Acute gastric anisakiasis: observations with endoscopic ultrasonography

Acute gastric anisakiasis: observations with endoscopic ultrasonography

Acute gastric anisakiasis: observations with endoscopic ultrasonography Takashi Okai, Ikurou Mouri, Yasushi Yamaguchi, Hideki Ohta, Yoshiharu Motoo, N...

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Acute gastric anisakiasis: observations with endoscopic ultrasonography Takashi Okai, Ikurou Mouri, Yasushi Yamaguchi, Hideki Ohta, Yoshiharu Motoo, Norio Sawabu,

MD MD MD MD MD MD

The thickened stomach wall of two patients with acute gastric anisakiasis was demonstrated by endoscopic ultrasonography (EUS). The advantage of using EUS in the differential diagnosis of the giant folds observed in the stomach is discussed. CASE 1

A 23-year-old man came to the hospital on January 17, 1990, with severe epigastric pain with urticaria. The pain began approximately 3 hours after eating slices of raw mackerel. Emergency endoscopy revealed an Anisakis larva in edematous folds of the stomach (Fig. 1). Using an Olympus GF-UM2 endoscope (Olympus, Tokyo, Japan), EUS was performed after removal of the worm with biopsy forceps. Thickening of the submucosal layer was clearly demonstrated, characterized by a homogeneous and relatively low echo level (Fig. 2). Although the second layer (deep mucosal layer) was increased slightly in thickness around the site of penetration by the larva, neither the muscularis propria nor serosal layers were affected. The symptoms disappeared the day after the endoscqpic removal of the larva. '

Figure 1. Endoscopic finding showing A, an Anisakis larva (arrow) between the edematous folds and B, the giant folds on the greater curvature of the corpus of the stomach.

CASE 2

On July 31, 1991, a 44-year-old woman came to our hospital with severe epigastric pain. She had eaten slices of raw mackerel 2 days before her visit. She had a history of acute gastric anisakiasis in June, 1990. Endoscopy disclosed an Anisakis larva in the edematous mucosa of the stomach (Fig. 3). EUS was performed before removal of the worm. As shown in Figure 4A, a short linear strong echo caused by the penetrating Anisakis was clearly visible on the mucosal surface of the stomach. Although the echo level ofthe thickened submucosal layer was relatively low at the penetration site, the internal echo of the thickened submucosal layer was generally homogeneous and showed a fine lamellar structure. The worm was removed with biopsy forceps and was scanned in a water bath to reconfirm the linear, strong echo observed in vivo. The same linear, strong echo was observed (Fig. 4C), and it was identified as the echo of the Anisakis larva itself (Fig. 4D). The patient's abdominal pain ameliorated soon after the removal. From the Department of Internal Medicine, Cancer Research Institute, Kanazawa University, Kanazawa, Japan. Reprint requests: Takashi Okai, MD, Department of Internal Medicine, Cancer Research Institute, Kanazawa University, 4-86 Yoneizumi, Kanazawa 921, Japan. 0016-5107/93/3903-0450$1.00 +.10

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Figure 2. EUS showing the thickened submucosal layer. Echo level of this thickened layer is relatively low at the site where the worm penetrated (arrows). The internal echo of the thickened submucosal layer is even and shows a lamellar appearance. Although the mucosal layer increases slightly in thickness around the penetrated site, both the muscularis propria and serosal layers are not affected. Abbreviations: m, mucosal layer; sm, submucosal layer; mp, muscularis propria. GASTROINTESTINAL ENDOSCOPY

Figure 3. Endoscopic finding showing A, an Anisakis larva penetrating gastric mucosa (arrows) and B, giant folds around the penetrated site.

DISCUSSION

Edematous and hypertrophic folds are common endoscopic findings in cases of acute gastric anisakiasis. 1-3 However, diffusely thickened folds mimicking gastric carcinoma of the linitis plastica type or a large gastric tumor simulating gastric leiomyoma have also been documented in some cases. 4 Thus the differentiation of this benign disease from malignant giant folds is important in clinical practice when endoscopic examination fails to detect Anisakis larva in the edematous gastic folds. In this report we have shown that the thickened stomach walls of patients with acute gastric anisakiasis consisted mostly of a thickened submucosal layer. Although the echo level of the thickened submucosal layer was relatively low at the penetration site, the internal echo of the thickened submucosal layer was generally homogeneous and showed a fine lamellar structure. These EUS findings are characteristic of acute gastric anisakiasis and are clearly different from findings in cases of gastric carcinoma of the linitis plastica type or malignant lymphoma. In the former, the thickening of the stomach wall is usually seen throughout all layers of the stomach wall. In addition, the echo level of the thickened stomach wall is usually VOLUME 39, NO.3, 1993

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Figure 4. EUS showing the thickened submucosal layer. A, A short linear strong echo caused by the penetrated Anisakis larva is clearly demonstrated on the luminal surface of the most thickened site of the stomach (arrow). Although the echo level ofthe thickened submucosal layer is relatively low at the penetrated site, the internal echo is generally even and shows a fine lamellar appearance. B, In addition, giants folds are seen around the penetrated site. C, The worm removed by a biopsy forceps is scanned again in a water bath. The same linear strong echo (arrow) is demonstrated. D, It is identified as the echo of an Anisakis larva itself. Abbreviations: m, mucosal layer; sm, submucosal layer; mp, muscularis propria.

