AJG – October, 2001
Further understanding of the changes in immunity elicited by pregnancy and of the natural history and outcome of chronic HCV in other situations with Th2 predominant response may improve our knowledge of immune mechanisms for HCV clearance. Claudia O. Zein, M.D. Haitham Abu-Lebdeh, M.D. Nizar N. Zein, M.D. Divisions of Gastroenterology and Hepatology and Endocrinology and Metabolism Mayo Clinic and Foundation Rochester, Minnesota
REFERENCES 1. Alter MJ, Kruszon-Moran D, Nainan OV, et al. The prevalence of hepatitis C virus infection in the United States, 1988 through 1994. N Engl J Med 1999;34:556 – 62. 2. Wietzke P, Schott P, Braun F, et al. Clearance of HCV RNA in a chronic hepatitis C virus-infected patient during acute hepatitis B superinfection. Liver 1999;19:348 –53. 3. Yoshikawa M, Morimoto Y, Shiroi A, et al. Spontaneous elimination of serum HCV-RNA after total gastrectomy for early gastric cancer in a patient with chronic hepatitis C. Am J Gastroenterol 2001;96:922–3. 4. Fontaine H, Nalpas B, Carnot F, et al. Effect of pregnancy on chronic hepatitis C: A case-control study. Lancet 2000;356: 1328 –9. 5. Romero-Gomez M, Suarez-Garcia E, Casanovas J, et al. Influence of pregnancy in chronic hepatitis C virus infection. Med Clin (Barc) 1998;111:641– 4. 6. Paternoster D, et al. Pregnancy and hepatitis C virus infection. Prenat Neonat Med 2000;5:42–7. 7. Gervais A, Bacq Y, Bernuau J, et al. Decrease in serum ALT and increase in serum HCV RNA during pregnancy in women with chronic hepatitis C. J Hepatol 2000;32:293–9. 8. Lin HH, Kao JH. Hepatitis C virus load during pregnancy and puerperium. Br J Obst Gynecol 2000;107:1503– 6. 9. Weetman A. The immunology of pregnancy. Thyroid 1999; 9:643– 6. 10. Nahmias AJ, Kourtis AP. The pregnant woman, placenta, fetus, and infectious agents. Clin Perinatol 1997;24:497–521. 11. Wegmann TG, Lin H, Guilbert L, Mosmann TR. Bidirectional cytokine interactions in the maternal-fetal relationship: Is successful pregnancy a Th2 phenomenon? Immunol Today 1993; 14:353– 6. 12. Lim KJH, Odukoya OA, Ajjan RA, et al. Profile of cytokine mRNA expression in peri-implantation human endometrium. Mol Hum Reprod 1998;4:77– 81. 13. Decker D, Schondrof M, Bildlingmaier F, et al. Surgical stress induces a shift in the type-1/type-2 T-helper cell balance, suggesting down-regulation of cell-mediated and up-regulation of antibody-mediated immunity commensurate to the trauma. Surgery 1996;119:316 –25. 14. Ishii K, Rosa D, Watanabe Y, et al. High titers of antibodies inhibiting the binding of envelope to human cells correlate with natural resolution of chronic hepatitis C. Hepatology 1998;28:1117–20.
Reprint requests and correspondence: Claudia O. Zein, M.D., Division of Gastroenterology and Hepatology, Mayo Clinic, 200 First Street Southwest, Rochester, MN 55905. Received May 1, 2001; accepted May 11, 2001.
Letters to the Editor
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Dysphagia and Maloney Dilations TO THE EDITOR: How can one dispute the disappointingly negative findings of the magnificent Mayo group’s sham controlled study (1) utilizing 18-mm (54 F) throughthe-scope balloon dilators in patients with dysphagia but without evident pathology? Sharing a problem seen in so many of my patients over the years, I have personally experienced major distal solid food dysphagia for 14 years! For some reason it favors nice restaurants or medical staff dinners in which I have about 30 – 45 seconds to escape before an overwhelming contraction evacuates the esophagus upward! A provocative barium esophagogram back at the beginning was normal. Two careful esophagogastroduodenoscopies since were also totally normal. A 52-F Maloney dilation failed spectacularly after 1 week! But a session with a 60-F (20 mm) Maloney produced 3– 4 years of total relief! Subsequently over the intervening years, four or five repeats of those 60-F Maloneys uniformly provided prolonged relief before gradual recurrence. I learned if milder, sometimes an ounce or two of hot water (less than McDonald’s coffee hot) produces instant relaxation and passage. I sense most of my dysphagic patients who share that lack of endoscopically evident anatomical causation have similarly responded to larger caliber dilators. But in such cases I rarely stop at a 54-F, and generally use a 56-F traversing the entire esophagus and then a 58-F/60-F (2 cm), usually with tip only into the stomach. The nice “feel” with the newer tungsten-filled Maloneys permits perception of “gripping” by an esophagus in “spasm.” Because I habitually rescope after increases in dilator size, one may see unexpected cricopharyngeal trauma with even a 54-F, precluding moving up to larger nonballoon dilators. At endoscopy, the lumen in the lower third of the esophagus may vanish, obliterated by intense spastic contractions. If the stomach is not above the diaphragm, after dilation one may see previously invisible distal rings, now made visible by fracture/trauma from bigger dilators. Many such large diameter “rings” are not dysphagic, unless an associated hypercontractile “spasm,” even ice induced. When treating most fixed rings and strictures, I find that a 54-F works very well. After far smaller dilators, relooks often reveal disruption, even deeper fractures. Relief is expected! Possibly one reason for my conflicting illusion of success is that “functional” dysphagia very possibly encompasses more of the distal esophagus; if so, ballooning only those few centimeters spanning a gastroesophageal junction is inadequate! I suspect even in that short, somewhat rare “hypercontractile sphincter” analogous to achalasia a 54-F is too small, often failing. In functional dysphagias, one “stretches” dysfunctional muscle! I suggest that therapeutic stretching most often requires longer and larger caliber dilators! Unless patients are unconscious, it seems impossible to “blind” such a Maloney/ Savary series, as compared to simply inflating–not inflating through-the-scope balloons. My lifetime of uncontrolled anecdotes suggests not only that such patient outcomes
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Letters to the Editor
differ by dilator types, but also that success most often requires significantly larger sizes! David E. Langdon, M.D. Department of Internal Medicine University of Texas at Dallas Southwestern Medical School Dallas, Texas
REFERENCE 1. Scolapio KS, Gostout CJ, Schroeder KW, et al. Dysphagia without endoscopically evident disease: To dilate or not? Am J Gastroenterol 2001;96:327–30. Reprint requests and correspondence: David E. Langdon, M.D., 3120 Matlock Road, Suite 201, Arlington, TX 76015. Received Apr. 23, 2001; accepted May 11, 2001.
