January 2004, VOLUME 182
NUMBER 1

Recommend & Share

January 2004, Volume 182, Number 1

Perspective

Imaging Manifestations of Abdominal Sarcoidosis

+ Affiliation:
1Both authors: Department of Radiology, University of North Carolina School of Medicine, Manning Dr., Old Clinic Bldg., Rm. 2016, Box 7510, Chapel Hill, NC 27599-7510.

Citation: American Journal of Roentgenology. 2004;182: 15-28. 10.2214/ajr.182.1.1820015

Next section

Sarcoidosis is a systemic inflammatory disease of unknown origin characterized by the formation of noncaseating granulomas. Virtually any organ system may be involved. Pulmonary changes are the most common manifestation, and the accompanying radiologic findings of bilateral hilar adenopathy with or without changes of interstitial lung disease are well known and characteristic. Involvement of abdominal viscera is less frequent, but when it occurs, it may mimic more common infectious or neoplastic conditions and result in unnecessary morbidity. We review our experience with the clinical and imaging manifestations of sarcoidosis in the abdomen.

Epidemiology, Etiology, and Pathology
Previous sectionNext section

Sarcoidosis occurs most commonly in the third to fifth decades of life and, in the United States, is slightly more common in women than men [1, 2]. Although sarcoidosis is seen worldwide, the frequency of the disease, organ system involved, acuity of presentation, and prognosis vary widely with geography and ethnicity. Areas with high prevalence include the United States, particularly the southeastern region, Sweden, Denmark, and Japan, whereas a low prevalence is noted in Spain, China, and South America [1]. In the United States, blacks are more commonly affected than whites, with an age-adjusted annual incidence rate of 35.5 per 100,000 for blacks and 10.9 per 100,000 for whites [2]. Pulmonary complications are the major cause of death in the United States; however, in Japan, cardiac involvement is a more common cause of mortality [1, 3]. Familial occurrence of the disease has been described and is more common among blacks than whites. Human leukocyte antigen analysis suggests a polygenic mode of risk inheritance [1].

Although the etiology of sarcoidosis is unknown, speculation has centered on the interaction of an unknown antigenic factor triggering an exaggerated cellular immune response in genetically susceptible individuals. Geographic variation in the organ system affected and the pattern of the illness suggest that there may be multiple antigenic triggers [1].

The presence of noncaseating granulomas is the pathologic hallmark of sarcoidosis. Although rare, central necrosis and cavitation have been reported in pulmonary lesions [4]. Diagnosis of sarcoidosis must be based on the entirety of the clinical presentation because noncaseating granulomas are also found in association with several other infectious agents (e.g., tuberculosis, histoplasmosis, brucellosis, and toxoplasmosis), occupational and environmental exposures (e.g., beryllium, talc, and fungi), autoimmune disorders (e.g., Wegener's granulomatosis and primary biliary cirrhosis), and neoplasia (e.g., lymphoma and solid tumors) [5]. This latter association is particularly relevant when sarcoidosis produces masslike lesions that mimic abdominal carcinomas. These granulomas, which are morphologically identical to sarcoids, can be seen both in the tumor itself as well as within regional nodes that may not contain tumors. Presumably the granulomas form in response to soluble antigenic factors derived from tumor cells eliciting an immunologic hypersensitivity reaction [6].

Symptoms associated with sarcoidosis are both systemic (e.g., fatigue, fever, or weight loss) and organ-specific (e.g., shortness of breath or cough). Löfgren's syndrome refers to the association of bilateral hilar adenopathy, fever, and erythema nodosum. Although it is commonly due to sarcoidosis, the syndrome can have other causes. Heerfordt's syndrome of parotid gland enlargement, fever, uveitis, and cranial nerve palsies is almost always produced by sarcoidosis, as is lupus pernio (indurated plaques on the cheeks, lips, nose, and ears) associated with pulmonary infiltrates and lytic lesions that affect the small bones of the hands and feet [7]. However, sarcoidosis frequently produces no symptoms. Estimates from autopsy research suggest that the number of cases of sarcoidosis may be 10 times more than the number of cases that are clinically apparent [8]. In a Japanese autopsy study, more than half of the individuals with sarcoidosis had not received a clinical diagnosis before death [3].

Abdominal Manifestations
Previous sectionNext section

Abdominal viscera are frequently involved in sarcoidosis, although this involvement usually does not produce symptoms. The liver and spleen are the most frequently involved viscera, with granulomata noted in 40–60% of patients in two autopsy series [3, 9]. Renal involvement is seen in 8–19% of patients. At autopsy, pancreatic, intestinal, and testicular sarcoidosis have been found in 5% or less of patients [3, 9]. In the following sections, we review in detail the reported appearance of abdominal sarcoidosis.

Liver

Liver involvement in sarcoidosis can be documented at biopsy in 24–94% of patients [10, 11]. Laboratory evidence of liver dysfunction is seen in 2–60% of patients, with the alkaline phosphatase level being most commonly affected. Despite these incidences, symptomatic liver disease occurs in less than 5% of patients with sarcoidosis. Portal hypertension and cirrhosis are rare [7].

The most common radiographic finding of hepatic sarcoidosis is hepatomegaly. In a review of 59 patients with sarcoidosis at our institution, we found that 29% of the patients had a liver span greater than 20 cm on CT, and 8% of the 59 exhibited marked hepatomegaly (liver span > 25 cm) [12]. Other studies on sarcoidosis have found similar results [13, 14], although in one study, only 4% of patients had enlarged livers for unknown reasons [15]. In most patients, the liver appears homogeneous; however, a pattern of multiple low-density intrahepatic septa on contrast-enhanced CT has also been described [16]. On sonography, a pattern of either diffuse increased homogeneous or heterogeneous echogenicity has been reported in patients with hepatic sarcoidosis [17].

Focal nodules are also noted in the livers of patients with hepatic sarcoidosis. Pathologically, these nodules are thought to represent the coalescence of small granulomas into macroscopically visible lesions. In our experience, these nodules are noted in 5% of patients [12]. In other studies, frequencies of focal nodules have ranged from 0% to 19% [1315]. The nodules are typically innumerable and diffusely distributed. The size of such nodules ranges from 1–2 mm to several centimeters [18, 19]. Hepatomegaly, splenic nodules, and adenopathy are frequently, but not invariably, associated with the presence of liver nodules [18]. In one study, 69% of patients with hepatic nodules also had splenic lesions [19]. Liver involvement by sarcoidosis typically responds to steroids. In one case report, hepatic nodules disappeared after 3 months of steroid therapy, although hepatomegaly remained [20]. We have seen a similar decrease in the size and visibility of hepatic and splenic nodules after 5 months of steroid therapy [18].

