UNASSIGNED: Thyrotoxicosis is related to cardiovascular mortality. This can be caused by several clinical manifestations involving the rare provocation of tricuspid regurgitation (TR) and mitral regurgitation (MR). However, there are still no clear data on thyrotoxic TR and/or MR. This study examines the progression of TR, MR, heart failure (HF) and pulmonary hypertension (PH) in response to the thyrotoxic heart manifestations, clinical characteristics and treatment approaches.
UNASSIGNED: A PRISMA-based systematic search was conducted using PubMed and other databases up to 17 June 2023. The outcomes of this study were TR, MR, HF and PH with their progression on follow-up, clinical characteristics and treatment approaches.
UNASSIGNED: A total of 57 case reports involving 62 patients (45.77 ± 13.41 years) were included in this study. They were predominantly women (n=50; 80.65%) and diagnosed with Graves\' disease (n=41; 75.81%). All patients were diagnosed with thyrotoxicosis, and this included 23 (37.10%) cases of thyroid storm. From echocardiographic studies, several patients improved clinically within the first 6 months of follow-up, including 20 TR patients (83.33%) in 6 months, nine MR patients (69.23%) in 3 months, eight HF patients (66.67%) in 2 months and 16 PH patients (76.19%) in 6 months.
UNASSIGNED: Several mechanisms are involved in thyrotoxic TR and/or MR, including the direct thyroid hormone effect and the indirect effect of other hyperthyroidism-associated factors. Patients with thyrotoxic TR and/or MR, including those with HF and PH, can experience clinical and structural improvements following hyperthyroidism treatment in the first 6 months.

BACKGROUND: Thyroid storm (TS), a life-threatening condition that can damage multiple organs, has limited therapeutic options. Hypercytokinemia is a suggested background, but the pathological condition is unclear and there are no appropriate animal models. We aimed to develop a TS mouse model by administration of triiodothyronine and lipopolysaccharide, and then to examine the effects of ghrelin on this model.
METHODS: We evaluated the use of serum IL-6 levels as a representative marker of hypercytokinemia in patients with TS. To establish the mouse model, preliminary experiments were conducted to determine the non-lethal doses of triiodothyronine and lipopolysaccharide when administered individually. As a TS model, C57BL/6 mice were administered with triiodothyronine 1.0 mg/kg (subcutaneously, once daily for seven consecutive days) and lipopolysaccharide 0.5 mg/kg (intraperitoneally, on day 7) to develop a lethal model with approximately 30% survival on day 8. We assessed the survival ratio, mouse sepsis scores and blood biomarkers (IL-6, metanephrine, alanine aminotransferase) and evaluated the effects of ghrelin 300 µg/kg on these parameters in TS model.
RESULTS: Serum IL-6 was increased in patients with TS compared with those with Graves\' disease as the diseased control (18.2 vs. 2.85 pg/mL, P < .05, n = 4 each). The dosage for the murine TS model was triiodothyronine 1.0 mg/kg and lipopolysaccharide 0.5 mg/kg. The TS model group had increased mouse sepsis score, serum IL-6, metanephrine and alanine aminotransferase. In this model, the ghrelin improved the survival rate to 66.7% (P < .01, vs. 0% [saline-treated group]) as well as the mouse sepsis score, and it decreased the serum IL-6 and metanephrine.
CONCLUSIONS: We established an animal model of TS that exhibits pathophysiological states similar to human TS with induction of serum IL-6 and other biomarkers by administration of T3 and LPS. The results suggest the potential effectiveness of ghrelin for TS in humans.

We present a case report on a spot diagnosis of Thyrotoxic Periodic Paralysis (TPP) with a unique first-person account of events from the patient. It illustrates the importance of pattern recognition and exemplifies how timely treatment enables quick resolution of a life-threatening medical emergency. Patient X\'s account affirms the condition\'s insidious onset and rapid deterioration. This case highlights the need for raising awareness of diseases that are more prevalent in specific ethnic groups and is particularly crucial for work in culturally diverse environments. We hope by sharing our experience, readers will be prompted to consider TPP as a differential diagnosis for acute limb weakness in an acute setting; with prompt testing of thyroid function and initiation of the appropriate treatments.

