scholarly journals Coexistence of Thyroid Hormone Resistance and Autoimmune Thyroid Disease: Not a Mere Coincidence

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A924-A925
Author(s):  
Helen Prathiba Gnanapragasam ◽  
Amrutha Idupuganti ◽  
Salman Zahoor Bhat
Keyword(s):  
Thyroid Hormone ◽  
Autoimmune Thyroiditis ◽  
Hashimoto’S Thyroiditis ◽  
Alpha Subunit ◽  
Hashimoto's Thyroiditis ◽  
Thyroid Peroxidase ◽  
Thyroid Autoantibodies ◽  
Hormone Resistance ◽  
Free T4 ◽  
Thyroid Hormone Resistance

Abstract Introduction: The coexistence of thyroid hormone resistance and autoimmune thyroiditis was initially thought to be a chance event. In a large cohort study, Barcoff et al. demonstrated an increased likelihood of thyroid autoantibodies in patients with thyroid hormone resistance (RTH). We report a unique case to epitomize the coexistence of these two conditions and discuss the postulated mechanisms. Clinical Case: A 22-year-old woman with a history of Hashimoto’s thyroiditis, attention deficit hyperactivity disorder, and migraine presented to the endocrinology clinic with symptoms of weight loss, fatigue, decreased appetite, and heat intolerance for 4 months. She was diagnosed with Hashimoto’s thyroiditis at age 12 with elevated TSH only and had been on levothyroxine 25 mcg since diagnosis. Physical exam demonstrated a body mass index of 34.14 kg/m2, blood pressure of 138/91 mmHg, pulse of 77 bpm, and an enlarged palpable thyroid gland. Laboratory investigations revealed elevated thyroid peroxidase (TPO) antibody at 234 IU/mL (<9) and thyroglobulin Antibody at 3 IU/mL (<1) with elevated free T4 of 3.76 ng/dL (0.61-1.36), elevated total T4 of 21.58 mcg/dL (6.09-12.23), increased T3 uptake of 51.2% uptake (32-48.4), and upper normal TSH of 3.99 uIU/mL (0.44-5.33). Elevated free T4 was confirmed by the equilibrium dialysis method at 6.2 ng/dL (0.9-2.2) with upper normal TSH at 3.77 uIU/mL. Thyroid ultrasound demonstrated thyromegaly and hypervascularity of the gland. TSH secreting pituitary adenoma was ruled out with a normal alpha subunit of 0.2 ng/ml (0.1-0.6) and molar ratio of the alpha subunit to TSH ratio <1 along with a normal pituitary MRI. She was not taking other medications or supplements. She was diagnosed with thyroid hormone resistance and is undergoing genetic testing to differentiate the THRB genetic mutations from Non-TR-RTH. Her symptoms improved after discontinuing her levothyroxine. Clinical Lesson: Our case highlights the importance of evaluating thyroid disorders properly before starting treatment and illustrates the coexistence of autoimmune thyroiditis with thyroid hormone resistance. Barcoff et al. demonstrated that there was an increased likelihood of thyroid autoantibodies with odds ratio = 2.36 (p = 0.002) in a large patient cohort with RTH, compared to their unaffected first-degree relatives. However, since there was no correlation in increased antibody with increased age and the duration of the disease, the proposed hypothesis did not substantiate chronic TSH stimulation inducing autoimmune response. The proposed mechanism is that the elevated TSH in RTH stimulates the immune system at the TRα level which was demonstrated in murine models with increased activation of thymic function in correlation with TSH level. More research is needed to understand the underlying mechanism of their coexistence.

scholarly journals Angioedema in a Patient with Autoimmune Thyroiditis – A Case Report