On contrast-enhanced CT, liver nodules appear as hypodense masses relative to adjacent normal parenchyma. Peripheral enhancement typically is not seen [18] (Fig. 1A, 1B, 1C, 1D). On MRI, the lesions are hypointense on all sequences and hypoenhancing relative to the background liver [17, 21] (Fig. 1A, 1B, 1C, 1D). Lesions are most conspicuous on the T2-weighted fat-saturated images and the early-phase gadolinium-enhanced T1-weighted images [21]. The periportal increase in signal intensity on T2-weighted images may reflect the tendency of sarcoid granulomas to appear along the portal tracts [17] (Fig. 2A, 2B, 2C, 2D). On sonography, nodules have been reported to be hypoechoic relative to the background liver [17], although we have also seen nodules that are hyperechoic (Figs. 3A, 3B and 4). The difference may depend on the echogenicity of the liver or the degree of fibrosis present in the granuloma. Although calcification is uncommon, we have seen it in a patient with long-standing disease.

figure
View larger version (50K)
Fig. 1A. 29-year-old man with pulmonary sarcoidosis who presented with malaise, anorexia, and abdominal discomfort. Liver biopsy showed noncaseating granulomata consistent with sarcoidosis. (Reprinted with permission from [21]) Contrast-enhanced CT scan shows hepatomegaly with innumerable small hypodense hepatic nodules. Portal adenopathy (arrows) is also present.

figure
View larger version (57K)
Fig. 1B. 29-year-old man with pulmonary sarcoidosis who presented with malaise, anorexia, and abdominal discomfort. Liver biopsy showed noncaseating granulomata consistent with sarcoidosis. (Reprinted with permission from [21]) T2-weighted fat-saturated image (B), T1-weighted fast low-angle shot image (C), and early-phase gadolinium-enhanced T1-weighted fast low-angle shot image (D) depict innumerable hypointense hepatic nodules. Nodules are most clearly seen on T2-weighted and gadolinium-enhanced images. Portal adenopathy (arrows) shows increased signal intensity on T2-weighted image, decreased signal intensity on T1-weighted images, and enhancement on gadolinium-enhanced T1-weighted images.

figure
View larger version (55K)
Fig. 1C. 29-year-old man with pulmonary sarcoidosis who presented with malaise, anorexia, and abdominal discomfort. Liver biopsy showed noncaseating granulomata consistent with sarcoidosis. (Reprinted with permission from [21]) T2-weighted fat-saturated image (B), T1-weighted fast low-angle shot image (C), and early-phase gadolinium-enhanced T1-weighted fast low-angle shot image (D) depict innumerable hypointense hepatic nodules. Nodules are most clearly seen on T2-weighted and gadolinium-enhanced images. Portal adenopathy (arrows) shows increased signal intensity on T2-weighted image, decreased signal intensity on T1-weighted images, and enhancement on gadolinium-enhanced T1-weighted images.

figure
View larger version (55K)
Fig. 1D. 29-year-old man with pulmonary sarcoidosis who presented with malaise, anorexia, and abdominal discomfort. Liver biopsy showed noncaseating granulomata consistent with sarcoidosis. (Reprinted with permission from [21]) T2-weighted fat-saturated image (B), T1-weighted fast low-angle shot image (C), and early-phase gadolinium-enhanced T1-weighted fast low-angle shot image (D) depict innumerable hypointense hepatic nodules. Nodules are most clearly seen on T2-weighted and gadolinium-enhanced images. Portal adenopathy (arrows) shows increased signal intensity on T2-weighted image, decreased signal intensity on T1-weighted images, and enhancement on gadolinium-enhanced T1-weighted images.

figure
View larger version (60K)
Fig. 2A. 64-year-old woman with hepatosplenic sarcoidosis. (Reprinted with permission from [21]) Multiple small hypodense splenic nodules are visible on contrast-enhanced CT scan.

figure
View larger version (52K)
Fig. 2B. 64-year-old woman with hepatosplenic sarcoidosis. (Reprinted with permission from [21]) T2-weighted fat-saturated image shows multiple small hypointense nodules in spleen and less conspicuous lesions in liver. Central periportal high signal intensity (arrows) is seen.

figure
View larger version (61K)
Fig. 2C. 64-year-old woman with hepatosplenic sarcoidosis. (Reprinted with permission from [21]) Unenhanced T1-weighted image does not show nodules well.

figure
View larger version (58K)
Fig. 2D. 64-year-old woman with hepatosplenic sarcoidosis. (Reprinted with permission from [21]) Splenic nodules are seen as hypoenhancing lesions on early-phase gadolinium-enhanced T1-weighted image.

figure
View larger version (67K)
Fig. 3A. 31-year-old woman with sarcoidosis. (Courtesy of Chong W, Chapel Hill, NC) Contrast-enhanced CT scan shows multiple hypodense hepatic nodules. Portal adenopathy (arrow) is also noted.

figure
View larger version (53K)
Fig. 3B. 31-year-old woman with sarcoidosis. (Courtesy of Chong W, Chapel Hill, NC) Sonogram shows hyperechoic hepatic nodules (arrows). K = kidney.

figure
View larger version (48K)
Fig. 4. 39-year-old woman with fatigue and elevated alkaline phosphatase level. Sonogram of liver shows diffuse inhomogeneous echotexture with areas of increased echogenicity (arrows) of varying sizes. Liver and cervical lymph node biopsies showed granulomatous inflammation consistent with sarcoidosis. (Courtesy of Mittelstaedt C, Chapel Hill, NC)

Biliary Tree

Sarcoidosis can involve the intra- or extra-hepatic biliary tree. Intrahepatic involvement typically occurs with granulomatous involvement of the portal triads, producing a cholestatic picture. Although this appearance may mimic that of primary biliary cirrhosis, the absence of antimitochondrial antibodies in sarcoidosis is a distinguishing feature [22]. Involvement of the extrahepatic ducts can produce strictures that mimic cholangiocarcinoma [23]. Enlarged portal nodes may also sufficiently compress the biliary tree to produce obstructive jaundice [24] (Fig. 5A, 5B, 5C). Resolution with steroids has been described in several case reports [25].

figure
View larger version (59K)
Fig. 5A. 56-year-old woman with jaundice. (Courtesy of Nelson RC, Durham, NC) ERCP image shows high-grade stenosis of extrahepatic biliary tree with prestenotic dilatation.

figure
View larger version (67K)
Fig. 5B. 56-year-old woman with jaundice. (Courtesy of Nelson RC, Durham, NC) Contrast-enhanced CT scans (C obtained 5 mm caudad to B) shows intrahepatic bile duct dilatation with multiple enlarged portal and celiac lymph nodes (arrows). Fine-needle aspiration of porta hepatis nodes revealed noncaseating granulomas consistent with sarcoidosis. Biliary stent is indicated by arrowhead.

figure
View larger version (62K)
Fig. 5C. 56-year-old woman with jaundice. (Courtesy of Nelson RC, Durham, NC) Contrast-enhanced CT scans (C obtained 5 mm caudad to B) shows intrahepatic bile duct dilatation with multiple enlarged portal and celiac lymph nodes (arrows). Fine-needle aspiration of porta hepatis nodes revealed noncaseating granulomas consistent with sarcoidosis. Biliary stent is indicated by arrowhead.

