- Email: [email protected]
spleen diameter ratio for non-invasive diagnosis of oesophageal varices: Is it useful in compensated cirrhosis?”
Correspondence / Digestive and Liver Disease 44 (2012) 962–966
Angelo Zullo ∗ Cesare Hassan Vincenzo Bruzzese Gastroenterology and Digestive Endoscopy, Nuovo Regina Margherita Hospital, Rome, Italy ∗ Corresponding
author at: Gastroenterologia ed Endoscopia Digestiva, PTP Nuovo Regina Margherita, Via E. Morosini 30, 00153 Rome, Italy. Tel.: +39 06 58446608; fax: +39 06 58446533. E-mail address: [email protected] (A. Zullo) Available online 8 July 2012
To conclude, we feel that independent validation of a diagnostic technique is always welcome; studies such as by Mangone et al. in compensated cirrhotics, as well as the thorough meta-analysis by Ying et al. [5], who found that the platelet count/spleen diameter ratio has a significantly greater (P = 0.031) accuracy in compensated cirrhosis than in all cirrhosis stages, might increase the possibility that an accepted, readily available, and inexpensive method such as the platelet count/spleen diameter ratio might be used in routine clinical practice. Conflict of interest statement None. Funding
doi:10.1016/j.dld.2012.06.002
Comment to “Platelet count/spleen diameter ratio for noninvasive diagnosis of oesophageal varices: Is it useful in compensated cirrhosis?” To the Editor: We read with great interest the article by Mangone et al. recently published in Digestive and Liver Disease evaluating the usefulness of the platelet count/spleen diameter for the non-invasive diagnosis of oesophageal varices and portal hypertensive gastropathy in patients with compensated cirrhosis [1]. Indeed, the authors are to be commended for having used the platelet count/spleen diameter ratio for the non-invasive diagnosis of any oesophagogastric endoscopic sign of portal hypertension. Overall, they observed that a platelet count/spleen diameter ratio above 936.4 had 76.6% and 74.5% negative predictive value for the presence of oesophageal varices and any sign of portal hypertension, respectively. To the best of our knowledge this is the first detailed report on the use of a non-invasive parameter for the diagnosis of any endoscopic sign of portal hypertension, and the results by Mangone et al. compare favourably with the results obtained in the relevant, unbiased, and technically accurate study which assessed liver stiffness measurement for the identification of cirrhotic patients with varices [2]. The main shortcoming of the study by Mangone et al., however, is the interpretation of their study results. In fact, the platelet count/spleen diameter ratio was initially devised, and subsequently validated, as a tool to reduce endoscopies by avoiding unnecessary and invasive examinations in patients who were unlikely to have oesophageal varices, and not as a parameter predictive of their presence [3]. In the study by Mangone et al., using the suggested 936.4 cut-off, upper digestive endoscopy would have been carried out in the 40 patients with a platelet count/spleen diameter ratio below this threshold (46.0% of the study population), thus saving 54% of endoscopies as compared to the current “screen all” practice, while among the 47 patients with a platelet count/spleen diameter ratio above 936.4 oesophageal varices would have been missed in 11 patients (23.4%)—and it might have been of interest to know the grade of these missed varices, as this was not reported. Noteworthy, this false negative rate using a non-invasive parameter is far lower than the one reported by Vizzutti et al. with the use of a non-invasive tool such as hepatic transient elastography at a threshold of 17.6 kPa (i.e., 37.5%), and is quite similar to the figure obtained by using a “minimally invasive” visual tool such as the oesophageal capsule endoscopy (i.e., 20%) in a French comparative multicentre study [4]. Despite these results, both hepatic transient elastography and oesophageal capsule endoscopy are commonly proposed as non-invasive methods to predict – or diagnose – the presence/absence of oesophageal varices.
