Letters to the Editor
nature publishing group
date of initial diagnosis of HCC and date of current RFA are also important variables for this study; because our study is a multicenter retrospective cohort study, matching these variables can decrease some confounders of selective patients from different centers. In future observational studies, we would like to use the approach of the propensity score-matching analysis.
CONFLICT OF INTEREST Guarantor of the article: Kuansheng Ma, MD, PhD. Specific author contributions: Xiaobin Feng and Kuansheng Ma drafted the article. Kuansheng Ma revised the manuscript and approved the final version. Financial support: None. Potential competing interests: None.
1
Institute of Hepatobiliary Surgery, Southwest Hospital, Third Military Medical University, Chongqing, China. Correspondence: Xiaobin Feng MD or Kuansheng Ma, MD, PhD, Institute of Hepatobiliary Surgery, Southwest Hospital, Third Military Medical University, No. 29 Gaotanyan Street, Shapingba District, Chongqing 400038, China. E-mail: [email protected] or [email protected]
Pancreatic Cancer in Patients With Recently Diagnosed Chronic Pancreatitis Bai-Rong Li, MD1, 2, 3, Gao-Ping Mao, MD1, Liang-Hao Hu, MD2, 3 and Zhao-Shen Li, MD2, 3 doi:10.1038/ajg.2015.107
REFERENCES 1. Facciorusso A, Muscatiello N, Di Leo A, Barone M. Combination therapy with sorafenib and radiofrequency ablation for hepatocellular carcinoma: a glimmer of light after the STORM trial? Am J Gastroenterol 2015;110:770–71 (this issue). 2. Huang J, Yan L, Cheng Z et al. A randomized trial comparing radiofrequency ablation and surgical resection for HCC conforming to the Milan criteria. Ann Surg 2010;252:903–12. 3. Hasegawa K, Aoki T, Ishizawa T et al. Comparison of the therapeutic outcomes between surgical resection and percutaneous ablation for small hepatocellular carcinoma. Ann Surg Oncol 2014;21(Suppl 3):S348–S355. 4. Nijkamp MW, van der Bilt JD, de Bruijn MT et al. Accelerated perinecrotic outgrowth of colorectal liver metastases following radiofrequency ablation is a hypoxia-driven phenomenon. Ann Surg 2009;249:814–23. 5. Pfeiffenberger J, Koschny R, Hoffmann K et al. Sorafenib treatment is save and may affect survival of recurrent hepatocellular carcinoma after liver transplantation. Langenbecks Arch Surg 2013;398:1123–8. 6. Alsina AE, Makris A, Nenos V et al. Can sorafenib increase survival for recurrent hepatocellular carcinoma after liver transplantation? A pilot study. Am Surg 2014;80:680–4. 7. Hua XD, He ZY. [Therapeutic effects of sorafenib combined with transcatheter arterial chemoembolization and microwave ablation on postsurgical recurrent hepatocellular carcinoma]. Zhonghua Zhong Liu Za Zhi 2012;34:790–2. 8. Wang SN, Chuang SC, Lee KT. Efficacy of sorafenib as adjuvant therapy to prevent early recurrence of hepatocellular carcinoma after curative surgery: A pilot study. Hepatol Res 2014;44:523–31. 9. Fukuda H, Numata K, Moriya S et al. Hepatocellular carcinoma: concomitant sorafenib promotes necrosis after radiofrequency ablation--propensity score matching analysis. Radiology 2014;272:598–604
© 2015 by the American College of Gastroenterology