Spleen

Fine-needle aspiration biopsy of the spleen has revealed granulomas in 24–59% of patients with sarcoidosis [26, 27]. Autopsy studies have similarly shown involvement in 38–77% of patients with the disease [7]. Although symptoms referable to the spleen itself are unusual, systemic complaints of fever, malaise, and weight loss are common, particularly in patients with splenomegaly [12]. In our experience, splenomegaly (greatest splenic dimension ≥ 14 cm) is seen in about a third of patients with sarcoidosis; marked splenomegaly (greatest splenic dimension ≥ 18 cm) is present in 6% of patients [12]. Other studies have reported finding splenomegaly in 25–60% of patients [1315].

At our institution, hypodense splenic nodules are seen in approximately 15% of patients with sarcoidosis [12]. Other studies have shown both lower (6%) [15] and higher (33%) [14] values, a variation that is probably linked to geographic and ethnic differences in study populations. Lesions are usually diffusely distributed and innumerable. Most nodules are between 0.1 and 3.0 cm, with a mean of approximately 1.0 cm [18, 19]. Isolated or predominant involvement of the spleen by nodules is more common than isolated or predominant hepatic nodular disease [18, 19]. Splenomegaly is common, although 17% of patients with nodules at our institution were found to have normal-size spleens [18]. Of our patients with hepatosplenic nodules, 76% also had concomitant abdominal lymphadenopathy [18]. Punctate calcifications are relatively uncommon in our experience but have been reported as affecting 16% of patients in one study [15].

The occurrence of nodular hepatosplenic sarcoid is more common during the first 5 years of sarcoidosis, with only six of 32 patients in one series having had the disease longer at the time that nodular hepatosplenic sarcoid was diagnosed [18]. Abdominal or systemic symptoms were also seen frequently in patients with nodular hepatosplenic sarcoidosis. In one study, they were present in 66% of the patients [18].

On contrast-enhanced CT, the splenic nodules are hypodense relative to adjacent normal spleen. Peripheral enhancement is not seen (Figs. 2A, 2B, 2C, 2D, 6A, 6B, 6C, 6D, and 7A, 7B). On MRI, the lesions are also hypointense on all sequences and hypoenhancing, although they become less conspicuous on delayed imaging, suggesting equilibration [21] (Figs. 2A, 2B, 2C, 2D and 8A, 8B, 8C). Lesions are best seen on early-phase gadolinium-enhanced T2-weighted fat-suppressed or T1-weighted images [21]. Data on the typical sonographic appearance are limited. In one report, lesions visible on contrast-enhanced CT were not seen on sonography, suggesting that the acoustic impedance of the granulomas was similar to that of normal splenic tissue [28]. We have noted that splenic nodules resulting from sarcoidosis show a slightly hyperechoic or inhomogeneous appearance (Figs. 6A, 6B, 6C, 6D and 8A, 8B, 8C), although hypoechoic nodules have also been reported [17].

figure
View larger version (66K)
Fig. 6A. 52-year-old woman with leukopenia and mild anemia. (Reprinted with permission from [12]) Contrast-enhanced CT scan shows mild splenomegaly with multiple small hypoattenuating nodules scattered diffusely throughout spleen.

figure
View larger version (68K)
Fig. 6B. 52-year-old woman with leukopenia and mild anemia. (Reprinted with permission from [12]) Sonogram of spleen shows splenomegaly with inhomogeneous echotexture.

figure
View larger version (95K)
Fig. 6C. 52-year-old woman with leukopenia and mild anemia. (Reprinted with permission from [12]) Photograph of gross specimen of spleen obtained at splenectomy shows multiple macroscopic nodules separated by thin bands of splenic parenchyma (arrow indicates one of many nodules).

figure
View larger version (147K)
Fig. 6D. 52-year-old woman with leukopenia and mild anemia. (Reprinted with permission from [12]) Photomicrograph of histopathologic specimen reveals multiple small granulomas (arrows) that have coalesced to form macroscopic nodules (N). (H and E, ×10)

figure
View larger version (61K)
Fig. 7A. 21-year-old woman with fatigue and elevated angiotensin-converting enzyme level. Contrast-enhanced CT scan shows multiple well-defined hypodense nodules scattered throughout spleen. Smaller and less well-defined hepatic nodules are observed, along with portal adenopathy (arrow).

figure
View larger version (115K)
Fig. 7B. 21-year-old woman with fatigue and elevated angiotensin-converting enzyme level. Photograph obtained at laparoscopy reveals white plaques studding liver, presumably corresponding to sarcoid granulomas.

figure
View larger version (77K)
Fig. 8A. 42-year-old woman with sarcoidosis. (Courtesy of Mittelstaedt C, Chapel Hill, NC) T2-weighted fat-saturated image (A) and gadolinium-enhanced T1-weighted image (B) reveal splenomegaly with hypointense and hypoenhancing splenic nodules.

figure
View larger version (71K)
Fig. 8B. 42-year-old woman with sarcoidosis. (Courtesy of Mittelstaedt C, Chapel Hill, NC) T2-weighted fat-saturated image (A) and gadolinium-enhanced T1-weighted image (B) reveal splenomegaly with hypointense and hypoenhancing splenic nodules.

figure
View larger version (64K)
Fig. 8C. 42-year-old woman with sarcoidosis. (Courtesy of Mittelstaedt C, Chapel Hill, NC) Sonogram shows splenomegaly with heterogeneous echotexture.

Abdominal Lymph Nodes

In our experience, abdominal adenopathy— defined as two or more nodes with a short axis greater than 1 cm or nodes in the retrocrural area with a short axis greater than 6 mm—is seen in approximately 30% of patients with sarcoidosis. Extensive adenopathy (node size > 2 cm and involvement of four or more sites) is found in approximately 10% of patients [12]. Other studies have shown similar or higher frequencies [14, 15]. In a study of 11 patients with abdominal or pelvic adenopathy from sarcoidosis, enlarged celiac artery nodes were seen in 82%; porta hepatis nodes, in 73%; paraaortic or paracaval nodes, in 73%; gastrohepatic ligament nodes, in 55%; mesenteric nodes, in 55%; superior mesenteric artery nodes, in 45%; and pelvic nodes, in 33%. Retrocrural nodes were involved in only 18% of the patients. In comparing the group of patients with sarcoidosis with a group of patients with non-Hodgkin's lymphoma, retrocrural nodes were involved significantly more frequently (70%) in the patients with lymphoma. No significant difference in the frequency of involvement at other nodal stations was found between the patients with lymphoma and the patients with sarcoidosis. Paraaortic and pelvic involvement was more commonly found in the lymphoma group; however, this difference between the two groups did not reach statistical significance in this relatively small series [14]. Mean node size was also significantly smaller in patients with sarcoidosis than in patients with lymphoma (mean ± SD, 2.6 ± 1.7 cm in sarcoidosis vs 8.0 ± 5.5 cm in lymphoma), but diameters of some nodes in patients with sarcoidosis were as large as 7.5 cm [14]. Confluent masses were also significantly less common in patients with sarcoidosis than in patients with lymphoma. In one series, masses were seen in only 9% of the patients with sarcoidosis but were seen in 50% of the patients with lymphoma [14].

