DOI: 10.1148/radiol.2453040999
(Radiology 2007;245:909-913.)
© RSNA, 2007
Case 127: Henoch-Schonlein Purpura1
Pamela T. Johnson, MD,
Karen M. Horton, MD and
Elliot K. Fishman, MD
1 From The Russell H. Morgan Department of Radiology and Radiological Science, Johns Hopkins School of Medicine, 601 N Caroline St, Room 3251, Baltimore, MD 21287. Received June 4, 2004; revision requested August 16; revision received January 11, 2005; final version accepted February 2.
Correspondence: Address correspondence to P.T.J. (e-mail: pjohnso5{at}jhmi.edu).
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HISTORY
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A 37-year-old man presented to his physician with sharp and continuous upper abdominal pain. Upper endoscopy was performed for evaluation and revealed Helicobacter pylori–negative gastritis. Treatment with a proton pump inhibitor failed to alleviate his symptoms. The patient subsequently developed diarrhea and dark stools, followed by a petechial rash that involved his lower extremities. At this point, he was admitted to an outside hospital for evaluation. Colonoscopy and repeat endoscopy revealed nothing that could account for his symptoms. After an observation period, he was discharged.
The patient's abdominal pain persisted and worsened. In addition, he felt feverish and developed joint pain, which was most severe in his knees and wrists. Three weeks after the initial episode, he was readmitted to the hospital with intractable abdominal pain and new onset of vomiting. At admission, a petechial rash with regions of purpura was noted on his thighs and calves. A similar rash with a maculopapular appearance was apparent on his upper extremities. Laboratory tests revealed an elevated erthrocyte sedimentation rate and a minimally elevated platelet count. Antinuclear antibody test results were negative. Intravenous contrast material–enhanced multidetector computed tomography (CT) of the abdomen and pelvis was performed the next day, with 120 mL of iohexol (Omnipque 350; GE Healthcare, Princeton, NJ) infused at a rate of 3 mL/sec.
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IMAGING FINDINGS
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Contrast-enhanced multidetector CT revealed several key findings. A long segment (estimated to be 25–30 cm) of proximal jejunal thickening was identified (Fig 1). The affected segment had mucosal enhancement and low attenuation in the submucosa owing to edema. A second thickened small-bowel segment was seen in the distal ileum (Fig 2), but the terminal ileum was normal (Fig 1). In addition, mesenteric edema and adenopathy were present (Fig 1). Minimal ascites (not shown) was identified in the pelvis. The mesenteric arteries and veins were well opacified and patent (Fig 1). No infarcts were seen in the kidneys or spleen.
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Figure 1a: Intravenous contrast-enhanced transverse multidetector CT images of the abdomen. (a) Jejunal wall thickening (arrow) of up to 1.5 cm. High attenuation within the wall reflects mucosal enhancement. (b) Patent superior mesenteric artery (black arrow) and mesenteric vein (white arrow), with thickened enhancing jejunum. (c) Enlarged mesenteric nodes and mesenteric inflammation (white arrows) adjacent to the abnormal jejunum. The superior mesenteric artery (black arrow) and mesenteric veins are patent. (d) Image obtained at the level of the cecum. In conjunction with a–c, this image shows that the diseased jejunum (arrow) extends over a long segment. (e) Image obtained at the level of the cecum shows normal terminal ileum (black arrow) and thickened small bowel (white arrow) with submucosal edema (target sign).
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Figure 1b: Intravenous contrast-enhanced transverse multidetector CT images of the abdomen. (a) Jejunal wall thickening (arrow) of up to 1.5 cm. High attenuation within the wall reflects mucosal enhancement. (b) Patent superior mesenteric artery (black arrow) and mesenteric vein (white arrow), with thickened enhancing jejunum. (c) Enlarged mesenteric nodes and mesenteric inflammation (white arrows) adjacent to the abnormal jejunum. The superior mesenteric artery (black arrow) and mesenteric veins are patent. (d) Image obtained at the level of the cecum. In conjunction with a–c, this image shows that the diseased jejunum (arrow) extends over a long segment. (e) Image obtained at the level of the cecum shows normal terminal ileum (black arrow) and thickened small bowel (white arrow) with submucosal edema (target sign).
