Systemic lupus erythematosus (SLE) is a condition in which autoimmune inflammation affects nearly every organ in the human body; it is characterized by a relapsing-remitting pattern. Systemic inflammation and tissue damage can arise from autoantibodies, the creation of immune complexes, and the deposition of autoantibodies, all defined as autoimmune diseases. Women of reproductive age are at a high risk of developing lupus, a chronic systemic condition. Among women between the ages of 15 and 44 years, the female-to-male ratio for the occurrence of lupus is as high as 13:1, while it is only 2:1 in children and in the elderly. In addition to accelerated atherosclerosis, SLE is associated with an increased risk of cardiovascular (CV) events such as coronary artery disease (CAD), peripheral artery disease (PAD), and cerebrovascular accident (CVA). Several SLE-specific processes, including impaired immunological regulation, impaired endothelial cell (EC) function, impaired vascular repair, hyperleptinemia, and traditional risk factors, contribute to early atherosclerosis in the disease. CAD can occur at any stage of the disease's progression, with younger individuals being much more at risk than their age-matched counterparts. This review article aims to provide a unique insight into the relationship between SLE and cardiovascular disease (CVD) by discussing the pathophysiological role of CVD in SLE, outlining screening criteria, and highlighting the treatment options for CVD in connection with SLE.
Multiple myeloma (MM) is the second most common hematologic malignancy that involves monoclonal immunoglobulin (Ig)-producing plasma cells. Due to its multifaceted clinical manifestations and complications, it draws attention to various medical specialties like neurology, nephrology, orthopedics, cardiology, etc. Renal failure (RF) is one of the most common and most serious complications of MM that can be caused either by excess immunoglobulins that are nephrotoxic or some other causes like hypercalcemia, infection, etc. In this review article, we have discussed the pathogenesis of RF in MM, described the different diagnostic tools to diagnose RF in MM, and explained different treatment modalities to treat RF in MM, including certain general measures (i.e., hydration, withholding any nephrotoxic agents), renal replacement therapy, serum free light chain (SFLC) removal by plasma exchange and high cut-off dialyzer (HCO-HD), chemotherapy, hematopoietic stem cell transplantation (HSCT), and renal transplantation.
Inflammatory bowel disease (IBD) is a chronic inflammatory gastrointestinal ailment that encompasses Crohn's disease (CD) and ulcerative colitis (UC). UC is an idiopathic, chronic inflammatory condition of the colonic mucosa that begins in the rectum and progresses proximally in a continuous way over a portion of the entire colon. Chronic inflammation is linked to cancer, and IBD-related chronic colonic inflammation raises the risk of colorectal cancer. Chronic inflammation has been linked to cancer, and chronic colonic inflammation caused by IBD increases the risk of colorectal cancer (CRC). When CRC arises in people with IBD, unlike sporadic CRC, the lesions are difficult to identify due to mucosal alterations produced by inflammation. The total prevalence of IBD-associated CRC is increasing due to the rapidly increasing frequency of IBD. Screening and surveillance colonoscopy in IBD patients is considered to allow for the early diagnosis of dysplasia and cancer, improving the prognosis of IBD-related CRC by giving patients proactive therapy. This article has reviewed literature pertaining to the mechanisms related to CRC development in UC and its clinical and therapeutic implications.
Cirrhosis is an end-stage liver disease that can cause changes in any component of the hemostatic system. The net effects of the complicated hemostatic changes have long been unknown due to concurrent changes in pro-and antihemostatic drivers. Coagulation disorders are caused by various factors, including decreased clotting and inhibitor factor synthesis, reduced clearance of activated factors, quantitative and qualitative platelet defects, hyperfibrinolysis, and increased intravascular coagulation. This review discusses the pathogenesis of coagulopathy and multiple studies related to its clinical presentations. This article also highlights an additional problem in the diagnostic and therapeutic approach to this group of patients: the fact that traditional coagulation tests and transfusional strategies may not be reliable for assessing and managing bleeding or thrombotic risks. Hence, multiple management options have been assessed for bleeding and thrombosis in liver disease.
Type 1 diabetes mellitus (T1DM) and celiac disease (CD) are one of the most recognized related autoimmune disorders as they share a common genetic background that has been found in the HLA genotype, more specifically DQ2 and DQ8 molecules. Studies have shown that environmental factors as early or late exposure to cereals in the first months of life or the acquired viral infections have been implicated in the risk of development of autoantigens. CD, in most cases, is asymptomatic; therefore, it goes underdiagnosed. As a result, it has been linked to late consequences as decreased growth, delayed puberty, and anemia. Also, CD has been considered an independent risk factor for nephropathy and retinopathy. Therefore, in T1DM patients, as high-risk individuals, a CD screening has been recommended, especially to analyze their joint management. A gluten-free diet has been studied and linked to possible benefits in glycemic control or decreasing the hypoglycemic episodes in T1DM and preventing in CD the late bowel mucosal damage as gluten has been well documented as the primary trigger of these autoimmune responses. This article has reviewed the concurrent occurrence of T1DM and CD regarding the pathogenesis, clinical overlaps, screening, and management options.
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