Nodal calcification is unusual in sarcoidosis. Enlarged abdominal lymph nodes may be the only abnormal finding on an imaging study, as was the case in approximately 50% of patients in one series [15]. Patients with lymphadenopathy tend to be younger (mean age in patients with adenopathy, 33 years; mean age in patients without lymphadenopathy, 43 years) [12] and are more likely to have symptoms than those without lymphadenopathy, although such symptoms may consist only of systemic distress such as fever, malaise, and weight loss. Nodal enlargement producing obstruction of adjacent structures has, however, been observed in the biliary tree and ureter. In one case report, a 27-year-old man with a known diagnosis of sarcoidosis presented with both jaundice and hydronephrosis from nodal compression. Resolution was observed after steroid therapy [29]. Chylous ascites has also been reported in one patient with extensive mesenteric and paraaortic adenopathy [30]. This patient did not respond to steroids, suggesting that fibrosis may have been present. One case of venous insufficiency in the small intestine resulting from sarcoid nodes compressing the mesenteric vein has also been described [31].

On CT, the nodes affected by sarcoidosis generally show homogeneous soft-tissue attenuation (Figs. 1A, 1B, 1C, 1D, 3A, 3B, 7A, 7B, and 9A, 9B). On MRI, these nodes appear hyperintense on T2-weighted fat-saturated images and show mild enhancement on gadolinium-enhanced images [21] (Fig. 1A, 1B, 1C, 1D). A fine hypointense speckled appearance of the nodes on T2-weighted fat-saturated images has been described, presumably reflecting macroscopic aggregation of granulomas [21] (Fig. 9A, 9B). Other authors have reported either homogeneously increased T2 signal in the nodes or a central low signal surrounded by peripheral high signal on T2-weighted imaging [32]. On sonography, nodes have been described as containing low-level echoes and increased through transmission, mimicking lymphoma [32]. Massive echolucent retrocardiac nodes resulting from sarcoidosis may simulate cor triatriatum [33]. We have seen a more nondescript appearance with a slightly hypoechoic echotexture compared with the liver (Fig. 10).

figure
View larger version (58K)
Fig. 9A. 34-year-old woman with sarcoidosis who presented with malaise, anorexia, weight loss, fever, and night sweats. (Reprinted with permission from [21]) Contrast-enhanced axial CT scan shows marked splenomegaly with gastric compression and extensive upper abdominal adenopathy (arrows).

figure
View larger version (57K)
Fig. 9B. 34-year-old woman with sarcoidosis who presented with malaise, anorexia, weight loss, fever, and night sweats. (Reprinted with permission from [21]) T2-weighted fat-saturated image reveals hyperintense lymphadenopathy (arrows), with suggestion of hypointense speckling.

figure
View larger version (55K)
Fig. 10. 42-year-old man with uveitis, bilateral hilar adenopathy, and pulmonary interstitial opacities. Sonogram shows enlarged slightly hypoechoic celiac lymphadenopathy (n), liver (L), and celiac axis (arrow). Biopsy of subcutaneous nodule revealed noncaseating granulomata consistent with sarcoidosis. (Courtesy of Mittelstaedt C, Chapel Hill, NC)

Pancreas

Sarcoid involvement of the pancreas is uncommon. Results of autopsy studies have suggested an incidence of 1%, although in one series, mild elevation in pancreatic amylase level was noted in 9% of patients [34, 35]. Clinically evident disease is rare and usually results from either direct infiltration of the gland or compression of pancreatic structures by enlarged peripancreatic nodes. Abdominal and back pain, weight loss, anorexia, jaundice, and pruritus are all reported and usually result from obstruction of the bile or pancreatic duct. Pancreatitis without an obstructive mass has also been reported and may result from direct gland involvement [36]. Sarcoid-associated hypercalcemia also may induce acute pancreatitis. Because prolonged sun exposure in patients with sarcoidosis may result in acute hypercalcemia, an episode of pancreatitis may be the initial presentation of sarcoidosis in patients on vacation in sunny climates [37]. Diabetes due to gland infiltration or pancreatitis also has been reported [38, 39].

The imaging manifestations of pancreatitis resulting from sarcoidosis are indistinguishable from those of pancreatitis caused by other conditions. Pancreatic mass lesions associated with sarcoidosis are rare but may mimic pancreatic adenocarcinomas in both their presentation and appearance. Lesions as large as 6–7 cm have been described [36, 40]. Associated narrowing or obstruction of the common bile duct as well as the portal and splenic veins also has been observed [41, 42]. Concomitant enlargement of peripancreatic nodes may be seen [40]. Typical lesions have been described as hypodense and hypo- or nonenhancing on CT [40, 43]. On sonography, the masses are hypoechoic [40]. Cholangiograms typically show a long, smoothly tapered narrowing rather than the more abrupt termination associated with tumor [43].

Percutaneous biopsy may be helpful in arriving at a diagnosis in cases of a pancreatic mass resulting from sarcoid, but it should be noted that sarcoidlike changes are occasionally seen in association with pancreatic neoplasms as well as with other tumors, both in the primary tumor and in regional nodes that may or may not contain tumor. This condition has been reported in approximately 4% of patients with carcinomas in various sites and 7% of patients with non-Hodgkin's lymphoma [6]. Most patients with pancreatic sarcoidosis respond to corticosteroids, so resection should be avoided if possible [43].

Luminal Gastrointestinal Tract

The most common site of sarcoid involvement in the gastrointestinal tract is the stomach, although reported locations range from the esophagus to the rectum. Symptomatic involvement of the luminal gastrointestinal tract by sarcoidosis is estimated to occur in less than 1% of patients [34]. Asymptomatic involvement may be more frequent. In a study of 60 asymptomatic patients with sarcoidosis, 10% were found to have gastric mucosal granulomas [44]. More extensive disease may result in abdominal pain, obstruction, bleeding, and malabsorption. Lesions typically respond to steroids [4547], although in some reported cases, the abnormal morphology remained, suggesting that fibrosis may persist after resolution of the granulomatous inflammation [46, 48].