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Figure 1c: Intravenous contrast-enhanced transverse multidetector CT images of the abdomen. (a) Jejunal wall thickening (arrow) of up to 1.5 cm. High attenuation within the wall reflects mucosal enhancement. (b) Patent superior mesenteric artery (black arrow) and mesenteric vein (white arrow), with thickened enhancing jejunum. (c) Enlarged mesenteric nodes and mesenteric inflammation (white arrows) adjacent to the abnormal jejunum. The superior mesenteric artery (black arrow) and mesenteric veins are patent. (d) Image obtained at the level of the cecum. In conjunction with a–c, this image shows that the diseased jejunum (arrow) extends over a long segment. (e) Image obtained at the level of the cecum shows normal terminal ileum (black arrow) and thickened small bowel (white arrow) with submucosal edema (target sign).
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Figure 1d: Intravenous contrast-enhanced transverse multidetector CT images of the abdomen. (a) Jejunal wall thickening (arrow) of up to 1.5 cm. High attenuation within the wall reflects mucosal enhancement. (b) Patent superior mesenteric artery (black arrow) and mesenteric vein (white arrow), with thickened enhancing jejunum. (c) Enlarged mesenteric nodes and mesenteric inflammation (white arrows) adjacent to the abnormal jejunum. The superior mesenteric artery (black arrow) and mesenteric veins are patent. (d) Image obtained at the level of the cecum. In conjunction with a–c, this image shows that the diseased jejunum (arrow) extends over a long segment. (e) Image obtained at the level of the cecum shows normal terminal ileum (black arrow) and thickened small bowel (white arrow) with submucosal edema (target sign).
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Figure 1e: Intravenous contrast-enhanced transverse multidetector CT images of the abdomen. (a) Jejunal wall thickening (arrow) of up to 1.5 cm. High attenuation within the wall reflects mucosal enhancement. (b) Patent superior mesenteric artery (black arrow) and mesenteric vein (white arrow), with thickened enhancing jejunum. (c) Enlarged mesenteric nodes and mesenteric inflammation (white arrows) adjacent to the abnormal jejunum. The superior mesenteric artery (black arrow) and mesenteric veins are patent. (d) Image obtained at the level of the cecum. In conjunction with a–c, this image shows that the diseased jejunum (arrow) extends over a long segment. (e) Image obtained at the level of the cecum shows normal terminal ileum (black arrow) and thickened small bowel (white arrow) with submucosal edema (target sign).
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DISCUSSION
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On the basis of the CT appearance of the bowel, the differential diagnosis included ischemia, small-bowel hemorrhage, infection, and Crohn disease. Since the mesenteric vessels were patent in this case, ischemia would have to be the result of small-vessel vasculitis, the sequela of arterial emboli, or secondary to a low-flow state. The latter was not supported by the patient's history, as no major hypotensive episode was reported. The involvement of both the long jejunum segment and the ileum segment can be seen in either embolic disease or vasculitis. In the absence of a clinical history supporting a diagnosis of emboli, such as history of atrial fibrillation, and with the lack of other organ involvement, such as splenic or renal infarcts, embolic disease was a less likely diagnosis. The degree of wall thickening (up to 15 mm) supported a cause of ischemia other than arterial compromise or low flow. Macari et al (1) compared the CT appearance of small-bowel ischemia with that of small-bowel hemorrhage and reported that ischemic bowel (primarily owing to nonocclusive low flow or superior mesenteric artery disease) showed wall thickening of 4 mm on average (range, 1–9 mm). It is important to recognize that vasculitis that affects small mesenteric arteries and small mesenteric veins can produce greater degrees of wall thickening than can mesenteric arterial disease (2–4).