To the Editor: We have read with great interest your recently published study on the presence and underlying pancreatic cancer (PaCa) in recently diagnosed chronic pancreatitis (CP) patients (1). This study excluded 18 patients who manifested PaCa within 3 years after CP diagnosis from the preexisting CP group; a 3-year duration was set as the exclusion period. Both of these criteria would lead to a lower PaCa incidence rate compared with that of the recently diagnosed CP group in the corresponding follow-up year. We would like to inquire about the reasons for these designations. The subgroup analysis regarding smoking and alcohol history does not seem to be sufficiently reasonable. PaCa incidence was lower among smokers and alcoholics in this research. The authors then concluded that PaCa is likely to be the cause of the symptoms and signs commonly regarded as CP. In our opinion, other points that may explain this result must be considered. First, rather than smoking and alcohol history, the current status of smoking and alcohol intake is more important for PaCa development, as previously reported (2,3). Anderson et al. (2) showed that abstinence from smoking decreases the risk of earlyonset PaCa among smokers. However, in the present study, cigarette and alcohol
use are presented as smoking and alcohol history but are assessed at the time the patients are entered into the database. Among recently diagnosed CP patients, a duration of at least 3 years had already passed between CP diagnosis and patient inclusion into the database. Thus, the status of smoking and alcohol intake for at least 3 years before CP diagnosis must be unknown. Changes in smoking and alcohol status may result in significant bias during subgroup analysis. Furthermore, to obtain more accurate results for related factors of PaCa misdiagnosis, subgroup analysis must include only patients who were diagnosed with PaCa within 2 years after CP diagnosis (41 patients) because alcohol and smoking may exert different effects on CP to PaCa progression and initial PaCa development. Diagnosis of PaCa at its early stages is difficult, and some early-stage pancreatic cancers are often misdiagnosed as CP (4–6). In the present study, most of the PaCa patients (74.51%, 38/51) were established within 1 year after CP diagnosis, similar to a previous study (66.27%, 338/510) (4). We expected more detailed results regarding the clinical stages of PaCa, the rate of surgical treatment, and survival durations after PaCa diagnosis. CONFLICT OF INTEREST The authors declare no conflict of interest.
REFERENCES 1. Munigala S, Kanwal F, Xian H et al. New diagnosis of chronic pancreatitis: risk of missing an underlying pancreatic cancer. Am J Gastroenterol 2014;109:1824–30. 2. Anderson MA, Zolotarevsky E, Cooper KL et al. Alcohol and tobacco lower the age of presentation in sporadic pancreatic cancer in a dose-dependent manner: a multicenter study. Am J Gastroenterol 2012;107:1730–9. 3. Brand RE, Greer JB, Zolotarevsky E et al. Pancreatic cancer patients who smoke and drink are diagnosed at younger ages. Clin Gastroenterol Hepatol 2009;7:1007–12. 4. Bang UC, Benfield T, Hyldstrup L et al. Mortality, cancer, and comorbidities associated with chronic pancreatitis: a Danish nationwide matched-cohort study. Gastroenterology 2014;146:989–94. 5. Li BR, Hu LH, Li ZS. Chronic pancreatitis and pancreatic cancer. Gastroenterology 2014;147:541–2. 6. Wang W, Liao Z, Li G et al. Incidence of pancreatic cancer in chinese patients with chronic pancreatitis. Pancreatology 2011;11:16–23.
