Status epilepticus in Hashimoto’s encephalopathy

Ercoli, Tommaso; Defazio, Giovanni; Muroni, Antonella

doi:10.1016/j.seizure.2019.06.020

Cited by 21 publications

(20 citation statements)

References 41 publications

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“…[23][24][25] TGAb and TPOAb positivity, especially almost 100% positivity for TPOAb, is one of the necessary criteria for the diagnosis of Hashimoto's encephalopathy. [26][27][28][29] However, it has not been determined whether antithyroid antibodies play a direct role in the pathogenesis of Hashimoto's encephalopathy or simply serve as a marker of autoimmune reactivity. [26][27][28][29] As an active form of vitamin D, 1,25dihydroxyvitamin D 3 can cooperate with vitamin D receptors to regulate calcium and phosphorus metabolism, control the proliferation and differentiation of cells and generate immunomodulatory effects.…”

Section: Discussionmentioning

confidence: 99%

“…[26][27][28][29] However, it has not been determined whether antithyroid antibodies play a direct role in the pathogenesis of Hashimoto's encephalopathy or simply serve as a marker of autoimmune reactivity. [26][27][28][29] As an active form of vitamin D, 1,25dihydroxyvitamin D 3 can cooperate with vitamin D receptors to regulate calcium and phosphorus metabolism, control the proliferation and differentiation of cells and generate immunomodulatory effects. 30 1,25 (OH) 2 D 3 down-regulates the expression of the major histocompatibility complex class II and stimulating molecules (CD40, CD80, CD86), increases the production of interleukin (IL)-10 and reduces the secretion of IL-12, thus repressing the Th 1 cell immune response.…”

Section: Discussionmentioning

confidence: 99%

“…23–25 TGAb and TPOAb positivity, especially almost 100% positivity for TPOAb, is one of the necessary criteria for the diagnosis of Hashimoto's encephalopathy. 26–29 However, it has not been determined whether antithyroid antibodies play a direct role in the pathogenesis of Hashimoto's encephalopathy or simply serve as a marker of autoimmune reactivity. 26–29…”

Section: Discussionmentioning

confidence: 99%

“…26–29 However, it has not been determined whether antithyroid antibodies play a direct role in the pathogenesis of Hashimoto's encephalopathy or simply serve as a marker of autoimmune reactivity. 26–29…”

Section: Discussionmentioning

confidence: 99%

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Effects of vitamin D on thyroid autoimmunity markers in Hashimoto’s thyroiditis: systematic review and meta-analysis

Zhang

Chen

et al. 2021

J Int Med Res

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Objective To perform a meta-analysis of randomized controlled trials to evaluate the efficacy of vitamin D supplementation on thyroid autoimmunity markers in Hashimoto’s thyroiditis (HT). Methods This meta-analysis included randomized controlled clinical trials identified by a systematic search of electronic databases (PubMed®, MEDLINE®, EMBASE, The Cochrane Library, China National Knowledge Infrastructure) from inception to August 2020. All studies included patients with HT that received vitamin D supplementation irrespective of the doses administered or the duration of treatment. The primary and secondary outcome measures were thyroid peroxidase antibody (TPOAb) and/or thyroglobulin antibody (TGAb) titres. Results Eight studies ( n = 652) were included. There was significant heterogeneity between the studies. Using a random-effect model, vitamin D supplementation reduced TPOAb titre (standardized mean difference [SMD]: –1.11; 95% confidence interval [CI]: 1–1.92, –0.29) and TGAb titre (SMD: –1.12; 95% CI: –1.96, –0.28). A subgroup analysis demonstrated that vitamin D supplementation for >3 months resulted in a decrease in TPOAb titre (SMD: –1.66, 95% CI: –2.91, –0.41) but treatment ≤3 months was ineffective. Treatment with vitamin D3 decreased TPOAb titre (SMD: –1.48; 95% CI: –2.53, –0.42) whereas vitamin D did not. Conclusion These data suggest that vitamin D reduces autoantibody titre in patients with HT.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Effects of vitamin D on thyroid autoimmunity markers in Hashimoto’s thyroiditis: systematic review and meta-analysis