2020 ◽  
Vol 47 (2) ◽  
pp. 34-37
Author(s):  
S. Dermendzhiev ◽  
A. Dzhambov ◽  
T. Dermendzhiev
Keyword(s):  
Autoimmune Thyroiditis ◽  
Hashimoto’S Thyroiditis ◽  
Immunoglobulin E ◽  
Thyroid Autoimmunity ◽  
Hormonal Control ◽  
Hashimoto's Thyroiditis ◽  
Thyroid Peroxidase ◽  
Normal Range ◽  
History Of ◽  
One Year

AbstractWe present a case of a 29-year-old Bulgarian woman with autoimmune thyroiditis and recurrent angioedema. The patient presented with a one-year-long history of recurrent angioedema and Hashimoto’s thyroiditis. Physical examination showed oedema surrounded by erythema on the forearms, and erythematous, itchy plaques spreading over her face, neck, chest, abdomen, and extremities. Blood tests showed elevated total immunoglobulin E (IgE). The patient had been diagnosed with Hashimoto’s thyroiditis and hypothyroidism. She had been taking levothyroxine 50 μg/d, resulting in a good hormonal control; however, her anti-thyroid peroxidase (anti-TPO) antibodies were high. She was started on methylprednisolone and antihistamines. In three weeks, we observed a good therapeutic response to the treatment and the lesions remitted. IgE dropped within normal range. Levels of anti-TPO antibodies were persistently high. In conclusion, patients with angioedema should be tested for thyroid autoimmunity. Further delve into the pathogenesis of angioedema in them is warranted in order to explore the possibility of an underlying atopy in those not responding to the standard treatment with levothyroxine.

scholarly journals Thyroid Hormone Resistance With Concurrent Papillary Thyroid Cancer

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A961-A962
Author(s):  
Dhivya Pahwa ◽  
Michael Howard Shanik
Keyword(s):  
Thyroid Cancer ◽  
Thyroid Hormone ◽  
Papillary Thyroid Carcinoma ◽  
Thyroid Carcinoma ◽  
Thyroid Hormone Receptor ◽  
Hormone Resistance ◽  
Papillary Thyroid ◽  
Free T4 ◽  
Thyroid Hormone Resistance ◽  
History Of

Abstract Introduction: Thyroid hormone resistance is a genetic mutation resulting in decreased receptor responsiveness. We present a case of thyroid hormone resistance with concurrent papillary thyroid cancer. Clinical Case: A 34-year-old man with a history of papillary thyroid carcinoma status post total thyroidectomy and radioactive iodine. He had transferred his care after moving to our area. He presented with persistently elevated TSH despite ongoing treatment with Levothyroxine 400 mcg daily. Upon presentation the patient reported intermittent palpitations and tremor. Vital signs revealed height of 74 inches, weight of 235 pounds, blood pressure of 112/64, and heart rate of 48. Physical examination revealed a well -healed scar on the neck without palpable lymphadenopathy. Bloodwork revealed TSH of 15.28 mIU/L and Free T4 of 2.8 ng/dL. The patient was maintained on Levothyroxine 400 mcg daily and educated on proper administration of the medication. Two months later, bloodwork revealed a TSH of 9.22 mIU/L with a Free T4 of 3.3 ng/dL. MRI of the pituitary revealed a 4mm hyper-intensity which likely represented a microadenoma. Resistance Thyroid Hormone (RTH) Mutation analysis was ordered which revealed a heterozygous mutation for the Thyroid Hormone Receptor (THR)-Beta gene. The mutation was detected at pArg438His indicating a single nucleotide substitution leading to the replacement of arginine by histidine at the p.438 of the translated protein on exon 10. The patient was maintained on Levothyroxine at 400 mcg daily. Discussion: Thyroid hormone resistance describes a constellation of symptoms from decreased tissue responsiveness to thyroid hormones. Literature reveals the prevalence of THR to be 1 in 40,000 individuals. It occurs due to mutation on the thyroid hormone receptor, most often found on the alpha or beta subunit. Frequently patients present with tachycardia and hyperactivity but it can also present with symptoms suggestive of hypothyroidism and goiter. Risk factors include family history of RTH mutation often with an autosomal dominant inheritance pattern. Patients with an elevated Free T4 with a non-suppressed TSH should be investigated with a genetic analysis of Resistance Thyroid hormone. A positive mutation would confirm the diagnosis. Close monitoring of symptoms as well as thyroid function tests should guide treatment. The concurrent diagnosis of thyroid hormone resistance in conjunction with papillary thyroid carcinoma in our patient is unique and makes management a challenge. The literature reveals few cases reported. Reference: DynaMed. (2018, November 30). Thyroid Hormone Resistance. Retrieved October 2, 2020, from https://www-dynamed-com.arktos.nyit.edu/topics/dmp~AN~T912485 Igata M, et al. Coexistence of resistance to thyroid hormone and papillary thyroid carcinoma. Endocrinol Diabetes Metab Case Rep. 2016;2016:160003. doi:10.1530/EDM-16-0003

