Journal of Autoimmune Disorders

Description

The association of an autoimmune thyroid disease with one or more other autoimmune diseases, with the exception of autoimmune Addison disease or hypoparathyroidism, is known as type 3 Polyendocrine Autoimmune Syndrome (PAS).During the investigation of primary hyperaldosteronism, vitiligo vulgaris and symptomless autoimmune hypothyroidism were discovered in this extremely uncommon case of type 3 PAS. An acquired condition known as generalized vitiligo is characterized by the progressive autoimmune loss of melanocytes from the affected areas, resulting in depigmented patches of skin, overlying hair, and oral mucosa. Even though vitiligo is probably the most common pigmentary disorder, research into its pathobiology, environmental triggers, and specific and effective therapeutic strategies has been hampered by a lack of a good laboratory animal model and a clinical definition that is not sufficiently clear.  

Association Studies of Candidate Genes

The characteristic depigmented lesions that are the hallmark of vitiligo are the result of a complex interaction between environmental, genetic, and immune factors. The recognition that vitiligo is a component of a broader, genetically determined autoimmune/auto-inflammatory diathesis has resulted from studies of the genetic epidemiology of generalized vitiligo over the past few years. Both allelic association studies of candidate genes and genome-wide linkage analyses to discover new genes have been used in attempts to identify genes involved in vitiligo susceptibility. These studies have begun to shed light on the pathogenesis of vitiligo. Future approaches to the treatment and prevention of vitiligo and the autoimmune diseases that are associated with it are anticipated to benefit from the discovery of novel therapeutic and preventative targets for the pathogenesis of vitiligo. Depigmentation of the skin is the hallmark of vitiligo, an acquired dermatological disorder characterized by the loss of epidermal melanocytes. In vitiligo, the mechanisms by which melanocytes are destroyed are still unknown. The mutant Smyth line (SL) of chickens is an animal model for studying autoimmune vitiligo that develops on its own. The purpose of this investigation was to ascertain whether an apoptotic mechanism is involved in the pathogenesis of depigmentation in Smyth line chicken vitiligo. In cryostat sections of two-week-old regenerating feathers, terminal deoxynucleotide transferase-mediated fluorescein-dUTP nick end labeling was used to detect in situ cell apoptosis. This increase was directly correlated with the changes in the number of TUNEL cells prior to, at the onset, and during depigmentation. In addition, some of these CD8 cells that were infiltrating were situated nearby or next to TUNEL cells. The co-occurrence of autoimmune diseases has been studied epidemiologically, which has aided in our understanding of autoimmunity. These observations suggest that enhanced apoptosis in the feather of SLV chickens is a pathogenic mechanism involved in the death of melanocytes and appears to be induced by infiltrating cytotoxic T lymphocytes CD8. Multiple autoimmune syndrome is characterized by the presence of three or more autoimmune disorders in a single patient. Environmental triggers and genetic susceptibility have been suggested to be involved in the unknown pathogenesis of multiple autoimmune syndromes. About 25% of people with autoimmune diseases are more likely to get other autoimmune diseases. The prevalence of their interactions with one another divides multiple autoimmune syndrome into three groups: types one, two, and three. This case emphasizes the need for on-going surveillance for the development of new autoimmune diseases in predisposed patients by presenting a novel combination of multiple autoimmune syndromes.

Co-Occurrence of Autoimmune Diseases

Generalized Vitiligo (GV) is a complicated condition in which the autoimmune destruction of melanocytes in the affected areas causes patchy depigmentation. The goal of GV genetic studies, which span six decades, is to discover the disease's biological mechanisms and pathways. The mode of inheritance and genetic epidemiology were the initial areas of study. Although some early genetic association studies of biological candidate genes were successful, most notably HLA and PTPN, many of these reports now appear to be false positives. These genes and pathways shed light on the underlying pathogen etic mechanisms and potential GV triggers, establish connections to other autoimmune diseases, and may hint at novel treatment and prevention strategies. Thus, the hopes and efforts of the early researchers who attempted to comprehend the genetic basis of vitiligo are supported by these findings. The autoimmune attack on skin melanocytes is thought to be the cause of the common DE pigmenting disorder known as vitiligo. Although there is some evidence that patients with vitiligo are more likely to have other autoimmune conditions than others, this evidence has not been systematically examined across the entire spectrum of autoimmune diseases. Our goal was to determine to whether patients with vitiligo and those without it were more likely to have autoimmune conditions. In accordance with MOOSE guidelines, a systematic review and meta-analysis were carried out and reported. Two reviewers were screened the studies and extracted the data. The proportion of patients with an autoimmune condition in patients with vitiligo and a comparator group was measured in observational studies. Using random effects models, pooled odds ratios and confidence intervals of 95 per cent were calculated. Thirty-nine studies were included. The overall quality of the evidence was poor, with a lot of heterogeneity and a high risk of bias in the majority of the studies. There were no studies that controlled for ethnicity, family history, the duration of vitiligo, or the severity of the disease. Given the bad quality of proof, making an end from the accessible information on presence of any relationship among vitiligo and other immune system diseases is preposterous.