Fighting thyrotoxicosis with therapeutic plasma exchange: A case report.

Thyrotoxicosis is the clinical condition resulting from an excess of thyroid hormones for any reason. The main causes are Graves-Basedow disease, toxic multinodular goitre and toxic adenoma. The medical treatment to control thyroid function includes antithyroid drugs, beta blockers, iodine solutions, corticosteroids and cholestyramine. Although therapeutic plasma exchange is not generally part of the therapy, it is an alternative as a preliminary stage before the definitive treatment. This procedure makes it possible to eliminate T4, T3, TSI, cytokines and amiodarone. In most cases, more than one cycle is necessary, either daily or every three days, until clinical improvement is observed. The effect on thyrotoxicosis is temporary, with an approximate duration of 24-48h. This approach has been proposed as a safe and effective alternative when the medical treatment is contraindicated or not effective, and when there is multiple organ failure or emergency surgery is required.

[The association between baseline TPOAb and/or TgAb positivity and thyroid immune-related adverse events in patients with malignancies following treatment with immune checkpoint inhibitors].

Objective: To investigate the association between positive anti-thyroid peroxidase antibody (TPOAb) and/or anti-thyroglobulin antibody (TgAb) and the occurrence of thyroid immune-related adverse events (irAEs) in patients with malignant tumors who treated with immune checkpoint inhibitors (ICIs). Methods: A case-control study. A total of 116 patients with malignant tumor who received ICIs treatment and underwent thyroid function evaluation at Peking Union Medical College Hospital from January 2017 to April 2023 were enrolled retrospectively, including 77 males and 39 females, with a median age of (M(Q1, Q3)) 63.0 (55.0, 70.0) years. The patients were divided into the euthyroid group (n=58) and the thyroid irAEs group (n=58) according to whether thyroid irAEs occurred after ICIs treatment. The clinical characteristics and baseline anti-thyroid antibodies associated with the occurrence of thyroid irAEs after ICIs treatment in patients with malignant tumors were evaluated. Variables with statistical significance in univariate analysis were included in multivariate logistic regression model to analyze the risk factors for thyroid irAEs in patients with malignant tumors who received ICIs treatment. Results: In irAEs group, therewore 4 (3.4%) cases of clinical thyrotoxicosis, 23(19.8%) cases of subclinical thyrotoxicosis, 23 (19.8%) cases of clinical hypothyroidism, and 8(6.9%) cases of subclinical hypothyroidism. The positive rate of anti-thyroid antibodies at baseline in the thyrioid irAEs group was higher than that in the euthyroid group［16/58（27.6%）vs 3/58（5.2%），P=0.001］. After at least one course of ICIs treatment, the incidence of thyroid irAEs in patients with positive anti-thyroid antibodies at baseline was 84.2% (16/19), whereas it was 43.3% (42/97) in patients with negative anti-thyroid antibodies(P=0.001). Univariate logistic regression analysis showed that gender (OR=2.812, 95%CI:1.257-6.293), baseline thyroid autoantibodies were positive (OR=6.984, 95%CI: 1.909-25.547), baseline TgAb positivity (OR=8.909, 95%CI: 1.923-41.280), and baseline TPOAb positivity (OR=7.304, 95%CI: 1.555-34.308) were associated with thyroid irAEs (all P<0.05). Multivariate logistic regression analysis indicated that baseline TgAb positivity (OR=7.637, 95%CI: 1.617-36.072) was a risk factor for thyroid irAEs (P=0.01). Conclusions: The incidence of thyroid irAEs is higher in patients who are positive for baseline TPOAb and/or TgAb compared to those who are negative for TPOAb and TgAb. Patients with positive TgAb at baseline are at high risk of developing thyroid irAEs.

Plasmapheresis in thyrotoxicosis: a single-center case series.

