Course Of Hyperthyroidism Research Articles

A sight into the pathogenesis and treatment of thyroid-associated ophthalmopathy

Introduction and aim. Thyroid-associated ophthalmopathy (TAO), often referred to as thyroid eye disease or Graves’ ophthalmopathy, is a syndrome characterized by autoimmune inflammation affecting the eye muscles, connective tissue, and orbital fat. The aim of this literature review is to present TAO and integrate the available data in the literature regarding the pathogenesis and treatment methods. Based on these, the authors aim to examine whether, despite the extensive knowledge already available on TAO, there are still issues to be investigated. Material and methods. In this literature review, books and scientific publications in both Polish and English languages have been assessed. The search criteria included keywords such as TAO, Graves’ disease, thyroid-associated ophthalmopathy. The evaluation covered the following databases: PubMed, Scopus, Google Scholar. Analysis of the literature. Typically, the eyeball is not involved, but in exceptional cases, corneal ulceration may occur, or inflammation of the optic nerve may ensue. TAO most commonly occurs in the course of hyperthyroidism in Graves’ disease, involving up to 25–50% of cases. The coexistence of autoantigens shared between the thyroid and orbital tissues is considered the primary cause of TAO when it occurs concurrently with hyperthyroidism, later in its course, or even preceding the manifestation of hyperthyroidism, with or without concurrent thyroid dysfunction. TAO is generally bilateral, although dominance on one side is often observed. Common symptoms include eye pain, photophobia, diplopia, varying degrees of proptosis, and impaired vision. The cornerstone of treatment lies in managing hyperthyroidism, as TAO cannot be cured without it. Conclusion. First-line treatment involves glucocorticoids, with radiation therapy as a supplementary option, and in cases unresponsive to pharmacological treatment, surgical intervention may be necessary.

AN ACUTE PSYCHOSIS REVEALING HYPERTHYROIDISM: A CASE REPORT

Psychiatric presentations may be a discovery circumstance for hyperthyroidism, but may also delay the diagnosis. The occurrence of psychotic disorders is rarely described during the course of hyperthyroidism. The link between these two conditions remains unclear. We report in this study a clinical case of psychotic disorders induced by hyperthyroidism.

A case of latent course of thyrotoxicosis with predominantly hepatic manifestations

Thyrotoxic hepatitis develops in 55-60% of patients with hyperthyroidism, it is often asymptomatic and diagnosed incidentally. The article describes a clinical case of thyrotoxic hepatitis in a 50-year-old female. The case seems to be rare as the overt signs of hyperthyroidism manifested in the patient 5 months later than the changes in liver function tests in blood. The current data on the epidemiology, pathogenesis and clinical picture of liver damage in thyrotoxicosis are represented in discussion.

OR11-3 Steroid Treatment in the Management of Destructive Thyrotoxicosis Induced by PD1 Blockade

Abstract Background Destructive thyroiditis is the most common endocrine immune related adverse event (iRAEs) in patients treated with anti-PD1/PD-L1 agents. Given its self-limited course, current guidelines recommend no treatment for this iRAE. Nevertheless in patients with enlarged thyroid volume and a poor performance status, thyrotoxicosis may be particularly severe and harmful. Aim of the study is to evaluate if steroid treatment might be useful in improving thyrotoxicosis in subjects with a poor performance status. Methods We conducted a case-control study, comparing the course of thyrotoxicosis of 4 patients treated with oral prednisone at the dosage of 25 mg/d (tapered to discontinuation in three weeks) and an enlarged thyroid volume to that of 8 patients with similar thyroid volume who were left untreated. Results No difference was found between the two groups at the onset of thyrotoxicosis (time 0) in demographic characteristics and in the levels of thyroid hormones. The levels of thyroid hormones were lower in subjects treated with prednisone compared to those untreated at time 7, 14, 21, 28, 35, 42, 60 and 90 days (P<0.05 at each time). The median time to remission of thyrotoxicosis was 24 days in patients treated with steroids and 92 days in untreated patients (P<0.001). At 6 months, the rate of evolution to hypothyroidism was similar in the 2 groups (4/4 in steroid group vs 7/8 in untreated group, P=0.74) and no difference was found in tumor progression (Progression free survival in treated group 5.1 months vs 5.0 months in untreated patients, P=0.89). Conclusion A short period of prednisone therapy is useful to restore more quickly euthyroidism in patients with a poor performance status and a severe destructive thyrotoxicosis induced by PD-1 blockade. This treatment does not impair the efficacy of immunotherapy. Presentation: Sunday, June 12, 2022 11:30 a.m. - 11:45 a.m.

