Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.11.1.8 (thyroid peroxidase)
3,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thyroid peroxidase antibody levels were measured in 409 patients who came to the thyroid pathology consultation of our Institution between September, 1990, and November, 1991, and were compared with a reference population. In the first 231 patients, we compared the results obtained with two commercial kits. The correlation coefficient between both populations of results was assessed to be 0.919. Only one of the kits was selected later ("Immutest anti-TPOR", Henning, Germany) because normal and pathological values overlapped to a lesser extent. In a population of controls (reference population). 4 cases out of 82 (4.8%) had values exceeding 100 U/ml (arbitrary units), this value being regarded as the boundary of normal conditions. Out of the 409 assays made in patients examined during the thyroid pathology consultation, 137 (33.5%) had pathological values ranging from 100 to 5000 U/ml and even more. Peroxidase antibodies are mainly found in patients with primary hypothyroidism (positive in 82% of cases) and graves' hyperthyroidism (positive in 81%). We have also observed the highest levels in these two conditions. In addition, we have demonstrated a group of patients with normal thyroid conditions who were positive for peroxidase antibodies, sometimes in a family with a history of thyroid pathology. These may be at higher risks to develop hypothyroidism in the future than the general population. A TRH test in some subjects and the clinical evolution of these patients lead us to advocating TPO antibody assay for screening on the first consultation. Endocrine surveillance is advisable in case of positive results.
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PMID:[Determination of thyroid peroxidase antibodies in common thyroid pathology. Methodological and clinical approach]. 802 44

The afferent cortical connections of individual cytoarchitectonic areas within the superior temporal sulcus (STS) of the rhesus monkey were studied by retrograde tracer techniques, including double tracer experiments. Rostral superior temporal polysensory (STP) cortex (area TPO-1) receives input from the rostral superior temporal gyrus (STG), cortex of the circular sulcus, and parahippocampal gyrus (PHG) (areas 35, TF, and TL). Mid-STP cortex (areas TPO-2 and -3) has input from the mid-STG, cortex of the mid-circular sulcus, caudal inferior parietal lobule (IPL), cingulate gyrus (areas, 23, 24, retrosplenial cortex), and mid-PHG (areas 28, TF, TH, and TL). Caudal STP cortex (area TPO-4) has afferent connections with the caudal STG, cortex of the caudal insula and caudal circular sulcus, caudal IPL, lower bank of the intraparietal sulcus (IPS), medial parietal lobe, cingulate gyrus, and mid- and caudal PHG (areas TF, TH, TL; prostriate area). The most rostral cortex of the lower bank of the STS (areas TEa and TEm), a presumed visual association area, receives input from the rostral inferotemporal (IT) region; more caudal portions of areas TEa and TEm have afferent connections with the caudal IT region, PHG, preoccipital gyrus, and cortex of the lower bank of the IPS.
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PMID:Parietal, temporal, and occipital projections to cortex of the superior temporal sulcus in the rhesus monkey: a retrograde tracer study. 802 52

Postpartum thyroiditis (PPT) affects half of the 10% of women who have elevated circulating thyroid autoantibodies during the postpartum year. Because of the similarities between PPT and Hashimoto's thyroiditis, the pathogenic role of complement in PPT has been investigated. Complement fixation by thyroid peroxidase antibodies (TPO Abs) (expressed as log reciprocal titer) in serum from euthyroid TPO Ab-positive women (n = 29) was 0.91 at 1 month postpartum and increased to 1.45 by 12 months postpartum; complement C3 activation, measured by enzyme-linked immunosorbent assay, in a similar group of women (n = 75) was 0.05 at delivery and increased to 0.33 by 6 months postpartum. In women with PPT, there was greater TPO Ab-related complement activation during the postpartum year; complement fixation increased from 1.00 at 1 month postpartum to 1.48 at 4 months postpartum (P < 0.005) (n = 25), and C3 activation increased from 0.11 at delivery to 0.63 at 6 months postpartum (P < 0.005) (n = 73). Bioactive TPO Ab (TPO Ab x C3 index) was significantly higher in PPT women (55 kilo international units of activity (kIU)/L at 6 months postpartum) (Hashimoto range, 30-108 kIU/L) compared with euthyroid TPO Ab-positive women (< 9 kIU/L at all time points; P < 0.005). Serum samples from TPO Ab-negative control women showed no interaction with complement in either assay at any time during the postpartum year (complement fixation < 0.7; complement C3 activation index < 0.01). This detailed examination of the role of complement in the pathogenesis of PPT shows that TPO Ab-driven complement fixation is a marker for thyroid dysfunction in TPO Ab-positive women. The levels of bioactive TPO Ab in PPT fall within the range seen in Hashimoto's thyroiditis, suggesting similarities in their pathology.
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PMID:The role of complement in the pathogenesis of postpartum thyroiditis. 804 54

