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Asymptomatic Giardiasis— an association with proton pump inhibitors?
3666
Letters to the Editor
cases of mixed hepatocellular jaundice have been previously published (5, 6). In the patient reported here other causes of acute liver injury were reasonably excluded by an extensive diagnostic work-up, although the long period of latency elapsed between the intake of the drug and the development of jaundice argues against the diagnosis of famotidineinduced hepatitis. However, it must be taken into account that jaundice was the only clinical manifestation in our patient and it was probably preceded by an asymptomatic period of hypertransaminasemia, which remained underdiagnosed. In any case, even though the etiological role of famotidine in our patient could be controversial, therapeutic decision would be difficult if he needs an antisecretory treatment in the future. At this respect, in a case of famotidine-induced hepatitis, reported by Hashimoto et al. (5), cimetidine was also followed by a symptomatic hepatitis and only omeprazole was shown to be safe. Consequently, physicians need to be aware of this rare but potentially serious side effect of famotidine and an alternative treatment with proton pump inhibitors, under close surveillance, should be prescribed when famotidine liver toxicity is strongly suspected.
AJG – Vol. 95, No. 12, 2000
Precolonoscopy Video TO THE EDITOR: The summary by Dr. Brand reported that an informational video decreased anxiety and increased knowledge in a group of patients scheduled for colonoscopy relative to a similar group that only received an informational booklet (1). We reported a similar project that supported some of this study’s findings (2). We randomized 93 consecutive patients undergoing colonoscopy into two groups, one receiving videotape information and the second a printed pamphlet. Groups were not different as a function of age, education, gender, previous colonoscopy experience, trait anxiety, or standard laboratory values. No difference was found between groups on our procedure information assessment. However, in the 57 patients (23 video, 34 printed) who had no prior colonoscopy experiences, potential physiological indices of stress (3) were lower in the videotape than the printed pamphlet group (hemoglobin t ⫽ 1.97, p ⫽ .05; hematocrit t ⫽ 1.73, p ⫽ .10; albumin t ⫽ 2.74, p ⫽ .009). As Dr. Brand declared, videotape preparation may reduce subjective anxiety and related physiological parameters better than written instructional materials, especially for naı¨ve colonoscopy patients.
M. Jime´nez-Sa´enz F. Argu¨elles-Arias J. M. Herrerı´as-Gutie´rrez Division of Gastroenterology Liver Unit University Hospital Virgen Macarena Sevilla, Spain J. A. Dura´n-Quintana Department of Pharmacology University Hospital Virgen Macarena Sevilla, Spain
REFERENCES 1. Andrade R, Lucena MI, Martı´n-Vivaldi R, et al. Acute liver injury associated with the use of ebrotidine, a new H2-receptor antagonist. J Hepatol 1999;31:641– 6. 2. Gasbarrini G, Gentiloni N, Febbraro S, et al. Acute liver injury related to the use of niperotidine. J Hepatol 1997;27:583– 6. 3. Garcia Rodriguez LA, Wallander MA, Stricker BHC. The risk of acute liver injury associated with cimetidine and other acid-suppressing anti-ulcer drugs. Br J Clin Pharmacol 1997;43:183– 8. 4. Marı`a VAJ, Victorino RMM. Development and validation of a clinical scale for the diagnosis of drug-induced hepatitis. Hepatology 1997;26:664 –9. 5. Hashimoto F, Davis RL, Egli D. Hepatitis following treatments with famotidine and then cimetidine. Ann Pharmacother 1994; 28:37–9. 6. Ament PW, Roth JD, Fox CJ. Famotidine-induced mixed hepatocellular jaundice. Ann Pharmacother 1994;28:40 –2. Reprint requests and correspondence: Manuel Jime´nez-Sa´enz, C/Antonio Cortes Llado 6, Edificio Madeira Esc 1-2° A, Sevilla 41004, Spain. Received July 18, 2000; accepted July 24, 2000.
