IN VIVO EFFECTS OF METHIMAZOLE AND THYROXINE ON THYROID MICROSOMAL ANTIBODY TITERS IN HASHIMOTO'S THYROIDITIS

Author(s):  
Rolf Jansson ◽  
Per Anders Dahlberg ◽  
Anders Karlsson
2017 ◽  
Vol 126 (05) ◽  
pp. 321-326 ◽  
Author(s):  
Robert Krysiak ◽  
Witold Szkróbka ◽  
Bogusław Okopień

Abstract Background Levothyroxine and selenomethionine were found to reduce thyroid antibody titers in patients with Hashimoto’s thyroiditis. The same effect was produced by intensive statin therapy. The aim of the present study was to assess whether hypolipidemic agents modulate the impact of thyroid hormone supplementation and selenomethionine on thyroid autoimmunity. Methods The study included 62 women with Hashimoto's thyroiditis treated for at least 6 months with levothyroxine and selenomethionine. On the basis of plasma lipids, women were divided into three groups: women with isolated hypercholesterolemia (group A; n=20), women with isolated hypertriglyceridemia (group B; n=17), and women with normal plasma lipids (group C; n=25). Group A were then treated with atorvastatin (20 mg daily), while group B received micronized fenofibrate (200 mg daily). Serum titers of thyroid peroxidase and thyroglobulin antibodies, as well as serum levels of thyrotropin, free thyroxine and free triiodothyronine were measured at the beginning of the study and 6 months later. Results Fenofibrate decreased triglycerides and increased HDL cholesterol, while simvastatin decreased total and LDL cholesterol. Fenofibrate reduced titers of thyroid peroxidase and, to a lesser extent, thyroglobulin antibodies. Atorvastatin tended to increase thyroid peroxidase antibodies. No changes in thyrotropin, free thyroxine and free triiodothyronine were observed in any treatment group. Fenofibrate-induced changes in thyroid antibody titers correlated with baseline antibody titers, as well as with treatment-induced changes in HDL cholesterol and insulin sensitivity. Conclusions The obtained results indicate that only fibrates may potentiate the effect of selenomethionine and levothyroxine on thyroid autoimmunity in women.


2005 ◽  
Vol 153 (1) ◽  
pp. 41-48 ◽  
Author(s):  
Sevim Gullu ◽  
Rifat Emral ◽  
Mehmet Bastemir ◽  
Arthur B Parkes ◽  
John H Lazarus

Background: Statins have apoptotic effects on many cell types. Hashimoto’s thyroiditis (HT) is an autoimmune disease in which cell-mediated autoimmune mechanisms are pathogenetically involved. Objective: The aim of this study was to evaluate the in vivo effects of Simvastatin on thyroid function, lymphocyte subtypes and also to investigate the apoptotic effects of Simvastatin, Mevastatin, Pravastatin and Cerivastatin on lymphocytes from patients with HT. Methods: In the first part of the study, 11 patients with HT and subclinical hypothyroidism (SH) were given Simvastatin (20 mg/day) for 8 weeks. Ten patients with SH and HT served as the control group. No treatment was given to controls. Thyroid function, C-reactive protein (CRP) levels and lymphocyte subtypes of both groups were determined before the study and after 8 weeks. In the second part of the study, the apoptotic effects of statins on lymphocytes were evaluated in patients with HT (n = 10) and normal subjects (n = 10) in vitro. Apoptosis was investigated by using Annexin-V and propidium iodide. Lymphocytes from patients and controls were incubated with different concentrations of Simvastatin, Cerivastatin, Mevastatin and Pravastatin. Results: An increase in serum free tri-iodothyronine and free thyroxine levels and a decrease in TSH levels were observed (P < 0.05) with Simvastatin treatment. CD4 + cells and B lymphocytes increased whilst CD8 + cells, natural killer cells and activated T lymphocytes decreased significantly in the treatment group (P < 0.05). The CRP level of the group also decreased with Simvastatin but it did not reach significance (P = 0.057). None of parameters was found to be different from the baseline in the control group. In in vitro experiments, apoptosis was observed in CD3 + (both in CD8 + and CD4 + cells) with all statins in both patient and control samples. Mevalonate, which was used in experiments, reversed apoptosis in some but not all samples. Conclusions: The results of this study suggested that Simvastatin is an immune modulatory agent and improves thyroid function in patients with HT. This effect is probably mediated via lymphocyte apoptosis as demonstrated with in vitro experiments and is not confined to Simvastatin since Mevastatin, Pravastatin and Cerivastatin also induced apoptosis in lymphocytes.


