Kenji Yokoi

Takayasu's Arteritis Associated with Antiphospholipid Antibodies Report of Two Cases

The authors describe 2 patients with Takayasus arteritis in whom lupus anticoagulant was positive and the titer of anticardiolipin antibody was elevated. One patient developed diffusely stenotic and occlusive changes in the multiple larger arteries. Histology of the small-sized arteries in another patient showed occlusive vasculitis without thrombosis, in addition to the findings in large-sized arteries compatible with Takayasus disease. These findings are uncommon in Takayasus arteritis. These findings suggest that antiphospholipid antibodies may have contributed to the pathogenesis of the extensive vasculopathy and may have triggered vasculitis in these patients.

High frequencies of human T-lymphotropic virus type I (HTLV-I) infection and presence of HTLV-II proviral DNA in blood donors with anti-thyroid antibodies.

To investigate the relationship between human T-lymphotropic virus (HTLV) types I and II and the pathogenesis of autoimmune thyroid diseases, we examined serum anti-thyroid antibodies in 1019 blood donors with or without serum anti-HTLV-I antibody as well as proviral DNA for HTLV-II in leukocyte DNA by the polymerase chain reaction in 395 blood donors with or without anti-thyroid antibodies. The frequency of donors with anti-HTLV-I antibody who also showed anti-thyroid antibodies (7.9%) tended to be higher than that (6.3%) among donors who did not have the anti-HTLV-I antibody. The frequency of anti-thyroid antibodies in 125 young male donors aged 16–39 years with anti-HTLV-I antibody (4.8%) was significantly higher (P<0.05) than that (0.6%) in 164 control donors without the antibody. In blood donors with anti-thyroid antibody, 25.0% of those with anti-HTLV-I antibody and 14.3% of those without the antibody had HTLV-II proviral DNA. In contrast, in donors without anti-thyroid antibody HTLV-II proviral DNA was detected in 2.3% of those with anti-HTLV-I antibody and in 0.6% of those without the anti body. Thus the detection rates in donors with anti-thyroid antibody were significantly higher (P<0.001) than those in donors without the antibody, regardless of HTLV-I infection. These results suggest that HTLV-I infection and the presence of HTLV-II proviral DNA may be independently related to the pathogenesis of autoimmune thyroid diseases.

Evidence of HTLV-I in thyroid tissue in an HTLV-I carrier with Hashimoto's thyroiditis

Human T-lymphotropic virus type I (HTLV-I) protein and messenger RNA (mRNA) for HTLV-I were examined in thyroid tissues from two patients with Hashimotos thyroiditis and serum anti-thyroid antibody. The virus envelope protein and signals for the mRNA were detected in many of the follicular epithelial cells of the thyroid tissue from one of the patients, respectively, by immunohistochemistry and in situ hybridization. PCR-Southern blotting revealed the presence of HTLV-I DNA in the thyroid tissue, in which the viral protein and mRNA were detected, although no virus particles were found in the epithelial cells by electron microscopy. HTLV-I virus was not present in the thyroid tissue from the second patient. The present findings suggest that infection of thyroid tissue with HTLV-I is associated with the pathogenesis of Hashimotos thyroiditis in some patients.

Scar formation in the cardiac conduction system of a patient with Takayasu's arteritis.

An autopsied case of Takayasus arteritis associated with complete atrioventricular (AV) block is described for the first time. The findings of scar formation and diffuse infiltration of lymphocytes into the cardiac conduction system, particularly the AV node, were similar to those in patients with connective tissue diseases or congenital complete heart block. The degree of AV block progressed with aggravation of the disease. These findings suggest that complete AV block may have been induced by acquired autoimmunity involving the cardiac conduction system.

Familial occurrence of two patients with malignant rheumatoid arthritis

Abstract. In Japan, patients with rheumatoid arthritis associated with severe extra‐articular manifestations due to vasculitis are diagnosed as having malignant rheumatoid arthritis. We report the occurrence of two cases of malignant rheumatoid arthritis in a Japanese family. Both patients, a father and son, expressed HLA‐DR4 (Dw15), and were infected with Epstein‐Barr virus. Moreover, the father developed malignant rheumatoid arthritis during reactivation of the Epstein‐Barr virus. An unaffected male family member with the same HLA haplotypes was not infected by the virus. The possible role of the virus infection in the pathogenesis of malignant rheumatoid arthritis in a genetically susceptible family is discussed.