302

PREVALENCE OF ANTI-HCV

against cell-to-cell transmission of HBVI and further inhibit the replication and expression of HBV, there would be time for the infants to produce a high enough suppression of viral replicationz Department of Epidemiology, First Military Medical College, Gaungzhou 510515, People’s Republic of China

SHI-XIN TANG GUANG-LIEH YU

1. London WT, O’Connell AP.

Transplacental transmission of hepatitis B virus. Lancet

1986; i: 1037-38. 2. Alexander GJM, Eddleston ALWF. Does maternal antibody to core antigen prevent

anti-HCV. HBc antibodies were found in 29% of anti-HCVpositive and 25 % of anti-HCV-negative HCC patients, and in 24% of cryptogenic CLD. The mean age of the patients was significantly lower in HBsAg positive than in alcoholic or anti-HCV-positive HCC (p < 0-05 and p < 0-001, respectively). These results partly contradict those reported by Bruix et al and Colombo et al. Although the prevalence of anti-HCV was greatest in cryptogenic and in NANB CLD it was very high in HCC. On the one hand there was no difference between the anti-HCV prevalence in HCC and in CLD when aetiology is taken into account; on the other hand, in HCC and in cryptogenic CLD, the rate of association between anti-HCV and anti-HBc does not differ. The mean age of HBsAg-positive patients with HCC was lower than that of patients with HCC was lower than that of patients with alcohol-abuserelated or anti-HCV-positive HCC. Our data suggest that the link between HCV and HCC and the relation between HCV and HCC and the relation between HCV and HBV and alcohol in the pathogenesis of the disease should be further evaluated. HCV seems to be an important factor in the pathogenesis of HCC, but probably only in patients with CLD unrelated to alcohol or to HBV, and only through cirrhosis, at least in Western countries.

Department of Gastroenterology, Institute of Internal Medicine, University of Padua; and Hospital Department of Blood Transfusion and Immunohaematology, 35100 Padua, Italy

M. CHIARAMONTE F. FARINATI S. FAGIUOLI S. ONGARO V. ANELONI N. DE MARIA R. NACCARATO

1. Bruix

J, Barrera JM, Calvet X, et al. Prevalence of antibodies to hepatitis C virus in Spanish patients with hepatocellular carcinoma and hepatic cirrhosis. Lancet 1989;

1004-06. M, Kuo G, Choo QL, et al. Prevalence of antibodies to hepatitis C virus in Italian patients with hepatocellular carcinoma. Lancet 1989; ii: 1006-08

ii:

2 Colombo

Intrauterine infection with hepatitis B virus SIR,—We agree with Dr Mitsuda and colleagues (Oct 14, p 886) that there are three possible causes of vaccination failure. First that hepatitis B virus (HBV) infection in utero made the child immunologically tolerant to HBV antigens; second, that early administration of hepatitis B immunoglobulin (HBIg) could have protected the child from viraemia; and third that the baby was genetically a low responder to the epitopes of the vaccine antigens and was horizontally infected. In our study of intrauterine infection with HBV acquired from HBsAg-positive mothers, we have found that 44% (12/27) of fetal livers were positive for HBV DNA; however, only 5 (19%) of the 27 fetuses were positive for HBsAg, HBcAg, or anti-HBcIgM. The results suggest that mother-to-child intrauterine transmission is an important route of HBV infection in China, perhaps also in other South-East Asian countries. Furthermore not all fetuses infected with HBV in utero express viral antigens; possibly because of the immaturity of fetal tissues. We think that only the fetuses that have been infected with HBV and express viral antigens come into contact with heterogeneous antigens early in embryonic development and become immunologically tolerant to HBV antigens. Thus HBV cannot be effectively eliminated and the babies will be HBsAg carriers after birth. By contrast, some fetuses infected with HBV but without expression of viral antigens can be protected by the use of HBIg plus hepatitis B vaccine as early as possible. Because HBIg may protect

recognition of transplacental transmission of hepatitis-B-virus infection? Lancet 1986, i: 296-97.

Erythema multiforme and herpes simplex virus SIR,—Your Dec 2 editorial did not address fully the treatment of erythema multiforme. The systemic use of potassium iodide 300 mg daily produced a pronounced improvement in 14 of 16 patients with erythema multiforme.1 The lesions began to resolve within a few days of treatment and did so completely within a week-the natural history of a self-limited eruption being healing within 2-3 weeks. In 6 of these patients erythema multiforme was associated with herpes simplex virus. Potassium iodide has also proved of therapeutic benefit in subacute nodular migratory panniculitis,2 erythema nodosum,3and Sweet’s syndrome.1 We have treated with substantial success seven patients with recurrent erythema nodosum, some of whom were unresponsive to steroids and aspirin. The treatment is well tolerated with rare side-effects of thyroid disturbances,’ allergic reactions,s and occasional initiation of erythema nodosum.6 The mechanism of action of potassium iodide is unclear but may include an immunosuppressive effect mediated by heparin3or suppression of the generation of polymorphonuclear leucocytederived oxygen intermediates.7 Potassium iodide was used therapeutically at the beginning of this century for various dermatological disorders,8 but its use for the illnesses we mention has been neglected in recent years although it remains the treatment of choice for cutaneous sporotrichosis.9 Potassium iodide is readily available and is inexpensive, unlike acyclovir; thus it may be a preferable treatement, especially in third-world countries. We hope that our report will revive interest in the addition of potassium iodide to the therapeutic arsenal. Department of Internal Medicine C, Kaplan Hospital, 76100 Rehovot, Israel

S. D. H. MALNICK L. GREEN

T, Danno K, Okamoto H, Miyachi Y, Imamura S. Potassium iodide in erythema nodosum and other erythematous dermatoses. J Am Acad Dermatol

1. Hono

2.

1983; 9: 77-81. Vilanova X, Aguade JP.

Subacute nodular migratory panniculitis.

Br J Dermatol 1959,

71: 45-50.

Whiting DA. Treatment of erythema nodosum and nodular vasculitis with potassium iodide. Br J Dermatol 1976; 94: 75-78.

3. Schul EJ,

RJ, Eaglstem WH, Allen CM. Treatment of granuloma annulare with potassium iodide. J Am Acad Dermatol 1984; 10: 904. Curd JG, Milgrom H, Stevenson DD. Potassium iodide sensitivity m four patients with hypocomplementemic vasculitis. Ann Intern Med 1979; 91: 853-57. Zone JJ, Horio T. Potassium iodide and vasculins Arch Dermatol 1981; 117: 758-59 Miyachi Y, Niwa Y. Effects of potassium iodide, colchicine and dapsone on the generaton of polymorphonuclear leucocyte-derived oxygen intermediates. Br J Dermatol 1982; 107: 209-14. Radcliffe-Crocker H Diseases of the skin, 3rd ed. Philadelphia: P. Blakiston’s Son

4. Laserio 5.

6. 7.

8.

1908: 81-82. 9. Bennett JE In Harrison’s principles of internal medicine, 11th ed. New York McGraw-Hill, 1987: 742-43.

CORRECTIONS Routine diagnostic testing. In the table in this letter by E. Leatham and D. Smithard (Dec 23/30, p 1528) the headings "yes" and "no" were transposed Decreased susceptibility of Neisseria gonorrhoeae to ciprofloxacin. In this letter by Dr W. R. Gransden and colleagues (Jan 6, p 51) the MIC in the final line should have read "0 03 mg/l".

Intrauterine infection with hepatitis B virus.

302 PREVALENCE OF ANTI-HCV against cell-to-cell transmission of HBVI and further inhibit the replication and expression of HBV, there would be time...
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