scholarly journals Stress-induced hashitoxicosis: case report and relative HLA serotype and genotype

2019 ◽  
Vol 65 (6) ◽  
pp. 830-833 ◽  
Author(s):  
Roberto Vita ◽  
Valeria Cernaro ◽  
Salvatore Benvenga
Keyword(s):  
Hashimoto’S Thyroiditis ◽  
Stressful Life Events ◽  
Normal Values ◽  
White Cell Count ◽  
Hashimoto's Thyroiditis ◽  
Stressful Event ◽  
Graves Disease ◽  
Thyroid Function Tests ◽  
Receptor Antibodies ◽  
Tsh Receptor Antibodies

SUMMARY OBJECTIVE Even though stress has been long known as a provocative factor for Graves’ disease, its relationship with Hashimoto's thyroiditis is more controversial. Studies on this topic are scanty. This paper aims to report a case of stress-induced Hashitoxicosis. RESULTS Here we report a case of Hashitoxicosis induced by a psychological stressful event in a 28-year-old woman with Hashimoto's thyroiditis. She had remained stably euthyroid for 12 years. She was first observed in April 2016, while euthyroid. She came back after 11 months because of fatigue and palpitations, in the absence of neck pain. Thyroid function tests revealed moderate thyrotoxicosis (undetectable TSH; FT4 36.94 pmol/L, normal values 9.0-24.46; FT3 13.50 pmol/L, normal values 3.07-6.14) with negative TSH-receptor antibodies. In the previous three months, she had experienced a psychological stressful event. Inflammatory markers were negative, and the white cell count was normal. Thyroid ultrasound revealed a modest increase in vascularization. Transient subclinical hypothyroidism ensued after seven weeks and spontaneously recovered. On the last visit, the patient was still on euthyroidism. (TSH 1.01 mU/L; FT4 9.22 pmol/L; FT3 3.98 pmol/L). We also performed HLA serotyping and genotyping. CONCLUSION This case demonstrates that, similarly to Graves’ disease, Hashitoxicosis can also be triggered by stressful life events.

Inhibition of thyrotropin-stimulated adenylate cyclase activation and growth of rat thyroid cells, FRTL-5, by immunoglobulin G from patients with primary myxedema: comparison with activities of thyrotropin-binding inhibitor immunoglobulins

1989 ◽  
Vol 120 (1) ◽  
pp. 99-106 ◽  
Author(s):  
B. Y. Cho ◽  
Y. K. Shong ◽  
H. K. Lee ◽  
C.-S. Koh ◽  
H. K. Min
Keyword(s):  
Hashimoto’S Thyroiditis ◽  
Thymidine Incorporation ◽  
Tsh Receptor ◽  
Hashimoto's Thyroiditis ◽  
Thyroid Cells ◽  
Rat Thyroid ◽  
Receptor Antibodies ◽  
Tsh Receptor Antibodies ◽  
Growth Inhibiting ◽  
Blocking Type

Abstract. We studied the blocking type TSH receptor antibodies in 28 patients with primary myxedema and 21 patients with goitrous Hashimoto's thyroiditis by measuring the ability of their IgGs to inhibit TSH binding to its receptor, and to inhibit TSH-stimulated cAMP increase and [3H] thymidine incorporation in a rat thyroid cell line, FRTL-5. The incidences of TSH binding inhibitor immunoglobulin, thyroid stimulation inhibiting immunoglobulin and thyroid growth inhibiting immunoglobulin in patients with primary myxedema were 54.6, 75 and 65.2%, respectively, against 14.3,0 and 17.7%, respectively, in goitrous Hashimoto's thyroiditis. The antibodies inhibited dose-dependently not only TSH stimulated but also Graves' IgG-stimulated cAMP increase and [3H] thymidine incorporation. The TSH binding inhibitor immunoglobulin activities in patients with primary myxedema were significantly correlated with both the thyroid stimulation inhibiting immunoglobulin (r = 0.665; P<0.01) and the thyroid growth inhibiting immunoglobulin (r = 0.618; P<0.01) activity. Thirteen patients whose TSH binding inhibitor immunoglobulin activities were more than 50% had both strong thyroid stimulation inhibiting immunoglobulin (75.1–100%) and thyroid growth inhibiting immunoglobulin (57.4–100%) activities. These data suggest that the vast majority of patients with primary myxedema have potent blocking type TSH receptor antibodies. These might play a role in primary myxedema causing hypothyroidism and thyroid atrophy through inhibiting TSH-stimulated cAMP generation.

