zation of a hemorrhage secondary to contrast extravasation at thetime of venous sampling. If performed appropriately, as in thiscase, adrenal scintigraphy has the advantage of being noninvasive,cost-effective and accurate in defining functionality of an adrenaltumor. When performed under dexamethasone suppression, itsefficacy exceeds that of CT and MRI especially in the diagnosis ofbilateral adrenal hyperplasia. Series of NP-59 scintigraphy yieldvaried results of efficacy due either to differences in techniques,dexamethasone suppression protocols, and variation in interpreterexperience. In our experience an accuracy as high as 94% andsensitivity of 96% has been noted (14).

When aldosteronism is biochemically confirmed (with highplasma or urinary aldosterone levels and suppressed plasmarenin activity), an evaluation for the site(s) of aldosteronehypersécrétionmust be initiated. CT scanning or adrenalscintigraphy usually correctly lateralize an aldosteronoma. CTscanning is used first as it is widely available and may besufficient when it yields an unequivocal result. NP-59 is mostuseful when CT results are equivocal, for the positive identification of bilateral hyperplasia and in problem cases such as thisone. Adrenal venous sampling is reserved for cases where boththe above tests fail to identify the adrenal abnormality.

Sampling in addition to being invasive, requires the administration of iodinated contrast and the skills of a highlyexperienced invasive radiologist. NP-59 scintigraphy plays animportant role in aldosteronism for tumor localization and thedifferentiation from bilateral adrenal hyperplasia. Additionallyas this case illustrates, scintigraphy can locate sites of residualadrenocortical function when there has been injury to one orboth adrenal glands. Adrenocortical radiopharmaceuticals arewidely available around the world, but in the United StatesNP-59 remains an Investigational New Drug and thus must beutilized as part of an experimental protocol which is a significant logistic hurdle in its widespread use.

REFERENCES1. Conn JW. Primary aldosteronism, a new clinical syndrome. J Lab Clin Med

I955;45:3-17.

2. Melby JC, Spark RF, Dale SL, Egdahl RH, Kahn PC. Diagnosis and localization ofaldosterone-producing adenomas by adrenal vein catheterization. N Eng/ J Med1967:277:1050-1057.

i. Bucht H, Bergstrom J, Lindholmer B, Wijnbladh Hj, Hokfelt catheterization of the leftadrenal vein for contrast injection and steroid analysis in a case of Conn's syndrome.

Ada MedScand 1964;176:233-241.

4. Kahn PC, Nickrosz LV. Selective angiography of the adrenal glands. Am J Roentgen1967;101:739-749.

5. Kahn PC, Kelleher MD, Egdahl RH, Melby JC. Adrenal arteriography and venographyin primary aldosteronism. Radiology 1971:101:71-78.

6. Blair RJ, Beierwalters WH, Lieberman LM, et al. Radiolabelled cholesterol as anadrenal agent. J NucíMed 1971;12:176-182.

7. Beierwalters WH, Lieberman LM, Ansari AN, Nishiyama H. Localization of humanadrenal glands in vivo by scintillation scanning. JAMA 1971;216:275-277.

8. Bookstein JJ, Conn JW, Reuter SR. Adrenal hemorrhage as a complication of adrenalvenography in primary aldosteronism. Radiology 1968;90:778-779.

9. Basmadjian GP, Hertzel KR, Ice RD, Beierwaltes WH. Synthesis of a new adrenalcortex imaging agent 6ß-m]-iodomethyl-19-norcholest-5(10)en-3j3-ol (NP-59). J

LabdCompd 1975:11:427-431.

10. Sarkar SD, Beierwalters WH, Ice RD, et al. A new and superior adrenal scanningagent, NP-59. J NucíMed 1974:16:1038-1042.

11. Shapiro B, Britton KE, Hawkins LA, Edwards CE. Clinical experience with 75Se-

selenomethylcholesterol adrenal imaging. Clin Endocrinol (Oxf) 1981:15:19-27.

12. Conn JW, Cohen EL, Herwig KR. The dexamethasone modified adrenal scintiscan inhyporeninemic aldosteronism (tumor versus hyperplasia). J Lab Clin Med 1976;88:841-855.

13. Guerin CK, Wahner HW, Gorman CA, Carpenter PC, Sheddy PF. Computedtomographic scanning versus radioisotope imaging in adrenocortical diagnosis. Am JMed 1983:75:653-657.

14. Gross MD, Shapiro B, Grekin RJ, et al. Scmtigraphic localization of adrenal lesions inprimary aldosteronism. Am J Med 1984:77:839-844.

15. Fischer CE, Turner FA, Horion R. Remission of primary hyperaldosteronism afteradrenal venography. N EnglJ Med 1971:285:334-335.

16. Taylor HC, Sacks CR. Primary aldosteronism: remission and development of adrenalinsufficiency after adrenal venography. Ann Intern Med 1976;85:207-209.