1990 ◽  
Vol 123 (5) ◽  
pp. 511-518 ◽  
Author(s):  
Jaeduk Noh ◽  
Noboru Hamada ◽  
Hifumi Saito ◽  
Midori Yoshimoto ◽  
Hiroyuki Iwasaki ◽  
...  

Abstract. Recently, thyroid microsomal antigen was identified as thyroid peroxidase, and thyroid microsomal antibody was found to inhibit thyroid peroxidase activity in vitro. We investigated the possibility that anti-microsomal antibody inhibits the iodination of tyrosine, in vivo. Immunoglobulin G with or without anti-microsomal antibody from hypothyroid patients with goitrous Hashimoto's thyroiditis inhibited thyroid hormone synthesis in cultured slices of normal human thyroid tissue. IgGs with anti-microsomal antibody inhibited 125I thyroidal uptake and thyroid hormone synthesis stimulated by TSH more than normal IgG did. However, the same results were obtained with IgGs without anti-microsomal antibody. This effect did not involve anti-microsomal antibody, anti-thyroglobulin antibody, TSH-binding inhibitor immunoglobulin, thyroid stimulation-blocking immunoglobulin, or the cAMP level of the thyroid tissue. The ratio of organic I to inorganic I with stimulation by TSH in slices incubated with IgG from hypothyroid patients with goitrous Hashimoto's thyroiditis or normal IgG was not significantly different, but was significantly higher in slices incubated with methylmercaptoimidazole. Therefore, IgG from hypothyroid patients with goitrous Hashimoto's thyroiditis mainly suppressed 125I thyroidal uptake, rather than inhibiting thyroid peroxidase activity. In addition, this IgG was present in the serum of 11 of the 12 hypothyroid patients with Hashimoto's thyroiditis studied. This IgG may be involved in the mechanism that causes hypothyroidism in some patients with goitrous Hashimoto's disease.


2021 ◽  
Author(s):  
Fatemeh Eftekharian ◽  
Gholamhossein Ranjbar Omrani ◽  
Mohammad Hossein Dabbaghmanesh ◽  
Reza Sahraei ◽  
Marzieh Bakhshayeshkaram ◽  
...  

Abstract Background The purpose of this study was to determine the association of sonographic parameters with the serum levels of anti-thyroid peroxidase (TPO), anti-thyroglobulin (Tg), and thyroid hormones in patients with Hashimoto's thyroiditis. Methods 149 patients (118 females, 31 males; aged 18–60 years; mean age: 38.60 ± 8.03 years) who were diagnosed with Hashimoto's thyroiditis were enrolled in the study. Blood sample was taken to measure the serum levels of free T3 and T4, thyroid stimulating hormone (TSH), anti-TPO antibody titers, and anti-Tg antibody titers. The thyroid sonography of each patient was classified into one of the five grades by real-time ultrasonography (US) based on echogenicity, thyroid size, and thyroid pattern. We evaluated whether a correlation existed between thyroid characteristics on US and serum levels of thyroid hormones, anti-TPO and anti-Tg. Results Nodular structures were detected in 54 (36.2%) patients (38 micronodular and 16 macros nodular). Echogenicity was recorded as isoechoic in 15 (10.07%) and hypoechoic in 119 (79.87%) subjects. Euthyroid ‎subjects had significantly thicker isthmus than overt and subclinical hypothyroid patients (p = 0.018). Mean serum TSH, anti-Tg and anti-TPO titers was significantly higher in patients with micronodules than those with micronodules and subjects without nodules (P < 0.05). Isthmus thickness had a significant negative correlation with FT4 and FT3 (P = 0.046; r = 0.11& P = 0.017; r = 0.15, respectively). Thyroid autoantibodies had positive significant correlations with different parameters of the thyroid volume (P < 0.05). Conclusions Thyroid’s US findings in addition to serum levels of anti-Tg and anti-TPO titers would be useful in diagnosis and evaluation of the severity and extent of Hashimoto's thyroiditis, but further evaluations are needed. Trial registration: Trial registry identifier IR.SUMS.REC.1395.S161 (2015/11/30).


