Letters to the Editor 1439

Letters to the Editor European Journal of Gastroenterology & Hepatology 2014, 26:1439–1443

Preventive cholecystectomy for gallbladder cancer in high-risk groups: primary or secondary prevention Pankaj K. Garga,b, Durgatosh Pandeya and Sandeep Sachdevac, a Department of Surgical Oncology, All India Institute of Medical Sciences, b Department of Surgery, University College of Medical Sciences and Guru Teg Bahadur Hospital, Delhi and cDepartment of Community Medicine, Sarojini Naidu Medical College, Agra, Uttar Pradesh, India Correspondence to Pankaj K. Garg, MS, DNB, MNAMS, Department of Surgery, University College of Medical Sciences and Guru Teg Bahadur Hospital, Dilshad Garden, Delhi 110095, India Tel: +91 11 22692536; fax: +91 11 22590495; e-mail: dr.pan[email protected] Received 9 August 2014 Accepted 13 August 2014

We read with interest the paper titled ‘Gallbladder cancers: associated conditions, histological types, prognosis, and prevention’ by Cariati et al. [1] published in your journal. The authors have aptly highlighted the role of preventive cholecystectomy in patients with risk factors such as large and longstanding (>3 cm) cholesterol or composite gallstones, xanthogranulomatous cholecystitis, and segmental adenomyomatosis to prevent the development of gallbladder cancer (GBC). They have classified preventive cholecystectomy in this setting as a strategy under secondary prevention. The Centre for Disease Control and Prevention (CDC) (http://www.cdc.gov/excite/skincancer/mod13.htm) describes three stages of disease prevention: primary prevention is the method used before the onset of disease so as to limit its occurrence; secondary prevention is one where preventive steps are taken after the onset of disease, but before the disease manifests symptomatically or advances; and tertiary prevention targets a patient who already has symptomatic disease. Primary prevention decreases both the incidence and the prevalence of disease as the preventive steps are initiated before the initiation of disease. Preventive cholecystectomy, as the name indicates, is performed to remove known risk factors such as gallstones for the development of GBC to prevent the occurrence of GBC; it must be remembered that GBC has not developed at the time of preventive cholecystectomy. Thus, preventive cholecystectomy must be qualified as the primary prevention in this scenario and not as secondary prevention. Primary prevention has always been inclusive of the ‘high-risk’ strategy and any intervention, that is, health education, medical, or surgical in this group where the disease (GBC in this context) has not developed should technically be tantamount to primary prevention. To support this notion, 0954-691X © 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins

another instance can be cited from the bilateral prophylactic mastectomy among breast cancer (BRCA) gene carrier women, wherein bilateral prophylactic mastectomy is considered as a means of primary prevention of the breast cancer [2]. Again, in this case, breast cancer has not developed in this group of patients; they only harbor the risk factors known to predispose to breast cancer. Secondary prevention is defined as early diagnosis and treatment of the disease; secondary detection would not change the incidence of the disease. Secondary prevention helps to reduce the morbidity and mortality of a given disease. Screening mammography is a good example of secondary prevention. Screening mammography helps to diagnose nonpalpable early breast cancer in an asymptomatic individual; this can lead to a more definitive and curative treatment that has the potential to decrease morbidity and mortality. Secondary prevention for GBC would include mass-scale imaging (for example, ultrasonography) to detect early GBC in an asymptomatic patient; early detection of GBC would render them candidates for curative surgery. Therefore, there is a need for unambiguous terminologies for the prevention and control of important noncommunicable diseases not just from the academic point of view but also from the point of view of policy making and resource allocation.

Acknowledgements Conflicts of interest

There are no conflicts of interest.

References 1


Cariati A, Piromalli E, Cetta F. Gallbladder cancers: associated conditions, histological types, prognosis, and prevention. Eur J Gastroenterol Hepatol 2014; 26:562–569. Lostumbo L, Carbine N, Wallace J, Ezzo J. Prophylactic mastectomy for the prevention of breast cancer. Cochrane Database Syst Rev 2004; 4: CD002748.

Misleading results in the diagnosis of atrophic gastritis Francesco Di Mario and Elisabetta Goni, Department of Clinical and Experimental Medicine, University of Parma, Parma, Italy Correspondence to Francesco Di Mario, MD, Department of Clinical and Experimental Medicine, University of Parma, Via Gramsci 14, 43125, Parma, Italy Tel: + 39 033564; e-mail: francesco[email protected] Received 8 August 2014 Accepted 14 August 2014

We read with interest the paper of McNicholl et al. [1] on the accuracy of GastroPanel in the diagnosis of chronic DOI: 10.1097/MEG.0000000000000212

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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.


Chronic atrophic gastritis


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.





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: psyoun[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

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Misleading results in the diagnosis of atrophic gastritis.

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