Human thyroid peroxidase (hTPO) was detected immunohistochemically in 61 normal, benign and malignant thyroid tissues with a monoclonal antibody (38E) against hTPO using paraffin-embedded sections. Thyroid peroxidase was expressed intensely not only in tissues from Graves disease and hyperfunctioning adenomas, but also in those from carcinomas, adenomas and Hashimoto's thyroiditis. The staining pattern of TPO in the follicular cells was a diffuse and fine granular one in the normal thyroids, Graves' thyroids and adenomas, but abnormal coarse granular deposits of TPO were characteristically identified in most of the papillary carcinomas and Hashimoto's thyroiditis. These coarse granular deposits of TPO suggested that qualitative or structural changes in the TPO molecule are present in carcinomas and Hashimoto's thyroiditis. Consequently, these qualitative changes in TPO may be responsible for the lack of biochemically measured TPO activity in these diseases. This finding may also be useful in distinguishing between benign and malignant thyroid tumors.
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PMID:Immunohistochemical demonstration of thyroid peroxidase (TPO) in human thyroid tissues from various thyroid diseases. 806 1

To refine the linkage map of mouse Chromosome (Chr) 12 and to define better the homology relationships between it and human chrs 2p and 14q, nine new anonymous DNA markers of Chr 12 were identified, and mouse loci homologous to the human D14S17, CHGA, HSPA2, RRM2, TPO, and ZFP50 ("KUP") genes were defined. The inheritance of DNA variants associated with these markers was followed in progeny of a reciprocal backcross between the C57BL/6J and SWR/J laboratory mouse strains and in recombinant inbred (RI) strains of mice. These data, combined with results of previous analyses of the backcross, allowed the construction of a 22-marker multilocus linkage map that spanned 58 cM. Use of this map to anchor the RI typing data collected in this and previous studies allowed the construction of a 79-marker map that spanned 66 cM and the identification of a framework of unambiguously ordered, extensively typed markers that should facilitate the use of RI mice in testing new markers for possible linkage to Chr 12.
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PMID:Refinement of the DNA marker maps of mouse chromosome 12. 808 80

An EIA for measuring anti-TPO autoantibodies (rhTPO-EIA) was developed using recombinant human TPO expressed in CHO cells and was compared with MC-HA generally used in laboratory routine work. rhTPO-EIA showed a satisfactory reproducibility in the intra-assay test and did not have an accidental error of lots. Almost equal number of healthy females and males were measured for their IgG binding to TPO to define a normal range of anti-TPO autoantibodies. After setting 20 IU/ml as an upper limit of normal range, sera from patient with thyroid disorders were measured for their anti-TPO autoantibodies. Chronic thyroiditis and Graves' disease were highly positive, while adenoma, thyroid cancer, SLE, and RA were low in their positivity. The positive rate of anti-TPO autoantibodies was compatible to those of previous reports in each disorder. Seventy-two sera from patients with chronic thyroiditis or Graves' disease were measured for their autoantibodies by both rhTPO-EIA and MC-HA and the results were compared between both methods. A correlation coefficient was 0.486. Following absorption with thyroglobulin, sera were measured again and as the results, the correlation coefficient increased to 0.723. Therefore, MC-HA was thought to be influenced in the presence of anti-thyroglobulin autoantibodies. Since rhTPO-EIA is excellent in quality and not affected by anti-thyroglobulin antibodies, it is useful and applicable to clinical diagnosis and observation of thyroid disorders.
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PMID:[Measurement of human thyroid peroxidase autoantibodies by enzyme immunoassay using recombinant human TPO]. 815 66

