J Clin Gastroenterol
Volume 49, Number 4, April 2015
Letters to the Editor
diverticulosis: a 5-year follow-up. Int J Colorectal Dis. 2012;27:179–185. 10. Tursi A, Elisei W, Picchio M, et al. Letter: diverticulosis in inflammatory bowel diseases. Aliment Pharmacol Ther. 2014;39:899–900.
MRI, CT Scan, and Ultrasound in the Diagnosis of Nonalcoholic Fatty Liver Disease FIGURE 2. Comparison of the inflammatory infiltrate, subdivided according to the type of inflammatory cells. E indicates eosinophils; H, histioid cells; L, lymphocytes; N, neutrophils; P, plasma cells; SCAD, segmental colitis associated with diverticulosis; UC, ulcerative colitis. Bars represent median.
may be considered a form of chronic intestinal inflammation occurring in a colon-harboring diverticula, rather than a simple complication of diverticular disease.4 In fact SCAD seems to need a long-lasting medical treatment linked to the severity of the disease to maintain remission,9 similar to that occurring in IBD. Considering that histologic parameters between SCAD and IBD overlap, could be challenging to differentiate between SCAD and IBD, especially with UC. In this way, combining clinical, endoscopic, and histologic parameters is mandatory to pose the correct diagnosis, considering that UC prevalence is low in diverticulosis,10 that SCAD affects only colonharboring diverticula, that histologic and endoscopic inflammation spares SCAD but not UC patients.4 Antonio Tursi, MD* Cosimo D. Inchingolo, MDw Marcello Picchio, MDz Walter Elisei, MDy Francesca Mangiola, MD8 Giovanni Gasbarrini, MD, PhD8 *Gastroenterology Service, ASL BAT wDepartment of Pathology, “Lorenzo Bonomo” Hospital, Andria, BarlettaAndria-Trani zDivision of General Surgery, “P. Colombo” Hospital ASL RMH, Velletri, yDivision of Gastroenterology, ASL RMH, Albano Laziale 8“Ricerca in Medicina Foundation” ONLUS, Rome, Italy
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REFERENCES 1. Lamps LW, Knapple WL. Diverticular disease-associated segmental colitis. Clin Gastroenterol Hepatol. 2007;5: 27–31. 2. Tursi A, Elisei W, Brandimarte G, et al. The endoscopic spectrum of segmental colitis associated with diverticulosis. Colorectal Dis. 2010;12:464–470. 3. Tursi A, Elisei W, Picchio M. Incidence and prevalence of inflammatory bowel diseases in gastroenterology primary care setting. Eur J Intern Med. 2013;24: 852–856. 4. Tursi A. Segmental colitis associated with diverticulosis: complication of diverticular disease or autonomous entity? Dig Dis Sci. 2011;56:27–34. 5. Haboubi NY, Alqudah M. Pathology and pathogenesis of diverticular disease and patterns of colonic mucosal changes overlying the diverticula. Dig Dis. 2012;30:29–34. 6. Makapugay LM, Dean PJ. Diverticular disease-associated chronic colitis. Am J Surg Pathol. 1996;20:94–102. 7. Rizzello F, Gionchetti P, D’Arienzo A, et al. Oral beclometasone dipropionate in the treatment of active ulcerative colitis: a double-blind placebocontrolled study. Aliment Pharmacol Ther. 2002;16:1109–1116. 8. Magro F, Langnerb C, Driessen A, et al. on behalf of the European Society of Pathology (ESP) and the European Crohn’s and Colitis Organisation (ECCO). European consensus on the histopathology of inflammatory bowel disease. J Crohns Colitis. 2013;7: 827–851. 9. Tursi A, Elisei W, Giorgetti GM, et al. Segmental colitis associated with