Inhibition by immunoglobulin G of synthesis of thyroid hormone in thyroid cultures from hypothyroid patients with goitrous Hashimoto's thyroiditis

1990 ◽  
Vol 123 (5) ◽  
pp. 511-518 ◽  
Author(s):  
Jaeduk Noh ◽  
Noboru Hamada ◽  
Hifumi Saito ◽  
Midori Yoshimoto ◽  
Hiroyuki Iwasaki ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Peroxidase Activity ◽  
Immunoglobulin G ◽  
Hashimoto’S Thyroiditis ◽  
Thyroid Tissue ◽  
Hashimoto's Thyroiditis ◽  
Thyroid Peroxidase ◽  
Hormone Synthesis ◽  
Microsomal Antibody ◽  
Hypothyroid Patients

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.

scholarly journals Thyroid Function in Rubinstein-Taybi Syndrome*

1997 ◽  
Vol 82 (10) ◽  
pp. 3264-3266
Author(s):  
David P. Olson ◽  
Ronald J. Koenig
Keyword(s):  
Mental Retardation ◽  
Thyroid Hormone ◽  
Binding Protein ◽  
Hormone Deficiency ◽  
Hormone Resistance ◽  
Creb Binding Protein ◽  
Normal Range ◽  
Free T4 ◽  
Genetic Syndrome ◽  
Thyroid Hormone Resistance

Abstract Rubinstein-Taybi syndrome (RTS) is a genetic syndrome characterized by broad thumbs and halluces, growth retardation, mental retardation, and craniofacial abnormalities. This condition recently was found to be caused by mutations in the gene encoding cAMP response element-binding protein (CREB)-binding protein. As CREB-binding protein has been shown to be a critical coactivator for thyroid hormone receptors, it is plausible that RTS would be characterized by thyroid hormone resistance. In fact, features of RTS, such as mental retardation and short stature, are consistent with thyroid hormone deficiency or resistance. To assess the function of the thyroid axis in RTS, free T4 and TSH were measured in 12 subjects with this syndrome. The free T4 level was normal in all 12 (mean ± sd, 0.97 ± 0.20 ng/dL; normal range, 0.73–1.79), as was the TSH level (2.24 ± 0.87 μU/mL; normal range, 0.3–6.5). Thus, overt thyroid hormone resistance does not appear to be a typical feature of RTS.

scholarly journals Thyroid Autoantibodies Are Rare in Nonhuman Great Apes and Hypothyroidism Cannot Be Attributed to Thyroid Autoimmunity

Endocrinology ◽  
2013 ◽  
Vol 154 (12) ◽  
pp. 4896-4907 ◽  
Author(s):  
Holly Aliesky ◽  
Cynthia L. Courtney ◽  
Basil Rapoport ◽  
Sandra M. McLachlan
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Autoimmunity ◽  
Great Apes ◽  
Normal Serum ◽  
Thyroid Peroxidase ◽  
Thyroid Autoantibodies ◽  
Free T4 ◽  
Hormone Levels ◽  
Free T3 ◽  
Thyroid Hormone Levels