Vasculitis conditions known to cause small-bowel ischemia include systemic lupus erythematosus and Henoch-Schonlein purpura (HSP). In patients with systemic lupus erythematosus, small-artery and venous vasculitis can result in ischemic bowel. CT findings may include symmetric bowel thickening involving multiple segments of the jejunum and ileum with a target sign or homogeneous enhancement, bowel dilatation, increased attenuation of the mesentery, and ascites (3). Patients with lupus can present with abdominal pain, arthralgia, and a skin rash (classically a facial rash, although a variety of rashes can occur). However, antinuclear antibody screening findings were negative in this patient, decreasing the likelihood of a diagnosis of systemic lupus erythematosus.
This patient was noted to have a petechial rash with purpura involving the extremities, which was characteristic of HSP. In patients with HSP, this type of rash commonly involves the lower extremities (5,6) but also may involve the upper extremities and trunk (5). The rash is classically petechial with purpura, and it can have a maculopapular appearance (5–7). Although HSP is more common in children, it can occur in adults. Identification of this rash with intestinal ischemia or hemorrhage in an adult should direct the clinical work-up toward a diagnosis of HSP.
With respect to the other considerations, small-bowel hemorrhage would be an uncommon finding in a young man who was not being administered anticoagulant therapy; however, bowel hemorrhage can occur in patients with vasculitis. Other causes include coagulopathy (such as hemophilia), disorders with thrombocytopenia (such as idiopathic thrombocytopenic purpura, leukemia, lymphoma, and myeloma), ischemic bowel, and trauma (8,9). The CT appearance of small-bowel hemorrhage has been described as circumferential homogeneous high-attenuation thickening (9). In this case, some sections of the thickened bowel had an appearance similar to that of hemorrhage; however, without a precontrast CT scan, it may be impossible to distinguish hematoma from thickened enhancing mucosa. A precontrast CT scan would show high attenuation in the region of a hematoma, and this area would not enhance after intravenous contrast material infusion (10). The target sign (Fig 1) may be identified in patients with hemorrhage, as well as in those with ischemia (10). The length of the diseased bowel may be helpful in distinguishing the cause, as Macari et al (1) showed that short (
15 cm) segment involvement favors a diagnosis of hemorrhage, while long (>30 cm) segment involvement is associated with ischemia. The length of the abnormal jejunum in this patient (estimated to be 25–30 cm) fell in the intermediate range but approached the length more characteristic of ischemia.
Infectious enteritis should be considered in the setting of small-bowel thickening. However, giardiasis usually involves the proximal bowel (duodenum, jejunum). The presence of distal disease in this patient makes giardiasis an unlikely diagnosis. Patients with Yersinia enterocolitis can present with diarrhea, rash, and arthritis; however, the terminal ileum is usually diseased (11).
Terminal ileum disease is also typically identified in patients with Crohn disease. However, multifocal involvement of segments of the jejunum and ileum is compatible with a diagnosis of Crohn disease, and a normal terminal ileum is not sufficient evidence to exclude this diagnosis. Mucosal hyperemia and submucosal edema in the bowel wall, mesenteric stranding, and adenopathy can all be seen in patients with Crohn disease. Patients with small-bowel Crohn disease can present with diarrhea and abdominal pain (12). However, gastrointestinal bleeding in patients with Crohn disease usually reflects colonic involvement (12–14). A small number of cases of cutaneous leukocytoclastic vasculitis have been reported in patients with Crohn disease; however, the skin manifestations most commonly associated with this disease are erythema nodosum and pyoderma gangrenosum (15).
In this patient, the degree of bowel wall thickening and protracted symptoms raised concern about ischemic bowel. After CT scanning, the patient underwent laparotomy. Approximately 30 cm of the small bowel—beginning in the proximal jejunum, 10 cm distal to the ligament of Treitz—was found to be edematous and ischemic. This segment was resected, and primary duodenojejunostomy was performed. Pathologic analysis revealed bowel ulceration and ischemic changes, which were of full thickness in sections. Diffuse acute vasculitis was identified in the submucosa. The patient was also examined by a member of the dermatology department, and skin biopsy was performed promptly. The biopsy revealed leukocytoclasia and small-vessel damage in the superficial dermis, with fibrinoid necrosis, neutrophilic and eosinophilic infiltration, and extravastated red blood cells. Immunoflouorescent staining was positive for immunoglobulin A. These results enabled us to confirm the diagnosis of HSP.
