1440
European Journal of Gastroenterology & Hepatology 2014, Vol 26 No 12
atrophic gastritis (CAG), appearing in the last issue of the journal. We strongly disagree on some important points mentioned below.
Patient enrollment Ninety-one patients were enrolled in six hospitals all over Spain. Moreover, the authors wrote that six patients could not be finally included in the study because of mishandling of samples.
Statistical analysis
The statistical power of the study appears to be completely inadequate to support the declared aim (85 patients; 14 CAG, distributed in three different subgroups, for 85 patients overall).
Acknowledgements Conflicts of interest
Biohit Oyj: educational grants, speaker invitations, and consultancy.
This means that only 14 patients per center were enrolled. This is of course completely inadequate for such a ‘multicenter’ study.
References
Chronic atrophic gastritis
2
The declared aim of the present study was to investigate the accuracy of GastroPanel in the diagnosis of CAG. In fact, only 17% out of 85 patients (14 patients) had CAG: six patients (7%) had antral CAG, five patients (6%) had body CAG, and only three patients (4%) had multifocal CAG. The diagnosis of atrophic gastritis by GastroPanel is made on the basis of the knowledge of the severity of the histological alteration; the lack of this crucial information seems important for the results. Indeed, the localization of body atrophic gastritis is characterized by low levels of pepsinogen I (PGI) and high levels of gastrin 17, with a negative predictive value for the first parameter of 96% [2]. Moreover, Rugge et al. [3] reported in a 12-year prospective study the prognostic value of pepsinogens in the diagnosis of gastric cancer as well as the close relationship with the OLGA staging for gastric atrophy. On the basis of these features, PGI and ratio PGI/PGII are considered ‘the best non-invasive test for the diagnosis of atrophic gastritis’ by Maastricht IV consensus [4], MAPS guidelines [5], and, more recently, the Kyoto consensus held in January 2014 (in press in Gut). Therefore, the results of the present study are not in agreement with the international literature on this topic (PGI 101.4 μg/l in corpus atrophy based on only five patients) and completely inadequate to support the strong title ‘Accuracy of GastroPanel for the diagnosis of atrophic gastritis’. Similarly, the diagnosis of antral atrophic gastritis is made on the basis of very low levels of gastrin 17 and the presumption of obtaining results only on the basis of six patients is convincing. Finally, the use of proton-pump inhibitors modifies both pepsinogens and gastrin 17 values. The reported lack of withdrawal of such drugs is confounding to assess the actual levels of such parameters.
1
3
4
5
McNicholl AG, Forné M, Barrio J, De la Coba C, González B, Rivera R, et al. Helicobacter pylori Study Group of the Asociación Española de Gastroenterología (AEG). Accuracy of GastroPanel for the diagnosis of atrophic gastritis. Eur J Gastroenterol Hepatol 2014; 26:941–948. Di Mario F, Cavallaro LG. Non-invasive tests in gastric diseases. Dig Liver Dis 2008; 40:523–530. Rugge M, de Boni M, Pennelli G, de Bona M, Giacomelli L, Fassan M, et al. Gastritis OLGA-staging and gastric cancer risk: a twelve-year clinicopathological follow-up study. Aliment Pharmacol Ther 2010; 31:1104–1111. Malfertheiner P, Megraud F, O’Morain CA, Atherton J, Axon AT, Bazzoli F, et al. European Helicobacter Study Group. Management of Helicobacter pylori infection: the Maastricht IV/Florence Consensus Report. Gut 2012; 61:646–664. Dinis-Ribeiro M, Areia M, de Vries AC, Marcos-Pinto R, Monteiro-Soares M, O’Connor A, et al. MAPS Participants; European Society of Gastrointestinal Endoscopy; European Helicobacter Study Group; European Society of Pathology; Sociedade Portuguesa de Endoscopia Digestiva. Management of precancerous conditions and lesions in the stomach (MAPS): guideline from the European Society of Gastrointestinal Endoscopy (ESGE), European Helicobacter Study Group (EHSG), European Society of Pathology (ESP), and the Sociedade Portuguesa de Endoscopia Digestiva (SPED). Virchows Arch 2012; 460:19–46.
