The Clinical Significance of the Complement-Fixation Test in Thyrotoxicosis

Buchanan, W. Watson; Koutras, D. A.; Crooks, J.; Alexander, W. D.; Brass, W.; Anderson, J. R.; Goudie, R. B.; Gray, Kathleen

doi:10.1677/joe.0.0240115

Cited by 63 publications

(15 citation statements)

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“…The diagnosis was established in all patients with the "clinical diagnostic index" described by Crooks et al (1959) and by the clinical response to antithyroid drugs. Confirmation of the diagnosis was obtained in 23 patients by estimation of the serum protein-bound iodine (P.B.I.).…”

Section: Patientsmentioning

confidence: 99%

“…The patients were matched with the above African group for sex, and as closely as possible for age, duration of antithyroid drug therapy before surgery, exophthalmos, and consistency of goiir . Round-cell infiltration was assessed in all cases by counting the number of low-power fields containing round-cell aggregates out of 50 fields for each gland (Buchanan et al 1962 …”

Section: Studiesmentioning

confidence: 99%

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Thyrotoxicosis in the African: Clinical and Immunological Observations

McGill¹

1971

BMJ

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Section: Patientsmentioning

confidence: 99%

Section: Studiesmentioning

confidence: 99%

Thyrotoxicosis in the African: Clinical and Immunological Observations

McGill¹

1971

BMJ

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“….Autoantibodies to cellular antigens such as thyroid microsomal antigen appear to be rare in these animals, although they have been reported in some OS chickens (Khoury et at., 1982) and in Rhesus monkeys immunized with aulologous thyroid preparations (Kite, Argue & Rose, 1966). In contrast, thyroid microsomal anlibodies occur frequently in human autoimmune thyroid disease and observations in vivo and in vitro suggest that their presence is closely associated with thyroid destruction and the development of hypolhyroidism (Buchanan et at., 1962: Forbes et at.. 1962Khoury etat., 1981;Hirola et ai. 1986).…”

Section: Introductionmentioning

confidence: 99%

Thyroid peroxidase and the induction of autoimmune thyroid disease

McLachlan

Atherton

Nakajima

et al. 1990

Clinical and Experimental Immunology

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SUMMARYAnimal models of autoimmune thyroid disease are associated with thyroglobulin (Tg) as autoantigen whereas in man the autoimmune response to microsomal antigen/thyroid peroxidase (TPO) appears to play a major role in thyroiditis. Consequently, we have compared the ability of TPO and Tg to induce Ihyroid autoantibodies and thyroid damage in mice known to be susceptible (CBA/J) or resistant (BALB/c) to thyroiditis induced using murinc Tg. Groups of three to five mice were immunized twice using Freund's complete adjuvant with 80-100/(g highly purified porcine (p) TPO, pTg, rai (r) Tg, human Tg. bovine serum albumin (BSA) or BSA+0 2 (.1% pTg (the level of Tg contamination of TPO). Four weeks after immunization with TPO. plasma from CBA/J (but nol BALB/c) mice contained IgG class antibodies which bound lo TPO-coated tubes in the presence or absence ofexcessTg (and could therefore be clearly distinguished from Tg antibodies) but there was no evidence of thyroiditis in cither strain of mice. In contrast, in CBA/J mice immunized with rTg and, to a lesser extent in mice that had received pTg, thyroid tissue was infiltrated with lymphoid cells and/or neutrophils and antibodies to pTg (but not pTPO) were present. Our observations demonstrate that induction of TPO antibody alone is insuHicicnt lo lead to ihyroiditis in CBA/J mice. Further, these studies emphasize ihe complex interactions between MHC and different thyroid antigens in the processes leading to thyroid destruction.

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“…The prevalence of thyroid failure due to autoimmune thyroiditis with increasing age is a well known phenomenon. Another plausible explanation is that the subjects may have had low titers of anti-thyroid antibodies, because we tested circulating antibodies with a serum dilution of 1:25, and the titer of anti-thyroid antibodies is related in most cases to the degree of lymphocytic infiltration in the thyroid [ 15].…”

Section: Discussionmentioning

confidence: 99%

Anti-Thyroid Antibodies in Patients with Hyperprolactinemia.

Ishibashi

Kuzuya²,

Sawada

et al. 1991

Endocrinol Japon

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Abstract. To clarify the possible role of prolactin in the regulation of immune responses in man, we measured circulating anti-thyroid antibodies in 172 normal subjects, 84 patients with prolactinoma and 63 patients with acromegaly with normal thyroid and adrenocortical functions. Frequencies of positive thyroidal microsome and thyroglobulin antibodies were significantly (p<0.05 and p<0.01, respectively) higher in women with prolactinoma (20.6% and 20.6%) than in normal women (7.5% and 4.7%). Men with prolactinoma had a significantly (p<0.05) higher frequency of positive thyroglobulin antibody (18.8%) than normal men (1.5%). When the subjects were divided by decade, women with prolactinoma in the 4th decade had significantly (p<0.05) higher frequencies of positive thyroidal microsome and thyroglobulin antibodies (30.8% and 30.8%) than normal women of corresponding age (3.7% and 3.7%). In contrast, there was no significant difference in the frequencies of positive anti-thyroid antibodies in patients with acromegaly and in normal subjects. Analysis of the peripheral lymphocyte population revealed that patients with prolactinoma had a higher percentage of B cells than normal subjects, while there was no significant difference in the percentages of total T lymphocytes or in the helper and suppressor T cell ratios in the two groups of subjects. These results suggest that prolactin regulates humoral immune responses in man directly by stimulating B lymphocytes or indirectly by inhibiting suppressor T lymphocyte activity.

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The Clinical Significance of the Complement-Fixation Test in Thyrotoxicosis

Cited by 63 publications

References 0 publications

Thyrotoxicosis in the African: Clinical and Immunological Observations

Thyrotoxicosis in the African: Clinical and Immunological Observations

Thyroid peroxidase and the induction of autoimmune thyroid disease

Anti-Thyroid Antibodies in Patients with Hyperprolactinemia.

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