BACKGROUND: Development of hypoparathyroidism (hypoPT) after total thyroidectomy (TT) may increase the risk of kidney-related morbidity. We aimed to examine the risk of hypoPT and chronic kidney disease (CKD) in patients undergoing TT in Denmark over a 20-year period.
METHODS: Using population-based registries, we identified all Danish individuals with TT between January 1998 and December 2017. We included a matched comparison cohort by randomly selecting 10 citizens for each patient, by sex and birth year. We calculated cumulative incidence and hazard ratio (HR) of CKD by Cox regression in patients with TT compared with the comparison cohort. Further, CKD risks were stratified by indications for TT and comorbidity groups according to Charlson Comorbidity Index.
RESULTS: We included 2421 patients with TT and 21.5% had hypoPT. After 10 years, the risk of developing CKD for hypoPT patients was 13.5% (95% CI:9.8-17.7), 11.6% (95% CI: 9.7-13.7) for patients without hypoPT, and 5.8% (95% CI: 5.3-6.2) for the comparison cohort. When compared with the matched comparison cohort, the adjusted HR for CKD in hypoPT patients was 3.23 (95% CI: 2.37-4-41) and 2.27 (1.87-2.75) for patients without hypoPT. For patients without previous comorbidities, the adjusted HR of CKD was higher than in patients with several comorbidities.
CONCLUSIONS: HypoPT was a frequent complication after TT and was associated with an increased risk of CKD. We also found an increased risk of CKD in patients with a normal parathyroid function after TT, which needs to be further evaluated.

UNASSIGNED: Preoperative iodine therapy in toxic nodular goiter (TNG) is discouraged as iodine may cause aggravation of hyperthyroidism. We aimed to examine if a short course of iodine treatment is safe to administer in TNG.
UNASSIGNED: Patients with TNG (n=20) and subclinical to mild hyperthyroidism (free (f)T4 <30 pmol/L) without complicating illnesses were included in this pre-post-intervention study at Karolinska University Hospital. All participants received Lugol\'s solution 5%, three oral drops thrice daily for 10 days. Heart rate, TSH, fT4, fT3 concentrations were collected before (day 0) and after treatment (day 10). Thyroid hormone concentrations were also measured at two time points during treatment to discover aggravations of hyperthyroidism. ThyPRO39se, a quality-of-life questionnaire, was filled out day 0 and day 10. Differences in heart rate, thyroid hormone concentrations, and quality-of-life before and after treatment were compared. Adverse reactions were reported.
UNASSIGNED: The median age was 63.5 years. Female to male ratio 19:1. FT4 and fT3 concentrations decreased (both p<0.001), and TSH concentration increased (p<0.001) after 10 days of treatment. There was no difference in heart rate. No aggravations of thyrotoxicosis were noticed in any of the participants. ThyPRO39se scores improved on three scales, including hyperthyroid symptoms, while the remaining scale scores were unchanged. Mild and transient symptoms related to or possibly related to treatment were observed in six participants.
UNASSIGNED: A short course of Lugol\'s solution improved thyroid hormone concentrations, reduced patient-reported hyperthyroid symptoms and was safe in TNG. Lugol\'s solution might be an option for preoperative treatment in TNG.
UNASSIGNED: https://www.clinicaltrials.gov, identifier NCT04856488.

Amiodarone is a class III anti-arrhythmic drug found to be effective in treating multiple life-threatening arrhythmias, including paroxysmal atrial fibrillation. Despite its effectiveness, amiodarone has been found to result in thyroid dysfunction. Amiodarone-induced thyrotoxicosis (AIT) is classified as type 1, which often develops in those with autoimmune hyperthyroid conditions, or type 2, which occurs because of destructive thyroiditis in an apparently normal thyroid. Differentiating between both types often poses a clinical and therapeutic dilemma, as AIT 1 is treated with thionamides, whereas AIT 2 requires steroids for treatment. We present a case of a patient with AIT who was treated empirically for both subtypes with methimazole and prednisone without clinical improvement. Methimazole was later stopped due to concern for agranulocytosis, and the patient was then treated with cholestyramine, metoprolol, and prednisone. Given persistent thyrotoxicosis, the decision was made to proceed with surgical intervention. The patient underwent a successful total thyroidectomy without complications. The patient\'s condition clinically improved post-surgery and was discharged home on post-operative day 2 in stable condition. Prednisone was tapered over two weeks, and he was started on a weight-based dose of levothyroxine. He continues to follow up in our clinic for postoperative hypothyroidism and is clinically and biochemically euthyroid.