Spontaneous rupture of eosinophilic liver abscess Se Young Janga, Won Young Taka, Young Oh Kweona, Suhyun Leea, Yu Rim Leea, Sunzoo Kimb, Hye Won Leeb and Soo Young Parka, Departments of aInternal Medicine and bPathology, Kyungpook National University School of Medicine, Daegu, Republic of Korea Correspondence to Soo Young Park, MD, PhD, Department of Internal Medicine, Kyungpook National University School of Medicine, 130 Dongdeok-ro, Jung-gu, 700-721 Daegu, Republic of Korea Tel: + 82 53 200 5516; fax: + 82 53 426 7883; e-mail: [email protected] Received 16 August 2014 Accepted 16 October 2014
Introduction Eosinophilic liver abscess is a rare disease with focal infiltration of eosinophils in the liver [1]. Etiologies are known to be associated with parasitic infection, allergic reaction, drug, tumor, and hypereosinophilic syndrome [1–3]. Although eosinophil infiltration can occur in other organs such as the stomach, lung, heart, and colon, the liver is the most frequently affected organ because of its anatomical position and high blood flow [4–6]. Eosinophilic liver abscess is usually diagnosed incidentally on screening abdominal ultrasound or computed tomography (CT) scans [1]. The clinical presentation of eosinophilic liver abscess is asymptomatic or nonspecific asthenia in most cases, but patients can present with acute abdominal pain or
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
Letters to the Editor 1441
fever [6,7]. Although most cases of eosinophilic liver abscess follow a relatively benign course, serious complications have been reported [8,9]. Here, we report a rare case of spontaneous rupture of eosinophilic liver abscess that was managed successfully by medical treatment.
further decreased to 10.8 g/dl in the next 8 h. Complete blood cell count was followed up every 8 h and there was no additional decrease in the Hb level. Systolic blood pressure was maintained around 110 mmHg without tachycardia after intravenous hydration. He was admitted to the intensive care unit under close observation.
Case report A 67-year-old man visited the emergency room for abrupt-onset abdominal pain that had persisted for 6 h. Pain initiated spontaneously without a precipitating cause. He had dull abdominal pain in the right upper quadrant abdomen that was aggravated by positional change and deep breathing. There was tenderness of the right upper abdomen without rebound tenderness. The patient had been taking 5 mg of amlodipine besylate (Norvasc; Pfizer, New York, New York, USA) and 100 mg of aspirin (Bayer, Leverkusen, Germany) once a day. He had been healthy and showed normal results on abdominal ultrasonography performed 1 year ago. Laboratory tests showed leukocytosis and eosinophilia. The white blood cell count was 11 330/μl (normal range, 4800–10 800/μl) and the eosinophil count was 7409/μl (65.4%). The hemoglobin (Hb) level was 12.8 g/dl (13–18 g/dl) and the platelet count was 263 × 103/μl (130–400 × 103/μl). On admission, his blood pressure was 98 mmHg in systole and 78 mmHg in diastole, with a pulse rate of 86 bpm. A CT scan of the abdomen showed subcapsular hematoma with an ill-defined, 2-cm-sized low-density lesion in segment 5 of the liver (Fig. 1a). Compared with 15.1 g/dl checked 4 months ago, his Hb level had decreased to 12.8 g/dl at presentation, and it
Over the next 5 days, we performed diagnostic paracentesis and liver biopsy for low-density lesion in segment 5 of the liver under ultrasound guidance. Aspirated fluid was grossly blood colored, and the Hb level and the white blood cell count were 11.2 g/dl and 1325/μl (eosinophil 65.4%), respectively. Histological findings of the biopsy specimen showed a granulomatous lobular inflammatory lesion composed of lymphocytes, plasma cells, numerous eosinophils, and central fibrinoid necrosis (Fig. 2). Although histopathologic findings and laboratory results were compatible with visceral larva migrans, no specific parasites were found in the enzymelinked immunosorbent assay (for Cysticercus spp., Paragonimus spp., Sparganum spp., Clonorchis spp., and Fasciola hepatica). He nonetheless took prescribed praziquantel and albendazole for parasitic infection. A followup CT scan performed after 3 months showed multiple new low-density lesions in liver segments 6 and 7, whereas the previous low-density lesion in segment 5 had disappeared (Fig. 1b). He was prescribed 900 mg triclabendazole (Fasinex Bolus; Hanpoong Industry Co., Ltd, Incheon, Republic of Korea) for 1 day. Six months later, the subcapsular fluid collection and lowdensity lesions resolved, with normalization of the eosinophil count (Fig. 1c).