1973 ◽  
Vol 74 (4) ◽  
pp. 675-684
Author(s):  
J. Földes ◽  
J. Takó ◽  
Cs. Bános ◽  
E. Gesztesi ◽  
J. Juhász

ABSTRACT Antibodies raised against the microsomal fraction of the thyroid epithelial cells have been shown to inhibit in vitro binding of LATS to the microsomal fraction and to diminish in vivo thyroid stimulating effects of both LATS and TSH. Antimicrosomal antibody is also likely to block in vivo binding of LATS to the thyroid, and to reduce its rate of elimination from the circulating blood. The results are consistent with the assumption that the receptor structures and site of action of LATS and TSH in the thyroid are identical. On the basis of these findings the possibility arises that high titres of antimicrosomal antibodies in the serum may interfere with the results of LATS bioassay in such patients. Moreover, it seems reasonable to assume that in Hashimoto's thyroiditis high levels of antimicrosomal antibodies reduce the TSH sensitivity of thyroid, leading to an enhanced secretion of TSH and promoting the development of hypothyroidism.


1987 ◽  
Vol 116 (1_Suppl) ◽  
pp. S86-S88 ◽  
Author(s):  
M. Londei ◽  
B. Grubeck-Loebenstein ◽  
C. Greenall ◽  
M. Turner ◽  
M. Feldmann

1978 ◽  
Vol 88 (4) ◽  
pp. 703-712 ◽  
Author(s):  
Ken Okamura ◽  
Kenjiro Inoue ◽  
Teruo Omae

ABSTRACT An interesting case of iodide induced goitre with immunological abnormalities is described. The patient who was sensitive to synthetic penicillin had previously been treated for exudative pleuritis, congestive heart failure and acute renal failure. Following recovery, he began to ingest large amounts of seaweed after which he developed goitrous hypothyroidism. It was of interest that the serum level of gamma-globulin increased, and subsequently the antithyroid microsomal antibody became strongly positive, suggesting that thyroidal autoimmune processes had been precipitated. Biopsy of the thyroid gland revealed chronic thyroiditis, with evidence suggesting extreme stimulation by TSH. High thyroidal uptake of 131I, positive perchlorate discharge test and biochemical analysis of the thyroidal soluble protein showed severe impairment of hormone synthesis following continuous accumulation of excess iodide. While there is evidence suggesting that increased iodide may be an important factor in the initiation of Hashimoto's thyroiditis, this may result from the marked increased sensitivity of Hashimoto's gland to the effects of iodine. Thus an occult lesion could be unmasked in this manner. The mechanism by which iodide mediates this effect is not clear.


1999 ◽  
pp. 452-456 ◽  
Author(s):  
F Bogazzi ◽  
L Bartalena ◽  
S Brogioni ◽  
A Burelli ◽  
L Manetti ◽  
...  