HSP is a small-vessel vasculitis that occurs more commonly in children than adults. While the literature states that the majority of those with HSP are younger than 10 years (5,7), some series have reported that adults older than 20 years may account for nearly 30% of those affected (16). Pathologically, HSP is characterized as a small-vessel vasculitis (5,17). Skin biopsy is often performed to enable confirmation of the diagnosis in adults (16), and it reveals leukocytoclastic vasculitis and immunoglobulin A deposits at the dermoepidermoid junction (7,17). Multiple organ systems may be affected. The skin disease is the first manifestation in many patients and eventually develops in 95%–100% of patients (5,6,16). Joint involvement occurs in 60%–84% of patients; gastrointestinal tract involvement, in 57%–76% of patients; and renal disease, in 20%–100% of patients (5,7). The American College of Rheumatology has defined four diagnostic criteria, two of which are necessary to distinguish HSP from other forms of vasculitis (16). These criteria are (a) age of 20 years or younger at onset, (b) palpable purpura, (c) gastrointestinal bleeding, and (d) biopsy evidence of granulocytes around small arteriolar and venular walls.
As in this case, gastrointestinal disease can precede the skin rash (16,18). The most common abdominal symptom is colicky pain, which may be associated with diarrhea, nausea, or vomiting (7,18,19). Melena is more common in adults than children (5). While gastrointestinal disease develops in approximately 60% of adults, it is present at disease onset in a minority of patients (5). The disease can affect any portion of the bowel distal to the esophagus (18). Ulceration may occur (6,18), and bowel wall thickening results from edema and intramural hemorrage (18–20).
While HSP can have a self-limited course, the results of a study involving 46 adults with HSP showed that 63% of adults, compared with 40% of children, required treatment (5). The radiology literature emphasizes the importance of recognizing this entity to avoid unnecessary surgery (18,19). In severe cases, medical therapy (corticosteroid treatment) may be necessary (5–7,17,21), and intravenous immunoglobulin therapy has been shown to be efficacious in a case of persistent bloody diarrhea (22). Despite the propensity for spontaneous remission of bowel disease, obstruction, ischemia, or infarct, irreducible intussusception and perforation are uncommon complications that may require surgery (5,7,17,20).
Reports on the appearance of HSP on abdominal CT images have been based on evaluation of small case series (18,19). A case report described duodenal and jejunal wall thickening, luminal narrowing, fold thickening, and ulceration (18). In a small series (19), bowel wall thickening was characterized as homogeneous and circumferential, with a mean maximum thickness of 9 mm (range, 7–12 mm). The target sign (Fig 1) was identified in two (29%) of seven patients evaluated (19). A pattern of multifocal bowel involvement with skip lesions on CT images has been described (18,19). The jejunum and ileum were involved in all seven patients included in the report by Jeong et al (19). Other findings included intestinal dilatation, enlarged mesenteric nodes (<1.5 cm), engorged mesenteric vessels, increased attenuation of the mesenteric fat, and ascites (19).
This patient presented with a rare complication of an uncommon disease: severe ischemic bowel in the setting of adult-onset HSP. The CT findings in this patient are similar to those described in the literature, with multifocal small-bowel thickening and associated mesenteric disease; however, the degree of bowel wall thickening and intractable pain prompted the surgical diagnosis of ischemic bowel. This case emphasizes the importance of forming radiologic interpretations with as much clinical information as possible.
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FOOTNOTES
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Authors stated no financial relationship to disclose.
| Part one of this case appeared 4 months previously and may contain larger images.