non-homogeneous, as indicated by the presence of irregular high echo points. 5-s In the latter, it has been reported that the second layer (deep mucosal layer) is always thickened, whether or not the deeper layers of the stomach are involved. Furthermore, it is emphasized that the echo level of the affected layer is characteristically low and homogeneous. 9-11 We may thus distinguish acute gastric anisakiasis from these malignant giant folds of the stomach whether or not the worm is detected. In summary, these EUS findings may become a new diagnostic tool for the differentiation of benign giant gastric folds from malignant hypertrophic gastric rugae. Furthermore, we can also distinguish acute gastric anisakiasis from Menetrier's disease, where the second layer (deep mucosal layer) is characteristically 451

thickened with fine or patchy high echo points. 12,13 However, further investigation with more patients needs to be carried out to assess the actual clinical value of EUS in the differential diagnosis of giant folds of the stomach. REFERENCES 1. Akasaka Y, Kizu M, Aoike A, et at. Endoscopic management of acute gastric anisakiasis. Endoscopy 1979;2:158-62. 2. Sugimachi K, Inokuchi K, Ooiwa T, et at. Acute gastric anisakiasis: analysis of 178 cases. JAMA 1985;253:1012-3. 3. Ikeda K, Kumashiro R, Kifune T. Nine cases of acute gastric anisakiasis. Gastrointest Endosc 1989;35:304-8. 4. Kitadai Y, Haruma K, Sumii K, et at. Two cases of vanishing tumor of the stomach due to anisakiasis [in Japanese). J Jap Soc Int Med 1987;76:1434-8. 5. Andriulli A, Recchia S, Angelis CDe, et al. Endoscopic ultrasonographic evaluation of patients with biopsy negative gastric linitis plastica. Gastrointest Endosc 1990;36:611-5. 6. Okai T, Yamakawa 0, Matsuda N, et al. Analysis of gastric car-

7. 8. 9. 10. 11. 12. 13.

cinoma growth by endoscopic ultrasonography. Endoscopy 1991;23:121-5. Bolondi L, Casanova P, Caletti GC, et al. Primary gastric lymphoma versus gastric carcinoma: endoscopic US evaluation. Radiology 1987;165:821-6. Botet JF, Lightdale CJ, Zauber AG, et al. Preoperative staging of gastric cancer: comparison of endoscopic US and dynamic CT. Radiology 1991;181:426-32. Caletti GC, Lorena Z, Bolondi L, et at. Impact of endoscopic ultrasonography on diagnosis and treatment of primary gastric lymphoma. Surgery 1988;103:315-20. Taal BG, den Hartog-Jager F, Burgers JMV, et at. Primary non-Hodgkin's lymphoma ofthe stomach: changing aspects and therapeutic choices. Eur J Cancer Clin OncoI1989;25:439-50. Fujishima H, Misawa T, MaruokaA, et al. Staging and follow-up of primary gastric lymphoma by endoscopic ultrasonography. Am J Gastroenterol 1991;86:719-24. Dancygier H. Endoscopic ultrasonography of the upper gastrointestinal tract. Baillieres Clin Gastroenterol 1991;5:19-36. Fujishima H, Misawa T, Chijiiwa Y, et aI. Scirrhous carcinoma of the stomach versus hypertrophic gastritis: findings at endoscopic US. Radiology 1991;181:197-200.

Recurrent cholangitis caused by the migration of pancreatic calculi associated with pancreas divisum Jean-Yves Robert, Jean-FranCfois Bretagne, Jean-Luc Raoul, Laurent Siproudhis, Denis Heresbach, Michel Gosselin,

MD MD MD MD MD MD

Biliary complications are commonly observed in chronic calcifying pancreatitis (CCP). They are mainly represented by common bile duct stenosis1 caused by pancreatitis or pseudocyst development. 2 These complications can be either asymptomatic or revealed by cholestasis,3 sepsis such as cholangitis, or liver abcess. 4 Despite the high frequency of pancreatic stones within the main pancreatic duct of patients with CCP,5,6 impaction or migration ofthese calculi into or through the main papilla have been, to the best of our knowledge, hitherto unreported. We report here the case of a 34-year-old man with CCP revealed by recurrent cholangitis caused by migration of pancreatic stones through the main papilla. CASE REPORT

In April 1990, a 34-year-old man with severe abdominal pain was admitted to our department. No history of alcohol From the Department of Hepato-gastroenterology and Digestive Endoscopy, University Hospital Pontchaillou, Rennes, France. Reprint requests: Prof. Dr. J.F. Bretagne, Department of Hepatogastroenterology, University Hospital Pontchaillou, 35033 Rennes, France. 0016-5107/93/3903-0452$1.00 +.10

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Figure 1. Ventral duct system of pancreas divisum showing characteristic features of chronic pancreatitis and small calculi within the main duct (May 1989).

or tobacco abuse and no pancreatic disease in family members existed. For 4 years preceding admission, the patient had, on three occasions, epigastric pain, fever, and transient jaundice for 24 hours. Similar abnormalities as seen on laboratory tests were observed at each attack. At the time of the third episode (June 1989), laboratory tests showed a leukocytosis of 18,000 cells/mm3 (90% neutrophilic polynuclear cells) and an elevation of urinary amylase without increased serum amylase levels. Liver function tests showed a mild cholestasis (alkaline phosphatase X 1.5N; total bilirubin X 2N) and increased transaminase levels (ALT X 20N; AST X ION). Ultrasonographic examination was normal, and the gallbladder was free of gallstones. ERCP after cannulation of the main papilla showed a short duct corresponding to the ventral part of pancreas divisum. The main duct and side branches were dilated and contained small stones, consistent with the diagnosis of chronic pancreatitis (Fig. 1). An attempt at biliary tract opacification failed, and cannulation of the accessory papilla was not attempted. The diagnosis GASTROINTESTINAL ENDOSCOPY