OBJECTIVE: Thyroid blood flow is greatly enhanced in untreated Graves' disease, but it is not known whether it is due to thyroid hormone excess or to thyroid hyperstimulation by TSH-receptor antibody. To address this issue in vivo patients with different thyroid disorders were submitted to color flow doppler sonography (CFDS). SUBJECTS AND METHODS: We investigated 24 normal subjects, and 78 patients with untreated hyperthyroidism (49 with Graves' hyperthyroidism, 24 with toxic adenoma, and 5 patients with TSH-secreting pituitary adenoma (TSHoma)), 19 patients with thyrotoxicosis (7 with thyrotoxicosis factitia, and 12 with subacute thyroiditis), 37 euthyroid patients with goitrous Hashimoto's thyroiditis, and 21 untreated hypothyroid patients with Hashimoto's thyroiditis. RESULTS: Normal subjects had CFDS pattern 0 (absent or minimal intraparenchimal spots) and mean intraparenchimal peak systolic velocity (PSV) of 4.8+/-1.2cm/s. Patients with spontaneous hyperthyroidism due to Graves' disease, TSHoma, and toxic adenoma had significantly increased PSV (P<0.0001, P=0.0004, P<0.0001 respectively vs controls) and CFDS pattern. Patients with Graves' disease had CFDS pattern II (mild increase of color flow doppler signal) in 10 (20%) and pattern III (marked increase) in 39 cases (80%). Mean PSV was 15+/-3cm/s. Patients with toxic adenoma had CFDS pattern I (presence of parenchymal blood flow with patchy uneven distribution) in 2 (8%), pattern II in 16 (70%) and pattern III in 5 (22%). Mean PSV was 11+/-2.4cm/s. Patients with TSHoma showed CFDS pattern I in one case (20%) and pattern II in 4 (80%). Mean PSV was 14.8+/-4.2cm/s. Patients with thyrotoxicosis had normal PSV (4.2+/-1. 1cm/s in subacute thyroiditis, 4+/-0.8cm/s in thyrotoxicosis factitia, P=not significant vs controls) and CFDS pattern 0. Untreated euthyroid patients with goitrous Hashimoto's thyroiditis had CFDS pattern 0, and mean PSV (4.3+/-0.9cm/s; P=not significant vs controls). Untreated hypothyroid patients with goitrous Hashimoto's thyroiditis had CFDS pattern I in 14 cases (67%), pattern II in 4 (19%) and pattern 0 in 3 (14%) and mean PSV (5.6+/-1. 4cm/s) was higher than that of controls (P=0.026). CONCLUSIONS: An increase in both intrathyroidal vascularity and blood velocity was observed in patients with spontaneous hyperthyroidism but not in thyrotoxicosis due to either ingestion of thyroid hormones or to a thyroidal destructive process. The slightly increased vascularity and blood velocity observed in patients with hypothyroid Hashimoto's thyroiditis suggests that thyroid stimulation by either TSH-receptor antibody or TSH is responsible for the increased thyroid blood flow.


1977 ◽  
Vol 84 (4) ◽  
pp. 759-767 ◽  
Author(s):  
Christian von Westarp ◽  
Andrew J. S. Knox ◽  
Vas V. Row ◽  
Robert Volpé

ABSTRACT Antibodies were raised to various sub-cellular fractions of human thyroids, (of Graves' disease, Hashimoto's thyroiditis, and non-toxic goitre). With one exception it was found that antibodies to the Graves' thyroid fractions cross-reacted with both the non-toxic goitre and Hashimoto's thyroiditis fractions. This exception was in the antiserum to the Graves' 105 000 × g pellet (Gr4) which contained an antibody (A-1) that could not be absorbed by either the non-toxic goitre (NTG) or the Hashimoto's (H) thyroid preparations. The antibody-antigen reaction between A-1 and Gr4 could be blocked by the addition of LATS (or TSH) to the antigen, thus suggesting that A-1 might be a LATS-like immunoglobulin. These results suggest that the TSH receptor may be antigenic and that an antibody to this receptor can be produced in vivo. Production of such an antibody to the TSH receptor would permit the development for the first time of a good animal model of Graves' disease.


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