Joseph K. Neumann, Ph.D. Puneet Goenka, M.D. James H. Quillen VA Medical Center Johnson City, Tennessee
REFERENCES 1. Brand RE. Relaxing with a precolonoscopy video! Am J Gastroenterol 2000;95:1128. 2. Goenka P, Manalo G, Jobson BJ, et al. Informed consent for colonoscopy by videotape vs. printed material—A prospective randomized comparative study of patients’ understanding and stress. Gastrointest Endosc 1999;49:AB52. 3. Muldoon MF, Herbert TB, Patterson SM, et al. Effects of acute stress on serum lipid levels, hemoconcentration, and blood viscosity. Arch Intern Med 1995;155:615–20. Reprint requests and correspondence: Joseph K. Neumann, Ph.D., Psychology Service (116B2), James H. Quillen VA Medical Center, P.O. Box 4000, Mountain Home, TN 37684. Received July 19, 2000; accepted July 24, 2000.
Asymptomatic Giardiasis— An Association With Proton Pump Inhibitors? TO THE EDITOR: Proton pump inhibitors are commonly prescribed for gastroesophageal reflux (GERD) and peptic ulcer disease. They are usually well tolerated with the commonest side effects reported as diarrhea and headaches in a minority of patients (1). An unusual case of Giardiasis is
AJG – December, 2000
described in a patient on chronic lansoprazole who had none of the typical risk factors associated with this infection. A 25-yr-old man with GERD refractory to histamine antagonists was referred for upper endoscopy (EGD). This was remarkable for esophagitis and he was treated with lansoprazole 30 mg b.i.d. with excellent relief of symptoms. His symptoms recurred each time he reduced his medications and he was also reluctant to consider surgery. EGD with small bowel biopsies was repeated as part of an IRBapproved study. This was grossly unremarkable but small bowel biopsies revealed Giardia Lamblia trophozoites. Repeat history revealed he had no diarrhea and none of the typical risk factors for Giardiasis such as immune deficiency, well-water use, overseas travel, or anal intercourse. His HIV test was negative and he was on no other medications. He was treated with metronidazole 500 mg b.i.d. for 5 days and remains asymptomatic on lansoprazole 30 mg b.i.d. He has declined follow-up endoscopy to confirm Giardia eradication. Three clinical syndromes have been described with Giardiasis—asymptomatic carriage, an acute self-limiting illness, and chronic diarrhea associated with malabsorption (2). It is difficult to be certain when this patient acquired Giardiasis. It may have predated proton pump inhibitor use or occurred during his 2 yr of therapy. Due to previous reports describing an association between proton pump inhibitors and bacterial overgrowth, the absence of other risk factors, and lansoprazole’s more profound effect on gastric acid inhibition compared to omeprazole, it was presumed that long-standing hypochlorhydria was this patient’s greatest risk factor for acquiring Giardiasis (3– 6). It remains unclear why he was asymptomatic. This may have been related to the inoculum of Giardia in his small bowel and his overall health and immune status. However, due to the lack of data on the outcome of asymptomatic untreated Giardiasis in adults and the patient’s wish to continue with chronic medical therapy for GERD, it was felt the benefits of treatment outweighed the risks. Sandeep Mukherjee, M.D. VAMC and SUNY Health Science Center Syracuse, New York
REFERENCES 1. Lansoprazole Product Information, TAP Pharmaceuticals, Inc., Deerfield, IL 60014-1595, U.S.A. 2. Lopez CE, Dykes AC, Juranek DD, et al. Waterborne giardiasis: A community wide outbreak of disease and a high rate of asymptomatic infection. Am J Epid 1980;112:495. 3. Gough A, Andrews D, Bacon PA, et al. Evidence of omeprazole induced small bowel bacterial overgrowth in patients with scleroderma. Br J Rheum 1995;34:976 –7. 4. Neal KR, Scott HM, Slack RCB, et al. Omeprazole as a risk factor for Campylobacter gastroenteritis—a case control study. Br J Med 1996;312:414 –5. 5. Goenka MK, Kochhar J, Chakrabarti A, et al. Candidia overgrowth after treatment of duodenal ulcer. A comparison of
Letters to the Editor
3667
cimetidine, famotidine and omeprazole. J Clin Gastroenterol 1996;23(1):7–10. 6. Schapira M, Roquet ME, Henrion J, et al. Severe non-typhoidal salmonellosis probably in relation with omeprazole treatment; report of two cases. Acta Gastroenterol Belgica 1996;59(2): 168 –71. Correspondence: Sandeep Mukherjee, M.D., University of Nebraska Medical Center, Division of Gastroenterology, 983285 Nebraska Medical Center, Omaha, NE 68198-3285. Received July 20, 2000; accepted July 24, 2000.