Lesions in the gastrointestinal tract show a varied appearance. Plaquelike lesions have been reported in the esophagus [45]. Gastric sarcoidosis may present as mucosal nodularity and thickened irregular folds, radiographic features that may be indistinguishable from those of Ménétrier's disease [45, 49] (Fig. 11). Apthous ulcers and larger ulcerations have been seen as well as linear and polypoid filling defects in the stomach [49] (Fig. 12A, 12B, 12C). A linitis plastica–type appearance has been identified and can mimic involvement by gastric adenocarcinomas [50] (Fig. 13A, 13B). In the small bowel, a circumferential obstructive process due to sarcoidosis also has been described in the duodenum [48, 51]. Colonic sarcoidosis may appear as irregular mass lesions mimicking carcinoma [5254] (Fig. 14A, 14B, 14C, 14D). Sarcoidosis in the appendix may produce appendicitis [51].

figure
View larger version (74K)
Fig. 11. 24-year-old man with epigastric pain and hematemesis. Spot image from upper gastrointestinal examination shows thickened gastric folds. Gastric biopsy revealed noncaseating granulomata consistent with sarcoidosis. (Courtesy of Levy A, Armed Forces Institute of Pathology, Washington, DC)

figure
View larger version (59K)
Fig. 12A. 36-year-old woman with nausea and vomiting. Radiograph obtained at upper gastrointestinal examination shows irregular gastric ulceration (U) with deformity and narrowing of gastric body and antrum (arrows).

figure
View larger version (61K)
Fig. 12B. 36-year-old woman with nausea and vomiting. Contrast-enhanced CT scan obtained through upper abdomen shows thickening of gastric antrum and body (arrows) with paraaortic adenopathy (arrowhead).

figure
View larger version (60K)
Fig. 12C. 36-year-old woman with nausea and vomiting. Contrast-enhanced CT scan obtained through lower abdomen shows mesenteric adenopathy (arrows) with thickening of cecum and terminal ileum (arrowhead). Because ulcerations proved refractory to therapy, antrectomy and Billroth's I anastomosis were performed along with ileocecal resection and liver biopsy. Histologic examination of pathology specimens showed granulomatous inflammation consistent with sarcoidosis.

figure
View larger version (63K)
Fig. 13A. 21-year-old woman with nausea, vomiting, and weight loss. Radiograph obtained at upper gastrointestinal examination shows antral narrowing and deformity. Biopsy revealed noncaseating granulomata.

figure
View larger version (60K)
Fig. 13B. 21-year-old woman with nausea, vomiting, and weight loss. Contrast-enhanced CT scan also shows mild mesenteric and paraaortic adenopathy (arrows).

figure
View larger version (58K)
Fig. 14A. 43-year-old man with right lower quadrant pain and weight loss. Compression spot film image obtained during barium enema shows irregular narrowing of cecal lumen. (Reprinted with permission from [54])

figure
View larger version (52K)
Fig. 14B. 43-year-old man with right lower quadrant pain and weight loss. Contrast-enhanced CT scan shows circumferentially thickened cecum. (Courtesy of Levy A, Armed Forces Institute of Pathology, Washington, DC)

figure
View larger version (56K)
Fig. 14C. 43-year-old man with right lower quadrant pain and weight loss. Abdominal sonogram also shows thickened cecum. At exploratory laparotomy, large cecal mass with extension into small bowel was noted with accompanying adenopathy. Right hemicolectomy was performed. Pathology showed noncaseating granulomatous inflammation involving ileum, colon, and lymph nodes, consistent with sarcoidosis. (Courtesy of Levy A, Armed Forces Institute of Pathology, Washington, DC)

figure
View larger version (185K)
Fig. 14D. 43-year-old man with right lower quadrant pain and weight loss. Photomicrograph of histopathologic specimen obtained from cecum shows chronic inflammatory changes in mucosa and noncaseating submucosal granulomas (arrows). (H and E, ×10) (Reprinted with permission from [54])

Exclusion of other causes of granulomatous inflammation, including fungal and mycobacterial diseases and Crohn's disease, is important. The appearance of pathologic specimens may offer some features with which to distinguish sarcoidosis from other entities. Sarcoidosis is frequently limited to the mucosa, whereas Crohn's disease is a transmural process [51]. Sarcoidosis is often accompanied by an elevated serum angiotensin-converting enzyme (ACE) level; unlike Crohns's disease, it responds rapidly to steroids. Concurrent involvement of other organ systems by sarcoidosis may also be helpful in determining the correct diagnosis.

Genitourinary Tract

Granulomatous involvement of the kidney has been reported in 7–22% of patients with sarcoidosis at autopsy [7]. Nephrotic syndrome, glomerulonephritis, and tubulointerstitial disease all have been reported but are rare. Nephromegaly or renal atrophy may result, depending on the extent and duration of involvement. Radiographically detectable renal masses are unusual [55]. Multiple 2- to 3-cm isodense masses that enhance less than the adjacent normal renal parenchyma have been reported in a patient with nodular involvement of the liver and spleen [56]. The renal deposits may mimic the appearance of lymphoma or metastasis (Figs. 15 and 16A, 16B).

figure
View larger version (69K)
Fig. 15. 34-year-old man with bilateral hypoenhancing renal masses (arrows). Fine-needle aspiration of left kidney showed findings compatible with sarcoidosis. (Courtesy of Levy A, Armed Forces Institute of Pathology, Washington, DC)

figure
View larger version (47K)
Fig. 16A. 35-year-old woman with abdominal pain. (Courtesy of Levy A, Armed Forces Institute of Pathology, Washington, DC) Contrast-enhanced CT scan shows heterogeneous mass involving left kidney with paraaortic adenopathy. Patient underwent left nephrectomy.

figure
View larger version (123K)
Fig. 16B. 35-year-old woman with abdominal pain. (Courtesy of Levy A, Armed Forces Institute of Pathology, Washington, DC) Photograph of gross specimen shows granulomatous mass. Microscopic pathologic findings were compatible with sarcoidosis.

Hydronephrosis may be caused by compression of the ureters by enlarged retroperitoneal nodes. Resolution of both the nodal enlargement and the hydronephrosis has been reported with administration of steroids [29].

The most frequent effect of sarcoidosis in the kidney is due to hypercalcemia or hypercalciuria. Nephrocalcinosis, nephrolithiasis, and interstitial calcium deposition all have been reported and may lead to renal failure. Radiographically detectable nephrocalcinosis is reported to occur in 1–4% of patients [15, 56]. Hypercalciuria is more common, being reported in 15–62% of patients. Hypercalcemia is noted in 3–11% of patients [7]. Increased conversion of 25-hydroxyvitamin D3 to active 1,25 dihydroxyvitamin D by granuloma macrophages causes disturbance in calcium metabolism. This overproduction then results in increased intestinal calcium absorption [57]. Most patients with hypercalcemia have radiographic evidence of pulmonary disease, although this occurrence is not consistently found [58]. Acute sunlight exposure may precipitate hypercalcemia by increasing the availability of substrate for this conversion. Such acute hypercalcemia may result in malaise, dehydration, or pancreatitis and may be the initial presentation of sarcoidosis [37].