965
None. References [1] Mangone M, Moretti A, Alivernini F, et al. Platelet count/spleen diameter ratio for non-invasive diagnosis of oesophageal varices: is it useful in compensated cirrhosis? Digestive and Liver Disease 2012;44:504–7. [2] Vizzutti F, Arena U, Romanelli RG, et al. Liver stiffness measurement predicts severe portal hypertension in patients with HCV-related cirrhosis. Hepatology 2007;45:1290–7. [3] Giannini E, Zaman A, Kreil A, et al. Platelet count/spleen diameter ratio for the noninvasive diagnosis of esophageal varices: results of a multicenter, prospective, validation study. American Journal of Gastroenterology 2006;101:2511–9. [4] Lapalus MG, Ben Soussan E, Gaudric M, et al. Esophageal capsule endoscopy vs. EGD for the evaluation of portal hypertension: a French prospective multicenter comparative study. American Journal of Gastroenterology 2009;104:1112–8. [5] Ying L, Lin X, Xie ZL, Hu YP, Shi KQ. Performance of platelet count/spleen diameter ratio for diagnosis of esophageal varices in cirrhosis: a meta-analysis. Digestive Diseases and Sciences 2012;57:1672–81.
Edoardo G. Giannini ∗ Vincenzo Savarino Gastroenterology Unit, Department of Internal Medicine, University of Genoa, Genoa, Italy ∗ Corresponding
author at: Gastroenterology Unit, Department of Internal Medicine, University of Genoa, Viale Benedetto XV, No. 6, 16132 Genoa, Italy. Tel.: +39 010 353 7950; fax: +39 010 353 8638. E-mail address: [email protected] (E.G. Giannini) Available online 18 June 2012
doi:10.1016/j.dld.2012.05.014
Acute recurrent pancreatitis and pancreas divisum: Appearances can be deceiving Sir, The role of pancreas divisum (PD) in inducing acute recurrent pancreatitis (ARP) is still under debate; whereas some authors consider PD a simple morphological anomaly of the pancreatic ductal system without any clinical consequences [1], others have reported that it is able to induce ARP as a result of relative outflow obstruction [2]. We believe that PD per se is not always a cause of ARP. Case 1: A 33-year-old male had had ARP since 1985. In May 2009, he was cholecystectomized for gallstones and subsequently experienced two other episodes of abdominal pain. When seen in February 2010 in our Pancreas Unit, he was in good general condition; the biochemical examinations revealed a slight increase of transaminases and no mutations of CFTR, PRSS1 and SPINK1 genes. Faecal elastase-1 (FE-1) and the oral glucose tolerance test (OGTT) were also normal. Magnetic resonance cholangiopancreatography (MRCP) showed the presence of PD and no chronic
Angelo Zullo ∗ Cesare Hassan Vincenzo Bruzzese Gastroenterology and Digestive Endoscopy, Nuovo Regina Margherita Hospital, Rome, Italy ∗ Corresponding
author at: Gastroenterologia ed Endoscopia Digestiva, PTP Nuovo Regina Margherita, Via E. Morosini 30, 00153 Rome, Italy. Tel.: +39 06 58446608; fax: +39 06 58446533. E-mail address: [email protected] (A. Zullo) Available online 8 July 2012
To conclude, we feel that independent validation of a diagnostic technique is always welcome; studies such as by Mangone et al. in compensated cirrhotics, as well as the thorough meta-analysis by Ying et al. [5], who found that the platelet count/spleen diameter ratio has a significantly greater (P = 0.031) accuracy in compensated cirrhosis than in all cirrhosis stages, might increase the possibility that an accepted, readily available, and inexpensive method such as the platelet count/spleen diameter ratio might be used in routine clinical practice. Conflict of interest statement None. Funding
doi:10.1016/j.dld.2012.06.002
Comment to “Platelet count/spleen diameter ratio for noninvasive diagnosis of oesophageal varices: Is it useful in compensated cirrhosis?” To the Editor: We read with great interest the article by Mangone et al. recently published in Digestive and Liver Disease evaluating the usefulness of the platelet count/spleen diameter for the non-invasive diagnosis of oesophageal varices and portal hypertensive gastropathy in patients with compensated cirrhosis [1]. Indeed, the authors are to be commended for having used the platelet count/spleen diameter ratio for the non-invasive diagnosis of any oesophagogastric endoscopic sign of portal hypertension. Overall, they observed that a platelet count/spleen diameter ratio above 936.4 had 76.6% and 74.5% negative predictive value for the presence of oesophageal varices and any sign of portal hypertension, respectively. To the best of our knowledge this is the first detailed report on