The great apes include, in addition to Homo, the genera Pongo (orangutans), Gorilla (gorillas), and Pan, the latter comprising two species, P. troglodytes (chimpanzees) and P. paniscus (bonobos). Adult-onset hypothyroidism was previously reported in 4 individual nonhuman great apes. However, there is scarce information on normal serum thyroid hormone levels and virtually no data for thyroid autoantibodies in these animals. Therefore, we examined thyroid hormone levels and TSH in all nonhuman great ape genera including adults, adolescents, and infants. Because hypothyroidism in humans is commonly the end result of thyroid autoimmunity, we also tested healthy and hypothyroid nonhuman great apes for antibodies to thyroglobulin (Tg), thyroid peroxidase (TPO), and the TSH receptor (TSHR). We established a thyroid hormone and TSH database in orangutans, gorillas, chimpanzees, and bonobos (447 individuals). The most striking differences are the greatly reduced free-T4 and free-T3 levels in orangutans and gorillas vs chimpanzees and bonobos, and conversely, elevated TSH levels in gorillas vs Pan species. Antibodies to Tg and TPO were detected in only 2.6% of adult animals vs approximately 10% in humans. No animals with Tg, TPO, or TSHR antibodies exhibited thyroid dysfunction. Conversely, hypothyroid nonhuman great apes lacked thyroid autoantibodies. Moreover, thyroid histology in necropsy tissues was similar in euthyroid and hypothyroid individuals, and lymphocytic infiltration was absent in 2 hypothyroid animals. In conclusion, free T4 and free T3 are lower in orangutans and gorillas vs chimpanzees and bonobos, the closest living human relatives. Moreover, thyroid autoantibodies are rare and hypothyroidism is unrelated to thyroid autoimmunity in nonhuman great apes.

Innapropriate TSH secretion: the challenging diagnosis

2016 ◽  
Vol 62 (5) ◽  
pp. 79-80 ◽  
Author(s):  
Nélson Cunha ◽  
Leonor Gomes ◽  
Luís Cardoso ◽  
Nuno Vicente ◽  
Diana Martins ◽  
...  
Keyword(s):  
Pituitary Adenoma ◽  
Thyroid Hormone ◽  
Genetic Test ◽  
Elevated Serum ◽  
Hormone Resistance ◽  
Free T4 ◽  
Resistance To Thyroid Hormone ◽  
Thyroid Hormone Resistance ◽  
Free T3 ◽  
Tsh Secretion