17. Eagen RT, Page MI. Adrenal insufficiency following bilateral adrenal venography.JAMA 1971:215:115-116.

18. Bayliss RI, Edwards MB, Starter F. Complications of adrenal venography. BrJ Radial1970:43:531-533.

19. Gross MD, Freitas JE, Swanson DP, Brady T, Beierwalters WH. The normaldexamethasone-suppression adrenal scan. J NucíMed 1979;20:1131-1135.

Gastric Antral Vascular Ectasia: A Case Report andReview of the LiteratureBarry E. Herman, John J. Vargo, Stephen Baum, Eugene D. Silverman and John EisoldTwin Rivers Gastroenterology Center, Easton, Pennsylvania; Cleveland Clinic Foundation, Cleveland, Ohio; St. VincentHospital and Health Center, Billings, Montana; Department of Radiology and Nuclear Medicine, National Naval MedicalCenter, Bethesda, Maryland; and Office of the Attending Physician, U.S. Capitol, Washington, D.C.

We present an 83-yr-old woman with a history of renal insufficiency,diabetes and idiopathic thrombocytopenic purpura (IIP) who experienced recurrent hemorrhage from gastric antral vascular ectasias(GAVE). Methods: Extensive evaluation consisting of barium smallbowel series, colonoscopy, abdominal CT scan and visceral angiography excluded other causes of bleeding. Results: After 99mTc-

labeled red cell imaging to localize the bleeding to the antrum, anantrectomy was performed. Seven months postsurgery, the patientexperienced no further hemorrhage. Conclusion: ""Tc-labeled

red cell scans can be used for the diagnosis of GAVE.

Received Mar. 6, 1995; revision accepted Oct. 8, 1995.For correspondence or reprints contact: Eugene D. Silverman, MD, Department of

Radiology, National Naval Medical Center, Bethesda, MD 20889-5600.The opinions and assertions contained herein are the private ones of the authors and

are not to be construed as official policy or as reflecting of the Department of Defense.

Key Words: gastricantralvascularectasias;technetium-99m-RBCs

J NucíMed 1996; 37:854-856

vJastric antral vascular ectasia (GAVE) is a rare conditionassociated with chronic iron deficiency anemia (1-5). GAVEusually occurs in elderly women and has been reported inassociation with achlorhydria (4) and cirrhosis (2). In 1984,Jabbari et al. (5) coined the condition with the term "watermelon" stomach (5) due to the characteristic linear antral

streaking seen endoscopically.Hemorrhage from GAVE (6) is rare. We describe a case of

GAVE with recurrent hemorrhage documented by a "'"Tc-

labeled red cell scan and reviewed the reported cases of thisentity.

854 THE JOURNALOF NUCLEARMEDICINE•Vol. 37 •No. 5 •May 1996

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FIGURE 1. Upper intestinalbarium meal with prominent antral folds.

CASE REPORTAn 83-yr-old woman developed substernal chest pressure and

exertional dyspnea. Evaluation revealed a hematocrit of 22.7%with normocytic indices, blood urea nitrogen of 26.8 mmole/liter(75 mg/dl) and serum creatinine of 176.8 mmole/liter (2.0 mg/dl).Stool was positive for occult blood. An upper endoscopy wasperformed revealing "beefy" antral folds. Colonoscopy was un

remarkable. The patient required repeated blood transfusions tomaintain her hematocrit. Abdominal CT and angiography of thesuperior mesenteric, inferior mesenteric and celiac arteries werenormal. Bone marrow biopsy demonstrated decreased erythroidelements with adequate iron stores. She failed treatment withranitidine and sucralfate, and continued to experience intermittentmelena.

Past medical history was significant for hypertension, noninsulindependent diabetes mellitus, idiopathic thrombocytopenic purpura,Paget's disease and mild renal insufficiency. The patient denied the

use of aspirin, nonsteroidal anti-inflammatory drugs, tobacco oralcohol. Medications included: insulin, sucralfate, ranitidine, dilti-azem and iron. Physical examination revealed pallor, a systolic

FIGURE 2. Technetium-99m-labeled red cell scan. (A) Normal vascularanatomy at 34-36 min. (B) Focus of activity appearing at 78-80 min to the

right of the midepigastrium represented bleeding from the antroduodenalarea (black arrow).

FIGURE 3. Several ectatic vessels containing microthrombi (Hematoxylinand eosin, 400x).

ejection murmur and hemoccult positive stools. Laboratory examination was remarkable for a normocytic normochromic anemia.