the use of a non-invasive parameter for the diagnosis of any endoscopic sign of portal hypertension, and the results by Mangone et al. compare favourably with the results obtained in the relevant, unbiased, and technically accurate study which assessed liver stiffness measurement for the identification of cirrhotic patients with varices [2]. The main shortcoming of the study by Mangone et al., however, is the interpretation of their study results. In fact, the platelet count/spleen diameter ratio was initially devised, and subsequently validated, as a tool to reduce endoscopies by avoiding unnecessary and invasive examinations in patients who were unlikely to have oesophageal varices, and not as a parameter predictive of their presence [3]. In the study by Mangone et al., using the suggested 936.4 cut-off, upper digestive endoscopy would have been carried out in the 40 patients with a platelet count/spleen diameter ratio below this threshold (46.0% of the study population), thus saving 54% of endoscopies as compared to the current “screen all” practice, while among the 47 patients with a platelet count/spleen diameter ratio above 936.4 oesophageal varices would have been missed in 11 patients (23.4%)—and it might have been of interest to know the grade of these missed varices, as this was not reported. Noteworthy, this false negative rate using a non-invasive parameter is far lower than the one reported by Vizzutti et al. with the use of a non-invasive tool such as hepatic transient elastography at a threshold of 17.6 kPa (i.e., 37.5%), and is quite similar to the figure obtained by using a “minimally invasive” visual tool such as the oesophageal capsule endoscopy (i.e., 20%) in a French comparative multicentre study [4]. Despite these results, both hepatic transient elastography and oesophageal capsule endoscopy are commonly proposed as non-invasive methods to predict – or diagnose – the presence/absence of oesophageal varices.
965
None. References [1] Mangone M, Moretti A, Alivernini F, et al. Platelet count/spleen diameter ratio for non-invasive diagnosis of oesophageal varices: is it useful in compensated cirrhosis? Digestive and Liver Disease 2012;44:504–7. [2] Vizzutti F, Arena U, Romanelli RG, et al. Liver stiffness measurement predicts severe portal hypertension in patients with HCV-related cirrhosis. Hepatology 2007;45:1290–7. [3] Giannini E, Zaman A, Kreil A, et al. Platelet count/spleen diameter ratio for the noninvasive diagnosis of esophageal varices: results of a multicenter, prospective, validation study. American Journal of Gastroenterology 2006;101:2511–9. [4] Lapalus MG, Ben Soussan E, Gaudric M, et al. Esophageal capsule endoscopy vs. EGD for the evaluation of portal hypertension: a French prospective multicenter comparative study. American Journal of Gastroenterology 2009;104:1112–8. [5] Ying L, Lin X, Xie ZL, Hu YP, Shi KQ. Performance of platelet count/spleen diameter ratio for diagnosis of esophageal varices in cirrhosis: a meta-analysis. Digestive Diseases and Sciences 2012;57:1672–81.
Edoardo G. Giannini ∗ Vincenzo Savarino Gastroenterology Unit, Department of Internal Medicine, University of Genoa, Genoa, Italy ∗ Corresponding
author at: Gastroenterology Unit, Department of Internal Medicine, University of Genoa, Viale Benedetto XV, No. 6, 16132 Genoa, Italy. Tel.: +39 010 353 7950; fax: +39 010 353 8638. E-mail address: [email protected] (E.G. Giannini) Available online 18 June 2012
doi:10.1016/j.dld.2012.05.014
Acute recurrent pancreatitis and pancreas divisum: Appearances can be deceiving Sir, The role of pancreas divisum (PD) in inducing acute recurrent pancreatitis (ARP) is still under debate; whereas some authors consider PD a simple morphological anomaly of the pancreatic ductal system without any clinical consequences [1], others have reported that it is able to induce ARP as a result of relative outflow obstruction [2]. We believe that PD per se is not always a cause of ARP. Case 1: A 33-year-old male had had ARP since 1985. In May 2009, he was cholecystectomized for gallstones and subsequently experienced two other episodes of abdominal pain. When seen in February 2010 in our Pancreas Unit, he was in good general condition; the biochemical examinations revealed a slight increase of transaminases and no mutations of CFTR, PRSS1 and SPINK1 genes. Faecal elastase-1 (FE-1) and the oral glucose tolerance test (OGTT) were also normal. Magnetic resonance cholangiopancreatography (MRCP) showed the presence of PD and no chronic