The purpose of this work was to study if TSH has a role in TPO antigen expression in vivo. Using the cytotoxicity assay we measured TPO expression and correlated it with TSH serum levels in 3 groups of rats: control, hypothyroid and hypothyroid supplemented with thyroxine. For comparative purposes, in the cytotoxicity assay we used rat monoclonal antiTPO or human sera with high titles for antiTPO antibodies. Hypothyroid rats showed marked elevations of TSH serum levels and TPO antigen expression in their thyrocytes when compared to the control and supplemented group. A positive correlation between TPO antigen and TSH levels was observed (r = 0.69, p < 0.001). There was an excellent correlation between TPO results using rat monoclonal or human sera antibodies (r = 0.94 p < 0.0001). It is concluded that TSH modulates TPO antigen expression. These data are of clinical relevance considering that TSH modulates the expression of other antigens that can maintain the immune response and perpetuate the immune disease in patients with Graves disease treated with antithyroid drugs. Thus, the avoidance of TSH hypersecretion with administration of thyroxine could be useful to treat these patients.
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PMID:[Experimental evidence that endogenous TSH modulates microsomal antigen expression: clinical implications]. 819 Nov 12

The purpose of this paper is to study some of the mechanisms by which antigen presentation, one of the first steps in the immune process, is modulated. Three different experiments are performed: a) Using thyroid tissue from patients operated on for Graves' Disease, spontaneous HLA-DR and TPO antigen expressions were measured through the Cytotoxicity Assay; these findings were correlated with the presence of antiTPO in the sera of these patients. It was found that only patients whose thyroid tissue spontaneously expressed both antigens had circulating antiTPO in their sera, thus demonstrating that dual expression is basic for antibody production. b) Blood samples from other Graves' patients were obtained; peripheral lymphocytes were isolated and cultured in complete media for 5 days, then supernatant was separated and IFN-g concentration was measured by a sandwich type RIA; the same procedure was done in 12 normal controls in order to compare the results. It was found that lymphocytes from Graves' patients secreted significantly more IFN-g than normal controls (20.9 +/- 13.54 U/ml vs 3.7 +/- 3.22 U/ml respectively, p < 0.001) confirming that they were sensitized, so this determination could be used as a marker of immune process, if other infectious conditions are excluded; also it was found that IFN-g hypersecretion persists once hyperthyroidism has been treated, pointing out that the immune abnormality is still present.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Importance of gamma-interferon and DR expression in autoimmune thyroid disease]. 819 Nov 31

TPO is the key enzyme involved in the thyroid hormone synthesis. The human TPO (hTPO) gene locates on chromosome 2 and consists of 17 exons and 16 introns. Compared with other peroxidases, hTPO is 42% homologous with granulocyte myeloperoxidase. Thyroid cells contain multiple TPO mRNA transcripts of various size. However, the reason is unknown. TTF-1 and TTF-2 are known to regulate TPO gene expression. Moreover, the other factors are becoming clear to regulate it. Congenital TPO defects result in hypothyroidism and goiter. Recent studies clarify a human mutation causing TPO deficiency.
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PMID:[Thyroid peroxidase (TPO) gene and pathogenic TPO mutation]. 819 71

Both in vivo and in vitro isotopic tests are available for the diagnosis of thyroid diseases. As in vitro tests, serum concentrations of T4, T3, free T4, free T3, TSH, TBG, and thyroglobulin (Tg) are determined by RIA or by IRMA. TSH receptor antibodies are measured by RRA for TSH. In order to differentiate blocking from stimulating antibodies, however, assessment of biological activity of the antibody by another type of method such as TSAb assay is required. Radioassays for anti-Tg and anti-TPO antibodies have recently been developed. The former assay is sensitive enough to make early diagnosis of Hashimoto's thyroiditis. The serum Tg measurement by a newly developed IRMA is applicable even in cases with anti-Tg antibodies. Radiolabeled T4-analogs are most frequently used in the RIA of free T4. A one-step labeled antibody method (Amerlex MAB kit) and a sensitive RIA with use of equilibrium dialysis (Model FT4 kit) have recently been in clinical application in our country. These two assays have an advantage of overcoming two major problems, effects of albumin and anti-T4 antibodies, that the analog method has. As in vivo isotopic tests, thyroid scintigraphy using 123I or 99mTc with the combined assessment of the thyroidal uptake rate of each radionuclide and tumor imaging are performed. The thyroid scintigraphy gives functional information, being useful for the differential diagnosis of destructive thyrotoxicosis from Graves' hyperthyroidism. Hypothyroid patients with increased 123I or 99mTc uptake are suspected highly to have dyshormonogenesis or reversible hypothyroidism due to iodine excess.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical nuclear medicine in thyroid diseases]. 819 36


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