Immunological Study on Autoimmune Postpartum Thyroiditis.
10.3349/ymj.1986.27.4.276
- Author:
Hyeon Man KIM
1
;
Kap Bum HUH
;
Hyun Chul LEE
;
Sung Kil LIM
;
Kiil PARK
;
Jung Koo YOUN
;
Sang Yong LEE
Author Information
1. Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Korea.
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
autoimmune postpartum thyroiditis;
lymphocyte subsets;
postpartum women
- MeSH:
Adult;
Antibody-Dependent Cell Cytotoxicity;
B-Lymphocytes/immunology;
Female;
Human;
Pregnancy;
Puerperal Disorders/immunology*;
T-Lymphocytes/immunology;
Thyroiditis, Autoimmune/immunology*
- From:Yonsei Medical Journal
1986;27(4):276-282
- CountryRepublic of Korea
- Language:English
-
Abstract:
Autoimmune postpartum thyroiditis (PPT) has been thought of as one of the organ-specific autoimmune diseases. The present study was designed to investigate whether the immunological changes during the postpartum period might induce this disease, by comparing the circulating lymphocyte subsets and antibody-dependent cell-mediated cytotoxicity (ADCC) between normal postpartum women and PPT patients. The results were as follows: 1) No significant differences in the circulating total T lymphocyte population, or suppressor T lymphocyte subsets, or in Th/Ts ratio were found among 25 PPT patients, 11 normal postpartum women and 11 normal non-pregnant women. 2) In PPT patients, helper T lymphocyte subsets were fewer in proportion than those of normal postpartum or non-pregnant women. However, B lymphocyte population (19.7 +/- 7.8%) and ADCC activity (.41 +/- 13) in PPT patients were comparable to those in normal postpartum women (18.3 +/- 4.8%, .42 +/- .11), although they were significantly greater than those in normal normal non-pregnant women (13.3 +/- 5.9%, .29 +/- .07). In conclusion, the enhancement of immune activities observed in PPT patients was comparable to that in normal postpartum women, suggesting that some other causative or triggering factors might be responsible for the occurrence of this disease.