Epididymal and testicular involvement by sarcoidosis has also been reported. Unilateral disease is most common, but bilateral involvement is not rare. On sonography, the resultant masses are described as homogeneously hypoechoic [59] (Fig. 17).

figure
View larger version (70K)
Fig. 17. 44-year-old man with bilateral testicular pain. Testicular sonogram reveals multiple bilateral hypoechoic masses. Excisional biopsy of right testicular mass was performed. Gross pathologic examination (not shown) revealed firm tan mass in wedge of testicular tissue. Microscopic examination (not shown) found confluent epithelioid granulomas compatible with sarcoidosis. (Courtesy of Levy A, Armed Forces Institute of Pathology, Washington, DC)

Abdominal Wall

Sarcoidosis can involve the skeletal muscle and produce either a nodular, myopathic, or myositic form. Radiographic changes described with the nodular form of sarcoidosis include nodules extending along the muscle fibers. The atrophic myopathic form is characterized by muscular atrophy and fatty infiltration [60]. Although the muscle is generally smaller than normal, pseudohypertrophy from abundant fatty infiltration has also been described. Involvement of the extremities is most common; however, sarcoidosis involving the musculature of the abdominal wall has been reported [61] (Fig. 18).

figure
View larger version (57K)
Fig. 18. CT scan obtained in 44-year-old man who presented with firm mass in right upper quadrant that corresponded to abnormal right rectus abdominis muscle. Note sarcoid nodule in subcutaneous fat. Biopsy of left internal oblique muscle showed noncaseating granulomas and increased connective tissue and fat consistent with sarcoid myopathy and pseudohypertrophy. (Reprinted with permission from [61])

Sarcoidosis also may involve the subcutaneous fat-producing nodules or a more diffuse infiltrative lesion. Slight enhancement of the lesion relative to the muscle is reported in the nodular form; little enhancement is seen in the diffuse form. Both forms show signal intensity similar to that of muscle on T1-weighted images and heterogeneously increased T2 signal [62].

Correlation of Abdominal Sarcoidosis with Pulmonary Involvement
Previous sectionNext section

Involvement of the abdominal viscera frequently occurs in the context of more extensive chest disease; however, abdominal sarcoidosis without pulmonary or mediastinal involvement is not rare. In a study at our institution, between 25% and 38% of patients who had sarcoidosis with abdominal adenopathy, hepatomegaly, or splenomegaly had normal findings on chest radiography [12]. This frequency persisted even when the abdominal findings of sarcoidosis were marked. Normal findings on chest radiographs were noted in one of three patients whose spleen size exceeded 18 cm, in two of five patients with marked adenopathy, and in two of four patients whose liver span exceeded 25 cm [12]. Similar findings have been observed in other studies in which the authors have concluded that there was no correlation between the degree of chest abnormality and the involvement of liver, spleen, or node [14, 15].

The extent of pulmonary involvement has been evaluated in patients with nodular hepatosplenic sarcoidosis both at initial presentation and on subsequent follow-up visits. In a study of 32 patients with nodular hepatosplenic sarcoidosis, 25% had normal chest radiographs. Sixty-one percent of patients had stage 1 or 2 findings on chest radiographs, and 14% had stage 3 or 4 findings on chest radiographs. In the subset of patients for whom follow-up was available, 74% had no change in stage, suggesting that the presence of radiographically visible splenic nodules does not portend a bad pulmonary prognosis [18]. Case reports of sarcoid in other abdominal viscera also suggest that there is no firm correlation between chest findings and abdominal disease [41, 43, 46, 52, 56, 62].

ACE Level, 67Gallium (Ga) Citrate Scintigraphy, FDG Positron Emission Tomography, and Abdominal Sarcoidosis
Previous sectionNext section

Several markers and techniques have been investigated for assessment of disease activity and location in sarcoidosis including serum ACE levels, 67Ga citrate scintigraphy, and FDG positron emission tomography (PET). Serum ACE is thought to be produced by the epithelioid cells within sarcoid granulomas. It is elevated in approximately 60% of patients with sarcoidosis, and its level is thought to reflect whole-body granuloma mass and disease activity [63, 64]. This supposition is supported by several studies of abdominal sarcoidosis and ACE levels. In one study, a linear relationship was observed between ACE level and spleen size as well as between ACE level and the presence of adenopathy and hepatosplenic nodules. The mean serum ACE level was noted to be 3.1 times the upper limits of a normal level in patients with sarcoidosis who had splenic nodules, whereas the mean ACE level was 1.3 times the normal level in patients with sarcoidosis who had no splenic nodules [12]. In another study of patients with nodular hepatosplenic sarcoidosis, the ACE level was elevated in 10 of 11 patients. The single patient in this study with a normal ACE level had been receiving 40–60 mg of prednisone, which may have suppressed the ACE [18].

Gallium-67 citrate is a nonspecific agent taken up by activated lymphocytes, mononuclear phagocytes, and neutrophils in the lung and other organs. Increased pulmonary uptake is reported in more than 90% of patients with active sarcoidosis and is thought to reflect disease activity [65, 66]. Extrapulmonary accumulation has also been reported in the lacrimal and parotid glands, nasopharynx, skin, bone, muscle, and abdominal nodes. Normal intense 67Ga uptake in the liver and spleen limits assessment of these organs [67]. Although 67Ga uptake is also seen in lymphoma and granulomatous infections, a positive finding on a 67Ga citrate scintigraphic scan may be helpful in selecting a site for diagnostic biopsy and in monitoring disease activity.

Increased FDG accumulation has been reported in sarcoidosis and in granulomatous infections. Such activity may mimic neoplastic disease, particularly in a patient in whom sarcoidosis is asymptomatic and undiagnosed. Increased FDG activity has also been found in extrathoracic sarcoidosis, including the liver, spleen, abdominal and inguinal nodes, muscle, skin, and subcutaneous tissue. Activity in these more unusual sites, particularly those in the abdomen, may mimic lymphoma [68].

Conclusion
Previous sectionNext section

Sarcoidosis has been reported in virtually every abdominal organ and compartment; the liver, spleen, and lymph nodes are the sites most commonly involved. Imaging findings usually consist of either homogeneous organomegaly or nodular infiltration. These infrequently seen lesions can mimic more serious neoplastic or infectious diseases on both radiologic and scintigraphic studies. Sarcoidosis should be included in the abdominal differential diagnosis in the appropriate clinical setting so that therapeutic misadventures can be avoided.

Address correspondence to D. M. Warshauer.