Zhang

Chen

et al. 2021

J Int Med Res

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“…Most patients respond well to steroid therapy with complete relief of symptoms, but they might have a relapse‐recovery period. Hence, treatment duration and factors associated with treatment failure remain to be established 3,4 …”

Section: Introductionmentioning

confidence: 99%

Challenges in corticosteroid dose regulation in a patient with autoimmune thyroid disease and neuropsychiatric syndrome: A running commentary

Bidaki

Saghafi

Ahrari

et al. 2021

Clinical Case Reports

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Hashimoto’s Encephalopathy: Case Series and Literature Review

Chaudhuri

Mukherjee

Chakravarty

2023

Curr Neurol Neurosci Rep

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Purpose of ReviewTo describe the clinical manifestations of Hashimoto's encephalopathy (HE) and discuss its pathogenesis in light of recent research. Recent FindingsThe pathogenesis of HE is uncertain. Available evidences point towards an autoimmune etiology due to vasculitis or other inflammatory process. Detection of thyroid antibodies -antithyroid peroxidase and anti-thyroglobulin are essential for diagnosis. Autoimmune encephalitis including Anti-IgLON5 disease needs to be excluded in suspected cases with appropriate tests for neuronal surface antibodies. Detection of thyroid autoantibodies is nonspecific, as these can be detected in some normal individuals and in other autoimmune diseases. In recent years, attention has turned to an aggressive form of Hashimoto's thyroiditis accompanied by elevated serum IgG4 levels in younger males with very high levels of thyroid antibodies. The role of the thyroid autoantibodies in the central nervous system (CNS) tissue damage remains unclear and these can act only as markers for diagnosis. Conversely, they have a role to play in determining the thyroid pathology -more glandular fibrosis associated with thyro-peroxidase antibody than with the thyroglobulin antibody. Summary HE is a syndrome characterized by altered mental status, confusion, hallucinations, delusions, and sometimes seizures, in association with high serum anti-thyroid antibody concentration that is usually responsive to glucocorticoid therapy. Diagnosis requires the exclusion of other causes of encephalopathies and encephalitis including autoimmune encephalitis associated with neuronal surface antibodies and paraneoplastic ones. Diagnosis also is dependent on the demonstration of thyroid autoantibodies in serum. Since there is no direct pathophysiologic link between antithyroid antibodies, Hashimoto thyroiditis and the cerebral syndrome, the nomenclature HE could be misleading. The response to steroids led to a renaming of the syndrome to steroid responsive encephalopathy associated with autoimmune thyroiditis (SREAT), though some cases do not respond to steroids. In recent years, attention has turned to an aggressive form of Hashimoto's thyroiditis accompanied by elevated serum IgG4 levels (IgG4-related disease). This is characterized by a higher incidence in men (5:1) than in women, onset at a younger age, more intense thyroid inflammation and higher antithyroid antibody titters. Such patients have excessive production of IgG4 + plasmacytes, which infiltrate various organs leading to their fibrosis and sclerosis, sometimes resulting in inflammatory tumors. HE is treated with corticosteroids along with treatment of the dysthyroid condition, if any.There are yet no guidelines regarding steroid dose and/or duration.

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Status epilepticus in Hashimoto’s encephalopathy

Cited by 21 publications

References 41 publications

Effects of vitamin D on thyroid autoimmunity markers in Hashimoto’s thyroiditis: systematic review and meta-analysis

Effects of vitamin D on thyroid autoimmunity markers in Hashimoto’s thyroiditis: systematic review and meta-analysis

Challenges in corticosteroid dose regulation in a patient with autoimmune thyroid disease and neuropsychiatric syndrome: A running commentary

Hashimoto’s Encephalopathy: Case Series and Literature Review

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