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References
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- Ha HK, Lee HJ, Yang SK, et al. Intestinal Behcet syndrome: CT features of patients with and without complications. Radiology 1998;209(2):449–454.[Abstract/Free Full Text]
- Blanco R, Martinez-Taboada VM, Rodriguez-Valverde V, et al. Henoch-Schonlein purpura in adulthood and childhood: two different expressions of the same syndrome. Arthritis Rheum 1997;40(5):859–864.[Medline]
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- Glick NS. Other inflammatory conditions. In: Gore RM, Levine MS, Laufer I, eds. Gastrointestinal radiology. Philadelphia, Pa: Saunders, 1994; 1145.
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- Mills JA, Michel BA, Bloch DA, et al. The American College of Rheumatology 1990 criteria for the classification of Henoch-Schonlein purpura. Arthritis Rheum 1990;33(8):1114–1121.[Medline]
- Savage CO, Harper L, Cockwell P, Adu D, Howie AJ. ABC of arterial and vascular disease: vasculitis. BMJ 2000;320(7245):1325–1328.[Free Full Text]
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- Jeong YK, Ha HK, Yoon CH, et al. Gastrointestinal involvement in Henoch-Schonlein syndrome: CT findings. AJR Am J Roentgenol 1997;168(4):965–968.[Abstract/Free Full Text]
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Congratulations to the 153 individuals and 11 resident groups that submitted the most likely diagnosis (Henoch-Schonlein purpura) for Diagnosis Please, Case 127. The names and locations of the individuals and resident groups, as submitted, are as follows:
Individual responses
- Jaleel P. Abdul, MD, Dammam, Saudi Arabia
- Hisashi Abe, MD, Suita, Osaka, Japan
- Gholamali Afshang, MD, Tinley Park, Ill
- Amr M. Ajlan, MBBS, Montreal, Quebec, Canada
- Erhan Akpinar, Ankara, Turkey
- Roger L. Antonelli, MD, Dayton, Ohio
- Jason B. Ashley, MD, London, Ontario, Canada
- Fahad Azzumeea, MBBS, Montreal, Quebec, Canada
- Asim K. Bag, MD, Birmingham, Ala
- Monica Ballesta Moratalla, MD, Valencia, Spain
- Thomas J. Barloon, MD, Iowa City, Iowa
- Paula Bartumeus, Valencia, Spain
- Ronald L. Becker, MD, Rolling Hills, Calif
- Bryan D. Berkey, MD, Tripler AMC, Hawaii
- Ronald N. Boyle, MD, La Plata, Md
- Adrian P. Brady, MB, Cork, Ireland
- Eric L. Bressler, MD, Minnetonka, Minn
- Douglas C. Brown, MD, Virginia Beach, Va
- Marcelo Cabrini, Lomas de Zamora, Argentina
- Antonio A. Cavalcanti, MD, São Paulo, Brazil
- Michael H. Childress, MD, Silver Spring, Md
- Alex T. Chuang, MD, Dallas, Tex
- Marco A. Cura, MD, San Antonio, Tex
- Paxton H. Daniel, MD, Fort Worth, Tex
- Marc G. De Baets, MD, Collina d'Oro, Switzerland
- Johannes F. De Villiers, MBChB, MMed, Gisborne, New Zealand
- Mustafa Kemal Demir, MD, Istanbul, Turkey
- Thaworn Dendumrongsup, MD, Songkla, Thailand
- Bart D'herde, Hasselt, Belgium
- Seyed A. Emamian, MD, PhD, Rockville, Md
- Juliet H. Fallah, MD, Clarendon Hills, Ill
