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High prevalence of serum antibodies to hepatitis C virus in patients with Hashimoto's thyroiditis

BMJ 1994; 309 doi: (Published 01 October 1994) Cite this as: BMJ 1994;309:846
  1. J C Duclos Vallee,
  2. C Johanet,
  3. J C Trinchet,
  4. P Deny,
  5. M F Laurent,
  6. F Duron,
  7. P Valensi,
  8. B Weil,
  9. J C Homberg,
  10. D Pateron,
  11. M Beaugrand
  1. Service d'Hepatogastroenterologie, Hopital Jean Verdier, 93140 Bondy Cedex, France Laboratoire d'Immunologie, Hopital Saint Antoine, 75012 Paris Service de Microbiologie, Hopital Avicenne, 93000 Bobigny Service de Medecine Nucleaire, Hopital Pitie Salpetriere, 75013 Paris Service d'Endocrinologie, Hopital Saint Antoine, 75012 Paris Service d'Endocrinologie, Hopital Jean Verdier, 93140 Bondy Laboratoire d'Immunologie Clinique, Hopital Cochin, 75014 Paris
  1. Correspodence to: Professor Beaugrand.
  • Accepted 16 July 1994

Given the reports of thyroid dysfunction and various autoimmune disorders such as Sjogren's syndrome in patients infected with hepatitis C virus,1, 2 we hypothesised a link between autoimmune thyroid disease, mainly Hashimoto's thyroiditis, and such infection. We looked for antibodies to hepatitis C virus in the serum of patients with thyroid disease.

Subjects, methods, and results

We studied stored serum samples from 200 patients (190 women) with thyroid disease (simple goitre (n=50), Graves' disease (n=50), and Hashimoto's thyroiditis (n=50) randomly selected from all patients seen at five centres between 1987 and 1992.

Thyroid function was assessed by standard radioimmunoassays for serum thyroxine, triiodothyronine, and thyroid stimulating hormone. Receptor antibodies for thyroid stimulating hormone were detected with radioreceptor assay (Trak-asay, Henning Laboratories, Berlin). Serum antibodies to thyroid microsome and thyroperoxidase were used to diagnose Hashimoto's thyroiditis, depending on the centre. Serum antibodies to thyroid microsome were detected with indirect immunoinflorescence assay by using cryostat sections of human thyroid or by passive haemagglutination with a commercial kit (Thymune-M, Wellcome Laboratories, Beckenham). Serum antibodies to thyroperoxidase were assessed by radioimmunoassay (Dynotest anti- TPO, Henning Laboratories, Berlin) and antibodies to thyroglobulin by passive haemagglutination (Thymune-T, Wellcome Laboratories, Beckenham).

A second generation enzyme linked immunosorbent assay (ELISA) (Diagnostics Pasteur, Marnes la Coquette, France) was used to detect antibodies to hepatitis C virus. Samples yielding positive results were retested with a second generation recombinant immunoblot assay (RIBA, Ortho Diagnostic Systems, Raritan, New Jersey). Serum concentrations of immunoglobulin G were assayed by laser nephelometry in the serum of patients with Hashimoto's thyroiditis.

Fisher's exact test and the Mann-Whitney U test were used for statistical analysis. Results are expressed as means (SD).

The table summarises the results of the assays. No significant difference was noted for age or serum concentration of immunoglobulin G in patients with Hashimoto's thyroiditis with or without hepatitis C virus antibodies.


We found a higher prevalence of serum hepatitis C virus antibodies in patients with Hashimoto's thyroiditis than in those with any other thyroid disease. Among patients with Hashimoto's thyroiditis those with a positive result on ELISA and a negative result on immunoblot assay had lower serum concentrations of immunoglobulin G than those with positive results in both tests, though this result was not significant. This suggests that false positive reactions because of high serum concentrations of immunoglobulin G are unlikely.

The disappearance of hepatitis C virus is followed by decreasing titres of serum hepatitis C virus antibodies, which become undetectable after several months or years of follow up,3 though those patients with negative results in both assays may have low titres of antibodies not recognised by the highly specific but less sensitive immunoblot assay. If the result of the immunoblot assay becomes negative before the ELISA result, a few of these patients may be in fact infected with hepatitis C virus. The high prevalence of such antibodies in patients with Hashimoto's thyroiditis compared with other groups of thyroid disease and with the normal population4 suggests that hepatitis C virus may be responsible for triggering Hashimoto's thyroiditis. The role of another agent or epidemiological factor related to hepatitis C virus, however, cannot be excluded.

Results of assays* for serum antibodies to hepatitis C virus in four groups of patients with thyroid disease

View this table:

Hepatitis C virus is not the first viral agent suspected of initiating an autoimmune thyroid process. Some viruses may be implicated in animals, and the role of retroviruses has been suggested in humans.5 The possible role of infection with hepatitis C virus in triggering Hashimoto's thyroiditis does not rule out other agents such as exoviruses or endoviruses,5 and other detailed studies of such associations are needed.

We thank Professor J P Luton for providing the serum samples.


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