Background. The elevation of thyroid hormone with a normal or elevated TSH occurs uncommonly. This has different causes and pose a diagnosis challenge namely between TSH-secreting pituitary adenoma (TSHoma) and resistance to thyroid hormone. The accurate diagnosis is essential, because delayed diagnosis of TSHoma can lead to tumour growth and poor surgical cure rates, whereas medical, surgical or radioablative treatments in patients with resistance to thyroid hormone are usually unnecessary and potentially harmful.Case Report. A 23-years-old women with palpitations, fatigue, insomnia and exophthalmia with elevated serum free T4 and TSH, medicated with methimazole 5mg 3id was sent to evaluation in endocrinology department. She did not report headaches or visual problems. Patient’s laboratory tests at admission: TSH 9,6 µUI/mL (0,4–4,0 µUI/mL), Free T4 2,1 pg/dL (0,8–1,9 pg/dL). After stopping anti-thyroid drug presented TSH 2,9 µUI/mL (0,4-4,0 µUI/mL), Free T4 3,7 pg/dL (0,8–1,9 pg/dL), Free T3 11 pg/mL (1,8–4,2 pg/mL); antithyroid peroxidase and antithyroglobulin antibodies and thyroid stimulating immunoglobulin were undetectable; thyroid ultrasound revealed small heterogeneous goiter; thyroid technetium scintigraphy showed diffuse glandular hyperfunctioning; Magnetic resonance imaging revealed a microadenoma with 7,5mm in the left side of pituitary. Remaining anterior pituitary hormones were within normal ranges. The thyrotropin-releasing hormone stimulation test was performed and revealed TSH at 0’ 1,7 µUI/mL, 20’ 14 µUI/mL and 60’ 11 µUI/mL, with free T4 2,3 pg/dL and free T3 5,9 pg/mL, which was consistent with thyroid hormone resistance syndrome. In this clinical setting genetic test was performed and revealed mutation in heterozygosity in THRβ gene: c.1030G>A, p.Gly344Arg. Patient’s mother was also tested and no mutation was found. Her father was not available to do the genetic test. No pituitary surgery or thyroidectomy was performed, nor were prescribed any anti-thyroid drugs.Conclusions. In this case, an innapropriate TSH secretion was identified and the clinical, biochemical and genetic investigations were consistent with resistance to thyroid hormone. Known that as many as 15% non-ill people may have a small, nonfunctioning pituitary adenoma, patients with thyroid hormone resistance may have incidentally abnormal imaging findings. The high level of clinical suspicion and the proper laboratory, genetic and radiological studies, conduct to a correct diagnosis and prevent unnecessary and potential harmful therapies.

scholarly journals Serum resolvin E1 levels and its relationship with thyroid autoimmunity in Hashimoto’s thyroiditis: a preliminary study

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Jing Song ◽  
Rongxin Sun ◽  
Yuanyuan Zhang ◽  
Jing Ke ◽  
Dong Zhao
Keyword(s):  
Hashimoto’S Thyroiditis ◽  
Protective Factor ◽  
Thyroid Autoimmunity ◽  
Hashimoto's Thyroiditis ◽  
Enzyme Linked Immunosorbent Assay ◽  
Thyroid Peroxidase ◽  
Healthy Controls ◽  
Omega 3 ◽  
Free T4 ◽  
Ordinal Logistic Regression Analysis

Abstract Background Omega-3 polyunsaturated fatty acids (PUFAs) produce lipid mediators with both anti-inflammatory and pro-resolution properties, including resolvins. The purpose of this study was to detect serum resolvin E1 (RVE1) levels in Hashimoto’s thyroiditis (HT) patients and healthy controls (HCs) and to evaluate the relationship of RVE1 with thyroid autoimmunity. Methods A total of 57 participants were recruited, including 30 untreated HT patients and 27 age- and sex‐matched HCs. The levels of RVE1 in serum were measured via enzyme-linked immunosorbent assay (ELISA). An electrochemiluminescence immunoassay was used for the measurement of thyroid-stimulating hormone (TSH), total T4 (TT4), TT3, free T4 (FT4), FT3, anti-thyroid peroxidase antibody (TPOAb) and anti-thyroglobulin antibody (TgAb) levels. Hemogram tests and routine biochemical analyses were performed on each sample. Results The serum level of RVE1 of HT patients (24.09, 15.76–34.38 pg/mL) was significantly lower than that of healthy controls (28.51, 20.76–51.23 pg/mL) (P = 0.027). RVE1 levels showed a downward trend with increasing TgAb levels (P for trend = 0.001). Multivariable ordinal logistic regression analysis showed that RVE1 levels were negatively correlated with increasing TgAb levels in both the unadjusted (OR = 0.9446, 95 % CI = 0.9111–0.9782, P = 0.002) and adjusted models (OR = 0.9380, 95 % CI = 0.8967–0.9811, P = 0.005). Conclusions Decreased RVE1 levels might be a sign that HT is associated with inflammatory resolution dysfunction. RVE1 may serve as a protective factor against increased TgAb levels.

