Thyroid dysfunction in a prospectively followed series of patients with progressive systemic sclerosis.

Thirty-nine patients with progressive systemic sclerosis (PSS) in stable clinical conditions were extensively evaluated for the presence of thyroid disease. Two patients had previously undetected hypothyroidism while 7 additional patients had normal serum thyroid hormone levels but an exaggerated TSH response to thyrotropin-releasing hormone (TRH) administration, consistent with subclinical hypothyroidism. Four of the 9 subjects with abnormal TRH responses had positive antithyroid antibodies and of the remaining 5, 4 had been on chlorambucil or prednisone. Basal TSH and TSH response to TRH were significantly higher in PSS patients as a group when compared to a control group and increased with increasing duration of PSS. Serum antithyroid antibodies (antithyroglobulin and/or antimicrosomal antibodies) were positive in 18% and thyroid scans were abnormal in 18% of the patients. The euthyroid sick syndrome was not seen. Our findings indicate an increased frequency of, sometimes previously unsuspected, clinical and subclinical hypothyroidism in stable PSS patients which appears to be autoimmune in nature and becomes more prevalent with increased PSS duration. Careful and regular monitoring of the thyroid function in PSS patients is advisable.

In vitro T lymphocyte proliferative response to Yersinia enterocolitica in Reiter's syndrome. Lack of response in other HLA-B27 positive individuals.

We assessed the in vitro T lymphocyte tritiated thymidine (3HTdr) incorporation response of Reiter's patients in the United States to a serotype 3 strain of Yersinia enterocolitica. The mean 3HTdr incorporation response to the formalin killed form of this strain was 27,409 +/- 5,488 counts per minute for 14 HLA-B27 positive Reiter's patients compared with 5,414 +/- 3,490 cpm for a control group of 11 HLA-B27 positive normal individuals (P less than 0.0005). This high response in Reiter's patients was observed with the formalin killed form of Y enterocolitica serotype 3, but not with a heat killed form or a rough mutant form derived from the same bacterial strain. Further, Y enterocolitica of a different serotype (serotype 8) which is not associated with reactive arthritis failed to induce the high proliferative response observed with the serotype 3 strain. This response indicates that T lymphocytes from spontaneous Reiter's patients are capable of recognizing and proliferating to determinant(s) on the formalin killed form of Y enterocolitica serotype 3. Since this bacterium is associated with Reiter's syndrome in Europe but not the United States, these data are consistent with the possibility that our patients have previously encountered these or similar determinants through unrecognized infection with other microorganisms.