The American Journal of GASTROENTEROLOGY
773
774
Letters to the Editor
1
Department of Gastroenterology, Air Force General Hospital, Beijing, China; 2Department of Gastroenterology, Changhai Hospital, The Second Military Medical University, Shanghai, China; 3Digestive Endoscopy Center, Changhai Hospital, The Second Military Medical University, Shanghai, China. Correspondence: Liang-Hao Hu, MD or Zhao-Shen Li, MD, Department of Gastroenterology and Digestive Endoscopy Center, Changhai Hospital, The Second Military Medical University, 168 Changhai Road, Shanghai 200433, China. E-mail: [email protected] or [email protected]
Response to Li et al. Satish Munigala, MD, MPH1, Fasiha Kanwal, MD, MS1, Hong Xian, PhD2, 3 and Banke Agarwal, MD1 doi:10.1038/ajg.2015.110
To the Editor: We would like to thank Li et al. “Pancreatic cancer in patients with recently diagnosed chronic pancreatitis” (1) for their interest and comments on our article. Unlike previous studies that were studying the longterm risk of pancreatic cancer (PaCa) in patients with chronic pancreatitis, our study focuses on short-term risk of PaCa following a new diagnosis of chronic pancreatitis (CP). In our data set, we observed an excess risk of PaCa in first 3 years following a new diagnosis of CP. To make sure that the base line risk of PaCa in patients with pre-existing CP in our patients is not artifactually higher due to excess of PaCa patients misdiagnosed as CP, we used a 3-year cutoff after new diagnosis of CP to define pre-existing CP. With regard to the issue about the history of smoking and alcoholism raised by Li et al., we believe that these do not apply to our article as those are pertinent only to the long-term risk of PaCa in patients with CP. Our study evaluated the risk of PaCa misdiagnosed as CP. We believe that patients without risk factors for CP such as smoking and alcohol intake have lower likelihood of CP, and hence are more likely to have a PaCa that is misdiagnosed as CP. In the recent study by Bang et al. (2) using Swedish registry, the short term-risk of PaCa was higher in patients with nonalcoholic CP (and not in those with alcoholic CP) most likely due to a higher proportion of misdiagnosis of PaCa patients as CP. The American Journal of GASTROENTEROLOGY
nature publishing group
CONFLICT OF INTEREST The authors declare no conflict of interest. REFERENCES 1. Li B-R, Mao G-P, Hu L-H et al. Pancreatic cancer in patients with recently diagnosed chronic pancreatitis. Am J Gastroenterol 2015;110:773–4. 2. Bang UC, Benfield T, Hyldstrup L et al. Mortality, cancer, and comorbidities associated with chronic pancreatitis: a Danish nationwide matched-cohort study. Gastroenterology 2014;146:989–94.
1
Division of Gastroenterology and Hepatology, Saint Louis University School of Medicine, St Louis, Missouri, USA; 2Veterans Affairs St Louis Health Care System, St Louis, Missouri, USA; 3 Department of Biostatistics, Saint Louis University School of Public Health, St Louis, Missouri, USA. Correspondence: Banke Agarwal, MD, Division of Gastroenterology and Hepatology, St Louis University School of Medicine, 3635 Vista Avenue FDT 9S, St Louis, Missouri 63110, USA. E-mail: [email protected]
Diverticular Disease of the Colon and Irritable Bowel Syndrome: It Is Time to Differentiate Antonio Tursi, MD1 doi:10.1038/ajg.2015.78
To the Editor: I read with extreme interest the article by Yamada et al. “Association Between the Location of Diverticular Disease and the Irritable Bowel Syndrome: A Multicenter Study in Japan” (1) about the higher risk of irritable bowel syndrome (IBS) in patients having bilateral but especially left-sided, but not right-sided, diverticular disease (DD) of the colon (odds ratio (OR) 3.1; 95% confidence interval (CI): 1.4–7.1; P=0.0060). Although a strong relationship between DD and IBS has been already reported (2,3), the most interesting finding of this report is that right-sided DD is not linked to IBS (OR 0.9; 95% CI: 0.5–1.9; P=0.8873). However, I mean that it is time to consider that this overlap is less
strong than previously thought, and that we now have clinical and laboratory instruments to differentiate between these two entities. First of all, it is important to correctly define these symptoms. Although patients with symptomatic diverticulosis undoubtedly share features with IBS, strictly speaking they cannot have IBS, as the definition of IBS specifically excludes “organic or structural lesions likely to be responsible for symptoms” (4). In this way, it seems to be appropriate to speak of “IBS-like” symptoms rather than “IBS”. This correct definition is also useful to pose a correct differential diagnosis. On 194 patients with symptomatic diverticulosis and screened for IBS by Rome III criteria, Cuomo et al. (5) showed recently that only nine patients with DD (10%) fulfilled the criteria for IBS (P24 h was significantly more frequent in DD than in IBS (P
nature publishing group
date of initial diagnosis of HCC and date of current RFA are also important variables for this study; because our study is a multicenter retrospective cohort study, matching these variables can decrease some confounders of selective patients from different centers. In future observational studies, we would like to use the approach of the propensity score-matching analysis.
