Celiac disease (CD) is a small intestinal inflammatory disease commonly seen in the Western population. It has been observed that patients with monoglandular and polyglandular autoimmunity have a higher prevalence of celiac disease. Hashimoto's thyroiditis (HT) and Graves' disease (GD), which mainly constitute the autoimmune thyroid diseases (AITD), characterized by lymphocytic infiltration of the thyroid parenchyma, are noted to be frequently associated with celiac disease. The fundamental mechanism of this frequent coexistence is thought to be a shared genetic background. Due to the subclinical nature of the celiac disease, the diagnosis is often missed or made coincidentally during screening. The rising prevalence of the celiac disease among AITD patients has urged researchers to investigate the link between the two. We reviewed the most recent and relevant literature on the intriguing relationship between celiac disease and thyroid autoimmunity. The objectives of this article were to study the shared genetic background, the incidence of CD in AITD, the effect of a gluten-free diet on AITD, and the need for routine screening of CD in AITD patients.

Anemia in heart failure patients is a relatively common finding and has been linked with an increased risk of hospital admissions, morbidities, and significant mortality making its correction a significant factor in improving the quality of life and clinical outcomes in those suffering from it. This review article has discussed the multifactorial pathophysiology, including iron deficiency, longstanding inflammation, abnormal levels of human erythropoietin (Epo), and the abnormal activation of the renin-angiotensinaldosterone system (RAAS) being the most significant. The diagnostic guidelines as well as research-based management modalities specifically with iron supplements and erythropoietin stimulating agents have also been discussed, although research done in this area has been limited and shown conflicting results.

Hutchinson-Gilford progeria syndrome (HGPS) is a premature aging condition that involves genetic mutations, resulting in debilitating phenotypic features. The present state of knowledge on the molecular pathways that contribute to the pathophysiology of HGPS and the techniques being tested in vitro and in vivo to combat progerin toxicity have been discussed here. Nuclear morphological abnormalities, dysregulated gene expression, DNA repair deficiencies, telomere shortening, and genomic instability are all caused by progerin accumulation, all of which impair cellular proliferative capability. In addition, HGPS cells and preclinical animal models have revealed new information about the disease's molecular and cellular pathways and putative mechanisms involved in normal aging. This article has discussed the understanding of the molecular pathways by which progerin expression leads to HGPS and how the advanced therapy options for HGPS patients can help us understand and treat the condition.

Multiple sclerosis (MS) is an immune-mediated demyelinating disease of the nervous system with incredibly intricate etiopathogenesis involving numerous genetic, epigenetic, and environmental risk factors. Major environmental risk factors include ultraviolet (UV) radiation, vitamin D, Epstein-Barr virus (EBV) infection, smoking, and high body mass index (BMI). Vitamin D, in particular, can be viewed as one piece of this puzzle, with various tabs and pockets, occupying a sequential site. In this article, we have briefly discussed the neuroimmunology of MS and the role of vitamin D in regulating immune responses. Various observational studies and clinical trials were reviewed and discussed according to stages of disease activity and course of the disease. The data reviewed in this article implied that serum vitamin D levels greatly influence the risk of developing MS and disease activity. Long-term follow-up studies indicated that low serum vitamin D levels correlate with worse disability outcomes. Since clinical trials did not provide significant evidence, the role of vitamin D in controlling disease activity remains unresolved. Larger clinical trials are needed to support the findings of observational studies and provide significant evidence in favour of vitamin D.

No abstract