The patient's hospital course was notable for recurrent upper

gastrointestinal bleeding despite acid suppression and sucralfate.She required in excess of 33 units of packed red blood cells. Upperendoscopy revealed large, erythematous antral folds and biopsyspecimens were read as acute gastritis. A barium small bowel seriesshowed thickened antral folds (Fig. 1). Because of persistentthrombocytopenia with platelet counts in the 40,000/cmm range, atrial of intravenous immunoglobulin G was initiated. Despite anincrease in the platelet count to greater than 200,000/cmm, episodicbleeding continued. A bleeding scan was performed utilizing thestandard modified in vitro technique. Thirty minutes after theintravenous administration of 20 mg of stannous pyrophosphate,10 ml of autologous red cells were harvested and incubated with30 mCi of [WrnTc]pertechnetate for 20 min and reinjected. Sequen

tial images were obtained for 90 min. A bleeding site was detectedin the antroduodenal area at approximately 70 min (Fig. 2A, B).The patient underwent antrectomy with Roux-en-Y anastamosisand splenectomy. Surgical specimen showed enlarged antral folds.

Histopathology of the antrum demonstrated findings consistentwith "hyperplastic mucosa." Upon further review, fibromuscular

hyperplasia, vascular ectasias and fibrin thrombi were noted (Fig.3). Seven months after surgery, the patient's hematocrit was 32%

and no recurrence of melena was reported.

DISCUSSIONCommon causes of upper gastrointestinal hemorrhage in

clude peptic ulcer disease, esophageal varices, gastritis, esoph-agitis and Mallory Weis tears. More unusual etiologies include:dieulafoy lesions, hemobilia, aortoduodenal fistulas, gastro-duodenal arteriovenous malformations and GAVE. GAVE hastraditionally been associated with iron deficiency anemia (7-5).Endoscopically, one may see erythematous streaking or diffuseerythema of the antrum with or without enlarged folds (5).Histologically fibromuscular hyperplasia, mild infiltration ofchronic inflammatory cells, prominent mucosal capillaries, andfibrin thrombi are characteristic (7,8) of this disorder. GAVE isfrequently misdiagnosed as gastritis by the endoscopist orpathologist who is not familiar with this entity.

There are 74 reported cases (1-6,9-37). Fifty-five arefemales and 18 are males (in one case gender not mentioned)with an average age of 69.6 yr. Initial hemoglobin levels were1.6 mmol/liter-7.5 mmol/liter [2.6-12.1 mg/dl (x = 7.3)] andthe duration of anemia was present for as long as 48 yr. Seven of23 upper gastrointestinal barium studies showed enlarged antral

GASTRICANTRALVASCULARECTASIASTUDY•Herman et al. 855

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folds (1,6,11,13,17,21,23). Twelve 51Cr-labeled red cell blood loss

studies were performed (1,3,4,9,14,17,19,26,28,30,32,34), ten ofwhich were positive with an average bleeding rate of 119 cc/day(normal less than 1-10 cc/day). One case reported a maximalrate of 258 cc/day (17) and another localized the bleeding to theantrum (26). There are three reports of negative 99mTc-labeled

red cell scans (27,31,37); 4 of 15 visceral angiograms performed demonstrated hypervascularity in the region of theantrum but no active bleeding was noted (1,13,16,31).

There are 15 detailed reports of melena in patients presentingwith GAVE (2,3,9,14,18,20,21,23,34,35,36). It appears thatpatients with GAVE and melena frequently have underlyingconditions which have been associated with anemia and bleeding diathesis. Of the reported cases 7 had cirrhosis, 3 valvularheart disease, 3 congestive heart failure, 1 nonsteroidal anti-inflammatory use, 1 mixed connective tissue disease and 1chronic renal insufficiency.

Although many conservative modalities for treating GAVEhave been implemented (supportive, acid suppression, sucral-fate, hormones, steroids, serotonin antagonists, electrocoagula-tion, heater probe), laser ablation (18,33,35) and antrectomyhave received the most attention.

Although the pathogenesis of GAVE is unknown, it isbelieved to be caused by repeated trauma and ischemia fromantroduodenal prolapse (75). Acute hemorrhage in GAVE mayresult from a superimposed bleeding diathesis which is presentin a majority the cases reporting melena. Our patient hadchronic renal insufficiency and idiopathic thrombocytopeniaand continued to bleed despite correction of her platelet count.

In most cases of GAVE, bleeding is slowed and intermittent.Labeled red blood cell bleeding scans have detected bleedingsites of 5 ml and offer the advantage of observations over 24 hr.In-vitro red cell techniques offer labeling efficiency of greaterthan 95% (40).

CONCLUSIONThis report shows how 99mTc-labeled red cell scanning

documents active hemorrhage from GAVE and emphasizes thepoint that GAVE should be considered in the differentialdiagnosis of a positive bleeding scan localizing a hemorrhage tothe antroduodenal area.

ACKNOWLEDGMENTSWe thank Renata Hirszel and Judy Glynn for their assistance in

the preparation of this manuscript and Dave Larson, MD, for hispreparation of the histology images.

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1996;37:854-856.J Nucl Med.   Barry E. Herman, John J. Vargo, Stephen Baum, Eugene D. Silverman and John Eisold  Gastric Antral Vascular Ectasia: A Case Report and Review of the Literature

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