Parenteral and Sexual Transmission Are Not Risk Factors for Acute Hepatitis E Infection in Hong Kong TO THE EDITOR: Hepatitis E infection (HEV) is responsible for most enterically transmitted non-A non-B hepatitis in developing countries. Recently, sporadic hepatitis E infection in patients with neither travel history to endemic areas nor contact history was reported in the United Kingdom. Higher seroprevalence of anti-HEV antibodies has been reported in patients undergoing hemodialysis (1), patients with hepatitis C, and HIV-infected homosexuals. These findings suggest that hepatitis E infection may be transmitted through sexual and parenteral routes. Unlike most parts of mainland China, the endemicity of hepatitis E infection is low in Hong Kong. The seroprevalence of HEV in the general population was 16.1%, and it accounts for 5.8 – 8% of patients with acute hepatitis (2). In Hong Kong, there is stringent quality control for drinking water, and drinking unboiled water is uncommon. To investigate the risk factors for hepatitis E infection in Hong Kong, we conducted a case-control study in a tertiary hospital. From January, 1996 to December, 1999, 1335 patients were referred to our Infectious Disease Unit for acute hepatitis. Diagnosis of acute hepatitis was based on the typical clinical and biochemical features. Risk factors including family and personal history of hepatitis, intake of shellfish, blood transfusion, tattooing, acupuncture, and high risk sexual activity were assessed by face-to-face interview on admission. Hepatitis E serology was performed for patients with negative serology for acute hepatitis A, B, and C. Eighty-seven patients (6.5%) were diagnosed to have acute HEV infection by the presence of serum IgM antibodies to HEV (EIA, Genelabs, Singapore) and they were recruited as cases. Ninety-seven patients (7.3%) with negative serology for hepatitis A, B, C, and E served as controls. Odds ratios
AJG – Vol. 96, No. 10, 2001
were was used to calculate the relative risk of each potential risk factor. HEV infection was significantly associated with the history of recent intake of shellfish (Table 1). None of the patients with HEV infection had a history of blood transfusion, acupuncture, or i.v. drug abuse. Nine patients (10%) with HEV infection had a history of sexual promiscuity. However, eight of these nine patients also had a recent history of intake of shellfish. Family members of nine patients (10%) with HEV infection had acute hepatitis of unknown cause that occurred more than 5 yr apart. To look for the possibility of coinfection of HEV and other hepatitis viruses, we also tested for HEV IgM in all patients with acute hepatitis A, B, or C between January and June, 1999. Of 58 patients with acute hepatitis A (positive hepatitis A virus IgM), 18 patients (31%) had HEV coinfection, whereas none of the patients with acute hepatitis B (positive hepatitis B surface antigen and hepatitis B core IgM) were positive for HEV IgM. No patient had positive serology for hepatitis C during this 6-month study period. Our results showed that in Hong Kong HEV is mainly enterically transmitted by shellfish consumption. There is no evidence of sexual or parenteral transmission for HEV infection. There are two possible explanations for the higher seroprevalence of anti-HEV among patients with positive HIV and hepatitis C. First, HEV can be transmitted by the same route, and so patients with these diseases are at higher risk. However, there have been no reports on the high incidence of acute hepatitis E infection among these patients. One may argue that the HEV infection may be subclinical. But it is not likely among adult patients who are usually symptomatic while developing acute hepatitis. Furthermore, coinfection of two hepatitis viruses or superinfection of one on the other may lead to even more severe diseases (3). The more likely explanation is the false positivity of the serological tests, which may account for this seroepidemiological phenomenon. Studies have shown that anti-HEV might be positive in known negative sera, and it may be due to cross-reactivity with other hepatitis viruses Table 1. Risk Factors for Acute Hepatitis E and Non-A to E Hepatitis
Risk Factors Intake of shellfish (%) Travel to endemic area (%) Family history of hepatitis (%) Sexual promiscuity (%) Intravenous drug user (%) Blood transfusion (%) * p ⬍ 0.01 by 2 test.
Hepatitis E (n ⫽ 87)
Non-A to E Hepatitis (n ⫽ 97)
Odds Ratios (95% CIs)
57 (66)
44 (45)
2.29 (1.26–4.15)*
34 (39)
26 (27)
1.75 (0.94–3.26)
9 (10)
19 (20)
0.47 (0.20–1.11)
9 (10)
13 (13)
0.75 (0.30–1.84)
0
3 (3)
0
1 (1)