CONFLICT OF INTEREST Guarantor of the article: Kuansheng Ma, MD, PhD. Specific author contributions: Xiaobin Feng and Kuansheng Ma drafted the article. Kuansheng Ma revised the manuscript and approved the final version. Financial support: None. Potential competing interests: None.
1
Institute of Hepatobiliary Surgery, Southwest Hospital, Third Military Medical University, Chongqing, China. Correspondence: Xiaobin Feng MD or Kuansheng Ma, MD, PhD, Institute of Hepatobiliary Surgery, Southwest Hospital, Third Military Medical University, No. 29 Gaotanyan Street, Shapingba District, Chongqing 400038, China. E-mail: [email protected] or [email protected]
Pancreatic Cancer in Patients With Recently Diagnosed Chronic Pancreatitis Bai-Rong Li, MD1, 2, 3, Gao-Ping Mao, MD1, Liang-Hao Hu, MD2, 3 and Zhao-Shen Li, MD2, 3 doi:10.1038/ajg.2015.107
REFERENCES 1. Facciorusso A, Muscatiello N, Di Leo A, Barone M. Combination therapy with sorafenib and radiofrequency ablation for hepatocellular carcinoma: a glimmer of light after the STORM trial? Am J Gastroenterol 2015;110:770–71 (this issue). 2. Huang J, Yan L, Cheng Z et al. A randomized trial comparing radiofrequency ablation and surgical resection for HCC conforming to the Milan criteria. Ann Surg 2010;252:903–12. 3. Hasegawa K, Aoki T, Ishizawa T et al. Comparison of the therapeutic outcomes between surgical resection and percutaneous ablation for small hepatocellular carcinoma. Ann Surg Oncol 2014;21(Suppl 3):S348–S355. 4. Nijkamp MW, van der Bilt JD, de Bruijn MT et al. Accelerated perinecrotic outgrowth of colorectal liver metastases following radiofrequency ablation is a hypoxia-driven phenomenon. Ann Surg 2009;249:814–23. 5. Pfeiffenberger J, Koschny R, Hoffmann K et al. Sorafenib treatment is save and may affect survival of recurrent hepatocellular carcinoma after liver transplantation. Langenbecks Arch Surg 2013;398:1123–8. 6. Alsina AE, Makris A, Nenos V et al. Can sorafenib increase survival for recurrent hepatocellular carcinoma after liver transplantation? A pilot study. Am Surg 2014;80:680–4. 7. Hua XD, He ZY. [Therapeutic effects of sorafenib combined with transcatheter arterial chemoembolization and microwave ablation on postsurgical recurrent hepatocellular carcinoma]. Zhonghua Zhong Liu Za Zhi 2012;34:790–2. 8. Wang SN, Chuang SC, Lee KT. Efficacy of sorafenib as adjuvant therapy to prevent early recurrence of hepatocellular carcinoma after curative surgery: A pilot study. Hepatol Res 2014;44:523–31. 9. Fukuda H, Numata K, Moriya S et al. Hepatocellular carcinoma: concomitant sorafenib promotes necrosis after radiofrequency ablation--propensity score matching analysis. Radiology 2014;272:598–604
© 2015 by the American College of Gastroenterology