BACKGROUND: Plasmapheresis represent an alternative therapeutic option for hyperthyroidism with thyroid storm or refractory cases. It provides a rapid decrease in plasma thyroid hormones and anti-thyroid antibodies. The aim of this paper was to report our single center's experience in managing particular situations of hyperthyroidism using apheresis. CASES PRESENTATION: The following case series describes three young African patients (two females, one male) aged 29, 37, and 25 years old, respectively, with Graves' disease who presented with drug ineffectiveness, drug-induced agranulocytosis, and thyroid storm with multi-organ failure. The three patients underwent plasmapheresis sessions leading to effective decline of thyroid hormone levels and offering a window for processing total thyroidectomy. DISCUSSION/CONCLUSION: The standard management of thyrotoxicosis and thyroid storm was usually codified by the concomitant use of antithyroid medication, iodine, beta-blockers, and corticosteroids. This medical preparation can be effective in most cases. However, drug toxicity or ineffectiveness can limit the use of such therapeutics. Our paper supports the efficiency and safety of therapeutic plasma exchange in the preoperative management of thyrotoxicosis.

Evaluation of the safety profile of the quadrivalent vaccine against human papillomavirus in the risk of developing autoimmune, neurological, and hematological diseases in adolescent women in Colombia.

BACKGROUND: Cervical cancer eradication is one of the main goals for 2030 by the World Health Organization, which can only be achieved with high vaccination rates against Human Papilloma Virus. In Colombia, more and better scientific evidence is required to increase confidence in vaccination. The objective of this study is to evaluate the safety profile of the quadrivalent vaccine against HPV in the risk of developing autoimmune, neurological, and hematological diseases in adolescent women in Colombia. METHODS: We designed a cohort study based on national HPV vaccination records and incident diagnostic data for the diseases of special interest during 2012 and 2021. We included adolescent women between 9 and 19 years old and compared vaccinated and non-vaccinated cohorts using an Inverse Probability of Treatment Weighting (IPWT) method for each scenario disease and follow-up period (180 and 360 days). FINDINGS: The Odds Ratio (OR) of developing diseases of interest was estimated during two follow up periods, 180 and 360 days after the follow-up index date (Vaccination Day). The OR for developing rheumatoid arthritis was 4·4; CI95% (1·74 - 11·14), juvenile idiopathic arthritis was 2·76 IC95% (1·50 - 5·11), idiopathic thrombocytopenic purpura was 2·54 IC95% (1·28 - 5·02) and thyrotoxicosis was 2·86 IC95% (1·03 - 7·95), when comparing the vaccinated versus unvaccinated population. However, the temporal distribution of cases incident did not reveal a clear difference between the cohorts, since the rate of appearance of new cases has a constant linear behavior for the two groups. INTERPRETATION: For rheumatoid arthritis, juvenile idiopathic arthritis, idiopathic thrombocytopenic purpura, and thyrotoxicosis; the application of the vaccine had an effect on the development of the disease. Nevertheless, our results should be interpreted with caution and be further studied, considering that the biological plausibility of the events occurred without a clear temporal pattern in relation to the exposure to the vaccine.

Association of COVID-19 Infection with Subsequent Thyroid Dysfunction: An International Population-Based Propensity Score Matched Analysis.

