- Email: [email protected]
Response to Drs. Singh et al.
1646
Letters to the Editor
Reprint requests and correspondence: Pankaj Singh, 76-04 270th Street, New Hyde Park, NY 11040. Received Nov. 6, 2000; accepted Jan. 8, 2001.
Response to Drs. Singh et al. TO THE EDITOR: We are deeply thankful for the interest and comments made by Singh and colleagues. We believe there was a mistake in the reading and analysis of our study, because we did not conclude that bacterial infection in cirrhotics is not dependent on the etiology. Our findings state clearly that bacterial infections are more frequent in alcoholic cirrhotics than in nonalcoholics (p ⫽ 0.02). Although it was not reported in our study, of 78 alcoholic cirrhotics with infection, 66 (84.7%) were drinking actively up to the moment of diagnosis of infection, and nine (11.5%) were abstinent. Information could not be confirmed for three (3.8%) patients. Dr. Singh and colleagues rightly state that acute exposure to ethanol impairs the immune system (1–3). However, it is still unclear whether such alterations in the immune system are reversible following the discontinuation of the chronic use of alcohol and how long it take for this to occur. Despite the fact that active alcoholism may be a predisposing factor for the acquisition of infections, many other factors are also responsible for the higher prevalence of bacterial infection in cirrhotics. Heitor Rosa, M.D. Ame´rico O. Silve´rio, M.D. Rafael F. Perini, M.D. Claudia Barruda, M.D. Department of Gastroenterology and Hepatology Federal University of Goia´s School of Medicine Goiaˆnia, Brazil
REFERENCES 1. Mirland B, Mirland J. Reduced Fc receptor function in human monocytes exposed to ethanol in vitro. Alcohol 1984;19:211–7. 2. Bode C, Kugler V, Bode JC. Endotoxemia in patients with alcoholic and non-alcoholic cirrhosis and in subjects with no evidence of chronic liver disease following acute alcohol excess. J Hepatol 1987;4:8 –14. 3. Singhal PC, Reddy K, Ding G, et al. Ethanol induced macrophage apoptosis: The role of TGF-. J Immunol 1991;162: 3031– 6.
Reprint requests and correspondence: Heitor Rosa, M.D., Federal University of Goia´s, School of Medicine, Rua 126, n. 21, Setor Sul, Goiaˆnia, GO 74093-080, Brazil. Received Dec. 26, 2000; accepted Jan. 8, 2001.
AJG – Vol. 96, No. 5, 2001
Re: Sørensen et al.: Low Dose Aspirin TO THE EDITOR: Dr. Sorensen and his group (1), in a retrospective analysis of low dose aspirin at the level of 150 mg/day, note the risk of upper GI bleeding with the low dose aspirin and other nonsteroidal drugs is high, at a rate ratio of 5.6, whereas the rate ratio is 2.6 in users of noncoated low dose aspirin as well as coated low dose aspirin. This study done retrospectively suggests that prophylactic low dose aspirin carries an increased risk of GI bleeding irrespective of whether it is coated or uncoated. I am pleased to note that the authors comment on a need to analyze the risk/benefit effect of low dose aspirin in any prophylactic treatment program, but retrospective study is never as convincing as a prospective study that is yet to be done with significant numbers of patients. In addition, dosing of 81 mg/day in coated or uncoated form is more commonly used in the United States and bears a dose-related phenomenon with GI toxicity (D. Petroski, unpublished data, May 10, 1993). Also, the type of coated aspirin studied was not mentioned (various products are available to physicians and the public for supervised or unsupervised use). Some suggest that enteric coating is not protective at a low dose (2). In summary, let us further analyze low dose prophylactic aspirin by establishing a good large prospective study and find the most effective and safest lowest dose aspirin needed. Let us not count out properly formulated enteric coating as an added safety feature just yet. Donald Petroski, M.D. MCP Hahnemann University School of Medicine Philadelphia, Pennsylvania
REFERENCES 1. Sørensen HT, Mellekjær L, Blott WJ, et al. Risk of upper gastrointestinal bleeding associated with use of low-dose aspirin. Am J Gastroenterol 2000;95:2218 –24. 2. Kelly JP, Kaufman D, Jurgelon JM, et al. Risk of aspirinassociated major upper gastrointestinal bleeding with entericcoated or buffered product. Lancet 1996;348:1413– 6. Reprint requests and correspondence: Donald Petroski, M.D., Brachfeld Medical Associates, 218C Sunset Road, Willingboro, NJ 08046-1192. Received Oct. 16, 2000; accepted Jan. 8, 2001.
