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Recently, thyroid autoantibodies were found to be associated with moyamoya disease (MMD). The ring finger protein 213 (RNF213) p.R4810K variant represents the most important susceptibility genotype of this disease, but its relationship with thyroid autoantibodies remains to be elucidated. Thus, in this study, we aimed to evaluate the clinical relevance of thyroid autoantibodies in each RNF213 genotype in patients with MMD. Included in this study were patients with MMD without a thyroid disease history and in euthyroid status; they were then classified into the mutated or nonmutated based on the RNF213 p.R4810K genotype and positive or negative based on thyroid autoantibody (thyroperoxidase and thyroglobulin) levels. Clinical data of each group were thereafter evaluated. Among the 209 patients, the mutated RNF213 p.R4810K variant and positive thyroid autoantibodies were detected in 155 and 41 patients, respectively. Positive thyroid autoantibodies were found to be more common in the nonmutated patients than in the mutated patients (31.5% vs. 15.5%; P = 0.011). In the mutated patients, as compared to autoantibody-negative patients, autoantibody-positive patients were determined to be more likely to have advanced disease with posterior cerebral artery involvement (54.2% vs. 29.0%; P = 0.017), white matter infarction (58.3% vs. 37.6%; P = 0.046), and a higher modified Rankin Scale at last visit (16.7% vs. 3.1%; P = 0.021). These results suggest that thyroid autoantibodies can act as an immunity inducer in patients with MMD lacking the susceptibility gene RNF213 p.R4810K variant. Moreover, the simultaneous presence of thyroid autoantibodies and the variant seems to aggravate the disease, which indicates synergy between thyroid autoantibodies and the variant.

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Thyroid hormone plays a critical role in fetal growth and development, and thyroid dysfunction during pregnancy is associated with several adverse outcomes, such as miscarriage and preterm birth. In this review, we introduce and explain three major changes in the revised Korean Thyroid Association (KTA) guidelines for the diagnosis and management of thyroid disease during pregnancy: first, the normal range of thyroid-stimulating hormone (TSH) during pregnancy; second, the treatment of subclinical hypothyroidism; and third, the management of euthyroid pregnant women with positive thyroid autoantibodies. The revised KTA guidelines adopt 4.0 mIU/L as the upper limit of TSH in the first trimester. A TSH level between 4.0 and 10.0 mIU/L, combined with free thyroxine (T4) within the normal range, is defined as subclinical hypothyroidism, and a TSH level over 10 mIU/L is defined as overt hypothyroidism regardless of the free T4 level. Levothyroxine treatment is recommended when the TSH level is higher than 4 mIU/L in subclinical hypothyroidism, regardless of thyroid peroxidase antibody positivity. However, thyroid hormone therapy to prevent miscarriage is not recommended in thyroid autoantibody-positive women with normal thyroid function.

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OBJECTIVES: Immune checkpoint inhibitors (ICIs) cause a variety of toxicities, including immune-related adverse events (irAEs), but there are no biomarkers to predict their development. Guidelines recommend measuring circulating cardiac troponin I (cTnI) during ICI therapy to detect related cardiotoxicities. Moreover, elevated cTnI has also been associated with worse outcomes in non-cardiac patients, including cancer. Thus here, we investigated whether cTnI levels were higher in patients with irAEs. METHODS: The study consisted of three groups; 21 cancer patients undergoing ICI immunotherapies who presented with irAEs, four patients without irAEs, and 20 healthy controls. Patient samples were assessed at baseline (n=25), during ICI treatment (n=25, median=6 weeks of treatment) and at toxicity (n=6, median=13 weeks of treatment). In addition to blood high sensitivity cardiac troponin I (hs-cTnI), anti-thyroglobulin (TG) and anti-thyroid peroxidase (TPO) antibodies were also quantitated to detect thyroid dysfunction, constituting the second leading toxicity (23.8%) after pneumonitis (28.6%). RESULTS: Four patients with irAEs (n=4/21; 19%) and one without irAEs (n=1/4; 25%) showed higher hs-cTnI levels at any time-point; the remaining had physiological levels. None of these patients developed cardiotoxicity. Concurrent elevated levels of anti-thyroid antibodies and hs-cTnI were detected in one patient with thyroid dysfunction (n=1/5, 20%). However, these antibodies were also elevated in three patients (n=3/16, 19%) with non-thyroid irAEs and in up to 40% of healthy controls. CONCLUSIONS: hs-cTnI was not elevated in patients with irAEs, but larger studies are needed to confirm these observations.