Background: The COVID-19 pandemic's impact on thyroid function is a growing concern. Previous studies have produced inconclusive results, and there is a lack of comprehensive research into the long-term risks of thyroid dysfunction following COVID-19 infection. Methods: In this retrospective cohort study, we used data from the TriNetX international database, which includes electronic health records from a broad, diverse patient population. We compared patients with COVID-19 (cases) to those without (controls), matching for age, sex, race, and comorbidities using propensity score matching. The primary outcome was the diagnosis of thyroid dysfunction (thyrotoxicosis or hypothyroidism) within a 12-month period, analyzed using hazard ratios (HRs) and Kaplan-Meier curves, and stratified by age and sex. Results: Initially, the study included 1,379,311 COVID-19 patients and 6,896,814 non-COVID-19 patients from the TriNetX database. After matching, the cohorts were comparable in demographics and baseline characteristics. This study consistently demonstrated a significant increase in the risk of thyroid dysfunction, including thyrotoxicosis and hypothyroidism, among COVID-19 patients compared to non-COVID-19 patients. In the short term (3 months postexposure), the COVID-19 group exhibited a HR of 2.07 (95% confidence interval [CI] 2.01-2.12) for thyroid dysfunction, which included both thyrotoxicosis (HR 2.10, CI 1.92-2.29) and hypothyroidism (HR 2.08, CI 2.01-2.13). This heightened risk persisted over the long term (up to 12 months), with HRs indicating an ∼2.01-fold increased risk for overall thyroid dysfunction, a 1.8-fold increased risk for thyrotoxicosis, and a 2.04-fold increased risk for hypothyroidism. Subgroup analysis, stratified by age and sex, revealed a notably higher risk of thyroid dysfunction in patients aged 65 and above (HR 2.18, CI 2.11-2.25), compared to those in the under-65 age group (HR 1.97, CI 1.91-2.03). Both male and female patients were associated with an elevated risk, with females showing a slightly higher association with thyroid dysfunction (HR 2.12, CI 2.06-2.16) compared to males (HR 1.76, CI 1.69-1.82). Conclusions: COVID-19 infection was associated with an increased risk of thyroid dysfunction, including thyrotoxicosis and hypothyroidism, regardless of age or sex, during a 12-month follow-up period. Further research is required to validate these findings.

Using Bedside Spectral Doppler Ultrasound for the Assessment of Patients With Thyrotoxicosis.

OBJECTIVE: To assess the bedside utility of Spectral Doppler Ultrasound (SDUS) in the initial evaluation of patients presenting with thyrotoxicosis. METHODS: This is a retrospective cross-sectional study of patients diagnosed with thyrotoxicosis at an academic outpatient endocrinology clinic from August 2019 to November 2022. The thyroid arteries' peak systolic velocities (PSV) were measured bilaterally using SDUS. PSV ≥40 cm/s in at least a single thyroid artery was considered a reasonable cut-off for Graves' disease and PSV of perinodular artery ≥ 25 cm/s for toxic adenoma. RESULTS: We identified 73 patients. Mean age ± standard deviation 45.2 ± 16.4 years, 54 (74.0%) were female, 49 (67.1%) were Caucasian, 23 (31.5%) were African American, and 1 (1.4%) was Asian. The confirmed diagnoses were 48 (65.8%) Graves' disease, 13 (17.8%) thyroiditis, four (5.5%) toxic adenoma, four (5.5%) amiodarone-induced thyroiditis type 2, 1 (1.4%) toxic multinodular goiter, 1 (1.4%) had an unremarkable repeat thyroid function testing, and two (2.7%) were unconfirmed. Diagnosis based on the SDUS initial assessment was accurate in 65 (89.0%) of the patients, and it was conclusive and confirmatory during the initial encounter in 55 (75.3%) of the patients before additional testing. A thyroid scan was obtained in nine (12.3%) patients. Incorrectly diagnosed patients were observed in two patients of each of the following categories: Graves' disease, thyroiditis, toxic adenoma, and unconfirmed diagnoses. CONCLUSIONS: SDUS can be a valuable, efficient, and cost-effective bedside tool in the initial assessment of patients presenting with thyrotoxicosis.

[Type 2 amiodarone-induced thyrotoxicosis: efficacy of glucocorticoid therapy, a retrospective analysis].

