Neurological Adverse Events Associated with COVID-19 Vaccination.

How to cite this article: Jadali Z. Neurological Adverse Events Associated with COVID-19 Vaccination. Indian J Crit Care Med 2023;27(2):154-155.

Psoriatic arthritis and COVID-19: a new challenge for rheumatologists and dermatologists.

COVID-19 has changed the global health system and has great impact on different types of medical specialties including, dermatology and rheumatology. This point is important because although these two specialties are distinct subfields of medicine, there is some overlap between them. The overlap can be described by a number of rheumatic diseases that have cutaneous manifestations and vice versa. A good example of this is psoriatic arthritis because, in up to 42% of people, cutaneous lesions and arthritis coexist. Interestingly, emerging reports have described the possible occurrence of psoriasis and psoriatic arthritis in COVID-19 patients. Although the exact mechanism is unclear, some common pathophysiological mechanisms may contribute to disease pathogenesis. Therefore, elucidation of shared pathological pathways that connect these diseases will be valuable for better diagnosis and the complete treatment of COVID-19 patients with cutaneous and rheumatologic diseases.

Pediatric Coronavirus Disease 2019: Why Is It Less Severe and Frequent in Children than Adults?

There is no abstract.

Renal Complications Following COVID-19 Vaccination.

There is no abstract.

Increased Mitochondrial DNA Copy Number and Oxidative Damage in Patients with Hashimoto's Thyroiditis.

BACKGROUND: The purpose of present study was to investigate mitochondrial DNA copy number (mtDNAcn) and mtDNA damage in peripheral blood of patients with Hashimoto's thyroiditis (HT) and healthy controls (HC). METHODS: The relative mtDNAcn and oxidative DNA damage in this case-control study were measured in peripheral blood of 50 patients with Hashimoto's thyroiditis and 50 healthy controls using quantitative real-time PCR. The study was conducted in Tehran University of Medical Sciences hospital, Tehran, Iran in 2018. RESULTS: HT patients had significantly higher mitochondrial DNA copy number and mitochondrial oxidative damage than the comparison group. CONCLUSION: These data suggest the possible involvement of mitochondria and oxidative stress in the pathophysiology of HT.

Unfulfilled Inflammatory Resolution: A Key Factor in the Pathogenesis of Psoriasis.

Recent literature has highlighted the importance of chronic inflammation in psoriasis pathogenesis. Non-resolving inflammation can trigger progressive tissue damage and inflammatory mediator release which in turn perpetuate the inflammatory cycle. Under normal conditions, inflammatory responses are tightly controlled through several mechanisms that restore normal tissue function and structure. Defects in regulatory mechanisms of the inflammatory response can result in persistent unresolved inflammation and further increases of inflammation. Therefore, this review focuses on defects in regulatory mechanisms of inflammatory responses that lead to uncontrolled chronic inflammation in psoriasis. Databases such as Pubmed Embase, ISI, and Iranian databases including Iranmedex, and SID were researched to identify relevant literature. The results of this review indicate that dysregulation of the inflammatory response may be a likely cause of various immune-mediated inflammatory disorders such as psoriasis. Based on current findings, advances in understanding the cellular and molecular mechanisms involved in inflammation resolution are not only improving our knowledge of the pathogenesis of chronic inflammatory diseases but also supporting the development of new therapeutic strategies.

Novel coronavirus(Covid19), Its renal manifestations, and complications.

No abstract.

Quantification of mitochondrial DNA damage and copy number in circulating blood of patients with systemic sclerosis by a qPCR-based assay.

BACKGROUND: Although not fully understood, oxidative stress has been implicated in the pathogenesis of different autoimmune diseases such as systemic sclerosis. Accumulating evidence indicates that oxidative stress can induce mitochondrial DNA (mtDNA) damage and variations in mtDNA copy number (mtDNAcn). OBJECTIVE: The aim of this study was to explore mtDNAcn and oxidative DNA damage byproducts in peripheral blood of patients with systemic sclerosis and healthy controls. METHODS: Forty six patients with systemic sclerosis and forty nine healthy subjects were studied. Quantitative real-time PCR used to measure the relative mtDNAcn and the oxidative damage (oxidized purines) of each sample. RESULTS: The mean mtDNAcn was lower in patients with systemic sclerosis than in healthy controls whereas the degree of mtDNA damage was significantly higher in cases as compared to controls. Moreover, there was a negative correlation between mtDNAcn and oxidative DNA damage. STUDY LIMITATIONS: The lack of simultaneous analysis and quantification of DNA oxidative damage markers in serum or urine of patients with systemic sclerosis and healthy controls. CONCLUSION: These data suggest that alteration in mtDNAcn and increased oxidative DNA damage may be involved in the pathogenesis of systemic sclerosis.

Th9 Cells as a New Player in Inflammatory Skin Disorders.

CD4+T cells are composed of different subpopulations that differ in developmental pathways, surface markers, and their products. Among the catalog of these cells is Th9 cell subset that has a great capacity of Interleukin (IL)-9 production. They could be involved in the pathogenic or protective immune responses. Therefore, it is important to know how Th9 cells and cytokines influence the function of the human immune system as multitasking machinery, both in isolation or after the interaction with other surrounding cells. Since an important characteristic of Th9 cells is their tropism for skin, this article reviews the physiological and pathophysiological functions of Th9 and its cytokines under normal conditions and inflammatory skin disorders.