Fig. 1
(a) Contrast-enhanced computed tomography (CT) scan of the abdomen shows subcapsular fluid collection with hemorrhage and multiple ill-defined low-density lesions in segment 5 of the liver. (b) Follow-up CT scan after 3 months shows the disappearance of the subcapsular hematoma and previous low-density lesions, and new lesions with the characteristic tubular tunnel shape in segments 6 and 7. (c) Follow-up CT scan at 6 months shows complete resolution of all lesions previously observed in the liver.
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
1442 European Journal of Gastroenterology & Hepatology 2014, Vol 26 No 12
Fig. 2
Histological findings of the liver biopsy with hematoxylin and eosin staining. (a) Low-power image shows a granulomatous lobular inflammatory reaction characterized by palisading fibroblasts and inflammatory cells surrounding extensive central fibrinoid necrosis (magnification, × 40) (b) Highpower image shows central fibrinoid necrosis and the prominence of the palisading fibroblasts. Outer inflammatory infiltrate contains numerous eosinophils, neutrophils, and lymphocytes (magnification, × 200).
Discussion There have been several reports of spontaneous liver rupture in patients with hemangioma, giant hepatic cyst, hypereosinophilic syndrome, and peliosis hepatis [9–12]. However, to our knowledge, this is the first case reporting spontaneous rupture of eosinophilic liver abscess.
F. hepatica as a causative agent [18]. Second, pathologic findings of a granulomatous reaction with numerous eosinophils surrounding areas of necrosis are suggestive of parasitic infection. Finally, the patient had a history of consuming uncooked meat, especially raw cow liver, which could explain the transmission route of the parasite.
Eosinophilic organ infiltration is known to develop in two ways [13]. First, in hypereosinophilic syndrome, it is a consequence of the eosinophilia itself. Moderate to severe eosinophilia often leads to organ infiltration, resulting in organ damage because of the release of cytotoxic granule proteins, such as eosinophil major basic protein and eosinophil cationic protein, as well as inflammatory lipid mediators [14,15]. The infiltrated organs could be the skin, lungs, brain, heart, and liver [14, 16]. The other cause of eosinophilic organ infiltration is direct parasitic invasion. Some parasitic infections, such as fascioliasis and toxocariasis, produce focal lesions in the hepatic parenchyma because of either direct penetration or hematogenous migration to the liver. As these lesions are caused by immature worms arrested during migration, they contain the parasites [14].
F. hepatica is a trematode flatworm that occurs worldwide. Herbivorous mammals are the definitive hosts and humans are incidental hosts. Humans acquire infection incidentally by eating aquatic vegetation containing metacercariae, which excyst in the duodenum and migrate through the intestinal wall, peritoneal cavity, and liver parenchyma into the biliary ducts, where they develop into adults [19]. During migration, multiple small confluent abscesses are formed, which are seen as tracts or tunnels on imaging findings [20]. The abscesses are best seen on portal venousphase CT because they do not show contrast enhancement and therefore are better seen in the normal enhancing liver parenchyma [20,21]. The treatment of choice for F. hepatica is triclabendazole [18]. It is known that F. hepatica responds poorly to praziquantel and albendazole, which are used widely for other parasitic infestations [22,23].