Steroid treatment in the management of destructive thyrotoxicosis induced by PD1 blockade.

ObjectiveDestructive thyroiditis is the most common endocrine immune-related adverse event (iRAEs) in patients treated with anti-PD1/PD-L1 agents. Given its self-limited course, current guidelines recommend no treatment for this iRAE. Nevertheless, in patients with enlarged thyroid volume and a poor performance status, thyrotoxicosis may be particularly severe and harmful. The aim of the study is to evaluate if steroid treatment might be useful in improving thyrotoxicosis in subjects with a poor performance status.MethodsWe conducted a retrospective study, comparing the course of thyrotoxicosis of four patients treated with oral prednisone at the dosage of 25 mg/day (tapered to discontinuation in 3 weeks) and an enlarged thyroid volume to that of eight patients with similar thyroid volume who were left untreated.ResultsThe levels of thyroid hormones were lower in subjects treated compared to those untreated at time of 7, 14, 21, 28, 35, 42, 60 and 90 days (P < 0.05 at each time). The time to remission of thyrotoxicosis was 24 days in patients treated with steroids and 120 days in untreated patients (P < 0.001). At 6 months, the rate of evolution to hypothyroidism was similar in the two groups (4/4 in the steroid group vs 7/8 in the untreated group, P = 0.74) and no difference was found in tumor progression (P = 0.89).ConclusionsOur preliminary data suggest that in patients with a poor performance status experiencing a severe destructive thyrotoxicosis induced by PD-1 blockade, a short period of administration of oral prednisone is effective in obtaining a quick reduction of the levels of thyroid hormones.

A case of thyrotoxicosis-induced anemia in a patient with painless thyroiditis

BackgroundThere have been several reports of secondary anemia associated with Graves’ disease. There are no reports of secondary anemia resulting from thyrotoxicosis due to painless thyroiditis (silent thyroiditis). We report the case of a patient with pancreatic diabetes who developed anemia caused by thyrotoxicosis due to painless thyroiditis.Case presentationThe patient was a 37-year-old man who visited the hospital complaining of fatigue, palpitations, and dyspnea. His hemoglobin was 110 g/l (reference range, 135–176), and mean corpuscular volume was 81.5 fl (81.7–101.6). His free thyroxine (FT4) was high, at 100.4 pmol/l (11.6–21.9); the free triiodothyronine (FT3) was high, at 27.49 pmol/l (3.53–6.14); TSH was low, at < 0.01 mIU/l (0.50–5.00); and TSH receptor antibody was negative. Soluble IL-2 receptor (sIL-2R) was high, at 1340 U/ml (122–496); C-reactive protein (CRP) was high, at 6900 μg/l (< 3000); and reticulocytes was high, at 108 109 /l (30–100). Serum iron (Fe) was 9.5 (9.1–35.5), ferritin was 389 μg/l (13–401), haptoglobin was 0.66 g/l (0.19–1.70. Propranolol was prescribed and followed up. Anemia completely disappeared by 12 weeks after disease onset. Thyroid hormones and sIL-2R had normalized by 16 weeks after onset. He developed mild hypothyroidism and was treated with L-thyroxine at 24 weeks.ConclusionsThis is the first case report of transient secondary anemia associated with thyrotoxicosis due to painless thyroiditis. The change in sIL-2R was also observed during the clinical course of thyrotoxicosis and anemia, suggesting the immune processes in thyroid gland and bone marrow.

