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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.

The majority of the medical fraternity is continuously involved in finding new therapeutic schemes, including antimalarial medications (AMDs), which can be useful in combating the 2019-nCoV: coronavirus disease (COVID-19). For many decades, AMDs have been widely used in the treatment of malaria and various other anti-inflammatory diseases, particularly to treat autoimmune disorders of the connective tissue. The review comprises in vitro and in vivo studies, original studies, clinical trials, and consensus reports for the analysis, which were available in medical databases (e.g., PubMed). This manuscript summarizes the current knowledge about chloroquine (CQ)/hydroxychloroquine (HCQ) and shows the difference between their use, activity, recommendation, doses, and adverse effects on two groups of patients: those with rheumatic and viral diseases (including COVID-19). In the case of connective tissue disorders, AMDs are prescribed for a prolonged duration in small doses, and their effect is observed after few weeks, whereas in the case of viral infections, they are prescribed in larger doses for a short duration to achieve a quick saturation effect. In rheumatic diseases, AMDs are well tolerated, and their side effects are rare. However, in some viral diseases, the effect of AMDs is questionable or not so noticeable as suggested during the initial prognosis. They are mainly used as an additive therapy to antiviral drugs, but recent studies have shown that AMDs can diminish the efficacy of some antiviral drugs and may cause respiratory, kidney, liver, and cardiac complications.

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.

Yersinia bacteria (Yersinia enterocolitica, Yersinia pseudotuberculosis) are commonly found in nature in all climatic zones and are isolated from food (mainly raw pork, unpasteurized milk, or contaminated water), soil, and surface water, rarely from contaminated blood. Yersinia infection occurs through sick or asymptomatic carriers and contact with the feces of infected animals. The invasion of specific bacterial serotypes into the host cell is based on the type 3 secretion system (T3SS), which directly introduces many effector proteins (Yersinia outer proteins—Yops) into the host cell. The course of yersiniosis can be acute or chronic, with the predominant symptoms of acute enteritis (rarely pseudo-appendicitis or septicemia develops). Clinical and laboratory diagnosis of yersiniosis is difficult. The infection requires confirmation by isolating Yersinia bacteria from feces or other biological materials, including lymph nodes, synovial fluid, urine, bile, or blood. The detection of antibodies in blood serum or synovial fluid is useful in the diagnostic process. The treatment of yersiniosis is mainly symptomatic. Uncomplicated infections (diarrhea and abdominal pain) usually do not require antibiotic therapy, which is indicated in severe cases. Surgical intervention is undertaken in the situations of intestinal necrosis. Given the diagnostic and therapeutic difficulties, this review discusses the prevalence of Y. enterocolitica and Y. pseudotuberculosis, their mechanisms of disease induction (virulence factors and host response), clinical manifestations, diagnostic and preventive methods, and treatment strategies in the context of current knowledge and available recommendations.

Knee osteoarthritis (OA) is a common degenerative joint disease affecting global health. Its increasing prevalence, particularly among aging populations, remains a leading cause of disability. Besides conventional pharmacological and surgical treatments, dietary interventions are promising strategies to alleviate OA symptoms and progression. Unfortunately, scientific evidence does not support many commonly used, misleading ideas about nutrition in knee OA. Recent data highlight the detrimental effects of high-carbohydrate and high-fat diets, particularly those rich in refined sugars and saturated fats, which exacerbate systemic inflammation and contribute to cartilage degradation. Conversely, diets rich in omega-3 fatty acids, polyphenols, and dietary fiber have shown anti-inflammatory and chondroprotective properties. A Mediterranean diet rich in these nutrients effectively prevents the development of OA and its comorbidities, including obesity and cardiovascular disease. The role of supplements, such as glucosamine, chondroitin, and vitamin D, is questioned due to the lack of evidence supporting their efficacy in treating knee OA. Despite dietary recommendations published annually, there is still a need to debunk many myths that are not confirmed by current evidence. The significant research gaps require more extensive, controlled studies to establish evidence-based dietary recommendations (particularly carbohydrates, dietary fiber, and antioxidant intake). This comprehensive review provides insight into the various indications for the impact of nutrition on knee OA, focusing on key nutrients such as carbohydrates, fats, proteins, antioxidants, and selected micronutrients, providing the clinician with ready-to-implement nutritional modifications. Such an analysis may help clinicians and patients incorporate dietary strategies into treating knee OA, emphasizing the need for personalized, sustainable approaches.