In the present case, parasitic infestation of the liver might be the cause of eosinophilic liver abscess, even though the enzyme-linked immunosorbent assay for parasites yielded negative results. Parasitic infestation in the liver, especially F. hepatica, may have been the etiologic agent for the following reasons. First, CT findings were consistent with the characteristic ‘tunnel-shaped low-density lesions’ in the liver reported previously for visceral larva migrans, and the lesions were migrating in the liver with time [3,17]. Resolution of the liver abscess after triclabendazole therapy also supports the possibility of
Conclusion
We report a very rare case of spontaneous rupture of eosinophilic liver abscess because of human fascioliasis. In hemodynamically stable patients, conservative treatment with transfusion, hydration, and bed rest could be treatment options. Efforts to correct the underlying cause of eosinophilic infiltration should be made subsequently. However, in hemodynamically unstable patients, active interventions such as transarterial selective embolization or surgery for hemostasis should be considered [9,24,25].
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
Letters to the Editor 1443
Acknowledgements
12
Conflicts of interest
There are no conflicts of interest.
13
References
14
1 Yoo SY, Han JK, Kim YH, Kim TK, Choi BI, Han MC. Focal eosinophilic infiltration in the liver: radiologic findings and clinical course. Abdom Imaging 2003; 28:326–332. 2 Lee WJ, Lim HK, Lim JH, Kim SH, Choi SH, Lee SJ. Foci of eosinophil-related necrosis in the liver: imaging findings and correlation with eosinophilia. Am J Roentgenol 1999; 172:1255–1261. 3 Jang HJ, Lee WJ, Lee SJ, Kim SH, Lim HK, Lim JH. Focal eosinophilic necrosis of the liver in patients with underlying gastric or colorectal cancer: CT differentiation from metastasis. Korean J Radiol 2002; 3:240–244. 4 Baek MS, Mok YM, Han WC, Kim YS. A patient with eosinophilic gastroenteritis presenting with acute pancreatitis and ascites. Gut Liver 2014; 8:224–227. 5 Abe K, Shimokawa H, Kubota T, Nawa Y, Takeshita A. Myocarditis associated with visceral larva migrans due to Toxocara canis. Intern Med 2002; 41:706–708. 6 Bhatia V, Sarin SK. Hepatic visceral larva migrans: evolution of the lesion, diagnosis, and role of high-dose albendazole therapy. Am J Gastroenterol 1994; 89:624–627. 7 Hassan HA, Majid RA, Rashid NG, Nuradeen BE, Abdulkarim QH, Hawramy TA, et al. Eosinophilic granulomatous gastrointestinal and hepatic abscesses attributable to basidiobolomycosis and fasciolias: a simultaneous emergence in Iraqi Kurdistan. BMC Infect Dis 2013; 13:91. 8 Kwon JW, Kim TW, Kim KM, Lee SH, Cho SH, Min KU, et al. Clinical features of clinically diagnosed eosinophilic liver abscesses. Hepatol Int 2011; 5:949–954. 9 Cheung YS, Wong S, Lam PK, Lee KF, Wong J, Lai PB. Spontaneous liver rupture in hypereosinophilic syndrome: a rare but fatal complication. World J Gastroenterol 2009; 15:5875–5878. 10 Gupta S, Agarwal V, Acharya AN. Spontaneous rupture of a giant hepatic hemangioma-report of a case. Indian J Surg 2012; 74:434–436. 11 Miliadis L, Giannakopoulos T, Boutsikos G, Terzis I, Kyriazanos ID. Spontaneous rupture of a large non-parasitic liver cyst: a case report. J Med Case Rep 2010; 4:2.