OBJECTIVE: Thyrotoxic periodic paralysis (TPP) is characterized by muscle paralysis and significant intracellular potassium movement resulting in hypokalemia. Since TPP is a rare condition, only a few studies have explicated the clinical characteristics of patients with this disease. This study aimed to elucidate the clinical characteristics of patients with TPP by comparing them with those with thyrotoxicosis without paralysis (non-TPP) and sporadic periodic paralysis (SPP).
METHODS: This was a single-center retrospective cohort study. Clinical data of patients with hyperthyroidism (n = 62) or periodic paralysis (n = 92) who were emergently admitted to our hospital was extracted from the electronic medical records and analyzed.
RESULTS: All patients in the TPP group (15 males and 2 females) had Graves\' disease, with 14 being newly diagnosed. The average serum potassium level on admission was 2.3±0.75 mEq/L. No significant correlation was observed among serum potassium level, amount of potassium required for normalization, and thyroid hormone levels. The TPP group showed significantly younger age, higher male ratio and body mass index (BMI), and lower serum potassium and phosphorus levels than the non-TPP group, which comprised 36 patients with Graves\' disease. No significant differences were observed between the TPP and SPP (n = 11) groups in terms of age, sex, BMI, serum electrolyte levels, potassium requirement for normalization, and recovery time.
CONCLUSIONS: Considering that most patients with TPP have undiagnosed Graves\' disease, distinguishing TPP from SPP based on clinical information and course alone is difficult in emergency settings. Therefore, for early detection and launch of specific treatment of Graves\' disease, screening for thyroid hormone and anti-thyroid stimulating hormone receptor antibody levels is necessary when treating patients with periodic paralysis.

This review summarizes the diagnosis and management of thyrotoxicosis in pregnancy. The diagnostic clinical and biochemical considerations used to distinguish the various etiologies of hyperthyroidism from appropriate physiologic changes during pregnancy will be outlined. Finally, the review will discuss the risks and benefits of available options for the treatment of thyrotoxicosis during pregnancy, to mitigate the risks of fetal hyperthyroidism.

BACKGROUND: Amiodarone takes a leading position in arrhythmological practice in the prevention and relief of various cardiac arrhythmias. Type 2 amiodarone-induced thyrotoxicosis is a frequent side effect of the drug. It is the most complex type of thyroid dysfunction both in terms of the severity of clinical manifestations, and in terms of understanding the mechanisms of pathogenesis, possibility of differential diagnosis and providing effective treatment. Due to the increasing life expectancy of the population, corresponding increase in the frequency of cardiac arrhythmias, the problem does not lose its relevance. Identification of predictors, assessment and prediction of the individual risk of developing this thyroid pathology is a necessity in daily clinical practice for making a reasonable decision when prescribing the drug, determining the algorithm for further dynamic monitoring of the patient.
OBJECTIVE: To evaluate the structure of amiodarone-induced thyroid dysfunction, prevalence, time and predictors of development type 2 amiodarone-induced thyrotoxicosis in a prospective cohort study. MATERIALS AND METHODS: The study involved 124 patients without thyroid dysfunction who received amiodarone therapy for the first time. Evaluation of the functional state of the thyroid gland was performed initially, after prescribing the drug for the first 3 months 1 time per month, in the future - every 3 months. The follow-up period averaged 12-24 months. The end of the observation occurred with the development of amiodaron-induced thyroid dysfunction or patient\'s refusal to further participate in the study. For the differential diagnosis of the type of amiodarone-induced thyrotoxicosis, the level of anti-TSH receptor antibodies and thyroid scintigraphy with technetium pertechnetate were determined. The type and frequency of thyroid dysfunction, time and predictors of development type 2 amiodarone-induced thyrotoxicosis were evaluated.
RESULTS: The structure of amiodarone-induced thyroid dysfunction was represented by hypothyroidism in 19,3% (n=24), type 1 thyrotoxicosis in 1,6% (n=2), type 2 thyrotoxicosis in 23,4% (n=29). The median time of its development was 92,0 [69,0;116,0] weeks; the average period of common survival - 150,2±12,6 weeks (95% CI: 125,5-175,0), median - 144±21,7 weeks (95% CI: 101,4-186,6). The main predictors of type 2 amiodarone-induced thyrotoxicosis were: age (OR=0,931; 95% CI: 0,895-0,968; p<0.001), BMI (OR=0,859; 95% CI: 0,762-0,967; p=0,012), time from the start of amiodarone therapy (OR=1,023; 95% CI: 1,008-1,038; p=0,003). Age ≤60 years was associated with increased risk of the dysfunction by 2.4 times (OR=2,352; 95% CI: 1,053-5,253; p=0,037), BMI≤26,6 kg/m2 - 2,3 times (OR=2,301; 95% CI: 1,025-5,165; p=0,043). CONCLUSION: The results allow to personalized estimate the risk of type 2 amiodarone-induced thyrotoxicosis and determine the patient\'s management tactic.

Endocrine emergencies encompass a group of conditions that occur when hormonal deficiency or excess results in acute presentation. If these endocrine disorders are not rapidly identified or if specific treatment is delayed, significant complications or even death may occur. This article outlines the basics of endocrine emergencies involving the thyroid, parathyroid, pituitary, pancreas, and adrenal glands. It discusses various causative factors, diagnostic approaches, and treatment modalities, emphasizing the significance of preventive measures. This article is aimed at guiding health care professionals, and this overview seeks to enhance understanding and improve patient outcomes in managing endocrine emergencies.