Thyrotoxic Hepatitis In A Patient With Subacute Thyroiditis: A Case Report

Subacute granulomatous thyroiditis (DeQuervain's disease) is a self-limiting inflammatory disease which is often diagnosed in the ”temporary thyrotoxicosis period" during the initial phases of the desease. Liver enzyme abnormalities can be seen in the course of thyrotoxicosis. The definition of "thyrotoxic hepatitis" is used to describe the elevation of liver enzymes after excluding other causes. In this case report, a female patient who developed thyrotoxic hepatitis in the course of her subacute thyroiditis, is reported to remind the importance of evaluating liver functions in the follow-up of subacute thyroiditis.

Prevalence and aetiology of thyrotoxicosis in patients with hyperemesis gravidarum presenting to a tertiary hospital in Cape Town, South Africa

The association between hyperemesis gravidarum (HG) and abnormal thyroid function is well known. The prevalence, aetiology and course of thyrotoxicosis in women with hyperemesis gravidarum (HG) wer...

Myocardial infarction as a first clinical manifestation of hyperthyroidism

Abstract Introduction Hyperthyroidism is a condition in which there is an increased secretion of thyroid hormones that exceeds the current needs of the body. Increased concentrations of hormones affect proper functioning of many organs and systems, including the cardiovascular system. Untreated hyperthyroidism may result in myocardial infarction (MI), which very rarely is its first clinical manifestation. Aim The aim of this work is to present the case of a male patient with no previous symptoms, in whom ST segment elevation myocardial infarction (STEMI) occurred as the first clinical manifestation of hyperthyroidism. Case study Presentation and analysis of the case of a 41-year-old male admitted with clinical and electrocardiographic features of anterior wall STEMI in the course of hyperthyroidism. Results and discussion The cause of ischemia and MI in patients with no previous coronary artery disease is not fully known. Probable predisposing factors may include increased serum thyroid hormone concentrations. It enhances the vasoconstrictor effect of catecholamines and hyperkinetic circulation, which may be the potential causes of ischemia. In addition, it predisposes to a hypercoagulable state, which is the cause of coronary thrombosis. Conclusions It is not only high cholesterol levels and anemia that are the possible causes of MI. Endocrine disorders, such as hyperthyroidism should always be taken into account.

May dental extraction trigger subacute thyroiditis?

Searchable abstracts of presentations at key conferences in endocrinology ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Concomitant Graves Hyperthyroidism with Thyrotrophin-Secreting Pituitary Adenoma

The relationship of autoimmune thyroid disease and TSH-producing pituitary tumor is rarely found. We report two patients with hyperthyroidism, a 27-year-old man and a 28-year-old woman, who were diagnosed with Graves hyperthyroidism with elevated free thyroxine (FT4), suppressed TSH and positive thyrotropin receptor autoantibodies. After treatment with antithyroid drugs, FT4 did not return to normal, and serum TSH levels were found to be above-normal range. Pituitary tumors were subsequently found via pituitary magnetic resonance imaging (MRI). We suggest that Graves hyperthyroidism concomitant with TSH-producing pituitary tumor be kept in mind, as it may confuse the therapeutic course of hyperthyroidism and make it more complicated.

PRE- AND POSTTREATMENT ULTRASONOGRAPHY OF THE THYROID GLAND IN HYPERTHYROID CATS

Ultrasonography is useful for assessing the morphology of the thyroid gland in hyperthyroid cats. Our aim was to describe the ultrasonographic changes of the thyroid gland in hyperthyroid cats after 131I therapy. Ultrasonography was performed in 15 hyperthyroid cats at initial presentation and 6 months after 131I using a multifrequency linear transducer set at 12 MHz. The following criteria were evaluated: length, width, height, volume, shape, homogeneity, and vascularity, using Power Doppler. Pretreatment, 10 cats had bilaterally abnormal thyroid lobes, four cats one abnormal lobe with the contralateral lobe being normal or reduced in size, and one cat with one normal lobe and one lobe not visible. Six months after 131I therapy, there was a reduction in median volume from 819 to 210 mm3, reduced rounding, reduced heterogeneity, and decreased vascularity. In conclusion, ultrasonography may be used to monitor thyroid changes in order to assess 131I treatment response. Further studies are necessary to determine whether ultrasonography could contribute to the detection of a relapsing course of hyperthyroidism.