Chlamydia trachomatis is an evasive pathogen that can prompt severe clinical manifestations in humans such as vaginitis, epididymitis, lymphogranuloma venereum, trachoma, conjunctivitis and pneumonia. If left untreated, chronic infections with C. trachomatis can give rise to long-lasting and even permanent sequelae. To shed some light on its widespread nature, data from original research, systematic reviews and meta-analyses from three databases was collected and analyzed in the context of chlamydial infection, related symptoms and appropriate treatment modalities. This review describes the bacterium’s pervasiveness on a global scale, especially in developing countries, and suggests ways to halt its transmission and spread. Infections with C. trachomatis often go unnoticed, as many individuals are asymptomatic and unaware of their diagnosis, contributing to a delay in diagnosis and treatment. The high prevalence of chlamydial infection highlights the need for a universal screening and detection method enabling immediate treatment at its onset. Prognosis is favorable with antibiotic therapy and education for high-risk groups and their sexual partners. In the future, a quick, easily accessible, and inexpensive test should be developed to diagnose and treat infected individuals early on. Along with a vaccine against C. trachomatis, it would halt the transmission and spread of the pathogen worldwide.

Recent studies have noted an increasing number of Kawasaki-like cases in the pediatric population following severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. In the literature, the condition is described as multiple inflammatory syndrome in children (MIS-C) or pediatric inflammatory syndrome (PIMS). A similar clinical course of Kawasaki disease (KD) and MIS-C causes difficulties in distinguishing between both conditions. However, the differential diagnosis is crucial since patients with MIS-C can present severe symptoms (myocardial dysfunction, fever, mucocutaneous symptoms) and require more extensive monitoring during treatment than children diagnosed with KD. Along with assessing epidemiological and genetic factors, it is imperative to estimate the risk of developing MIS-C in KD patients with confirmed SARS-CoV-2 infection. Genetic predispositions, such as the ITPKC gene polymorphism in KD, ACE deletion (D) polymorphism in SARS-CoV-2, and inborn errors of immunity (IEIs) in MIS-C affect the regulation of immune system complex clearances and cellular adaptations. The virus has a tropism for both vascular and respiratory cells, which further causes additional symptoms necessitating standard therapy with antithrombotic treatment. The diagnostic criteria for KD, MIS-C, and SARS-CoV-2 help differentiate each condition and optimize treatment strategies. Unfortunately, long-term outcomes in KD patients who develop MIS-C due to SARS-CoV-2 infection have been inadequately documented due to the timing of the pandemic, further displaying the need for longitudinal studies in these patients. This review underlines the differences in diagnosis and treatment of KD and MIS-C. Overall, children with KD may develop MIS-C in the setting of SARS-CoV-2 infection, but further research is needed to outline specific etiologies, prognostic factors, and diagnoses.

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.

Rheumatoid arthritis (RA) is the most common chronic autoimmune arthropathy. If the disease is aggressive or left untreated, it becomes debilitating, affects a patient’s functionality, and reduces the quality of life. Disease-modifying anti-rheumatic drugs (DMARDs), both conventional, targeted, and biological, decrease the disease progression and are key components of effective treatment. Recently, there has been a continuous debate about the possible carcinogenicity of various DMARDs. Lung cancer is a leading cause of cancer death worldwide. The available data show an increased risk of lung cancer in RA patients, but the link between RA and cancer is poorly understood. Carcinogenesis in RA seems to be related to chronic inflammation, familial predisposition, risky behaviors (e.g., smoking), and iatrogenic complications. The main mechanisms of carcinogenic processes in patients with RA are the up-regulation of interleukin-6 (IL-6) cytokine production and wingless/integrated WNT signaling. Up-regulation of WNT5A is an important mechanism that links chronic inflammatory pathways to carcinogenesis observed in RA patients. Concomitant up-regulation of transcription factor STAT3 promotes cell proliferation and inhibits apoptosis. Conversely, suppressed inflammatory processes by DMARDs may decrease the risk of lung cancer. In this article, we discuss the molecular mechanisms of lung cancer in RA and the role of DMARDs in this process. Furthermore, we analyze the molecular effect of drug-induced cancer, which affects transcription factors and thus modulates carcinogenic processes. Finally, we describe risk factors and present preventive and therapeutic approaches.

Glucocorticoids (GCs) are essential and effective medications commonly prescribed to patients with autoimmune disorders and inflammatory diseases. However, they often adversely affect bone health, including a rapid bone mineral density reduction and an increased bone fracture rate. An estimated 30% of long-term GC users develop secondary osteoporosis [glucocorticoid-induced osteoporosis (GIO)], whereas the measurement and prevention for GC-treated patients are sometimes clinically overlooked in clinical practice. Fortunately, many guidelines for GIO-related fracture risk assessment have been established, and several new drugs that benefit primary osteoporosis patients may also serve as potential GIO therapeutic options. Because of the broad application of GCs in clinical practice and the growing prevalence of GIO, increasing with the dose and time of GC administration, awareness of GIO development is crucial for implementing preventive therapy promptly and effectively. In this paper, we discuss the pathomechanisms of GIO and bone health problems depending on the method and route of GC administration in various groups of patients. Various treatment regimens are broadly analyzed, highlighting the most crucial aspects and new therapeutic options.