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Sommacale D, Palladino E, Tamby EL, Diebold MD, Kianmanesh AR. Spontaneous hepatic rupture in a patient with peliosis hepatis: a report of one case. Int J Surg Case Rep 2013; 4:508–510. Jang IY, Yang YJ, Cho HJ, Choi Y, Shin EH, Kang DU, Kim TB. Eosinophilic organ infiltration without eosinophilia or direct parasite infection. Korean J Intern Med 2014; 29:126–129. Roufosse F, Weller PF. Practical approach to the patient with hypereosinophilia. J Allergy Clin Immunol 2010; 126:39–44. Simon D, Wardlaw A, Rothenberg ME. Organ-specific eosinophilic disorders of the skin, lung, and gastrointestinal tract. J Allergy Clin Immunol 2010; 126:3–13, quiz 4–5. Tefferi A. Blood eosinophilia: a new paradigm in disease classification, diagnosis, and treatment. Mayo Clin Proc 2005; 80:75–83. Pulpeiro JR, Armesto V, Varela J, Corredoira J. Fascioliasis: findings in 15 patients. Br J Radiol 1991; 64:798–801. Hien TT, Truong NT, Minh NH, Dat HD, Dung NT, Hue NT, et al. A randomized controlled pilot study of artesunate versus triclabendazole for human fascioliasis in central Vietnam. Am J Trop Med Hyg 2008; 78:388–392. Centers for Disease Control and Prevention. Parasites - fascioliasis (Fasciola infection). Available at: http://www.cdc.gov/parasites/fasciola/biology.html. [Accessed 12 August 2014]. Kabaalioğlu A, Cubuk M, Senol U, Cevikol C, Karaali K, Apaydin A, et al. Fascioliasis: US, CT, and MRI findings with new observations. Abdom Imaging 2000; 25:400–404. Andresen B, Blum J, von Weymarn A, Bürge M, Steinbrich W, Duewell S. Hepatic fascioliasis: report of two cases. Eur Radiol 2000; 10:1713–1715. Keiser J, Sayed H, el-Ghanam M, Sabry H, Anani S, el-Wakeel A, et al. Efficacy and safety of artemether in the treatment of chronic fascioliasis in Egypt: exploratory phase-2 trials. PLoS Negl Trop Dis 2011; 5:e1285. Keiser J, Utzinger J. Chemotherapy for major food-borne trematodes: a review. Expert Opin Pharmacother 2004; 5:1711–1726. Leung KL, Lau WY, Lai PB, Yiu RY, Meng WC, Leow CK. Spontaneous rupture of hepatocellular carcinoma: conservative management and selective intervention. Arch Surg 1999; 134:1103–1107. Wicke C, Pereira PL, Neeser E, Flesch I, Rodegerdts EA, Becker HD. Subcapsular liver hematoma in HELLP syndrome: evaluation of diagnostic and therapeutic options – a unicenter study. Am J Obstet Gynecol 2004; 190:106–112.
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
European Journal of Gastroenterology & Hepatology 2014, Vol 26 No 12
atrophic gastritis (CAG), appearing in the last issue of the journal. We strongly disagree on some important points mentioned below.
Patient enrollment Ninety-one patients were enrolled in six hospitals all over Spain. Moreover, the authors wrote that six patients could not be finally included in the study because of mishandling of samples.
Statistical analysis
The statistical power of the study appears to be completely inadequate to support the declared aim (85 patients; 14 CAG, distributed in three different subgroups, for 85 patients overall).
Acknowledgements Conflicts of interest
Biohit Oyj: educational grants, speaker invitations, and consultancy.
This means that only 14 patients per center were enrolled. This is of course completely inadequate for such a ‘multicenter’ study.