The T393C Polymorphism of the Gαs Gene (GNAS1) is Associated with the Course of Graves' Disease

Genotypes of the T393C SNP of GNAS1, a gene that encodes for the Galphas subunit of G proteins have been significantly associated with the clinical course in a variety of cancers. Since this SNP may also influence the course of Graves' disease (GD) and, especially, Graves' ophthalmopathy (GO), we determined genotype and allele frequency in a series of 359 patients, which were referred to our clinic within 6 months of the onset of GO. Among them, 336 patients also suffered from associated hyperthyroidism. Data on relapse and remission rates 12 months after termination of a 1 year antithyroid drug therapy was available for 276 patients. As controls, 820 healthy individuals were recruited. Our data suggest that the T393C SNP does not represent a risk factor for the development of both GD and GO. It was, however, significantly associated with the course of hyperthyroidism (p=0.013) and a similar trend was evident for the course of GO (p=0.093). Homozygous TT carriers showed a significantly increased risk (p=0.03) for hyperthyroidism to relapse (OR 2.4; 95% CI 1.1-5.4). Also, the TT genotype was associated with significantly increased serum TRAb levels (CC+CT: 5.4 IU/l vs. TT: 9.3 IU/l). This is probably caused by increased G-Protein susceptibility to TSHR-mediated stimulation through TRAb. Genotyping of the T393C SNP of GNAS1 may become a useful additional tool to predict the clinical course of GD and GO. This may allow the clinician to identify patients at risk for more severe courses of disease and to come to more timely decisions for treatment.

Detection of serum fibrosis markers in patients with autoimmune thyroid diseases

Obecfive To study the clinical significance of detecting serum proeollagen type Ⅲ(PCⅢ) and hyaluronie acid(HA)in patients with autoimmune thyroid diseases(AITD).Methods According to the thyroid function,the 114 patients with AITD were divided into hyperthyroidism group(38),hypothyroidism group(35),and sub-hypothyroidism group(41).In addition,40 healthy persons were served as controls.The level of serum PCⅢ was determined with ELISA and that of serum HA with RIA.The level of FT3,FT4 and sTSH were detected by immumnofluorometric assay.Results Serum FT3(18.35±6.19)pmol/L]and FT4[(76.28±23.49)pmol/L]level of patients with hyperthyroidism were obviously higher than those of the controls[(4.75±0.31),(16.12±3.27) pmol/L],but serum sTSH[(0.15±0.07)mU/L]was obviously lower than that of the control[(3.78±0.15)mU/L],the differences were statically significant(P＜0.01).Serum FT3[(3.36±0.26)pmol/L]and FT4 [(6.37±2.19) pmol/L]level of patients with hypothyroidism were both lower than those of the controls(P＜0.05).but serum sTSH[(44.58±13.29)mU/L]was obviously higher than that of the control(P＜0.01).Serum FT3 [(4.86±0.45)pmol/L]and FT4[(15.26±2.78)pmol/L]level of patients with sub-hypothyroidism had no statistical difference compared with those of the controls(P＞0.05),but serum sTSH[(14.26±4.73)mU/L] was obviously higher than that of the controls(P＜0.01).The level of sernm PCⅢ[(4.63±1.22)μg/L]in pafients with hyperthyroidism was significantly higher than that of any other group(P＜0.05).There waB no statistical significant difference in PCⅢ among the patients with hypothyroidism,the patients with sub-hypothyroidism and controls [(3.64±1.12),(3.54±1.17)and(3.56±1.07)μg/L],respectively(P＞0.05).The level of serum HA [(31.13±10.28)μg/L]in patients with hypothyroidism was significantly higher than that of any other group(P＜0.05).There was no statistical significant difference in HA among the patients with hyperthyroidism,the patients with sub-hypothyroidism and controls[(22.24±7.22),(22.43±7.99)and(23.09±9.19)μg/L,respectively,P＞0.05].Conclusions It is very significant to understand myocardial fibrosis early through detecting sernm PCⅢ in patients with hyperthyroidism.Measurement of serum PCⅢ and HA will be useful to discovery hepatic fibrosisearly in patients with a long course of hyperthyroidism. Key words: Thyroid diseases; Collagen type Ⅲ; Hyaluronic acid