To the Editor: We have read with great interest your recently published study on the presence and underlying pancreatic cancer (PaCa) in recently diagnosed chronic pancreatitis (CP) patients (1). This study excluded 18 patients who manifested PaCa within 3 years after CP diagnosis from the preexisting CP group; a 3-year duration was set as the exclusion period. Both of these criteria would lead to a lower PaCa incidence rate compared with that of the recently diagnosed CP group in the corresponding follow-up year. We would like to inquire about the reasons for these designations. The subgroup analysis regarding smoking and alcohol history does not seem to be sufficiently reasonable. PaCa incidence was lower among smokers and alcoholics in this research. The authors then concluded that PaCa is likely to be the cause of the symptoms and signs commonly regarded as CP. In our opinion, other points that may explain this result must be considered. First, rather than smoking and alcohol history, the current status of smoking and alcohol intake is more important for PaCa development, as previously reported (2,3). Anderson et al. (2) showed that abstinence from smoking decreases the risk of earlyonset PaCa among smokers. However, in the present study, cigarette and alcohol
use are presented as smoking and alcohol history but are assessed at the time the patients are entered into the database. Among recently diagnosed CP patients, a duration of at least 3 years had already passed between CP diagnosis and patient inclusion into the database. Thus, the status of smoking and alcohol intake for at least 3 years before CP diagnosis must be unknown. Changes in smoking and alcohol status may result in significant bias during subgroup analysis. Furthermore, to obtain more accurate results for related factors of PaCa misdiagnosis, subgroup analysis must include only patients who were diagnosed with PaCa within 2 years after CP diagnosis (41 patients) because alcohol and smoking may exert different effects on CP to PaCa progression and initial PaCa development. Diagnosis of PaCa at its early stages is difficult, and some early-stage pancreatic cancers are often misdiagnosed as CP (4–6). In the present study, most of the PaCa patients (74.51%, 38/51) were established within 1 year after CP diagnosis, similar to a previous study (66.27%, 338/510) (4). We expected more detailed results regarding the clinical stages of PaCa, the rate of surgical treatment, and survival durations after PaCa diagnosis. CONFLICT OF INTEREST The authors declare no conflict of interest.
REFERENCES 1. Munigala S, Kanwal F, Xian H et al. New diagnosis of chronic pancreatitis: risk of missing an underlying pancreatic cancer. Am J Gastroenterol 2014;109:1824–30. 2. Anderson MA, Zolotarevsky E, Cooper KL et al. Alcohol and tobacco lower the age of presentation in sporadic pancreatic cancer in a dose-dependent manner: a multicenter study. Am J Gastroenterol 2012;107:1730–9. 3. Brand RE, Greer JB, Zolotarevsky E et al. Pancreatic cancer patients who smoke and drink are diagnosed at younger ages. Clin Gastroenterol Hepatol 2009;7:1007–12. 4. Bang UC, Benfield T, Hyldstrup L et al. Mortality, cancer, and comorbidities associated with chronic pancreatitis: a Danish nationwide matched-cohort study. Gastroenterology 2014;146:989–94. 5. Li BR, Hu LH, Li ZS. Chronic pancreatitis and pancreatic cancer. Gastroenterology 2014;147:541–2. 6. Wang W, Liao Z, Li G et al. Incidence of pancreatic cancer in chinese patients with chronic pancreatitis. Pancreatology 2011;11:16–23.