References
Chronic atrophic gastritis
2
The declared aim of the present study was to investigate the accuracy of GastroPanel in the diagnosis of CAG. In fact, only 17% out of 85 patients (14 patients) had CAG: six patients (7%) had antral CAG, five patients (6%) had body CAG, and only three patients (4%) had multifocal CAG. The diagnosis of atrophic gastritis by GastroPanel is made on the basis of the knowledge of the severity of the histological alteration; the lack of this crucial information seems important for the results. Indeed, the localization of body atrophic gastritis is characterized by low levels of pepsinogen I (PGI) and high levels of gastrin 17, with a negative predictive value for the first parameter of 96% [2]. Moreover, Rugge et al. [3] reported in a 12-year prospective study the prognostic value of pepsinogens in the diagnosis of gastric cancer as well as the close relationship with the OLGA staging for gastric atrophy. On the basis of these features, PGI and ratio PGI/PGII are considered ‘the best non-invasive test for the diagnosis of atrophic gastritis’ by Maastricht IV consensus [4], MAPS guidelines [5], and, more recently, the Kyoto consensus held in January 2014 (in press in Gut). Therefore, the results of the present study are not in agreement with the international literature on this topic (PGI 101.4 μg/l in corpus atrophy based on only five patients) and completely inadequate to support the strong title ‘Accuracy of GastroPanel for the diagnosis of atrophic gastritis’. Similarly, the diagnosis of antral atrophic gastritis is made on the basis of very low levels of gastrin 17 and the presumption of obtaining results only on the basis of six patients is convincing. Finally, the use of proton-pump inhibitors modifies both pepsinogens and gastrin 17 values. The reported lack of withdrawal of such drugs is confounding to assess the actual levels of such parameters.
1
3
4
5
McNicholl AG, Forné M, Barrio J, De la Coba C, González B, Rivera R, et al. Helicobacter pylori Study Group of the Asociación Española de Gastroenterología (AEG). Accuracy of GastroPanel for the diagnosis of atrophic gastritis. Eur J Gastroenterol Hepatol 2014; 26:941–948. Di Mario F, Cavallaro LG. Non-invasive tests in gastric diseases. Dig Liver Dis 2008; 40:523–530. Rugge M, de Boni M, Pennelli G, de Bona M, Giacomelli L, Fassan M, et al. Gastritis OLGA-staging and gastric cancer risk: a twelve-year clinicopathological follow-up study. Aliment Pharmacol Ther 2010; 31:1104–1111. Malfertheiner P, Megraud F, O’Morain CA, Atherton J, Axon AT, Bazzoli F, et al. European Helicobacter Study Group. Management of Helicobacter pylori infection: the Maastricht IV/Florence Consensus Report. Gut 2012; 61:646–664. Dinis-Ribeiro M, Areia M, de Vries AC, Marcos-Pinto R, Monteiro-Soares M, O’Connor A, et al. MAPS Participants; European Society of Gastrointestinal Endoscopy; European Helicobacter Study Group; European Society of Pathology; Sociedade Portuguesa de Endoscopia Digestiva. Management of precancerous conditions and lesions in the stomach (MAPS): guideline from the European Society of Gastrointestinal Endoscopy (ESGE), European Helicobacter Study Group (EHSG), European Society of Pathology (ESP), and the Sociedade Portuguesa de Endoscopia Digestiva (SPED). Virchows Arch 2012; 460:19–46.
Spontaneous rupture of eosinophilic liver abscess Se Young Janga, Won Young Taka, Young Oh Kweona, Suhyun Leea, Yu Rim Leea, Sunzoo Kimb, Hye Won Leeb and Soo Young Parka, Departments of aInternal Medicine and bPathology, Kyungpook National University School of Medicine, Daegu, Republic of Korea Correspondence to Soo Young Park, MD, PhD, Department of Internal Medicine, Kyungpook National University School of Medicine, 130 Dongdeok-ro, Jung-gu, 700-721 Daegu, Republic of Korea Tel: + 82 53 200 5516; fax: + 82 53 426 7883; e-mail: [email protected] Received 16 August 2014 Accepted 16 October 2014
Introduction Eosinophilic liver abscess is a rare disease with focal infiltration of eosinophils in the liver [1]. Etiologies are known to be associated with parasitic infection, allergic reaction, drug, tumor, and hypereosinophilic syndrome [1–3]. Although eosinophil infiltration can occur in other organs such as the stomach, lung, heart, and colon, the liver is the most frequently affected organ because of its anatomical position and high blood flow [4–6]. Eosinophilic liver abscess is usually diagnosed incidentally on screening abdominal ultrasound or computed tomography (CT) scans [1]. The clinical presentation of eosinophilic liver abscess is asymptomatic or nonspecific asthenia in most cases, but patients can present with acute abdominal pain or
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
Letters to the Editor 1441
fever [6,7]. Although most cases of eosinophilic liver abscess follow a relatively benign course, serious complications have been reported [8,9]. Here, we report a rare case of spontaneous rupture of eosinophilic liver abscess that was managed successfully by medical treatment.
