ABSTRACT
This study comprehensively explores the complexities of rheumatoid arthritis during pregnancy and its impact on offspring. Through an extensive review of existing literature, we investigate maternal and fetal risks, including adverse pregnancy outcomes and developmental issues in offspring. Utilizing reputable databases such as PubMed, Google Scholar, and Science Direct, we meticulously examined studies exploring the connection between rheumatoid arthritis and pregnancy complications, with a focus on outcomes for offspring. We excluded studies lacking sufficient data or peer review. Synthesizing findings from selected studies, we identified common themes and patterns, presenting results in a clear, organized manner. Our examination reveals a heightened likelihood of preterm birth and preeclampsia among pregnant individuals with rheumatoid arthritis, often correlated with disease activity. Furthermore, we highlight the impact on fetal and neonatal outcomes, such as low birth weight, underscoring the importance of meticulous disease management throughout pregnancy. Balancing the necessity of disease-modifying agents with potential risks, and consideration of medication safety is paramount. A multidisciplinary approach involving rheumatologists and obstetricians is crucial for optimizing outcomes. In conclusion, this synthesis underscores the nuanced challenges of rheumatoid arthritis in pregnancy. A comprehensive understanding and personalized, multidisciplinary approach to an organization is essential for informed decision-making in clinical practice. Our review contributes to ongoing discourse, providing insights for enhanced patient care and guiding future research endeavors.
ABSTRACT
Rheumatoid arthritis (RA) is an autoimmune systemic inflammatory disorder that is mostly characterised by progressive symmetrical joint destruction, particularly in the wrist and fingers, while it may also affect additional joints and several organs, such as the skin, heart, blood vessels, and lungs. It is identified by raised anti-rheumatoid factor and anti-cyclic citrullinated peptide antibodies. The chemical mediators involved in the activity of RA are IL-1ß, TNF-α, and IL-6. Pregnancy exerts a positive effect on RA that helps to modulate the disease condition. Different hypotheses are recommended to explain the ameliorating effect of pregnancy in RA. RA cannot be completely cured. The treatment goal is the attrition of pain and inflammation and the further progression of the disease. Long-term management of RA is carried out using disease-modifying antirheumatic drugs (DMARDs). Therapy of acute flares can be done with Non-steroidal anti-inflammatory drugs (NSAIDs) accompanied by ad interim usage of glucocorticoids. Biologic response modifiers are also available; they act by abolishing the activity of T- cells. However, it is necessary to select the correct treatment regimen when it comes to the management of RA in pregnancy.
Subject(s)
Antirheumatic Agents/therapeutic use , Arthritis, Rheumatoid/drug therapy , Arthritis, Rheumatoid/metabolism , Disease Management , Pregnancy Complications/drug therapy , Pregnancy Complications/metabolism , Anti-Inflammatory Agents, Non-Steroidal/pharmacology , Anti-Inflammatory Agents, Non-Steroidal/therapeutic use , Antirheumatic Agents/pharmacology , Arthritis, Rheumatoid/immunology , Biological Products/pharmacology , Biological Products/therapeutic use , Female , Glucocorticoids/pharmacology , Glucocorticoids/therapeutic use , Humans , Pregnancy , Pregnancy Complications/immunology , Synovial Membrane/drug effects , Synovial Membrane/immunology , Synovial Membrane/metabolismABSTRACT
BACKGROUND: There is a comprehensive body of experimental and clinical evidence suggesting that exogenous supplementation of natural antioxidants or augmentation of endogenous antioxidants attenuates the damage caused by myocardial infarction. OBJECTIVE: To evaluate the cardioprotective effects of Cl-chalcone and F-chalcone against ischemia/reperfusion (I/R)-induced myocardial infarction in rats. METHODS: Myocardial infarct size was measured using the staining agent 2,3,5-triphenyltetrazolium chloride. Malondialdehyde was measured in serum and heart tissue, and superoxide dismutase and catalase in heart tissue were measured spectrophotometrically. RESULTS: I/R resulted in significant cardiac necrosis, indicated by a rise in the end products of myocardial lipid peroxidation (malondialdehydes). A loss of antioxidative enzymes (superoxide dismutase and catalase) in heart tissue was also observed in animals subjected to in vivo myocardial I/R injury. DISCUSSION: The present study demonstrated that treatment with Cl-chalcone and F-chalcone significantly limited infarct size, partially but significantly attenuated the level of lipid peroxidation and moderated the loss of antioxidant reserves in rats subjected to 30 min coronary artery occlusion followed by a 4 h reperfusion in comparison with I/R groups. CONCLUSIONS: The results of the present study suggest that chalcones have cardioprotective activity against I/R-induced myocardial infarction in rats.