BACKGROUND: Type 2 amiodarone-induced thyrotoxicosis remains a significant problem of endocrinology and cardiology. Due to the increase a life expectancy of the population, the prevalence of cardiac arrhythmias and prescribing of amiodarone are increasing. Thyrotoxicosis aggravates the existing cardiovascular disease in patients, leads to the progression of left ventricular dysfunction, relapses of arrhythmias, increasing the risk of adverse outcomes. The tactic of further management of patients is complicated: it is necessary to resolve the issue of canceling or continuing the use of antiarrhythmic drugs necessary for a patient with a history of cardiac arrhythmia, as well as competent therapy of the thyroid pathology that has arisen. Oral glucocorticoids are the first-line drugs for the treatment of patients with moderate and severe type 2  amiodarone-induced thyrotoxicosis. Despite the appearance of clinical recommendations, opinions on the management of patients are differ, both among cardiologists and among endocrinologists. Often thyrostatics are prescribed to patients simultaneously with glucocorticoids, although it doesn't have pathogenetic basis. AIM: To evaluate the efficacy of various therapy options in patients with type 2 amiodarone-induced thyrotoxicosis. MATERIALS AND METHODS: The retrospective study included 38 patients (20 men and 18 women aged 35 to 85 years) with type 2 amiodarone-induced thyrotoxicosis. All patients underwent an analysis of anamnestic, anthropometric data, complex laboratory and instrumental diagnostics. According to the treatment options, 3 groups were retrospectively formed: without therapy (n=19), taking glucocorticoids (n=11) and combination of glucocorticoids and thyrostatics (n=8). The follow-up period was 6-18 months, including the treatment. The efficacy of treatment in the groups was evaluated by the time of reaching euthyroidism on the background of glucocorticoid therapy and duration of thyrotoxicosis; the search was conducted for potential predictors of delayed response to glucocorticoid therapy and long-term course of thyrotoxicosis. RESULTS: The average age was 62.0 [52.9; 66.3] years. The level of free thyroxine was significantly decreased after 1 month from the start of therapy in both groups: from 38.1 [32.1; 58.4] to 23.4 [19.6; 29.3] pmol/l (p<0.001) in the group taking glucocorticoids; from 73.9 [42.2; 75.6] to 39.3 [22.4; 47.2] pmol/l (p<0.001) in the combination therapy group. The time of reaching euthyroidism was longer in the combination therapy group (p=0.047), didn't depend on the dose (p=0.338) and duration of taking thiamazole (p=0.911), the delayed response to therapy correlated with age (p=-0.857; p=0.007) and time interval from the appearance of clinical symptoms of thyrotoxicosis to the start of glucocorticoid therapy (p=0.881; p<0.001). CONCLUSION: The results demonstrate the dependence of glucocorticoid response on the age of the patient and start time of therapy relative to the duration of thyrotoxicosis, inexpediency of additional prescribing thyrostatics in type 2 amiodarone-induced thyrotoxicosis.

Paraneoplastic Hyperthyroidism Secondary to a Chemotherapy-Induced Surge in ß-hCG in a Patient with Non-Seminomatous Germ Cell Tumor.

Thyrotoxicosis as the presenting syndrome of an underlying ß-hCG-secreting malignancy is well described. It has been previously theorized, but not reported, that the surge of ß-hCG secondary to chemotherapy induction may inadvertently trigger thyrotoxicosis. After thorough review, this is the first documented case of such event in peer-reviewed medical literature published in the English language. This is a case of a 21-year-old male with stage IIIc non-seminomatous germ cell tumor who developed paraneoplastic hyperthyroidism within 4 days of the first cycle of chemotherapy. Management considerations are suggested based on this case and review of the literature.

Monitoring thyroid function during amiodarone use.

Amiodarone is an antiarrhythmic drug used to treat cardiac tachyarrhythmias. It has many adverse effects, with thyroid dysfunction one of the most notable. Through various mechanisms, both thyrotoxicosis and hypothyroidism can occur secondary to amiodarone therapy. There are two types of amiodarone-induced thyrotoxicosis: type 1 occurs in those with pre-existing thyroid disease and is treated with thionamide, whereas type 2 occurs in those without and is treated with glucocorticoids. Patients with amiodarone-induced hypothyroidism may be given levothyroxine to replace thyroid hormone, but in some cases, the appropriate management may be cessation of amiodarone.

Retracting the thyroid matters: Who develops asymptomatic transient thyrotoxicosis after parathyroidectomy.