scholarly journals SAT-518 Progression of Graves Disease to Hashimoto’s Thyroiditis Following Alemtuzumab Therapy for Multiple Sclerosis

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Brandon Rapier ◽  
Frank Gargasz ◽  
Omar Suheil Zmeili
Keyword(s):  
Multiple Sclerosis ◽  
Thyroid Function ◽  
Hashimoto’S Thyroiditis ◽  
Thyroid Nodules ◽  
Hashimoto's Thyroiditis ◽  
Graves Disease ◽  
Thyroid Function Tests ◽  
Thyroid Disorder ◽  
Free T4 ◽  
Free T3

Abstract Introduction: Alemtuzumab, an anti-CD52 monoclonal antibody used in the treatment of relapsing-remitting multiple sclerosis is most commonly associated with Graves disease, but autoimmune hypothyroidism may also be seen. We present an unusual case where both were present in the same patient and progression from hyperthyroidism to hypothyroidism was seen within only a few months. Clinical Case: A 33-year-old female referred to Endocrinology clinic for evaluation of hyperthyroidism. She was complaining of palpitations, tremors, increased sweating, heat intolerance, and unintentional weight loss for 3 months. She received 2 cycles of alemtuzumab treatments over the last 21 months for her multiple sclerosis. Last treatment was 8 months before she developed hyperthyroid symptoms. Patient had no prior history of thyroid disorder. Thyroid stimulating hormone (TSH) level was within normal range before alemtuzumab was administered. TSH was monitored periodically and was normal till 8 months after receiving alemtuzumab therapy. Physical exam was remarkable for diffuse enlarged thyroid, not tender, without palpated thyroid nodules but with thyroid bruit. No proptosis was present. Thyroid function tests obtained by her primary care physician were consistent with hyperthyroidism. Patient found to have suppressed TSH &lt;0.015 IU/mL [0.465 - 4.680IU/mL], elevated total T3 372ng/dL [97-169ng/dL], and elevated total T4 &gt;24.9 ug/dL [5.5 - 11.0 ug/dL]. Further workup revealed elevated Free T3, 10.90 [2.77 - 5.27 pg/mL] and elevated free T4 &gt; 6.99 ng/dL [0.78 - 2.19 ng/dL]. Thyrotropin receptor antibody (TR Ab) was elevated as well at 3.43 IU/L [&lt;1.75 IU/L]. Pregnancy test was negative. Thyroid ultrasound demonstrated goiter with no focal thyroid nodules seen. She was started on methimazole 10 mg daily. One month later, TSH was elevated at 31.58 though she only took methimazole for one week and then discontinued due to rash and pruritus. At that time, she reported severe fatigue and 25 lbs weight gain. Repeated labs one month later showed elevated TSH, 60.978 IU/ML, low free T4 0.08 pg/mL and low free T3 0.72 ng/dL. Thyroid peroxidase Antibody (TPO Ab) was obtained and was 5308.8 IU/mL [0.0 - 5.5 IU/mL]. She was started on levothyroxine 100 mcg daily. Two months later, levothyroxine dose was increased to 112 mcg daily due persistent TSH elevated. At subsequent visit, patient was euthyroid with normal TSH 3.191IU/mL and normal free T4 1.48 ug/dL. Conclusion: This case was unique in that the patient developed both TR Ab and TPO Ab after alemtuzumab therapy which resulted in Grave’s disease followed by Hashimoto’s thyroiditis. The case highlights the importance of continuous monitoring of thyroid function in patients treated with alemtuzumab given the unpredictable autoimmune phenomena which may occur.