Guillain-Barre´ Syndrome With Acute Hepatitis E TO THE EDITOR: Landry Guillain-Barre´ syndrome (GBS) is an acute polyradiculoneuropathy of uncertain cause. It is generally benign and numerous infectious agents and immunological mechanisms are said to play a role. Although there are many reports linking acute hepatitis and GBS, to our knowledge, this is the first report of GBS in a hepatitis E patient. A 50-yr-old man presented with anorexia, malaise, nausea, vomitings, jaundice, and high-colored urine of 4 days duration. On physical examination he was found to be jaundiced and have mildly tender hepatomegaly, but showed no features of chronic liver disease or encephalopathy. On the 5th hospital day he developed generalized paraesthesias and weakness of the lower limbs. The weakness progressed quickly and within 2 days the patient had become bedridden. Neurological examination revealed generalized muscle weakness (grade II–III muscle power in all groups of upper and lower limbs), hypotonia, areflexia, impaired proprioception in all limbs, and bilateral Laseague’s sign. Laboratory investigations revealed elevated transaminase levels (AST 1064 U/L, ALT 114 U/L) with serum bilirubin of 14.2 mg%. A complete blood count, electrolytes, and renal function tests were normal. Prothrombin time was prolonged (INR 2.4). Abdominal ultrasound demonstrated only slight hepatomegaly. Serological study showed IgM antibodies to hepatitis E while hepatitis B surface antigen, antibodies to hepatitis C, and IgM anti-HAV were absent. Cerebrospinal fluid (CSF) analysis showed an elevated protein concentration (186 mg/dl) without cellular response. Neurophysiological studies demonstrated generalized alteration in nerveconduction velocity and an increased F-response conduction time. All findings were consistent with demyelinating type of polyradiculoneuropathy. Two weeks after onset neurological improvement began, jaundice was also showing regression. One month later, the patient was symptom free with normal transaminase levels. It is well known that cases of acute viral hepatitis may, although rarely, be complicated by neurological manifestations. Guillain-Barre´ syndrome has been documented with hepatitis B virus, hepatitis A virus, and non-A, non-B hep-
Letters to the Editor
cases of mixed hepatocellular jaundice have been previously published (5, 6). In the patient reported here other causes of acute liver injury were reasonably excluded by an extensive diagnostic work-up, although the long period of latency elapsed between the intake of the drug and the development of jaundice argues against the diagnosis of famotidineinduced hepatitis. However, it must be taken into account that jaundice was the only clinical manifestation in our patient and it was probably preceded by an asymptomatic period of hypertransaminasemia, which remained underdiagnosed. In any case, even though the etiological role of famotidine in our patient could be controversial, therapeutic decision would be difficult if he needs an antisecretory treatment in the future. At this respect, in a case of famotidine-induced hepatitis, reported by Hashimoto et al. (5), cimetidine was also followed by a symptomatic hepatitis and only omeprazole was shown to be safe. Consequently, physicians need to be aware of this rare but potentially serious side effect of famotidine and an alternative treatment with proton pump inhibitors, under close surveillance, should be prescribed when famotidine liver toxicity is strongly suspected.
AJG – Vol. 95, No. 12, 2000
Precolonoscopy Video TO THE EDITOR: The summary by Dr. Brand reported that an informational video decreased anxiety and increased knowledge in a group of patients scheduled for colonoscopy relative to a similar group that only received an informational booklet (1). We reported a similar project that supported some of this study’s findings (2). We randomized 93 consecutive patients undergoing colonoscopy into two groups, one receiving videotape information and the second a printed pamphlet. Groups were not different as a function of age, education, gender, previous colonoscopy experience, trait anxiety, or standard laboratory values. No difference was found between groups on our procedure information assessment. However, in the 57 patients (23 video, 34 printed) who had no prior colonoscopy experiences, potential physiological indices of stress (3) were lower in the videotape than the printed pamphlet group (hemoglobin t ⫽ 1.97, p ⫽ .05; hematocrit t ⫽ 1.73, p ⫽ .10; albumin t ⫽ 2.74, p ⫽ .009). As Dr. Brand declared, videotape preparation may reduce subjective anxiety and related physiological parameters better than written instructional materials, especially for naı¨ve colonoscopy patients.