further decreased to 10.8 g/dl in the next 8 h. Complete blood cell count was followed up every 8 h and there was no additional decrease in the Hb level. Systolic blood pressure was maintained around 110 mmHg without tachycardia after intravenous hydration. He was admitted to the intensive care unit under close observation.
Case report A 67-year-old man visited the emergency room for abrupt-onset abdominal pain that had persisted for 6 h. Pain initiated spontaneously without a precipitating cause. He had dull abdominal pain in the right upper quadrant abdomen that was aggravated by positional change and deep breathing. There was tenderness of the right upper abdomen without rebound tenderness. The patient had been taking 5 mg of amlodipine besylate (Norvasc; Pfizer, New York, New York, USA) and 100 mg of aspirin (Bayer, Leverkusen, Germany) once a day. He had been healthy and showed normal results on abdominal ultrasonography performed 1 year ago. Laboratory tests showed leukocytosis and eosinophilia. The white blood cell count was 11 330/μl (normal range, 4800–10 800/μl) and the eosinophil count was 7409/μl (65.4%). The hemoglobin (Hb) level was 12.8 g/dl (13–18 g/dl) and the platelet count was 263 × 103/μl (130–400 × 103/μl). On admission, his blood pressure was 98 mmHg in systole and 78 mmHg in diastole, with a pulse rate of 86 bpm. A CT scan of the abdomen showed subcapsular hematoma with an ill-defined, 2-cm-sized low-density lesion in segment 5 of the liver (Fig. 1a). Compared with 15.1 g/dl checked 4 months ago, his Hb level had decreased to 12.8 g/dl at presentation, and it
Over the next 5 days, we performed diagnostic paracentesis and liver biopsy for low-density lesion in segment 5 of the liver under ultrasound guidance. Aspirated fluid was grossly blood colored, and the Hb level and the white blood cell count were 11.2 g/dl and 1325/μl (eosinophil 65.4%), respectively. Histological findings of the biopsy specimen showed a granulomatous lobular inflammatory lesion composed of lymphocytes, plasma cells, numerous eosinophils, and central fibrinoid necrosis (Fig. 2). Although histopathologic findings and laboratory results were compatible with visceral larva migrans, no specific parasites were found in the enzymelinked immunosorbent assay (for Cysticercus spp., Paragonimus spp., Sparganum spp., Clonorchis spp., and Fasciola hepatica). He nonetheless took prescribed praziquantel and albendazole for parasitic infection. A followup CT scan performed after 3 months showed multiple new low-density lesions in liver segments 6 and 7, whereas the previous low-density lesion in segment 5 had disappeared (Fig. 1b). He was prescribed 900 mg triclabendazole (Fasinex Bolus; Hanpoong Industry Co., Ltd, Incheon, Republic of Korea) for 1 day. Six months later, the subcapsular fluid collection and lowdensity lesions resolved, with normalization of the eosinophil count (Fig. 1c).
Fig. 1
(a) Contrast-enhanced computed tomography (CT) scan of the abdomen shows subcapsular fluid collection with hemorrhage and multiple ill-defined low-density lesions in segment 5 of the liver. (b) Follow-up CT scan after 3 months shows the disappearance of the subcapsular hematoma and previous low-density lesions, and new lesions with the characteristic tubular tunnel shape in segments 6 and 7. (c) Follow-up CT scan at 6 months shows complete resolution of all lesions previously observed in the liver.