The American Journal of GASTROENTEROLOGY
773
774
Letters to the Editor
1
Department of Gastroenterology, Air Force General Hospital, Beijing, China; 2Department of Gastroenterology, Changhai Hospital, The Second Military Medical University, Shanghai, China; 3Digestive Endoscopy Center, Changhai Hospital, The Second Military Medical University, Shanghai, China. Correspondence: Liang-Hao Hu, MD or Zhao-Shen Li, MD, Department of Gastroenterology and Digestive Endoscopy Center, Changhai Hospital, The Second Military Medical University, 168 Changhai Road, Shanghai 200433, China. E-mail: [email protected] or [email protected]
Response to Li et al. Satish Munigala, MD, MPH1, Fasiha Kanwal, MD, MS1, Hong Xian, PhD2, 3 and Banke Agarwal, MD1 doi:10.1038/ajg.2015.110
To the Editor: We would like to thank Li et al. “Pancreatic cancer in patients with recently diagnosed chronic pancreatitis” (1) for their interest and comments on our article. Unlike previous studies that were studying the longterm risk of pancreatic cancer (PaCa) in patients with chronic pancreatitis, our study focuses on short-term risk of PaCa following a new diagnosis of chronic pancreatitis (CP). In our data set, we observed an excess risk of PaCa in first 3 years following a new diagnosis of CP. To make sure that the base line risk of PaCa in patients with pre-existing CP in our patients is not artifactually higher due to excess of PaCa patients misdiagnosed as CP, we used a 3-year cutoff after new diagnosis of CP to define pre-existing CP. With regard to the issue about the history of smoking and alcoholism raised by Li et al., we believe that these do not apply to our article as those are pertinent only to the long-term risk of PaCa in patients with CP. Our study evaluated the risk of PaCa misdiagnosed as CP. We believe that patients without risk factors for CP such as smoking and alcohol intake have lower likelihood of CP, and hence are more likely to have a PaCa that is misdiagnosed as CP. In the recent study by Bang et al. (2) using Swedish registry, the short term-risk of PaCa was higher in patients with nonalcoholic CP (and not in those with alcoholic CP) most likely due to a higher proportion of misdiagnosis of PaCa patients as CP. The American Journal of GASTROENTEROLOGY
nature publishing group
CONFLICT OF INTEREST The authors declare no conflict of interest. REFERENCES 1. Li B-R, Mao G-P, Hu L-H et al. Pancreatic cancer in patients with recently diagnosed chronic pancreatitis. Am J Gastroenterol 2015;110:773–4. 2. Bang UC, Benfield T, Hyldstrup L et al. Mortality, cancer, and comorbidities associated with chronic pancreatitis: a Danish nationwide matched-cohort study. Gastroenterology 2014;146:989–94.
1
Division of Gastroenterology and Hepatology, Saint Louis University School of Medicine, St Louis, Missouri, USA; 2Veterans Affairs St Louis Health Care System, St Louis, Missouri, USA; 3 Department of Biostatistics, Saint Louis University School of Public Health, St Louis, Missouri, USA. Correspondence: Banke Agarwal, MD, Division of Gastroenterology and Hepatology, St Louis University School of Medicine, 3635 Vista Avenue FDT 9S, St Louis, Missouri 63110, USA. E-mail: [email protected]
Diverticular Disease of the Colon and Irritable Bowel Syndrome: It Is Time to Differentiate Antonio Tursi, MD1 doi:10.1038/ajg.2015.78
To the Editor: I read with extreme interest the article by Yamada et al. “Association Between the Location of Diverticular Disease and the Irritable Bowel Syndrome: A Multicenter Study in Japan” (1) about the higher risk of irritable bowel syndrome (IBS) in patients having bilateral but especially left-sided, but not right-sided, diverticular disease (DD) of the colon (odds ratio (OR) 3.1; 95% confidence interval (CI): 1.4–7.1; P=0.0060). Although a strong relationship between DD and IBS has been already reported (2,3), the most interesting finding of this report is that right-sided DD is not linked to IBS (OR 0.9; 95% CI: 0.5–1.9; P=0.8873). However, I mean that it is time to consider that this overlap is less
strong than previously thought, and that we now have clinical and laboratory instruments to differentiate between these two entities. First of all, it is important to correctly define these symptoms. Although patients with symptomatic diverticulosis undoubtedly share features with IBS, strictly speaking they cannot have IBS, as the definition of IBS specifically excludes “organic or structural lesions likely to be responsible for symptoms” (4). In this way, it seems to be appropriate to speak of “IBS-like” symptoms rather than “IBS”. This correct definition is also useful to pose a correct differential diagnosis. On 194 patients with symptomatic diverticulosis and screened for IBS by Rome III criteria, Cuomo et al. (5) showed recently that only nine patients with DD (10%) fulfilled the criteria for IBS (P24 h was significantly more frequent in DD than in IBS (P