2014 Wolters Kluwer Health, Inc. All rights reserved.
To the Editor: We read with great interest the World Gastroenterology Organisation global guidelines: nonalcoholic fatty liver disease and nonalcoholic steatohepatitis1 (NASH) and would like to commend the authors for their straightforward overview of the epidemiology, diagnosis, and treatment of nonalcoholic fatty liver disease (NAFLD). In this response to the guideline, we would like to comment on the procedure set forth for the diagnosis of NAFLD. Although we largely agree with the methodology presented, we would like to respectfully suggest reconsideration of the diagnostic algorithm section described in figure 2. The guidelines suggest the use of computed tomography (CT) when ultrasound (US) imaging is not informative. CT has been shown to have limited sensitivity in measuring hepatic steatosis compared with US.2 CT scan can be affected by other factors such as iron and fibrosis deposition. It has also been shown to be less accurate in detecting mild steatosis compared with more advanced steatosis.3 In addition, the use of radiation means that CT is unsuitable for use in children or for longitudinal follow-up in clinical trials and patient care. US is machine and operator dependent, has low positive predictive value, is affected by edema and extrahepatic adipose tissue, is difficult to perform in obese patients, and has limited sensitivity when steatosis is 20 g without any gender difference. However, according to guidelines, it is generally accepted as >30 g/d for men and >20 g/d for women.2 Therefore, improper use of this cutoff value could have led to patient selection bias in the original study. Second, there are several studies investigating serum/plasma and intracellular concentrations of water-soluble vitamins (vitamins B1, B3, B6, Cyetc.) and minerals (magnesium, seleniumyetc.) in MetS subjects.3–6 According to these studies, deficiencies of these vitamins and minerals were found to be associated with IR and increased risk for type-2 diabetes. These deficiencies may be secondary to decreased dietary intake or functional deficits resulting from coexisting diseases (conditions causing steatorrhea or severe chronic diarrhea such as Crohn’s disease, ulcerative colitis, celiac disease, short bowel syndromeyetc.). Moreover, an independent relationship between decreased serum magnesium levels and NASH was found in a study by Rodrı´ guez-Herna´ndez et al.7 Therefore, in such studies, evaluating NASH patients with coexisting MetS components, assessing plasma levels of certain vitamins and minerals involved in the development of NASH will provide more significant results and substantially improve the value of the article. Third, ordinal logistic regression analysis could be performed to determine the power of IR to predict the degree of fibrotic and inflammatory activity. In conclusion, using proper cutoff values would provide more reliable results. The assessment of certain vitamin and minerals, and performing ordinal logistic regression analysis for IR would improve the credibility of the whole article. Erdim Sertoglu, MD* Metin Uyanik, MDw Huseyin Kayadibi, MDz *Biochemistry Laboratory, Ankara Mevki Military Hospital, Anittepe Dispensary Ankara wBiochemistry Laboratory, Corlu Military Hospital, Tekirdag zBiochemistry Laboratory, Adana Military Hospital, Adana, Turkey
2014 Wolters Kluwer Health, Inc. All rights reserved.
Volume 49, Number 4, April 2015
Letters to the Editor
diverticulosis: a 5-year follow-up. Int J Colorectal Dis. 2012;27:179–185. 10. Tursi A, Elisei W, Picchio M, et al. Letter: diverticulosis in inflammatory bowel diseases. Aliment Pharmacol Ther. 2014;39:899–900.
MRI, CT Scan, and Ultrasound in the Diagnosis of Nonalcoholic Fatty Liver Disease FIGURE 2. Comparison of the inflammatory infiltrate, subdivided according to the type of inflammatory cells. E indicates eosinophils; H, histioid cells; L, lymphocytes; N, neutrophils; P, plasma cells; SCAD, segmental colitis associated with diverticulosis; UC, ulcerative colitis. Bars represent median.
may be considered a form of chronic intestinal inflammation occurring in a colon-harboring diverticula, rather than a simple complication of diverticular disease.4 In fact SCAD seems to need a long-lasting medical treatment linked to the severity of the disease to maintain remission,9 similar to that occurring in IBD. Considering that histologic parameters between SCAD and IBD overlap, could be challenging to differentiate between SCAD and IBD, especially with UC. In this way, combining clinical, endoscopic, and histologic parameters is mandatory to pose the correct diagnosis, considering that UC prevalence is low in diverticulosis,10 that SCAD affects only colonharboring diverticula, that histologic and endoscopic inflammation spares SCAD but not UC patients.4 Antonio Tursi, MD* Cosimo D. Inchingolo, MDw Marcello Picchio, MDz Walter Elisei, MDy Francesca Mangiola, MD8 Giovanni Gasbarrini, MD, PhD8 *Gastroenterology Service, ASL BAT wDepartment of Pathology, “Lorenzo Bonomo” Hospital, Andria, BarlettaAndria-Trani zDivision of General Surgery, “P. Colombo” Hospital ASL RMH, Velletri, yDivision of Gastroenterology, ASL RMH, Albano Laziale 8“Ricerca in Medicina Foundation” ONLUS, Rome, Italy