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
1442 European Journal of Gastroenterology & Hepatology 2014, Vol 26 No 12
Fig. 2
Histological findings of the liver biopsy with hematoxylin and eosin staining. (a) Low-power image shows a granulomatous lobular inflammatory reaction characterized by palisading fibroblasts and inflammatory cells surrounding extensive central fibrinoid necrosis (magnification, × 40) (b) Highpower image shows central fibrinoid necrosis and the prominence of the palisading fibroblasts. Outer inflammatory infiltrate contains numerous eosinophils, neutrophils, and lymphocytes (magnification, × 200).
Discussion There have been several reports of spontaneous liver rupture in patients with hemangioma, giant hepatic cyst, hypereosinophilic syndrome, and peliosis hepatis [9–12]. However, to our knowledge, this is the first case reporting spontaneous rupture of eosinophilic liver abscess.
F. hepatica as a causative agent [18]. Second, pathologic findings of a granulomatous reaction with numerous eosinophils surrounding areas of necrosis are suggestive of parasitic infection. Finally, the patient had a history of consuming uncooked meat, especially raw cow liver, which could explain the transmission route of the parasite.
Eosinophilic organ infiltration is known to develop in two ways [13]. First, in hypereosinophilic syndrome, it is a consequence of the eosinophilia itself. Moderate to severe eosinophilia often leads to organ infiltration, resulting in organ damage because of the release of cytotoxic granule proteins, such as eosinophil major basic protein and eosinophil cationic protein, as well as inflammatory lipid mediators [14,15]. The infiltrated organs could be the skin, lungs, brain, heart, and liver [14, 16]. The other cause of eosinophilic organ infiltration is direct parasitic invasion. Some parasitic infections, such as fascioliasis and toxocariasis, produce focal lesions in the hepatic parenchyma because of either direct penetration or hematogenous migration to the liver. As these lesions are caused by immature worms arrested during migration, they contain the parasites [14].
F. hepatica is a trematode flatworm that occurs worldwide. Herbivorous mammals are the definitive hosts and humans are incidental hosts. Humans acquire infection incidentally by eating aquatic vegetation containing metacercariae, which excyst in the duodenum and migrate through the intestinal wall, peritoneal cavity, and liver parenchyma into the biliary ducts, where they develop into adults [19]. During migration, multiple small confluent abscesses are formed, which are seen as tracts or tunnels on imaging findings [20]. The abscesses are best seen on portal venousphase CT because they do not show contrast enhancement and therefore are better seen in the normal enhancing liver parenchyma [20,21]. The treatment of choice for F. hepatica is triclabendazole [18]. It is known that F. hepatica responds poorly to praziquantel and albendazole, which are used widely for other parasitic infestations [22,23].
In the present case, parasitic infestation of the liver might be the cause of eosinophilic liver abscess, even though the enzyme-linked immunosorbent assay for parasites yielded negative results. Parasitic infestation in the liver, especially F. hepatica, may have been the etiologic agent for the following reasons. First, CT findings were consistent with the characteristic ‘tunnel-shaped low-density lesions’ in the liver reported previously for visceral larva migrans, and the lesions were migrating in the liver with time [3,17]. Resolution of the liver abscess after triclabendazole therapy also supports the possibility of
Conclusion
We report a very rare case of spontaneous rupture of eosinophilic liver abscess because of human fascioliasis. In hemodynamically stable patients, conservative treatment with transfusion, hydration, and bed rest could be treatment options. Efforts to correct the underlying cause of eosinophilic infiltration should be made subsequently. However, in hemodynamically unstable patients, active interventions such as transarterial selective embolization or surgery for hemostasis should be considered [9,24,25].
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
Letters to the Editor 1443
Acknowledgements
12
Conflicts of interest
There are no conflicts of interest.
13
References
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