Transient hyperthyroidism after total parathyroidectomy for tertiary hyperparathyroidism: A report of two cases

Surgical removal of enlarged parathyroid glands is the treatment of choice in most cases of tertiary renal hyperparathyroidism. Complications of this surgical procedure are rare. We report two cases of patients who developed acute hyperthyroidism after total parathyroidectomy with parathyroid autotransplantation for refractory tertiary hyperparathyroidism. The patients had no history or biochemical or radiologic evidence of thyroid disease. They were not taking drugs affecting thyroid function. Thyroid function (thyroid stimulating hormone, free T(3) and free T(4)) was measured preoperatively, immediately after surgery and again three months later. Total parathyroidectomy was successful in both patients. Circulating levels of parathyroid hormone were at the lower limit of normal values. Postoperative thyroid function tests demonstrated acute hyperthyroidism with a rapid increase in free T(3) and T(4) levels above normal and a drop in thyroid stimulating hormone below normal in both patients. The course of hyperthyroidism was short (normalization of fT(3) and fT(4) values within 14-21 days). Neither patient had symptoms of thyrotoxicosis. Transient hyperthyroidism may be an under-recognized complication of total parathyroidectomy for tertiary hyperparathyroidism. These patients should be monitored with thyroid function tests and assessed for clinical signs attributable to thyrotoxicosis.

Hypokalemic paralysis is not just a hypokalemic paralysis

Although the commonest form of hypokalemic paralysis is the hereditary variety, some patients during course of thyrotoxicosis or with chronic potassium depletion, may exhibit episodic weakness. Approach to the patient with hypokalemic paralysis should be a careful search for the etiology and potassium replacement therapy. In this report, two hypokalemic paralysis cases are described. Case 1 is a 29-year-old Caucasian male who developed thyrotoxic periodic paralysis. Case 2 is a 50-year-old female who experienced hypokalemic paralysis due to primary aldosteronism. Hypokalemic paralysis usually carries an underlying secret problem. Emergency department workers should give importance to etiological differentiation.

Intrahepatic cholestasis in subclinical and overt hyperthyroidism: two case reports

IntroductionNon-specific abnormalities in liver function tests might accompany the clinical course of hyperthyroidism. Hyperthyroidism can cause the elevation of hepatic enzymes and bilirubin. Jaundice is rare in overt hyperthyroidism, especially in subclinical hyperthyroidism. On the other hand, the use of anti-thyroid drugs has rarely been associated with toxic hepatitis and cholestatic jaundice.Case presentationHere we present two cases of cholestasis that accompanied two distinct forms of clinical hyperthyroidism. The first patient had a clinical presentation of severe cholestasis in the absence of congestive failure related to hyperthyroidism. The second case had developed intrahepatic cholestasis in the presence of subclinical hyperthyroidism, and improved with rifampicin treatment.ConclusionHyperthyroidism should be a consideration in non-specific liver dysfunction.