Challenging diagnosis of thyroid hormone resistance initially as Hashimoto’s thyroiditis

2019 ◽  
Vol 32 (2) ◽  
pp. 203-206 ◽  
Author(s):  
Tong Wooi Ch’ng ◽  
Vivian L. Chin
Keyword(s):  
Thyroid Hormone ◽  
Hashimoto’S Thyroiditis ◽  
Hashimoto's Thyroiditis ◽  
Heterozygous Mutation ◽  
Thyroid Peroxidase ◽  
Thyroid Function Tests ◽  
Resistance To Thyroid Hormone ◽  
Hyperactivity Disorder ◽  
Thyroid Peroxidase Antibody ◽  
High Index Of Suspicion

Abstract Background Resistance to thyroid hormone (RTH) commonly presents with goiter, attention deficit hyperactivity disorder (ADHD), short stature and tachycardia. However, due to its variable presentation with subtle clinical features, a third of the cases are mistreated, typically as hyperthyroidism. Case presentation A 15-year-old female with ADHD and oligomenorrhea was initially diagnosed as Hashimoto’s thyroiditis but found to have a rare heterozygous mutation in c803 C>G (p Ala 268 Gly) in the THRβ gene, confirming resistance to thyroid hormone. Conclusions Fluctuating thyroid function tests in addition to thyroid peroxidase antibody (TPO Ab) positivity complicated the diagnosis of RTH, initially diagnosed as Hashimoto’s thyroiditis. A high index of suspicion is needed to prevent misdiagnosis and mistreatment.

scholarly journals Alexithymia, Emotional Distress, and Perceived Quality of Life in Patients With Hashimoto’s Thyroiditis

2021 ◽  
Vol 12 ◽  
Author(s):  
Gabriella Martino ◽  
Andrea Caputo ◽  
Carmelo M. Vicario ◽  
Ulla Feldt-Rasmussen ◽  
Torquil Watt ◽  
...  
Keyword(s):  
Quality Of Life ◽  
Hashimoto’S Thyroiditis ◽  
Hashimoto's Thyroiditis ◽  
Thyroid Peroxidase ◽  
Thyroid Autoantibodies ◽  
Somatic Anxiety ◽  
Somatic Illness ◽  
Significant Difference ◽  
Toxic Goiter

Emotion-processing impairment represents a risk factor for the development of somatic illness, affecting negatively both health-related quality of life (HRQoL) and disease management in several chronic diseases. The present pilot study aims at (i) investigating the associations between alexithymia and depression, anxiety, and HRQoL in patients with Hashimoto’s thyroiditis (HT); (ii) examining the association between these three psychological conditions together with HRQoL, and thyroid autoantibodies status as well as thyroid echotexture in patients with HT; and (iii) comparing the intensity of all these clinical psychological features in patients with HT versus controls. Twenty-one patients with serologically or ultrasonographically verified HT and 16 controls with non-toxic goiter or postsurgical hypothyroidism were recruited for this study. Serum thyrotropin (TSH) and free thyroxine, as well as thyroid autoantibodies (thyroglobulin antibodies and thyroid peroxidase antibodies), were assayed. Alexithymia, depression, anxiety, and HRQoL were assessed with Toronto Alexithymia Scale; Beck Depression Inventory, second edition; Hamilton Anxiety Rating Scale; and Health Survey Short-Form 36, respectively. A negative relationship between the difficulty to describe feelings and the cognitive component of depression was found (r = -0.46, p = 0.04). Besides, patients with seronegative HT had lower somatic anxiety than patients with HT who tested positive (r = -0.68, p = 0.01 and r = -0.59, p = 0.04, respectively). Besides, no statistically significant difference was found between patients with HT and controls with regard to somatic anxiety. The present study suggests the relevance of alexithymia in patients suffering from HT, which may be intertwined with a possible state of underreported depression that is mainly expressed through physical complaints. Promoting the capability to describe and communicate feelings could contribute to psychological elaboration and coping with the disease and, consequently, to the improvement of self-management and perceived HRQoL.

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