scholarly journals SAT-482 Simultaneous Hashimoto/Graves Disease or Prolonged Hashitoxicosis? A Diagnostic Challenge with Therapeutic Implications

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Carlos A Penaherrera ◽  
Valentina Rodriguez
Keyword(s):  
Hashimoto’S Thyroiditis ◽  
Vital Signs ◽  
Simultaneous Presentation ◽  
Hashimoto's Thyroiditis ◽  
Graves Disease ◽  
Thyroid Function Tests ◽  
Childbearing Age ◽  
Diagnostic Challenge ◽  
Mixed Condition ◽  
Therapeutic Implications

Abstract Background: Some individuals with Hashimoto’s thyroiditis (HT), characterized by anti-TPO antibodies (Abs), can also have positive TSI Abs in up to 20% of cases, without necessarily having Graves disease (GD). Patients with signs of both hyper-and-hypothyroidism with positivity to these two Abs can pose a diagnostic and therapeutic dilemma, as their course is often unpredictable. Clinical Case: A 49-year-old woman was diagnosed with hypothyroidism and took levothyroxine (LT4) for about 1 year, after which she developed symptoms of hyperthyroidism and was switched to methimazole (MMI), which she only took for 1 year. At her initial visit at our clinic she had been off of MMI for 12 months and she was biochemically hyperthyroid (TSH of 0.01 mcIU/ml, f-T4 of 2.26 ng/dl). TSI Abs were positive at 461, but she also tested positive for anti-TPO at 673. Thyroid receptor Abs (TRAb) were also elevated at 54.8. Her vital signs were stable, but she had marked proptosis and complained of eye dryness, so MMI was restarted. A RAIU scan could not be obtained, but a thyroid US showed a heterogeneous and hypervascular gland. On MMI, her thyroid function tests normalized, and her eye disease vastly improved over 2 years. Her MMI dose was progressively decreased until it was stopped completely. On re-evaluation a few months later, she had newly elevated TSH of 8.7 mcIU/ml and low f-T4 of 0.87 ng/dl, with no symptoms of hypothyroidism, so we opted for management with active surveillance instead of starting her on LT4. Her TSI level improved to 240, but remains elevated. Discussion: It is unclear if our patient has a mixed condition with features of both GD and HT, or if she has HT with a very prolonged hyperthyroid phase (hashitoxicosis). Extended periods of hashitoxicosis have been described, the longest reported lasted for 2 years[1]. Simultaneous presentation of GD and HT is very rare, with only a few cases described in the literature. RAIU scan is often diagnostic, showing increased uptake as seen in GD, but patchy areas of decreased uptake can also be seen. In our case it is likely that HT and GD were coexisting, with GD masking the hypothyroidism, until the former remitted with MMI, and her HT took over. Though no RAIU scan was available, the TSI positivity, clinical response of her hyperthyroidism to MMI and the presence of orbitopathy rule in favor of co-existing GD. Decision to treat with LT4 should be weighed against the risk of causing recurrence of hyperthyroidism. Special considerations should be taken in women of childbearing age due to the difficult management that overlapping hyper/hypothyroidism would entail during pregnancy. References: 1. Shahbaz, A et al. Prolonged Duration of Hashitoxicosis in a Patient with Hashimoto’s Thyroiditis: A Case Report and Review of Literature. Cureus. 2018; 10(6):e2804

Impact of the serum thyroglobulin concentration on the diagnostics of benign and malignant thyroid diseases