Hyperthyroidism after parathyroid exploration

We hypothesized that hyperthyroidism after parathyroid exploration may be an underreported phenomenon with a course more severe than recognized previously. We examined pre- and postoperative thyroid function and outcomes in 199 consecutive patients who, since March 2000, had parathyroid exploration for primary sporadic hyperparathyroidism (HPTH). We excluded patients with prior thyroid or parathyroid surgery, preoperative thyroid medication, concurrent total thyroidectomy, or follow-up <5 months. Of 125 patients with normal preoperative serum thyroid-stimulating hormone levels, 39 (31.2%) were hyperthyroid postoperatively. Mean thyroid-stimulating hormone levels (mean +/- SD) dropped with operation from 2.0 +/- 1.1 microIU/mL to 1.2 +/- 1.4 microIU/mL (P < .0001). Nineteen patients (15%) reported symptoms 1 to 2 weeks after operation. The clinical course of hyperthyroidism typically was short, but 5 patients (4%) had symptomatic hyperthyroxinemia requiring medical therapy. Hyperthyroidism was independent of age, severity of HPTH, anatomic/pathologic features, operative time, and other measures of operative difficulty, but was associated with lithium therapy, bilateral exploration, and absence of concurrent thyroid lobectomy. Risk of hyperthyroidism may be underappreciated after routine parathyroid surgery for HPTH. Use of lithium and degree of dissection appear contributory. Patients undergoing parathyroid exploration need counseling and surveillance for hyperthyroidism, which may be reduced by minimizing the extent of parathyroid surgery.

Graves' disease—associated changes in the serum lysosomal glycosidases activity and the glycosaminoglycan content

Background: This study was undertaken to elucidate the influence of Graves' hyperthyroidism upon the metabolism of proteoglycans (PGs), the extracellular matrix (ECM) components. We determined the serum activity of lysosomal hydrolases contributing to GAGs degradation ( N-acetyl-β- d-glucosaminidase, β- d-glucuronidase, β- d-galactosidase, α- d-mannosidase, β- d-xylosidase and α- l-fucosidase). An effect of Graves' hyperthyroidism on total serum GAGs content was also analysed. Methods: Blood samples were taken from 30 patients with newly diagnosed Graves' disease, prior to antithyroid treatment and after attainment of euthyroid state, as well as from 30 healthy individuals. Results: The activity of all investigated enzymes involved in GAGs degradation was found markedly increased in blood serum of patients with hyperthyroidism, except for α- d-mannosidase, which was not significantly modified. Antithyroid treatment with thiamazole resulted in normalization of the lysosomal glycosidases activity, so they no longer differed from the healthy subjects. The total glycosaminoglycans content in blood serum of patients with newly diagnosed untreated Graves' disease significantly increased compared to control group. Following thiamazole therapy total serum amount of GAGs decreased significantly, but was still markedly increased as compared to serum of healthy individuals. Conclusions: The obtained results indicate that Graves' hyperthyroidism is associated with extracellular matrix components' alterations. Furthermore, we suggest that general increase of the serum lysosomal glycosidases activity and serum GAG concentration may both result from the same reason, i.e. excessive reactive oxygen species formation in the course of hyperthyroidism due to Graves' disease.

Doppler ultrasonography in predicting relapse of hyperthyroidism in Graves' disease

Purpose: To determine whether Doppler ultrasonography could be useful in the prediction of relapse of hyperthyroidism in patients with Graves' disease. Material and Methods: Forty patients with Graves' disease confirmed by laboratory tests were examined for a number of blood flow parameters in the inferior thyroid artery before and after they were subjected to proper antithyroid drug treatment. Data were retrospectively reviewed and compared with findings for a control group of 16 age-matched subjects. Results: Significantly increased blood flow parameters were observed both in patients with active hyperthyroidism before treatment and in euthyroid patients who presented a relapse shortly after withdrawal of proper antithyroid drug treatment versus normal controls. Conversely, no significant differences were observed between patients who remained in stable remission and normal controls. Conclusion: Our results support the concept that Doppler ultrasonography evaluation of patients with Graves' disease may contribute to the detection of a relapsing course of hyperthyroidism.