M. Jime´nez-Sa´enz F. Argu¨elles-Arias J. M. Herrerı´as-Gutie´rrez Division of Gastroenterology Liver Unit University Hospital Virgen Macarena Sevilla, Spain J. A. Dura´n-Quintana Department of Pharmacology University Hospital Virgen Macarena Sevilla, Spain
REFERENCES 1. Andrade R, Lucena MI, Martı´n-Vivaldi R, et al. Acute liver injury associated with the use of ebrotidine, a new H2-receptor antagonist. J Hepatol 1999;31:641– 6. 2. Gasbarrini G, Gentiloni N, Febbraro S, et al. Acute liver injury related to the use of niperotidine. J Hepatol 1997;27:583– 6. 3. Garcia Rodriguez LA, Wallander MA, Stricker BHC. The risk of acute liver injury associated with cimetidine and other acid-suppressing anti-ulcer drugs. Br J Clin Pharmacol 1997;43:183– 8. 4. Marı`a VAJ, Victorino RMM. Development and validation of a clinical scale for the diagnosis of drug-induced hepatitis. Hepatology 1997;26:664 –9. 5. Hashimoto F, Davis RL, Egli D. Hepatitis following treatments with famotidine and then cimetidine. Ann Pharmacother 1994; 28:37–9. 6. Ament PW, Roth JD, Fox CJ. Famotidine-induced mixed hepatocellular jaundice. Ann Pharmacother 1994;28:40 –2. Reprint requests and correspondence: Manuel Jime´nez-Sa´enz, C/Antonio Cortes Llado 6, Edificio Madeira Esc 1-2° A, Sevilla 41004, Spain. Received July 18, 2000; accepted July 24, 2000.
Joseph K. Neumann, Ph.D. Puneet Goenka, M.D. James H. Quillen VA Medical Center Johnson City, Tennessee
REFERENCES 1. Brand RE. Relaxing with a precolonoscopy video! Am J Gastroenterol 2000;95:1128. 2. Goenka P, Manalo G, Jobson BJ, et al. Informed consent for colonoscopy by videotape vs. printed material—A prospective randomized comparative study of patients’ understanding and stress. Gastrointest Endosc 1999;49:AB52. 3. Muldoon MF, Herbert TB, Patterson SM, et al. Effects of acute stress on serum lipid levels, hemoconcentration, and blood viscosity. Arch Intern Med 1995;155:615–20. Reprint requests and correspondence: Joseph K. Neumann, Ph.D., Psychology Service (116B2), James H. Quillen VA Medical Center, P.O. Box 4000, Mountain Home, TN 37684. Received July 19, 2000; accepted July 24, 2000.
Asymptomatic Giardiasis— An Association With Proton Pump Inhibitors? TO THE EDITOR: Proton pump inhibitors are commonly prescribed for gastroesophageal reflux (GERD) and peptic ulcer disease. They are usually well tolerated with the commonest side effects reported as diarrhea and headaches in a minority of patients (1). An unusual case of Giardiasis is
AJG – December, 2000
described in a patient on chronic lansoprazole who had none of the typical risk factors associated with this infection. A 25-yr-old man with GERD refractory to histamine antagonists was referred for upper endoscopy (EGD). This was remarkable for esophagitis and he was treated with lansoprazole 30 mg b.i.d. with excellent relief of symptoms. His symptoms recurred each time he reduced his medications and he was also reluctant to consider surgery. EGD with small bowel biopsies was repeated as part of an IRBapproved study. This was grossly unremarkable but small bowel biopsies revealed Giardia Lamblia trophozoites. Repeat history revealed he had no diarrhea and none of the typical risk factors for Giardiasis such as immune deficiency, well-water use, overseas travel, or anal intercourse. His HIV test was negative and he was on no other medications. He was treated with metronidazole 500 mg b.i.d. for 5 days and remains asymptomatic on lansoprazole 30 mg b.i.d. He has declined follow-up endoscopy to confirm Giardia eradication. Three clinical syndromes have been described with Giardiasis—asymptomatic carriage, an acute self-limiting illness, and chronic diarrhea associated with malabsorption (2). It is difficult to be certain when this patient acquired Giardiasis. It may have predated proton pump inhibitor use or occurred during his 2 yr of therapy. Due to previous reports describing an association between proton pump inhibitors and bacterial overgrowth, the absence of other risk factors, and lansoprazole’s more profound effect on gastric acid inhibition compared to omeprazole, it was presumed that long-standing hypochlorhydria was this patient’s greatest risk factor for acquiring Giardiasis (3– 6). It remains unclear why he was asymptomatic. This may have been related to the inoculum of Giardia in his small bowel and his overall health and immune status. However, due to the lack of data on the outcome of asymptomatic untreated Giardiasis in adults and the patient’s wish to continue with chronic medical therapy for GERD, it was felt the benefits of treatment outweighed the risks. Sandeep Mukherjee, M.D. VAMC and SUNY Health Science Center Syracuse, New York
