, the serum bilirubin levels are only mildly elevated in Dubin-Johnson syndrome and in the two rat models of the disease, suggesting alternative canalicular secretion pathways for bilirubin conjugates.395 Members of the mrp family, other than Mrp2, have been described in the rat bile canaliculi.396,397 Whether these mrps accept bilirubin glucuronides as substrates needs to be studied. MRP3 is expressed in the basolateral domain of the hepatocyte plasma membrane in patients with Dubin-Johnson syndrome. The activity of this transporter contributes to the conjugated hyperbilirubinemia by actively pumping bilirubin conjugates from liver to blood in these patients.140 Thus the accumulation of conjugated bilirubin in the plasma of Dubin-Johnson syndrome patients may not be caused by passive “leakage” only, but also by active transport of bilirubin conjugates out of the hepatocytes.

Inheritance

Dubin-Johnson syndrome is rare, but occurs in both sexes and in virtually all races. The syndrome occurs frequently (1 : 1300) in Persian Jews,376 in whom it is associated with clotting factor VII deficiency.398,399 It had been difficult to ascertain the inheritance pattern from clinical analysis,377 but with respect to urinary coproporphyrin excretion (see the following paragraph), Dubin-Johnson syndrome is inherited as an autosomal recessive characteristic.400,401

Urinary Coproporphyrin Excretion

Urinary coproporphyrin I excretion is increased in patients with Dubin-Johnson syndrome to a greater degree than in patients with other hepatobiliary disorders.401 Of the two isomers of coproporphyrin, isomers I and III, coproporphyrin III is a precursor of heme, whereas other porphyrin isomers are metabolic byproducts of unknown significance and are excreted in urine and bile.400 Normally, approximately 75% of total urinary coproporphyrin is coproporphyrin isomer III. In Dubin-Johnson syndrome, total urinary coproporphyrin excretion is normal, but more than 80% is coproporphyrin I (Fig. 62-8).401,402 Although neonates normally have elevated urinary content of coproporphyrin I as compared with adults, levels are not as high as those seen in Dubin-Johnson syndrome.403 In obligate heterozygotes (e.g., unaffected parents, children of subjects with Dubin-Johnson syndrome), total urinary coproporphyrin excretion was reduced by 40% of normal.401,403 The mechanism of the abnormal urinary porphyrin excretion and its relationship to the organic anion transport defect are not known. When the history and physical examination are consistent, the urinary coproporphyrin excretion pattern is diagnostic of Dubin-Johnson syndrome. However, the overlap of results in carriers with those in controls401 makes identification of heterozygotes difficult.

Animal Models

Mutant Corriedale Sheep

This mutant strain has an inherited defect that closely resembles the Dubin-Johnson syndrome. Biliary excretion of conjugated bilirubin, glutathione-conjugated BSP, iopanoic acid, and ICG is decreased, whereas taurocholate transport is normal.403,404 The secretion of the organic cation procainamide ethobromide is unaffected406 and, interestingly, the secretion of unconjugated BSP is unimpaired.405 These sheep have a mild hyperbilirubinemia, with 60% of the bilirubin being conjugated. The liver is pigmented as in Dubin-Johnson syndrome,406 but the histologic results are otherwise normal. Total urinary coproporphyrin excretion is normal with increased excretion of coproporphyrin isomer I and decreased isomer III excretion.

TR− Rats and Ehbr Rats

These rats have a hepatic excretory abnormality that strongly resembles that of the mutant Corriedale sheep and patients with Dubin-Johnson syndrome. The biliary excretion of conjugated bilirubin and many other organic anions is impaired.407-409 As in Dubin-Johnson syndrome, coproporphyrin I constitutes a major fraction of the total urinary coproporphyrins.407 As explained previously, the Mrp2 gene defect of TR− and EHBR rats has been characterized. Different single-nucleotide deletions cause an absence of canalicular Mrp2 expression in these two animal models.182,410

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Which of the following imaging modalities often requires the use of intravenous contrast media for studies of the abdomen?

Computed tomography (CT) is one of the most frequently utilized imaging modalities in medicine due to its ability to evaluate for a wide range of pathologies. The use of contrast agents, intravenous (IV) or oral, improves image quality by further delineating anatomical structures.

Which projection or position will best demonstrate free intraperitoneal air in the abdomen?

The most useful position for detecting free intraperitoneal air is the left lateral decubitus position.

What is the recommended kVp range using a digital system for an abdomen projection?

Results indicate optimum tube voltages of 70 kVp for abdomen and pelvis (with an optimum range 70–120 kVp), and 100 kVp (optimum range 80–120 kVp) for lumbar spine.

In which region or compartment of the abdomen is the pancreas located?

The pancreas is located deep in the abdomen (belly). Part of the pancreas is sandwiched between the stomach and the spine. The other part is nestled in the curve of the duodenum (first part of the small intestine).

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