RESUMEN
We intended to investigate the presence and medical application of serum hypoxia-inducible factor-1 alpha (HIF-1α) along with the already known systemic inflammatory markers and the new one's inflammatory indices, the proportion of mean corpuscular volume and lymphocytes (MCVL) and the cumulative inflammatory index (IIC), for patients with ulcerative colitis (UC). We sought to establish correlations that may be present between the serum levels of HIF-1α and these inflammatory indices, as well as their relationship with disease activity and the extent of UC, which can provide us with a more precise understanding of the evolution, prognosis, and future well-being of patients. Serum samples were collected from 46 patients diagnosed with UC and 23 controls. For our assessment of the serum levels of HIF-1α, we used the Enzyme-Linked Immunosorbent Assay (ELISA) technique. Thus, for HIF-1α we detected significantly higher values in more severe and more extensive UC. When it came to MCVL and IIC, we observed statistically significant differences between the three groups being compared (Severe, Moderate, and Mild). Our study highlighted that HIF-1α correlated much better with a disease activity score, MCVL, and IIC. With MCVL and IIC, a strong and very strong correlation had formed between them and well-known inflammation indices. By examining the ROC curves of the analyzed parameters, we recognized that TWI (accuracy of 83.70%) provides the best discrimination of patients with early forms of UC, followed by HIF-1α (73.90% accuracy), MCVL (70.90% accuracy), and PLR (70.40%). In our study, we observed that HIF-1α, MCVL, and PLR had the same sensitivity (73.33%) but HIF-1α had a much better specificity (60.87% vs. 58.70%, and 54.35%). Also, in addition to the PLR, HIF-1α and MCVL can be used as independent predictor factors in the discrimination of patients with early forms of UC.
RESUMEN
BACKGROUND: We aimed to analyze the presence and clinical use of serum 8-iso-prostaglandin F2-alpha (8-iso-PGF2α) as an oxidative stress marker and some inflammatory status biomarkers (tumor necrosis factor-alpha (TNF-α), interleukin 6 (IL-6), IL-10, high-sensitivity C-reactive protein (hs-CRP), and pentraxin-3 (PTX3)) for patients with preeclampsia (PE). METHODS: Sixty pregnant women, including thirty diagnosed with PE and thirty who were healthy (NP), were included in this study. For the assessment of serum levels of biomarkers, we used the Enzyme-Linked Immunosorbent Assay (ELISA) technique. RESULTS: Our preliminary study showed that the expression level of serum 8-iso-PGF2α in the PE group was higher than in the PE after delivery (PE-AD) group (742.00 vs. 324.00 pg/mL, p < 0.0001). Groups of preeclamptic patients (PE + PE-AD) expressed significantly elevated levels for all of the assessed inflammatory mediators as compared to NP. Significant strong positive correlations with 8-iso-PGF2α levels were found for systolic blood pressure (SBP), and TNF-α (Spearman's rho = 0.622, p-value = 0.020 and rho = 0.645, p-value = 0.002, respectively). Our study demonstrates that 8-iso-PGF2α and PTX3 have the greatest diagnostic value for pregnant women with PE. CONCLUSIONS: 8-iso-PGF2α and PTX3 can be used as independent predictor factors, along with already-known cytokines, that could represent a prophylactic way to help clinicians identify or predict which pregnant women will develop PE.
RESUMEN
Ankylosing spondylitis (AS) is a progressive common autoimmune inflammatory disease, part of the spondylarthritis group, characterized, besides clinical spinal and peripheral joint inflammation, by enthesitis and new bone formation, that can lead to severe functional impairment. Beyond intensive and continuous research on the pathogenic process extensively performed in recent years, their impact on therapeutic management remains open to future development. Better knowledge of AS pathogenesis have shown results progressively and studies are being performed to advance our current understanding of the disease. It is well known that tumor necrosis factor (TNF) exerts a central role, along with interleukin-17 (IL-17) and interleukin-23 (IL-23), demonstrated by several clinical studies. Similar to other rheumatic inflammatory conditions, SA is associated with an early process of systemic bone loss, both trabecular and cortical, consecutive osteopenia, osteoporosis, and high fracture risk. Current personalized therapeutic options benefit from new published data, to prevent future complications and to improve quality of life.
RESUMEN
Rheumatoid arthritis (RA) is classified as an inflammatory, chronic autoimmune and disabling disease based on the intricate interplay between environmental and genetic factors. With a prevalence ranging from 0.3 to 1%, RA is the most prevalent inflammatory joint disease observed in adults. Disruption of immune tolerance becomes evident when abnormal stimulation of the innate and adaptive immune system occurs. This cascade of events causes persistent joint inflammation, proliferative synovitis and, ultimately, damage of the underlying cartilage as well as the subchondral bone, leading to permanent joint destruction, deformity and subsequent loss of function. With cytokines being the key to a multitude of biological processes, including inflammation, hematopoiesis and overall immune response, one must inevitably look at the main pathways through which a significant number of those molecules exert their function. Janus kinase/signal transducers and activators of transcription (JAK/STATs) represent one such pathway and, recently, JAK inhibitors (JAKinibs) have shown promise in the treatment of several inflammatory diseases, including RA. This narrative review focuses on the intricate signaling pathways involved as well as on the clinical aspects and safety profiles of JAKinibs approved for the treatment of RA.