References
Previous sectionNext section
1. Hunninghake GW, Costabel U, Ando M, et al. Statement on sarcoidosis. Am J Respir Crit Care Med 1999; 160:736 –755 [Google Scholar]
2. Rybicki BA, Major M, Popovich J Jr, Miliarik MJ, Iannuzzi MC. Racial differences in sarcoidosis incidence: a five year study in a health maintenance organization. Am J Epidemiol 1997; 145:234 –241 [Google Scholar]
3. Iwai K, Tachibana T, Hosoda Y, Matsui Y. Sarcoidosis autopsies in Japan: frequency and trend in the last 28 years. Sarcoidosis 1988; 5:60 –65 [Google Scholar]
4. Shadid S, ter Maaten JC. Sarcoidosis: a great mimicker. J Intern Med 2002; 251:174 –176 [Google Scholar]
5. Newman LS, Rose CS, Maier LA. Sarcoidosis. N Engl J Med 1997; 336:1224 –1234 [Google Scholar]
6. Brincker H. Sarcoid reactions in malignant tumours. Cancer Treat Rev 1986; 13:147 –156 [Google Scholar]
7. Lynch JP III. Extrapulmonary sarcoid. Semin Respir Infect 1998; 13:229 –254 [Google Scholar]
8. Hagerstrand I, Linell F. The prevalence of sarcoidosis autopsy material from a Swedish town. Acta Med Scand 1964; 425[suppl]:171 –174 [Google Scholar]
9. Longcope WT, Freiman DG. A study of sarcoidosis based on a combined investigation of 160 cases including 30 autopsies from the Johns Hopkins Hospital and Massachusetts General Hospital. Medicine (Baltimore) 1952; 31:1 –132 [Google Scholar]
10. Lehmuskallio E, Hannuksela M, Halme H. The liver in sarcoidosis. Acta Med Scand 1977; 202:289 –293 [Google Scholar]
11. Klatskin G. Hepatic granulomata: problems in interpretation. Ann N Y Acad Sci 1976; 278:427 –432 [Google Scholar]
12. Warshauer DM, Dumbleton SA, Molina PL, Yankaskas BC, Parker LA, Woosley JT. Abdominal CT findings in sarcoidosis: radiologic and clinical correlation. Radiology 1994; 192:93 –98 [Google Scholar]
13. Deutch SJ, Sandler MA, Tankanow LB. Abdominal lymphadenopathy in sarcoidosis. J Ultrasound Med 1987; 6:237 –242 [Google Scholar]
14. Britt AR, Francis IR, Glazer GM, Ellis JH. Sarcoidosis: abdominal manifestations at CT. Radiology 1991; 178:91 –94 [Google Scholar]
15. Folz SJ, Johnson CD, Swensen SJ. Abdominal manifestations of sarcoidosis in CT studies. J Comput Assist Tomogr 1995; 19:573 –579 [Google Scholar]
16. Tsukada T, Katayama N, Taniguchi M, et al. Liver sarcoidosis showing low-density intrahepatic septa on postcontrast computed tomography. Gastroenterol Jpn 1993; 28:730 –733 [Google Scholar]
17. Kessler A, Mitchell DG, Israel HL, Goldberg BB. Hepatic and splenic sarcoidosis: ultrasound and MR imaging. Abdom Imaging 1993; 18:159 –163 [Google Scholar]
18. Warshauer DM, Molina PL, Hamman SM, et al. Nodular sarcoidosis of the liver and spleen: analysis of 32 cases. Radiology 1995; 195:757 –762 [Google Scholar]
19. Scott GC, Berman JM, Higgins JL Jr. CT patterns of nodular hepatic and splenic sarcoidosis: a review of the literature. J Comput Assist Tomogr 1997; 21:369 –372 [Google Scholar]
20. Nakata K, Iwata K, Kojima K, Kanai K. Computed tomography of liver sarcoidosis. J Comput Assist Tomogr 1989; 13:707 –708 [Google Scholar]
21. Warshauer DM, Semelka RC, Ascher SM. Nodular sarcoidosis of the liver and spleen: appearance on MR images. J Magn Reson Imaging 1994; 4:553 –557 [Google Scholar]
22. Ishak KG. Sarcoidosis of the liver and bile ducts. Mayo Clin Proc 1998; 73:467 –472 [Google Scholar]
23. Rezeig MA, Fashir BM. Biliary tract obstruction due to sarcoidosis: a case report. Am J Gastroenterol 1997; 92:527 –528 [Google Scholar]
24. Albu E, Saraiya RJ, Carvajal SJ, Sehonanda A, Balar N, Gerst PH. Sarcoidosis presenting as obstructive jaundice. Am Surg 1995; 61:516 –517 [Google Scholar]
25. Arsuaga JE, Oleaga JA, Rothstein KD, Haskal ZJ. SCVIR annual meeting film panel session: diagnosis and discussion of case 6—Society of Cardiovascular and Interventional Radiology. J Vasc Interv Radiol 2000; 11:792 –795 [Google Scholar]
26. Taavitsainen M, Koivuniemi A, Helminen J. Aspiration biopsy of the spleen in patient with sarcoidosis. Acta Radiol 1987; 28:723 –725 [Google Scholar]
27. Selroos O, Koivunen E. Usefulness of fine-needle aspiration biopsy of spleen in diagnosis of sarcoidosis. Chest 1983; 83:193 –195 [Google Scholar]
28. Franquet T, Oteo JA, Cozcolluela R, Casas JM. Multinodular splenic sarcoidosis: discordant CT and sonographic findings. AJR 1991; 156:1113 –1114 [Google Scholar]
29. Fraioli P, Montemurro L, Castrignano L, Rizzato G. Retroperitoneal involvement in sarcoidosis. Sarcoidosis 1990; 7:101 –105 [Google Scholar]
30. Provenza JM, Bacon BR. Chylous ascites due to sarcoidosis. Am J Gastroenterol 1991; 86:92 –95 [Google Scholar]
31. Schwarzchild W, Myerson RM. Venous insufficiency of the small intestine secondary to sarcoidosis of mesenteric lymph nodes. Am J Gastroenterol 1968; 50:69 –72 [Google Scholar]
32. Bach DB, Vellet AD. Retroperitoneal sarcoidosis. AJR 1991; 156:520 –522 [Abstract] [Google Scholar]
33. Walsh TK, Vacek JL, Bellinger RL. Sarcoidosis mimicking cor triatriatum: echolucency of adenopathy due to sarcoidosis. Am J Med 1985; 78:501 –505 [Google Scholar]
34. Mayock RL, Bertrand P, Morrison CE, Scott JH. Manifestations of sarcoidosis: analysis of 145 patients with a review of nine series selected from the literature. Am J Med 1963; 35:67 –89 [Google Scholar]
35. McCormick PA, O'Donnell M, McGeeney K, FitzGerald O, McCormick DA, FitzGerald MX. Sarcoidosis and the pancreas. Ir J Med Sci 1988; 157:181 –183 [Google Scholar]
36. Siavelis HA, Herrmann ME, Aranha GV, Garcia G, Eubanks T, Reyes CV. Sarcoidosis and the pancreas. Surgery 1999; 125:456 –461 [Google Scholar]
37. Cronin CC, Dinneen SF, O'Mahony S, Bredin CP, O'Sullivan DJ. Precipitation of hypercalcemia in sarcoidosis by foreign sun holidays: report of four cases. Postgrad Med J 1990; 66:307 –309 [Google Scholar]
38. Boruchowicz A, Maunoury V, Crinquette JF, Cappoen JP. Diabetes: an ignored complication of sarcoidosis. (letter) Am J Gastroenterol 1995; 90:681 [Google Scholar]
39. Cronin CC, Dinneen SF, Mitchell TH, Shanahan FL. Sarcoidosis, the pancreas, and diabetes mellitus. (letter) Am J Gastroenterol 1995; 90:2068 [Google Scholar]
40. Sagalow BR, Miller CL, Wechsler RJ. Pancreatic sarcoid mimicking pancreatic cancer. J Clin Ultrasound 1988; 16:131 –134 [Google Scholar]
41. Bacal D, Hoshal VL Jr, Schaldenbrand JD, Lampman RM. Sarcoidosis of the pancreas: case report and review of the literature. Am Surg 2000; 66:675 –678 [Google Scholar]
42. Toda K, Souda S, Yoshikawa Y, Momiyama T, Ohshima M. Narrowing of the distal common bile duct and the portal vein secondary to pancreatic sarcoidosis. Am J Gastroenterol 1994; 89:1259 –1291 [Google Scholar]
43. Frank JL, Goldman M, Nathanson I, et al. Surgical management of pancreatic sarcoid. Eur J Surg 2001; 167:68 –72 [Google Scholar]
44. Palmer ED. Note on silent sarcoidosis of the gastric mucosa. J Lab Clin Med 1958; 52:231 [Google Scholar]
45. Levine MS, Ekberg O, Rubesin SE, Gatenby RA. Gastrointestinal sarcoidosis: radiographic findings. AJR 1989; 153:293 –295 [Abstract] [Google Scholar]
46. Rauf A, Davis P, Levendoglu H. Sarcoidosis of the small intestine. Am J Gastroenterol 1988; 83:187 –189 [Google Scholar]
47. Fleming RH, Nuzek M, McFadden DW. Small intestinal sarcoidosis with massive hemorrhage: report of a case. Surgery 1994; 115:127 –131 [Google Scholar]
48. Noel JM, Katona IM, Pineiro-Carrero VM. Sarcoidosis resulting in duodenal obstruction in an adolescent. J Pediatr Gastroenterol Nutr 1997; 24:594 –598 [Google Scholar]
49. Farman J, Ramirez G, Rybak B, Lebwohl O, Semrad C, Rotterdam H. Gastric sarcoidosis. Abdom Imaging 1997; 22:248 –252 [Google Scholar]
50. Bellan L, Semelka R, Warren CP. Sarcoidosis as a cause of linitis plastica. Can Assoc Radiol J 1988; 39:72 –74 [Google Scholar]
51. Stampfl DA, Grimm IS, Barbot DJ, Rosato FE, Gordon SJ. Sarcoidosis causing duodenal obstruction: case report and review of gastrointestinal manifestations. Dig Dis Sci 1990; 35:526 –532 [Google Scholar]
52. Hilzenrat N, Spanier A, Lamoureux E, Bloom C, Sherker A. Colonic obstruction secondary to sarcoidosis: nonsurgical diagnosis and management. Gastroenterology 1995; 108:1556 –1559 [Google Scholar]
53. Kohn NN. Sarcoidosis of the colon. J Med Soc N J 1980; 77:517 –518 [Google Scholar]
54. Smirniotopoulos JG, Lonergan GJ, Abbott RM, et al. Image interpretation session: 1998—cecal and pulmonary sarcoidosis. RadioGraphics 1999; 19:223 –225 [Google Scholar]
55. Gazaigne J, Mozziconacci JG, Mornet M, Provendier B. Epididymal and renal sarcoidosis. Br J Urol 1995; 75:413 –414 [Google Scholar]
56. Hughes JJ, Wilder WM. Computed tomography of renal sarcoidosis. J Comput Assist Tomogr 1988; 12:1057 –1058 [Google Scholar]
57. Sato A. Renal dysfunction in patients with sarcoidosis. Intern Med 1996; 35:523 –524 [Google Scholar]
58. Sander S, Buller GK, Perazella MA. Hypercalcemia, sarcoidosis, and normal chest radiographs. Am J Med 1995; 99:437 –438 [Google Scholar]
59. Yamamoto N, Hasegawa Y, Miyamoto K, Ikeda T, Kuriyama M, Kawada Y. Bilateral epididymal sarcoidosis: case report. Scand J Urol Nephrol 1992; 26:301 –303 [Google Scholar]
60. Otake S. Sarcoidosis involving skeletal muscle: imaging findings and relative value of imaging procedures. AJR 1994; 162:369 –375 [Abstract] [Google Scholar]
61. Levine CD, Miller JJ, Stanislaus G, Wachsberg RH, Simmons MZ. Sarcoid myopathy: imaging findings. J Clin Ultrasound 1997; 25:515 –517 [Google Scholar]
62. Shinozaki T, Watanabe H, Aoki J, Fukuda T, Shirakura K, Takagishi K. Imaging features of subcutaneous sarcoidosis. Skeletal Radiol 1998; 27:359 –364 [Google Scholar]
63. Gilbert S, Steinbrech D, Landas S, Hunninghake G. Amounts of angiotensin-converting enzyme mRNA reflect the burden of granulomas in granulomatous lung disease. Am Rev Respir Dis 1993; 148:483 –486 [Google Scholar]
64. Maliarik MJ, Rybicki BA, Malvitz E, et al. Angiotensin-converting enzyme gene polymorphism and risk of sarcoidosis. Am J Respir Crit Care Med 1998; 158:1566 –1570 [Google Scholar]
65. Gupta RG, Bekerman C, Sicilian L, Oparil S, Pinsky SM, Szidon JP. Gallium 67 citrate scanning and serum angiotensin-converting enzyme levels in sarcoidosis. Radiology 1982; 144:895 –899 [Google Scholar]
66. Alavi A, Palevsky HI. Gallium-67-citrate scanning in the assessment of disease activity in sarcoidosis. J Nucl Med 1992; 33:751 –755 [Google Scholar]
67. Rohatgi PK, Singh R, Vieras F. Extrapulmonary localization of gallium in sarcoidosis. Clin Nucl Med 1987; 12:9 –16 [Google Scholar]
68. Lewis PJ, Salama A. Uptake of fluorine-18-fluorodeoxyglucose in sarcoidosis. J Nucl Med 1994; 35:1647 –1649 [Google Scholar]