Copyright
r
REFERENCES 1. Lamps LW, Knapple WL. Diverticular disease-associated segmental colitis. Clin Gastroenterol Hepatol. 2007;5: 27–31. 2. Tursi A, Elisei W, Brandimarte G, et al. The endoscopic spectrum of segmental colitis associated with diverticulosis. Colorectal Dis. 2010;12:464–470. 3. Tursi A, Elisei W, Picchio M. Incidence and prevalence of inflammatory bowel diseases in gastroenterology primary care setting. Eur J Intern Med. 2013;24: 852–856. 4. Tursi A. Segmental colitis associated with diverticulosis: complication of diverticular disease or autonomous entity? Dig Dis Sci. 2011;56:27–34. 5. Haboubi NY, Alqudah M. Pathology and pathogenesis of diverticular disease and patterns of colonic mucosal changes overlying the diverticula. Dig Dis. 2012;30:29–34. 6. Makapugay LM, Dean PJ. Diverticular disease-associated chronic colitis. Am J Surg Pathol. 1996;20:94–102. 7. Rizzello F, Gionchetti P, D’Arienzo A, et al. Oral beclometasone dipropionate in the treatment of active ulcerative colitis: a double-blind placebocontrolled study. Aliment Pharmacol Ther. 2002;16:1109–1116. 8. Magro F, Langnerb C, Driessen A, et al. on behalf of the European Society of Pathology (ESP) and the European Crohn’s and Colitis Organisation (ECCO). European consensus on the histopathology of inflammatory bowel disease. J Crohns Colitis. 2013;7: 827–851. 9. Tursi A, Elisei W, Giorgetti GM, et al. Segmental colitis associated with
2014 Wolters Kluwer Health, Inc. All rights reserved.
To the Editor: We read with great interest the World Gastroenterology Organisation global guidelines: nonalcoholic fatty liver disease and nonalcoholic steatohepatitis1 (NASH) and would like to commend the authors for their straightforward overview of the epidemiology, diagnosis, and treatment of nonalcoholic fatty liver disease (NAFLD). In this response to the guideline, we would like to comment on the procedure set forth for the diagnosis of NAFLD. Although we largely agree with the methodology presented, we would like to respectfully suggest reconsideration of the diagnostic algorithm section described in figure 2. The guidelines suggest the use of computed tomography (CT) when ultrasound (US) imaging is not informative. CT has been shown to have limited sensitivity in measuring hepatic steatosis compared with US.2 CT scan can be affected by other factors such as iron and fibrosis deposition. It has also been shown to be less accurate in detecting mild steatosis compared with more advanced steatosis.3 In addition, the use of radiation means that CT is unsuitable for use in children or for longitudinal follow-up in clinical trials and patient care. US is machine and operator dependent, has low positive predictive value, is affected by edema and extrahepatic adipose tissue, is difficult to perform in obese patients, and has limited sensitivity when steatosis is 20 g without any gender difference. However, according to guidelines, it is generally accepted as >30 g/d for men and >20 g/d for women.2 Therefore, improper use of this cutoff value could have led to patient selection bias in the original study. Second, there are several studies investigating serum/plasma and intracellular concentrations of water-soluble vitamins (vitamins B1, B3, B6, Cyetc.) and minerals (magnesium, seleniumyetc.) in MetS subjects.3–6 According to these studies, deficiencies of these vitamins and minerals were found to be associated with IR and increased risk for type-2 diabetes. These deficiencies may be secondary to decreased dietary intake or functional deficits resulting from coexisting diseases (conditions causing steatorrhea or severe chronic diarrhea such as Crohn’s disease, ulcerative colitis, celiac disease, short bowel syndromeyetc.). Moreover, an independent relationship between decreased serum magnesium levels and NASH was found in a study by Rodrı´ guez-Herna´ndez et al.7 Therefore, in such studies, evaluating NASH patients with coexisting MetS components, assessing plasma levels of certain vitamins and minerals involved in the development of NASH will provide more significant results and substantially improve the value of the article. Third, ordinal logistic regression analysis could be performed to determine the power of IR to predict the degree of fibrotic and inflammatory activity. In conclusion, using proper cutoff values would provide more reliable results. The assessment of certain vitamin and minerals, and performing ordinal logistic regression analysis for IR would improve the credibility of the whole article. Erdim Sertoglu, MD* Metin Uyanik, MDw Huseyin Kayadibi, MDz *Biochemistry Laboratory, Ankara Mevki Military Hospital, Anittepe Dispensary Ankara wBiochemistry Laboratory, Corlu Military Hospital, Tekirdag zBiochemistry Laboratory, Adana Military Hospital, Adana, Turkey
2014 Wolters Kluwer Health, Inc. All rights reserved.