2000 ◽  
Vol 39 (05) ◽  
pp. 133-138 ◽  
Author(s):  
W. Dembowski ◽  
H.-J. Schroth ◽  
K. Klinger ◽  
Th. Rink
Keyword(s):  
Hashimoto’S Thyroiditis ◽  
Thyroid Volume ◽  
Nodular Goiter ◽  
Thyroid Diseases ◽  
Hashimoto's Thyroiditis ◽  
Graves Disease ◽  
Normal Range ◽  
Serum Thyroglobulin ◽  
Diffuse Goiter ◽  
Hyperthyroid Patients

Summary Aim of this study is to evaluate new and controversially discussed indications for determining the thyroglobulin (Tg) level in different thyroid diseases to support routine diagnostics. Methods: The following groups were included: 250 healthy subjects without goiter, 50 persons with diffuse goiter, 161 patients with multinodular goiter devoid of functional disorder (108 of them underwent surgery, in 17 cases carcinomas were detected), 60 hyperthyroid patients with autonomously functioning nodular goiter, 150 patients with Hashimoto’s thyroiditis and 30 hyperthyroid patients with Graves’ disease. Results: The upper limit of the normal range of the Tg level was calculated as 30 ng Tg/ml. The evaluation of the collective with diffuse goiter showed that the figure of the Tg level can be expected in a similar magnitude as the thyroid volume in milliliters. Nodular tissue led to far higher Tg values then presumed when considering the respective thyroid volume, with a rather high variance. A formula for a rough prediction of the Tg levels in nodular goiters is described. In ten out of 17 cases with thyroid carcinoma, the Tg was lower than estimated with thyroid and nodular volumes, but two patients showed a Tg exceeding 1000 ng/ml. The collective with functional autonomy had a significantly higher average Tg level than a matched euthyroid group being under suppressive levothyroxine substitution. However, due to the high variance of the Tg values, the autonomy could not consistently be predicted with the Tg level in individual cases. The patients with Hashimoto’s thyroiditis showed slightly decreased Tg levels. In Graves’ disease, a significantly higher average Tg level was observed compared with a matched group with diffuse goiter, but 47% of all Tg values were still in the normal range (< 30 ng/ml). Conclusion: Elevated Tg levels indicate a high probability of thyroid diseases, such as malignancy, autonomy or Graves’ disease. However, as low Tg concentrations cannot exclude the respective disorder, a routine Tg determination seems not to be justified in benign thyroid diseases.

A sensitive method for assaying thyroid stimulating immunoglobulins of Graves' disease: use of the guanyl nucleotide-amplified thyroid adenylate cyclase assay

1983 ◽  
Vol 103 (3) ◽  
pp. 345-351 ◽  
Author(s):  
E. Macchia ◽  
P. Carayon ◽  
G. F. Fenzi ◽  
S. Lissitzky ◽  
A. Pinchera
Keyword(s):  
Adenylate Cyclase ◽  
Hashimoto’S Thyroiditis ◽  
Plasma Membranes ◽  
Hashimoto's Thyroiditis ◽  
Graves Disease ◽  
Tissue Preparation ◽  
Thyroid Cells ◽  
Significant Stimulation ◽  
Adenylate Cyclase Stimulation ◽  
Sensitive Method