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Background: Although thyroid radiology has been conducted in patients with sickle cell anemia (SCA), to our knowledge, there is no report of thyroid gland assessment using ultrasonographic shear wave elastography (US-SWE). Objectives: To determine values for ultrasonographic US-SWE of the thyroid in patients with SCA and correlations between thyroid elasticity and biochemical variables used to evaluate thyroid function. Methods: Prospective case-control observational study of 36 patients with SCA and 33 healthy volunteer controls. US-SWE measurements of thyroid gland parenchyma and biochemical parameters of the participants were obtained and compared, and the diagnostic accuracy of elasticity was determined. Results: The thyroid volume was smaller in patients with SCA than that in controls (P = 0.001). Compared with the controls, the patients with SCA had significantly lower serum levels of free triiodothyronine (fT3) (P = 0.004) and thyroglobulin (Tg) (P = 0.001) and significantly higher levels of thyroid-stimulating hormone (P = 0.028). Thyroid stiffness was significantly higher in the left lobe (LL) of the patients with SCA than in the controls (P = 0.003). In the patients with SCA, we found a significant correlation between right lobe (RL) and LL stiffness and serum levels of Tg (RL [r = -0.439] and LL [r = -0.484]; P = 0.021) and fT3 (RL [r = -0.463] and LL [r = -0.386]; P = 0.012). Receiver operating characteristic (ROC) curve analysis of thyroid elasticity that represented a diagnosis of SCA found a cutoff of >7.31 kPa, a sensitivity of 52.0%, and a specificity of 72.0% for the RL (P = 0.316, area under the curve [AUC] 0.570), and a cutoff of >8.06 kPa, a sensitivity of 58.0%, and a specificity of 84.0% for the LL (P = 0.011, AUC 0.680). Conclusions: US-SWE can be used to follow up thyroid changes in patients with SCA.

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Reversible splenial lesion syndrome (RESLES) is a rare clinical imaging syndrome caused by various etiologies and has no specific clinical manifestations, of which magnetic resonance imaging is characterized by reversible splenial lesion. Its etiology is complex, with infection more common, rare due to thyroid disease.The clinical data of a patient of RESLES with significantly increased anti-thyroid antibody are reported to enrich the etiology and further improve the understanding of the disease.

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Early menarche is associated with adverse health outcomes during adolescence as well as breast and other reproductive cancers later in adulthood. However, the causes of early menarche and the pathways through which they operate are not fully understood. Though maternal thyroid function during pregnancy affects child growth, and rapid childhood growth is associated with a decreased age at menarche, the relationship between prenatal maternal thyroid function and daughters' age at menarche has not been examined. We conducted a mediation analysis in a historical cohort of 260 mother-child pairs to estimate the total and indirect effects of maternal prenatal thyroid function on daughters' age at menarche. No association was observed between thyroid stimulating hormone (TSH) or anti-thyroid peroxidase antibodies (ATPO) and daughters' age at menarche. Using a sample-specific, a-priori cutoff at the 10th percentile, low levels of maternal free thyroxine (FT4) were associated with earlier daughter age at menarche, with a hazard ratio (95 % CI) of 1.70 (1.02, 2.84) comparing the bottom 10th percentile with the top 90th percentile of exposure levels. Higher maternal FT4 was associated with rapid child weight gain from ages 5-9, and rapid child weight gain from ages 5-9 was associated with earlier age at menarche; the estimated indirect effect of this pathway was null. While maternal FT4 is associated with earlier age at menarche in daughters, this is not mediated by rapid weight gain in our study population, suggesting that maternal FT4 is operating through a different pathway.

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OBJECTIVES: The thymus plays a central role in immune tolerance, which prevents autoimmunity. Myasthenia gravis (MG) is commonly associated with thymoma or thymus hyperplasia, and it can coexist with autoimmune thyroid diseases. However, the role of the thymus in thyroid autoimmunity remains to be clarified, which we investigated here. STUDY DESIGN: The study design entailed the inclusion of consecutive MG patients and the measurement of anti-thyroid autoantibodies at baseline and, limited to autoantibody-positive patients, also at 24 and 48 weeks. One hundred and seven MG patients were studied. The main outcome measure was the behaviour of anti-thyroglobulin autoantibodies (TgAbs) and anti-thyroperoxidase autoantibodies (TPOAbs) over time in relation to thymectomy. RESULTS: Serum TgAbs and/or TPOAbs were detected in ∼20% of patients in the absence of thyroid dysfunction. The prevalence of positive serum TgAbs and/or TPOAbs decreased significantly (p = 0.002) over the follow-up period in patients who underwent thymectomy, but not in patients who were not thymectomized. When the analysis was restricted to TgAbs or TPOAbs, findings were similar. On the same line, there was a general trend towards a reduction in the serum concentrations of anti-thyroid autoantibodies in patients who underwent thymectomy, which was significant for TPOAbs (p = 0.009). CONCLUSIONS: Our findings suggest a role of the thymus in the maintenance of humoral thyroid autoimmunity.