BACKGROUND: Hyperthyroidism after parathyroidectomy is not a well-understood complication. We sought to determine the incidence and risk factors of hyperthyroidism after parathyroidectomy. MATERIALS AND METHODS: This is a prospective study of 91 patients undergoing parathyroidectomy. Pre- and post-operative thyroid-stimulating hormone(TSH) and free thyroxine(T4) levels at two-week follow-ups were collected. Bivariate analyses were conducted to compare demographics, laboratory results, and intraoperative findings between patients with normal and suppressed post-parathyroidectomy TSH. RESULTS: Twenty-two(24.2 â€‹%) patients had suppressed TSH after parathyroidectomy and 2(2.2 â€‹%) reported symptoms of hyperthyroidism. All hyperthyroidism resolved within 6 weeks. No patients required medical treatment. Compared to the normal TSH group, the suppressed TSH group had significantly more bilateral explorations(91.0 â€‹% vs. 58.0 â€‹%, p â€‹= â€‹0.006), and superior parathyroid resections(95.5 â€‹% vs. 65.2 â€‹%, p â€‹= â€‹0.006). CONCLUSION: Transient hyperthyroidism is common following parathyroidectomy, which is likely associated with intraoperative thyroid manipulation. Gentle retraction of thyroid glands in parathyroidectomy is warranted, especially during superior parathyroid gland resection.

Amiodarone-induced thyrotoxicosis: Should surgery be considered?

Amiodarone is the most widely prescribed antiarrhythmic drug worldwide, but induces thyrotoxicosis or hypothyroidism in 15 to 20% of patients. Hyperthyroidism is less frequent than hypothyroidism, and two types of thyrotoxicosis are distinguished according to presence of underlying thyroid disease. Diagnosis is made in case of low TSH and high levels of T3 and T4. Initial treatment is based on anti-thyroid drugs and/or glucocorticoids. Some patients do not respond to medication, which increases the time spent with hyperthyroidism. A long interval between diagnosis and euthyroidism and low left ventricular ejection fraction (LVEF) are predictive of major adverse cardiovascular events. Here, after describing the current state of knowledge of amiodarone-induced thyrotoxicosis, we analyze the literature on the impact of surgery. We suggest that early surgery should be the first option in case of ineffective medical treatment or LVEF<40%. In expert centers, surgical morbidity is no longer different than in other indications for thyroidectomy.

Comparison of pathophysiology in subclinical hyperthyroidism with different etiologies.

Subclinical hyperthyroidism (SHyper) is defined as normal levels of free thyroxine (fT4) and free triiodothyronine (fT3) with suppressed levels of TSH. Previous studies have reported the individual pathophysiology of endogenous SHyper patients and athyreotic patients receiving TSH suppression therapy with levothyroxine; however, apparently no studies have compared the two conditions. Five-hundred-forty untreated endogenous SHyper patients and 1,024 patients receiving TSH suppression therapy who underwent total thyroidectomy for papillary thyroid carcinoma were sampled. Thyroid hormone profiles and peripheral indices related to thyrotoxicosis were investigated in endogenous SHyper patients, athyreotic patients receiving TSH suppression therapy, and healthy participants. Endogenous SHyper patients showed significantly higher thyroid hormone levels (fT4 [p < 0.001] and fT3 [p < 0.001]), and peripheral indices showed a significant tendency towards thyrotoxicosis (strong TSH suppression: alkaline phosphatase [ALP, p < 0.001], creatinine [Cre, p < 0.001], pulse rate [p < 0.05]; and mild TSH suppression: Cre [p < 0.05]) than healthy participants. In contrast, athyreotic patients receiving TSH suppression therapy showed a significant tendency towards thyrotoxicosis than healthy participants only when TSH was strongly suppressed (fT3 [p < 0.001] and Cre [p < 0.001]). Endogenous SHyper patients showed significantly higher fT3 levels (p < 0.001) than athyreotic patients receiving TSH suppression therapy; however, there was a significant tendency towards thyrotoxicosis only when TSH was strongly suppressed (ALP [p < 0.05] and pulse rate [p < 0.05]). The effects of endogenous SHyper and TSH suppression therapy on target organ function are different. Although the serum thyroid hormone profile is similar to that of the thyrotoxic state, athyreotic patients receiving TSH suppression therapy with mildly suppressed serum TSH levels are not thyrotoxic.