REFERENCES 1. Lansoprazole Product Information, TAP Pharmaceuticals, Inc., Deerfield, IL 60014-1595, U.S.A. 2. Lopez CE, Dykes AC, Juranek DD, et al. Waterborne giardiasis: A community wide outbreak of disease and a high rate of asymptomatic infection. Am J Epid 1980;112:495. 3. Gough A, Andrews D, Bacon PA, et al. Evidence of omeprazole induced small bowel bacterial overgrowth in patients with scleroderma. Br J Rheum 1995;34:976 –7. 4. Neal KR, Scott HM, Slack RCB, et al. Omeprazole as a risk factor for Campylobacter gastroenteritis—a case control study. Br J Med 1996;312:414 –5. 5. Goenka MK, Kochhar J, Chakrabarti A, et al. Candidia overgrowth after treatment of duodenal ulcer. A comparison of
Letters to the Editor
3667
cimetidine, famotidine and omeprazole. J Clin Gastroenterol 1996;23(1):7–10. 6. Schapira M, Roquet ME, Henrion J, et al. Severe non-typhoidal salmonellosis probably in relation with omeprazole treatment; report of two cases. Acta Gastroenterol Belgica 1996;59(2): 168 –71. Correspondence: Sandeep Mukherjee, M.D., University of Nebraska Medical Center, Division of Gastroenterology, 983285 Nebraska Medical Center, Omaha, NE 68198-3285. Received July 20, 2000; accepted July 24, 2000.
Guillain-Barre´ Syndrome With Acute Hepatitis E TO THE EDITOR: Landry Guillain-Barre´ syndrome (GBS) is an acute polyradiculoneuropathy of uncertain cause. It is generally benign and numerous infectious agents and immunological mechanisms are said to play a role. Although there are many reports linking acute hepatitis and GBS, to our knowledge, this is the first report of GBS in a hepatitis E patient. A 50-yr-old man presented with anorexia, malaise, nausea, vomitings, jaundice, and high-colored urine of 4 days duration. On physical examination he was found to be jaundiced and have mildly tender hepatomegaly, but showed no features of chronic liver disease or encephalopathy. On the 5th hospital day he developed generalized paraesthesias and weakness of the lower limbs. The weakness progressed quickly and within 2 days the patient had become bedridden. Neurological examination revealed generalized muscle weakness (grade II–III muscle power in all groups of upper and lower limbs), hypotonia, areflexia, impaired proprioception in all limbs, and bilateral Laseague’s sign. Laboratory investigations revealed elevated transaminase levels (AST 1064 U/L, ALT 114 U/L) with serum bilirubin of 14.2 mg%. A complete blood count, electrolytes, and renal function tests were normal. Prothrombin time was prolonged (INR 2.4). Abdominal ultrasound demonstrated only slight hepatomegaly. Serological study showed IgM antibodies to hepatitis E while hepatitis B surface antigen, antibodies to hepatitis C, and IgM anti-HAV were absent. Cerebrospinal fluid (CSF) analysis showed an elevated protein concentration (186 mg/dl) without cellular response. Neurophysiological studies demonstrated generalized alteration in nerveconduction velocity and an increased F-response conduction time. All findings were consistent with demyelinating type of polyradiculoneuropathy. Two weeks after onset neurological improvement began, jaundice was also showing regression. One month later, the patient was symptom free with normal transaminase levels. It is well known that cases of acute viral hepatitis may, although rarely, be complicated by neurological manifestations. Guillain-Barre´ syndrome has been documented with hepatitis B virus, hepatitis A virus, and non-A, non-B hep-