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Urticaria is defined as the sudden appearance of erythematous, itchy wheals of variable size, with or without angioedema (AE) (swelling of the deeper layers of the skin). Its classification depends on time course of symptoms and the presence of eliciting factors. When it lasts less than 6 weeks it is classified as acute urticaria (AU), and if the symptoms persist for more than 6 weeks, it is classified as chronic urticaria (CU). Current International Guidelines also classify CU as chronic spontaneous urticaria (CSU) and inducible urticarial, according to the absence or presence of environmental triggering factors. CSU is defined as urticaria and/or angioedema in which there is no evidence of a specific eliciting factor. CSU is associated with autoimmunity in 30-45% of the cases, sharing some immunological mechanisms with other autoimmune diseases, and is associated with autoimmune thyroid disease (ATD) in about 4.3%-57.4% patients. Several studies suggest that adequate therapy with anti-thyroid drugs or levothyroxine in early stages of ATD and CSU, may help to remit the latter; but there is still a lack of double-blind, placebo-controlled studies that support this hypothesis in patients without abnormal thyroid hormone levels. The objective of this review is to describe the pathophysiology of chronic spontaneous urticaria and its association with autoimmune thyroid disease.

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Anti-LGI1 encephalitis is an autoimmune encephalitis with antibodies against leucine-rich glioma-inactivated 1 (LGI1), first described in 2010. It is a non-frequent and poorly understood entity that represents the second most frequent cause of autoimmune encephalitis. This entity is characterized by the presence of limbic encephalitis, hyponatremia, and faciobrachial dystonic seizures. Herein, we present the case of a male patient with an onset of epileptic seizures (generalized tonic-clonic seizure), and involuntary dystonic movements that affect the right side of his face and right upper limb associated with mental disorder, and affectation of higher functions. The electroencephalogram showed continuous generalized slowing of the background activity. The brain magnetic resonance imaging showed signal hyperintensity at the level of both mesial temporal lobes and hippocampi and in the head of the right caudate nucleus. Anti-thyroglobulin antibodies were positive, and he was initially diagnosed as Hashimoto's encephalopathy (HE). However, the response to corticosteroids was not completed as it is usually observed in HE. For that, antibodies for autoimmune encephalitis were tested, and the anti-LGI1 antibodies were positive in serum and cerebrospinal fluid. HE is an important differential diagnosis to consider. Furthermore, the presence of Anti-thyroglobulin antibodies should not be taken as the definitive diagnostic criteria, since these antibodies could be associated with other autoimmune encephalopathies, which include in addition to anti-LGI1, anti-NMDA and anti-Caspr2.

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Depression is a leading contributor to the global burden of diseases. Despite advances in research, challenges still exist in managing this disorder. Sufferers of autoimmune diseases are often observed to suffer from depression more often than healthy individuals, an association that cannot be completely accounted for by the impact of the disease on the individual. An association between autoimmunity and depressive symptoms also appears to exist in populations with subclinical symptoms. Moreover, researchers have successfully developed murine models illustrating the ability of autoantibodies to induce depressive-like symptoms. This paper will provide an overview of the association between autoantibodies and occurrence of depressive symptoms. Though current evidence appears to support a role for autoantibodies in the pathogenesis of depression, the majority of studies have examined this relationship cross-sectionally, therefore failing to establish a temporal association. Nonetheless, this novel theory meshes with older and newer neurochemical theories of depression. A better understanding of the immuno-pathogenesis underlying depression presents opportunities for more targeted treatment approaches and more timely and appropriate measures of detection.

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Objective To analyze the relationship between serum Th1/Th2 cytokines levels and autoantibodies against thyroid, and explore the role of Th1/Th2 cellular immunity imbalance in the pathogenesis of autoimmune thyroid diseases(AITD). Methods 21 patients with Graves'desease(GD), 18 cases with Hashimoto's thyroiditis(HT), 17 cases with non-toxic nodular goiter(NTNG) and 20 healthy subjects were enrolled in this study. The serum concentrations of their Th1 cytokines (IFN-?,IL-2) and Th2 cytokines (IL-4,IL-10) were assayed by ELISA. The serum levels of their thyrotropin receptor antibodies(TRAb), thyroglobulin antibodies (TGAb) and thyroid peroxidase antibodies(TPOAb) were measured by routine methods. The relationship between the serum Th1, Th2 cytokines levels and serum TRAb, TGAb, TPOAb levels were analyzed. Results The serum levels of IL-4 and IL-10 in patients with GD were significantly higher than those in patients with HT,NTNG and healthy subjects(P