Peroxisome proliferator-activated receptors are expressed in many tissues, including adipocytes, hepatocytes, muscles and endothelial cells; however, the affinity depends on the isoform of PPAR, and different distribution and expression profiles, which ultimately lead to different clinical outcomes. Because they play an important role in lipid and glucose homeostasis, they are called lipid and insulin sensors. Their actions are limited to specific tissue types and thus, reveal a characteristic influence on target cells. PPARα mainly influences fatty acid metabolism and its activation lowers lipid levels, while PPARγ is mostly involved in the regulation of the adipogenesis, energy balance, and lipid biosynthesis. PPARβ/δ participates in fatty acid oxidation, mostly in skeletal and cardiac muscles, but it also regulates blood glucose and cholesterol levels. Many natural and synthetic ligands influence the expression of these receptors. Synthetic ligands are widely used in the treatment of dyslipidemia (e.g. fibrates - PPARα activators) or in diabetes mellitus (e.g. thiazolidinediones - PPARγ agonists). New generation drugs - PPARα/γ dual agonists - reveal hypolipemic, hypotensive, antiatherogenic, anti-inflammatory and anticoagulant action while the overexpression of PPARβ/δ prevents the development of obesity and reduces lipid accumulation in cardiac cells, even during a high-fat diet. Precise data on the expression and function of natural PPAR agonists on glucose and lipid metabolism are still missing, mostly because the same ligand influences several receptors and a number of reports have provided conflicting results. To date, we know that PPARs have the capability to accommodate and bind a variety of natural and synthetic lipophilic acids, such as essential fatty acids, eicosanoids, phytanic acid and palmitoylethanolamide. A current understanding of the effects of PPARs, their molecular mechanisms and the role of these receptors in nutrition and therapeutic treatment are delineated in this paper.

The presence of antinuclear antibodies (ANA) is mainly associated with connective tissue diseases (CTD). In addition, their presence is found in healthy people. These antibodies are more common in women and the elderly. Some drugs and xenobiotics are also important for the development of autoimmunity and ANA synthesis. Moreover, the deficiency of vitamin D in the body of patients correlates with occurrence of these antibodies. Unlike the healthy group, a positive ANA count was observed in patients with atopic dermatitis (AD) and in people with immune disorders. Antinuclear antibodies in low counts are also found in the course of chronic bacterial or viral infection and in patients with hematological malignancies. Also the possibility of false positive results, which may be caused by the choice of method used to determine antibodies, should be borne in mind. Taking into account all these factors, it is concluded that the ANA result itself has no diagnostic value.

Fibromyalgia (FM) is characterized by chronic widespread musculoskeletal pain associated with sleep problems, fatigue, depression, and anxiety. The persistence of pain, impairment of cognitive function, and negative impact on the psychological state have caused a detrimental effect on the patients’ quality of life. However, to date, the treatment and mechanisms of this disease are yet to be established. Oxidative stress might play a critical role in FM pathophysiology. Increased levels of prooxidative factors such as nitric oxide, lipid peroxidation, and mitophagy can cause pain sensitization in fibromyalgia. Numerous studies have supported the hypothesis of beneficial antioxidative effects in FM. Due to the lack of effective therapy for fibromyalgia, many treatments are sought to reduce pain and fatigue and improve patients’ quality of life. This manuscript discusses the impact of various antioxidative procedures that can diminish fibromyalgia symptoms, such as hyperbaric oxygen therapy, modification of dietary habits, and physical activity.

Arterial stiffness is often increased in overweight/obese subjects before the development of hypertension. It is also one of the earliest indicators of increased cardiovascular disease risk and can be considered a good predictor of the development of subclinical cardiovascular dysfunction. Arterial stiffness is a significant prognostic factor influencing cardiovascular risk, which dietary habits can modify. Obese patients should use the caloric-restricted diet because it augments aortic distensibility, diminishes pulse wave velocity (PWV), and increases the activity of endothelial nitric oxide synthases. High intake of saturated fatty acids (SFA), trans fats, and cholesterol, typical for the Western diet, impairs endothelial function and raises brachial-ankle PWV. The replacement of SFA with monounsaturated (MUFA) or polyunsaturated fatty acids (PUFA) derived from seafood and plants diminishes the risk of arterial stiffness. The dairy product intake (excluding butter) decreases PWV in the general population. The high-sucrose diet causes toxic hyperglycemia and increases arterial stiffness. Complex carbohydrates with a low glycemic index (including isomaltose) should be recommended to keep vascular health. The high sodium intake (>10 g/day), particularly associated with low potassium consumption, has a deleterious effect on arterial stiffness (↑ baPWV). Since vegetables and fruits are good sources of vitamins and phytochemicals, they should be recommended in patients with high PWV. Thus, the dietary recommendation to prevent arterial stiffness should be similar to the Mediterranean diet, which is rich in dairy products, plant oils, and fish, with a minimal red meat intake and five servings of fruits and vegetables daily.

Background: Granulomatosis with polyangiitis (GPA) presents a wide spectrum of manifestations from the common respiratory symptoms to infrequent neurological and cardiac complications. The challenge in diagnosis and management makes the rapidly progressive disorder one of the most challenging dilemmas in clinical medicine. Method: An extensive electronic literature search was done using multiple databases (e.g. PubMed) from January 2007 to August 2017 to gather information on the etiopathogenesis, clinical presentation, and current treatment management plan of GPA. The language used was English. Search items included ‘Granulomatosis with Polyangiitis symptoms,’ ‘Wegener’s Granulomatosis,’ and ‘Treatment of Granulomatosis with Polyangiitis’ for the databases. Inclusion criteria consisted of published articles in the English language which reported on the clinical manifestations of GPA, as well as on the treatment of the disease. Exclusion criteria included articles that: (1) did not specifically report on GPA vasculitis but also focused on discussion of other vasculitis such as MPA or Churg-Strauss; (2) reported on treatment/symptoms of GPA prior to 2007. Result: This review provides an overview of work undertaken in key areas of GPA research, including its complex multifactorial etiology, clinical manifestations, treatment strategies, and treatment-related adverse effects. Conclusion: Major advances in the understanding and treatment of GPA over recent decades have contributed to the notable decline in morbidity and mortality of patients. The ultimate goal is an improved prognosis through outcome measures which assesses the disease control with minimal adverse effects of intensive immunosuppressive regimens, an integral part of the clinical approach to improve the quality of life of GPA patients.

Systemic sclerosis (SSc) is an autoimmune connective tissue disorder of unknown etiology. This disease is characterized by a large variety of clinical patterns, which include the fibrosis of skin and visceral organs causing a variety of clinical manifestations. Genetic and environmental factors participate in the etiology of this disease; however, recently many studies underline the oxidative background influencing the course and complications of this disease. Reactive oxygen species (ROS) synthesized in SSc can mediate extra- and intracellular oxidative processes affecting endothelial cells and fibroblasts. The estimation of prooxidative markers in the pathogenesis of SSc can enable the identification of useful markers for disease activity and, thus, may help in planning appropriate therapy focusing on the fibrotic or vascular pattern. Recently, many attempts have been made to find antioxidative molecules (nutritional and pharmacological) reducing the prooxidant state in a variety of cells—mainly in endothelium and proliferating fibroblasts. This paper presents both the background of oxidative stress processes in systemic sclerosis mediated by different mechanisms and the evidence suggesting which of the dietary and pharmacological antioxidants can be used as therapeutic targets for this disease.