Fundic Gland Polyps and Gynecological Malignancies TO THE EDITOR: We read with interest the article by McGarrity et al. that appeared in a recent issue (1). The authors report the occurrence of a giant polyp of the prox-
Letters to the Editor
Reprint requests and correspondence: Pankaj Singh, 76-04 270th Street, New Hyde Park, NY 11040. Received Nov. 6, 2000; accepted Jan. 8, 2001.
Response to Drs. Singh et al. TO THE EDITOR: We are deeply thankful for the interest and comments made by Singh and colleagues. We believe there was a mistake in the reading and analysis of our study, because we did not conclude that bacterial infection in cirrhotics is not dependent on the etiology. Our findings state clearly that bacterial infections are more frequent in alcoholic cirrhotics than in nonalcoholics (p ⫽ 0.02). Although it was not reported in our study, of 78 alcoholic cirrhotics with infection, 66 (84.7%) were drinking actively up to the moment of diagnosis of infection, and nine (11.5%) were abstinent. Information could not be confirmed for three (3.8%) patients. Dr. Singh and colleagues rightly state that acute exposure to ethanol impairs the immune system (1–3). However, it is still unclear whether such alterations in the immune system are reversible following the discontinuation of the chronic use of alcohol and how long it take for this to occur. Despite the fact that active alcoholism may be a predisposing factor for the acquisition of infections, many other factors are also responsible for the higher prevalence of bacterial infection in cirrhotics. Heitor Rosa, M.D. Ame´rico O. Silve´rio, M.D. Rafael F. Perini, M.D. Claudia Barruda, M.D. Department of Gastroenterology and Hepatology Federal University of Goia´s School of Medicine Goiaˆnia, Brazil
REFERENCES 1. Mirland B, Mirland J. Reduced Fc receptor function in human monocytes exposed to ethanol in vitro. Alcohol 1984;19:211–7. 2. Bode C, Kugler V, Bode JC. Endotoxemia in patients with alcoholic and non-alcoholic cirrhosis and in subjects with no evidence of chronic liver disease following acute alcohol excess. J Hepatol 1987;4:8 –14. 3. Singhal PC, Reddy K, Ding G, et al. Ethanol induced macrophage apoptosis: The role of TGF-. J Immunol 1991;162: 3031– 6.
Reprint requests and correspondence: Heitor Rosa, M.D., Federal University of Goia´s, School of Medicine, Rua 126, n. 21, Setor Sul, Goiaˆnia, GO 74093-080, Brazil. Received Dec. 26, 2000; accepted Jan. 8, 2001.
AJG – Vol. 96, No. 5, 2001
Re: Sørensen et al.: Low Dose Aspirin TO THE EDITOR: Dr. Sorensen and his group (1), in a retrospective analysis of low dose aspirin at the level of 150 mg/day, note the risk of upper GI bleeding with the low dose aspirin and other nonsteroidal drugs is high, at a rate ratio of 5.6, whereas the rate ratio is 2.6 in users of noncoated low dose aspirin as well as coated low dose aspirin. This study done retrospectively suggests that prophylactic low dose aspirin carries an increased risk of GI bleeding irrespective of whether it is coated or uncoated. I am pleased to note that the authors comment on a need to analyze the risk/benefit effect of low dose aspirin in any prophylactic treatment program, but retrospective study is never as convincing as a prospective study that is yet to be done with significant numbers of patients. In addition, dosing of 81 mg/day in coated or uncoated form is more commonly used in the United States and bears a dose-related phenomenon with GI toxicity (D. Petroski, unpublished data, May 10, 1993). Also, the type of coated aspirin studied was not mentioned (various products are available to physicians and the public for supervised or unsupervised use). Some suggest that enteric coating is not protective at a low dose (2). In summary, let us further analyze low dose prophylactic aspirin by establishing a good large prospective study and find the most effective and safest lowest dose aspirin needed. Let us not count out properly formulated enteric coating as an added safety feature just yet. Donald Petroski, M.D. MCP Hahnemann University School of Medicine Philadelphia, Pennsylvania
REFERENCES 1. Sørensen HT, Mellekjær L, Blott WJ, et al. Risk of upper gastrointestinal bleeding associated with use of low-dose aspirin. Am J Gastroenterol 2000;95:2218 –24. 2. Kelly JP, Kaufman D, Jurgelon JM, et al. Risk of aspirinassociated major upper gastrointestinal bleeding with entericcoated or buffered product. Lancet 1996;348:1413– 6. Reprint requests and correspondence: Donald Petroski, M.D., Brachfeld Medical Associates, 218C Sunset Road, Willingboro, NJ 08046-1192. Received Oct. 16, 2000; accepted Jan. 8, 2001.
Fundic Gland Polyps and Gynecological Malignancies TO THE EDITOR: We read with interest the article by McGarrity et al. that appeared in a recent issue (1). The authors report the occurrence of a giant polyp of the prox-