- Susan M. Fanapour, DO, Lombard, Ill
- Virginia Fattal Jaef, MD, Rosario, Argentina
- Brett D. Ferdinand, MD, Livingston, NJ
- Luis G. Ferrer, MD, Valencia, Spain
- Ricardo B. Fonseca, MD, Nashville, Tenn
- Angeles Franco Lopez, Madrid, Spain
- Akira Fujikawa, MD, Setagaya, Tokyo, Japan
- Ann S. Fulcher, MD, Midlothian, Va
- Rajneesh Galwa, Jaipur, India
- Ram P. Galwa, MD, Chandigarh, India
- Douglas J. Gardner, MD, Windsor, Ontario, Canada
- William G. Gawman, MD, Waterloo, Ontario, Canada
- Carlos R. Gimenez, MD, New Orleans, La
- Mark G. Goldshein, MD, Andover, Mass
- Francisco Jose Gonzalez, Santander, Spain
- Bruno Miguel Graca, MD, Coimbra, Portugal
- Aleksandar Grgic, MD, Zweibruecken, Germany
- Flavius F. Guglielmo, MD, Basking Ridge, NJ
- Pramod K. Gupta, MD, Plano, Tex
- Adam R. Guttentag, MD, Philadelphia, Pa
- Ehsan A. Haider, MBBCh, Montreal, Quebec, Canada
- Ferris M. Hall, MD, Brookline, Mass
- Srinivasan Harish, MBBS, Burlington, Ontario, Canada
- Yuusuke Hirokawa, MD, Kyoto, Japan
- Brian H. Hu, MD, Nashua, NH
- Alberto C. Iaia, MD, Wilmington, Del
- Waleed M. Ibrahim, MD, Columbus, Ohio
- Rathachai Kaewlai, MD, Boston, Mass
- Kiriakos Kalampoukas, MD, Halandri, Greece
- Andrew J. Kapustin, MD, Charlotte, NC
- Masako Kataoka, MD, Cambridge, United Kingdom
- Takuji Kiryu, MD, PhD, Gifu, Japan
- Steven A. Klein, MD, Shrewsbury, Mass
- Kusuma Kurmayagari, Montreal, Quebec, Canada
- Mario A. Laguna, MD, Milwaukee, Wis
- Pierre A. Lambrechts, MD, Meise, Belgium
- Martin Lecompte, MD, Manotick, Ontario, Canada
- Karl J. Lehmann, MD, Karlsruhe, Germany
- Myron M. Levitt, MD, Scotch Plains, NJ
- Donald R. Lewis, Jr, MD, Huntington, WVa
- John T. Lim, MD, Newport Coast, Calif
- David A. Lisle, MBBS, Brisbane, Australia
- Jaime Llauger, MD, Barcelona, Spain
- Patricia A. Lowry, MD, Chattanooga, Tenn
- Edward Lubat, MD, Englewood, NJ
- Naganathan B. Mani, MD, Miami, Fla
- Michael B. Martin, MD, Austin, Tex
- Daniel L. Martins, MD, São Paulo, Brazil
- Uma Mahesh Matapathi, MD, Hyderabad, India
- Satoshi Matsushima, MD, Tokyo, Japan
- Waldir H. Maymone, MD, Rio de Janeiro, Brazil
- Frank J. McKowne, MD, Vancouver, Wash
- Sunil L. Mehta, MD, Mississauga, Ontario, Canada
- Nikolaos Michailidis, Thessaloniki, Greece
- Manabu Minami, MD, PhD, Yokohama, Japan
- Mansour Mirfakhraee, MD, Shreveport, La
- Jose Mondello, MD, Buenos Aires, Argentina
- Srikanth M. Narayanaswamy, MBBS, MRCPch, Plymouth, United Kingdom
- Tammam N. Nehme, MD, East Wenatchee, Wash
- Christopher C. Ng, MD, Nashville, Tenn
- Soheil Niku, MD, San Diego, Calif
- Mizuki Nishino, MD, Boston, Mass
- Hiroshi Nobusawa, MD, PhD, Ota, Tokyo, Japan
- Vijayanadh Ojili, MD, Montreal, Quebec, Canada
- Cinthia D. Ortega, MD, São Paulo, Brazil
- Klaus Orth, Aachen, Germany
- Marc G. Ossip, MD, Toronto, Ontario, Canada
- Neeraj J. Panchal, MD, San Diego, Calif
- Matteo Passamonti, MD, Lodi, Italy
- Narendrakumar P. Patel, MD, Newburgh, NY