Recommended Articles

Imaging Manifestations of Abdominal Sarcoidosis

Full Access, , , ,
American Journal of Roentgenology. 2004;183:171-173. 10.2214/ajr.183.1.1830171
Citation | Full Text | PDF (2222 KB) | PDF Plus (2278 KB) 
Full Access, ,
American Journal of Roentgenology. 2014;203:1192-1204. 10.2214/AJR.13.12386
Abstract | Full Text | PDF (1122 KB) | PDF Plus (1179 KB) | Erratum 
Full Access, ,
American Journal of Roentgenology. 2013;200:W116-W123. 10.2214/AJR.12.8493
Abstract | Full Text | PDF (1186 KB) | PDF Plus (1211 KB) 
Full Access, , , , , , , , ,
American Journal of Roentgenology. 2018;211:76-86. 10.2214/AJR.18.19704
Abstract | Full Text | PDF (1227 KB) | PDF Plus (1279 KB) | Supplemental Material 
Full Access
American Journal of Roentgenology. 2017;209:826-835. 10.2214/AJR.17.17973
Abstract | Full Text | PDF (978 KB) | PDF Plus (1060 KB) 
Full Access, , , , ,
American Journal of Roentgenology. 2014;202:479-492. 10.2214/AJR.13.11463
Abstract | Full Text | PDF (1418 KB) | PDF Plus (1472 KB)