Abstract. The purpose of this study was to develop and validate a sensitive method for evaluating adenylate cyclase stimulation by thyroid-stimulating antibodies (TSAb), based on the measurement of thyroid membrane adenylate cyclase activity in the presence of a non-hydrolyzable GTP analogue, guanyl-5'-yl imidodiphosphate (Gpp(NH)p). The addition of Gpp(NH)p (10−5 m) produced a 10-fold increase of the sensitivity of the system for both TSH and TSAb. Immunoglobulin G preparations from sera of 30 patients with Graves' disease were tested for the adenylate cyclase stimulation either in the presence or in the absence of Gpp(NH)p: a significant stimulation was observed in 27/30 patients when the GTP analogue was added to the system, while only 20/30 patients were positive in the absence of the nucleotide. The advantage of Gpp(NH)p addition was also evident in a large series which included 57 patients with Graves' disease, 15 with Hashimoto's thyroiditis or primary myxoedema and 22 normal subjects. In fact, 88% of patients with Graves' disease resulted positive, while no significant stimulation was elicited by Hashimoto's thyroiditis, primary myxoedema and by normal immunoglobulins. The sensitivity achieved in our system which employs thyroid plasma membranes was similar to that obtained by other investigators with the use of thyroid slices or thyroid cells in primary culture. Furthermore, methods based on thyroid plasma membranes are supposed to have a better reproducibility, since the same tissue preparation, if appropriately stored, may be used in several different tests.

scholarly journals Defect of a subpopulation of natural killer immune cells in Graves’ disease and Hashimoto’s thyroiditis: normalizing effect of dehydroepiandrosterone sulfate

2005 ◽  
Vol 152 (5) ◽  
pp. 703-712 ◽  
Author(s):  
Sebastiano Bruno Solerte ◽  
Sara Precerutti ◽  
Carmine Gazzaruso ◽  
Eleonora Locatelli ◽  
Mauro Zamboni ◽  
...  
Keyword(s):  
Nk Cells ◽  
Hashimoto’S Thyroiditis ◽  
Nk Cell ◽  
Secretory Activity ◽  
Thyroid Diseases ◽  
Hashimoto's Thyroiditis ◽  
Graves Disease ◽  
Autoimmune Thyroid Diseases ◽  
Autoimmune Thyroid ◽  
Tnf Α

Background: The study of the natural killer (NK) immune compartment could provide important findings to help in the understanding of some of the pathogenetic mechanisms related to autoimmune thyroid diseases (Graves’ disease (GD) and Hashimoto’s thyroiditis (HT)). Within this context, it was suggested that alterations in NK cell cytotoxicity (NKCC) and NK production of cytokines might occur in subjects with GD and HT, whereas the normalization of NK functions could potentially contribute to the prevention of the onset or the progression of both diseases. Objective: Due to the hypothesis of alterations in NK in autoimmune thyroid diseases, we were interested to evaluate NKCC in GD and HT patients and to modulate NK function and secretory activity with cytokines and dehydroepiandrosterone sulfate (DHEAS) in an attempt to normalize NK cell defect. Design: We studied 13 patients with recent onset Graves’ disease, 11 patients with Hashimoto’s thyroiditis at first diagnosis and 15 age-matched healthy subjects. Methods: NK cells were concentrated at a density of 7.75 × 106 cells/ml by negative immunomagnetic cell separation and validated by FACScan as CD16 + /CD56 + cells. NK cells were incubated with interleukin-2 (IL-2) and interferon-β (IFN-β) and co-incubated with DHEAS at different molar concentrations for measuring NKCC and the secretory pattern of tumor necrosis factor-α (TNF-α) from NK cells. Results: Lower spontaneous, IL-2- and IFN-β-modulated NKCC was demonstrated in GD and HT patients compared with healthy subjects (P < 0.001). A decrease in spontaneous and IL-2-modulated TNF-α release from NK cells was also found in both groups of patients (P < 0.001). The co-incubation of NK cells with IL-2/IFN-β + DHEAS at different molar concentrations (from 10−8 to 10−5 M/ml/NK cells) promptly normalized NKCC and TNF-α secretion in GD and HT patients. Conclusions: A functional defect of a subpopulation of NK immune cells, involving both NKCC and the secretory activity, was demonstrated in newly-diagnosed GD and HT patients. This defect can be reversed by a dose-dependent treatment with DHEAS. The impairment of NK cell activity in autoimmune thyroid diseases could potentially determine a critical expansion of T/B-cell immune compartments leading to the generation of autoantibodies and to the pathogenesis of thyroid autoimmunity.

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