- Suresh K. Patel, MD, Chicago, Ill
- Yeliz Pekcevik, Izmir, Turkey
- Ivan Pilate, Brussels, Belgium
- Sudhakar N. Pipavath, MD, Seattle, Wash
- Sanjay P. Prabhu, MBBS, Melbourne, Australia
- Ilias Primetis, MD, Athens, Greece
- Claudio P. Ramos, MD, Juiz de Fora, Brazil
- Daniel C. Rappaport, MD, Toronto, Ontario, Canada
- Matthew C. Rheinboldt, MD, Nashville, Tenn
- Manoel D. Rocha, MD, São Paulo, Brazil
- Tsutomu Sakamoto, MD, Tokyo, Japan
- Hatice Tuba Sanal, MD, San Diego, Calif
- Debra M. Sarasohn, MD, New York, NY
- Steven M. Schultz, MD, Fort Worth, Tex
- Mustafa Secil, MD, Izmir, Turkey
- Hidekazu Seo, MD, Hamamatsu, Shizuoka, Japan
- Matthew P. Shapiro, MD, Charlottesville, Va
- Hideki Shima, MD, Tokyo, Japan
- Taro Shimono, MD, Osaka, Sayama, Japan
- Annamaria Skacelova, MD, Veazie, Me
- Darrin S. Smith, MD, Visalia, Calif
- Annemie Snoeckx, MD, Zandhoven, Belgium
- James D. Sprinkle, Jr, MD, Spotsylvania, Va
- Evan Stein, MD, PhD, New York, NY
- Subramanian Subramanian, MD, New Delhi, India
- Kouichi Sugiyama, Numazu, Japan
- Norio Takahashi, MD, Fukui, Japan
- Yukihisa Takayama, MD, Columbus, Ohio
- Ken Tamai, Kyoto, Japan
- Douglas L. Teich, MD, Brookline, Mass
- Osman Temizoz, Edirne, Turkey
- Kazuma Terauchi, Fujieda, Shizuoka, Japan
- Ross L. Titton, MD, Voorhees, NJ
- Eugene Tong, MD, Austin, Tex
- William C. Torreggiani, MB, Dublin, Ireland
- Ozgur Tosun, Ankara, Turkey
- Ricardo H. Trueba, MD, Buenos Aires, Argentina
- Panagiotis V. Tsirkinidis, MD, Athens, Greece
- Baris I. Turkbey, MD, Baltimore, Md
- Eleni Vafeiadou, Thessaloniki, Greece
- Piet K. Vanhoenacker, MD, Moorsel, Belgium
- Elida Vazquez, MD, Barcelona, Spain
- Nanda Venkatanarasimha, MBBS, MRCP, Plymouth, United Kingdom
- Ricardo Luis Videla, Córdoba, Argentina
- Christopher P. Vittore, MD, Belvidere, Ill
- James S. Walsh, MD, Edinburgh, United Kingdom
- Michael Weber, MD, Berlin, Germany
- Jeffrey H. West, MD, Jacksonville, Fla
- Kaneko You, Gifu, Japan
- Stanko Yovichevich, MD, Sydney, Australia
- Joe Yut, Olathe, Kan
- Jeffrey H. Zapolsky, MD, Oshkosh, Wis
Resident group responses
- Armed Forces Medical College Radiology Residents, Mumbai, Maharashtra, India
- Baylor University Medical Center Radiology Residents, Dallas, Tex
- Diagnostico Medico Radiology Residents, Buenos Aires, Argentina
- Fukushima University Radiology Residents, Fukushima, Japan
- Fundacion Jimenez Diaz Radiology Residents, Madrid, Spain
- Hospital das Clinicas da Faculdade de Medicina da Universidade de São Paulo Radiology Residents, São Paulo, Brazil
- Kyoto City Hospital Radiology Residents, Kyoto, Japan
- Penn State Milton S. Hershey Medical Center Radiology Residents, Hershey, Pa
- Prince of Songkla University Radiology Residents, Songkla, Thailand
- University of Pennsylvania Radiology Residents, Philadelphia, Pa
- Virginia Commonwealth University Radiology Residents, Richmond, Va
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HISTORY
IMAGING FINDINGS
