Potassium is the predominant intracellular cation, with its extracellular concentrations maintained between 3. 5 and 5 mM. Among the different potassium disorders, hypokalaemia is a common clinical condition that increases the risk of life-threatening ventricular arrhythmias. This review aims to consolidate pre-clinical findings on the electrophysiological mechanisms underlying hypokalaemia-induced arrhythmogenicity. Both triggers and substrates are required for the induction and maintenance of ventricular arrhythmias. Triggered activity can arise from either early afterdepolarizations (EADs) or delayed afterdepolarizations (DADs). Action potential duration (APD) prolongation can predispose to EADs, whereas intracellular Ca2+ overload can cause both EADs and DADs. Substrates on the other hand can either be static or dynamic. Static substrates include action potential triangulation, non-uniform APD prolongation, abnormal transmural repolarization gradients, reduced conduction velocity (CV), shortened effective refractory period (ERP), reduced excitation wavelength (CV × ERP) and increased critical intervals for re-excitation (APD–ERP). In contrast, dynamic substrates comprise increased amplitude of APD alternans, steeper APD restitution gradients, transient reversal of transmural repolarization gradients and impaired depolarization-repolarization coupling. The following review article will summarize the molecular mechanisms that generate these electrophysiological abnormalities and subsequent arrhythmogenesis.
Uveitis is the most common ophthalmological disorder in the field of rheumatology, accounting for a significant proportion of visual morbidity, both locally and internationally. Causative factors can be divided into infectious and noninfectious etiologies. The diagnosis of uveitis is a major challenge due to heterogeneity in presentation. The disease course may be acute monophasic, recurrent, or chronic relapsing. Complications include posterior synechiae, secondary cataract, ocular hypertension or glaucoma, macular edema, retinal vascular occlusion, epiretinal membrane, and so on, and ultimately visual loss. Antimicrobial therapy is indicated for infection, whereas noninfectious uveitis warrants a combination of steroids, immunosuppressives, and anti-inflammatory agents. With the advancement of biologics, treatment strategies in chronic, noninfectious uveitis have had multiple breakthroughs, particularly in treatment-resistant cases. This article provides a review of the diagnostic approach to uveitis based on symptomatology and ophthalmological findings, and discussion of relevant treatment modalities and strategies.
Objectives There are concerns for COVID-19 vaccination in causing thyroid dysfunction and triggering thyroid autoimmunity. Also, data on the impact of pre-existing thyroid autoimmunity on COVID-19 vaccination efficacy are limited. We evaluated the impact of COVID-19 vaccination on thyroid function and antibodies, and the influence of pre-existing thyroid autoimmunity on neutralizing antibody (NAb) responses. Methods Adults without history of COVID-19 or thyroid disorders who received COVID-19 vaccination between 14 June 2021 and 8 August 2021 at three vaccination centers were recruited. All participants received two doses of vaccines. Thyroid-stimulating hormone (TSH), free thyroxine (fT4), free triiodothyronine (fT3), anti-thyroid peroxidase (anti-TPO) and anti-thyroglobulin (anti-Tg) antibodies were measured at baseline and 8 weeks after the first dose of vaccination. Post-vaccination NAb against SARS-CoV-2 receptor-binding domain was measured. Results In total, 215 individuals were included (129 BNT162b2 [60%] and 86 CoronaVac [40%] recipients): mean age 49.6 years, 37.2% men, and 12.1% positive for anti-TPO/anti-Tg at baseline. After vaccination, TSH levels did not change (p=0.225), but fT4 slightly increased (from 12. 0±1.1 to 12.2±1.2 pmol/L, p<0. 001) and fT3 slightly decreased (from 4.1±0.4 to 4. 0±0.4 pmol/L, p<0. 001). Only 3 patients (1.4%) had abnormal thyroid function after vaccination: two occurred among BNT162b2 recipients - both were subclinical thyrotoxicosis (TSH 0.32mIU/L, fT4 11.51pmol/L and fT3 4.40pmol/L; TSH 0.34mIU/L, fT4 12.67pmol/L and fT3 4.22pmol/L; both were anti-TPO and anti-Tg negative before and after vaccination); one occurred among CoronaVac recipients - isolated mild low fT3 (TSH 0.90mIU/L, fT4 9.94pmol/L and fT3 2.33pmol/L; anti-TPO/Tg negative before and after vaccination). All three recipients were asymptomatic. Both anti-TPO and anti-Tg titers increased modestly after vaccination (anti-TPO: from 7.50 [IQR: 5.90-11.2] to 9.80 IU/mL [IQR: 7.80-13.1], p<0. 001; anti-Tg: from 12.4 [IQR: 11.1-14.9] to 15.7 IU/mL [IQR: 14.2-18.2], p<0. 001), without significant changes in anti-TPO/Tg positivity. Changes in thyroid function and anti-thyroid antibodies were generally consistent between BNT162b2 and CoronaVac recipients, although anti-TPO titer rise was greater after BNT162b2 (p<0. 001). NAb responses were similar between individuals with and without pre-existing thyroid autoimmunity (p=0.855). Conclusion COVID-19 vaccination was associated with a modest increase in anti-thyroid antibody titers. Anti-TPO increase was greater among BNT162b2 recipients. However, there was no clinically significant thyroid dysfunction 8 weeks post-vaccination. NAb responses were not influenced by pre-existing thyroid autoimmunity. Our results provided important reassurance to people to proceed to COVID-19 vaccination. Presentation: No date and time listed
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