TIM-3 genetic variants and risk of Behçet disease in the Iranian population.

BACKGROUND: Behçet disease is a prototypical systemic autoimmune disease, caused by a complex interplay between environmental and genetic factors. The transmembrane immunoglobulin and mucin domain-3 (TIM-3) is a distinct member of the TIM family that is preferentially expressed on Th1 cells and plays a role in Th1-mediated autoimmune or inflammatory diseases, such as Behçet disease. OBJECTIVE: The aim of this study was to test the potential association between TIM-3 gene polymorphisms and Behçet disease. METHODS: Two single-nucleotide polymorphisms of TIM-3 (rs9313439 and rs10515746) were genotyped in 212 patients with Behçet disease and 200 healthy controls. Typing of the polymorphisms was performed using multiplex PCR amplification. RESULTS: There were no significant differences in allele and genotype frequencies between the Behçet disease patients and controls who were successfully genotyped. Similar results were also found after stratification by gender, age, or clinical features. STUDY LIMITATIONS: Lack of studies on various racial or ethnic groups and small sample size. CONCLUSION: This study failed to demonstrate any association between the tested TIM-3 polymorphisms and Behçet disease.

Enhanced Th17 Responses in Patients with Autoimmune Hepatitis.

BACKGROUND T cells are major players in chronic inflammatory diseases such as autoimmune hepatitis (AIH). However, it is not clear which subset of T cells participates in the pathophysiology of the disease. The aim of this study was to assess the expression profile of signature transcription factor and cytokines of T helper 17 (Th17) cells in patients with AIH. METHODS A total of 24 patients with AIH and 24 normal subjects were recruited in the study. Comparison of gene expression patterns between the patients and normal subjects was done by quantitative real-time reverse transcriptase polymerase chain reaction (qRT-PCR). RESULTS The results showed that retinoic acid receptor-related orphan receptors gamma (RORÉ£t), interleukin-17A (IL-17A), and interleukin-22 (IL-22) mRNA expression were increased greatly in the patients group compared with the normal controls group (p < 0.05). CONCLUSION Deregulated production of Th17-related molecules may be associated with the pathogenesis of AIH.

Single Nucleotide Polymorphisms of FCRL3 in Iranian Patients with Behcet's Disease.

BACKGROUND: Both genetic and environmental factors influence, susceptibility to autoimmune disorders including Behcet's disease (BD). FCRL3 (Fc receptor like 3 genes), a novel immunoregulatory gene, has recently been reported as a new promising candidate gene for general autoimmunity. This study was conducted to explore the potential association of FCRL3 polymorphisms with BD. METHODS: This study was conducted from 2010 to 2015 in Tehran University of Medical Sciences, Tehran, Iran. Four single-nucleotide polymorphisms of FCRL3 (rs7528684, rs11264799, rs945635, and rs3761959) were genotyped in 220 patients and 220 healthy controls. Typing of the polymorphisms in this case-control study was carried out using polymerase chain reaction-restriction fragment length polymorphism analysis. RESULTS: Analysis of the alleles revealed a significantly lower frequency of the A allele at the -169 site (rs7528684) in BD patients compared with that in controls (P=0.000, 66.4% versus 82%, χ2= 30.23). Moreover, a significant lower frequency of AA genotype and higher frequency of GG genotype was recorded for rs7528684. There was also relationship between posterior uveitis as a clinical sign of disease and polymorphism of allele A at the -169 site (P=0.015). CONCLUSION: This study revealed a significant difference in both allele and genotype frequency at position -169 of FCRL3 gene between Iranian patients with BD and normal subjects. These data suggest FCRL3 gene polymorphisms might be the autoimmunity risk factor for BD.

Increased Expression of Aryl Hydrocarbon Receptor in Peripheral Blood Mononuclear Cells of Patients with Autoimmune Hepatitis.

BACKGROUND Previous studies have indicated an elevated level of serum Interleukin (IL)-22 in patients with autoimmune hepatitis (AIH). However, there are no experimental data on the master transcription factor (aryl hydrocarbon receptor) that plays an important role in the development of T helper type 22 (Th22) cells as major producers of IL-22. The aim of the present study was to examine the expression of aryl hydrocarbon receptor in patients with AIH and in normal controls. METHODS Levels of mRNA transcripts were measured in the peripheral blood mononuclear cells of 18 patients with AIH and compared with 18 normal controls by a quantitative real-time polymerase chain reaction. RESULTS mRNA expression of aryl hydrocarbon receptor was significantly higher in patients with AIH compared with the healthy control group (P = 0.006). CONCLUSION Th22 cells may play an important role in the pathogenesis of AIH.

Vitiligo patients show significant up-regulation of aryl hydrocarbon receptor transcription factor.

IL-22 has been implicated in the pathogenesis of vitiligo. However, the role of aryl hydrocarbon receptor transcription factor that acts as a master regulator of IL-22-producing Th22 cells is not fully understood. The goal of this study was to investigate the expression pattern of aryl hydrocarbon receptor in peripheral blood mononuclear cells of patients with vitiligo and in normal controls. Transcript levels were determined by a reverse transcription quantitative real-time polymerase chain reaction. Aryl hydrocarbon receptor mRNA expression was drastically increased in patients with vitiligo compared to healthy controls (P = 0.000). Th22 cells may contribute to abnormal immune responses underlying vitiligo.