Clinical Use and Therapeutic Potential of IVIG/SCIG, Plasma-Derived IgA or IgM, and Other Alternative Immunoglobulin Preparations

Intravenous and subcutaneous immunoglobulin preparations, consisting of IgG class antibodies, are increasingly used to treat a broad range of pathological conditions, including humoral immune deficiencies, as well as acute and chronic inflammatory or autoimmune disorders. A plethora of Fab- or Fc-mediated immune regulatory mechanisms has been described that might act separately or in concert, depending on pathogenesis or stage of clinical condition. Attempts have been undertaken to improve the efficacy of polyclonal IgG preparations, including the identification of relevant subfractions, mild chemical modification of molecules, or modification of carbohydrate side chains. Furthermore, plasma-derived IgA or IgM preparations may exhibit characteristics that might be exploited therapeutically. The need for improved treatment strategies without increase in plasma demand is a goal and might be achieved by more optimal use of plasma-derived proteins, including the IgA and the IgM fractions. This article provides an overview on the current knowledge and future strategies to improve the efficacy of regular IgG preparations and discusses the potential of human plasma-derived IgA, IgM, and preparations composed of mixtures of IgG, IgA, and IgM

Increased P-wave dispersion in patients with newly diagnosed lichen planus

OBJECTIVE: Lichen planus is a chronic inflammatory autoimmune mucocutaneous disease. Recent research has emphasized the strong association between inflammation and both P-wave dispersion and dyslipidemia. The difference between the maximum and minimum P-wave durations on an electrocardiogram is defined as P-wave dispersion. The prolongation of P-wave dispersion has been demonstrated to be an independent risk factor for developing atrial fibrillation. The aim of this study was to investigate P-wave dispersion in patients with lichen planus. METHODS: Fifty-eight patients with lichen planus and 37 age- and gender-matched healthy controls were included in this study. We obtained electrocardiographic recordings from all participants and used them to calculate the P-wave variables. We also assessed the levels of highly sensitive C-reactive protein, which is an inflammatory marker, and the lipid levels for each group. The results were reported as the means ± standard deviations and percentages. RESULTS: The P-wave dispersion was significantly higher in lichen planus patients than in the control group. Additionally, highly sensitive C-reactive protein, LDL cholesterol, and triglyceride levels were significantly higher in lichen planus patients compared to the controls. There was a significant positive correlation between highly sensitive C-reactive protein and P-wave dispersion (r = 0.549, p<0.001) in lichen planus patients. CONCLUSIONS: P-wave dispersion increased on the surface electrocardiographic measurements of lichen planus patients. This result may be important in the early detection of subclinical cardiac involvement. Increased P-wave dispersion, in terms of the tendency for atrial fibrillation, should be considered in these patients

Atrial Fibrillation and Epicardial Adipose Tissue

Atrial fibrillation (AF) is associated with increased cardiovascular morbidity and mortality with projections that it will affect 8–12 million people in the United States by 2050. Obesity has been identified as an important independent risk factor for AF, with weight loss leading to decreased AF burden and improved arrhythmia free survival. The precise mechanisms by which obesity contributes to AF remain poorly understood. However, it has recently been speculated that epicardial adipose tissue (EAT) may be a key mediator between obesity and AF. EAT is a visceral fat depot with anatomic contiguity to the myocardium. Under physiological conditions, EAT plays an important protective role via mechanical, metabolic, and thermogenic functions. However, under pathophysiological conditions, it may contribute to development of AF through various mechanisms including fatty infiltration, fibrosis, inflammation, oxidative stress, atrial remodelling, and genetic factors. EAT has been shown in multiple studies to be a risk factor for development of AF and predictor of recurrence after catheter ablation. The mechanisms directly linking EAT to the pathogenesis of AF also are uncertain. Multiple pharmacologic options have been proposed to target EAT; however, the efficacy of targeted reduction in EAT requires further investigation