Osteoarthritis (OA) is a significant public health issue. According to the World Health Organization, it is the leading health condition with the fastest rate of growth and the second leading cause of disability1. According to the World Health Organization Scientific Group on Rheumatic Diseases, 10% of people in the world who are 60 or older have major clinical issues that can be linked to OA2,3. Three hundred million people worldwide and 30.8 million adults in the United States are thought to have OA. It results in pain, loss of function, and a lower quality of life (QOL) and is the main contributor to disability in older adults4. OA was previously considered merely a “wear and tear” condition. It was previously believed that inflammation resulted from the joint’s articular cartilage being destroyed due to chronic overload and poor biomechanics. Stiffness, edema, and decreased mobility followed as a result of this. It is currently recognized that OA is a complex process that involves various metabolic and inflammatory factors, which contribute to the development and progression of the condition5,6. One of the major pathologic changes observed in OA joints is the gradual loss and damage of the cartilage lining the joint, which leads to the thickening of the bone under the cartilage (subchondral bone) and the formation of bone spurs (osteophytes). There is also varying inflammation of the synovial membrane that lines the joint, as well as deterioration of the ligaments and cartilage within the joint itself. OA may also result in the enlargement of the joint capsule7. Although the exact cause of the development of OA is still unknown, some variables are thought to be influencing factors (such as aging, obesity, inflammation, trauma, joint overuse, metabolic disorders, heredity, etc8,9). Cardinal symptoms include discomfort, brief morning stiffness, and crepitus on joint motion, which can cause instability and physical disability and impede mobility lifestyle excellence (QOL). According to the attribution to known causative factors, such as trauma, operations on the joint structures, and abnormal joints at birth, to mention a few, OA can be divided into 2 categories: primary (or idiopathic) and secondary (based on the presence of these factors). Several risk factors contribute to primary OA, with advancing age and weight being the most significant. Knee misalignment, increased biomechanical joint loading, genetics, and low-grade systemic inflammation, as recently indicated, are additional risk factors10. The nonpharmacologic management of OA and the advancement of general health rely heavily on education, exercise, and weight reduction11. Simple analgesia both paracetamol and nonsteroidal anti-inflammatory drugs (NSAIDs) are evidence-based drugs for symptom relief in OA. Paracetamol is the first-line pharmacologic medication for the treatment of OA indicated by all worldwide recommendations. NSAIDs are efficient OA therapy options. NSAIDs, including COX-2 selective inhibitors, can lessen pain and functional impairment in knee OA better than a placebo, according to a meta-analysis12. In short-term studies, NSAIDs are linked to more negative side effects than paracetamol. In patients with OA, COX-2 selective inhibitors are just as efficacious as traditional nonselective NSAIDs. Compared with traditional NSAIDs, they have been linked with substantially fewer upper gastrointestinal complications and slightly less dyspepsia, at least in patients not taking low-dose aspirin. Although the majority of aspirin-induced asthma patients tolerate them well, they do have a pattern of nephrotoxicity and drug interactions that is comparable to that of conventional NSAIDs11. Topical NSAIDS can be used in the short run to treat OA of the knee and hand. These, however, were less efficient than NSAIDs taken orally. Due to the profundity of the hip joint, their effectiveness in treating hip OA is debatable. Topical NSAIDs are typically well-taken, and systemic side effects are extremely rare. However, 10%–15% of individuals may experience local adverse events11. In an animal study, a drug compound named R805/CX-011 demonstrated promise for reducing the excruciating hyperinflammation associated with OA. The results of this study were published in Science Translational Medicine. The medication may interfere with GP130, a critical cell receptor instructing the immune system to fight infections or viruses. The receptor summons assailants in reaction to fragments of fragmented cartilage from our joints, causing hyper inflammation in the joints and the crippling chronic pain and stiffness that over 32 million U.S. individuals with OA experience. Although there is no treatment, doctors advise joint replacement surgery and over-the-counter medicines, physical therapy, exercise, and weight loss to reduce symptoms7. It may be possible to stop the hyper-inflammatory response that characterizes OA by blocking only one of the numerous signaling cascades that GP130 activates, either by medication or genetic change. Also, there were indications in the animal models that the therapies might result in tissue repair and regeneration. Up to 70 patients will test R805/CX-011 for the treatment of OA in a clinical trial that combines safety and preliminary efficacy. Physical therapy and nonsteroidal anti-inflammatory medicines are currently the main treatments for OA. However, these treatments are frequently insufficient to treat the condition’s severe pain-causing osteophytes and microscopic bone spikes that develop on constantly inflamed joints. R805/CX-011 injections may be a less costly, less invasive approach that could postpone or even reduce the need for joint replacement surgery7. In conclusion, OA is a prevalent joint condition that primarily affects diarthrodial joints and is associated with increased socioeconomic impact due to the aging population. The cardinal symptoms of OA can cause instability and physical disability, leading to a decline in the QOL. The nonpharmacologic management of OA relies heavily on education, exercise, and weight reduction, whereas simple analgesia, including paracetamol and NSAIDs, are evidence-based drugs for symptom relief in OA. The drug compound R805/CX-011 has shown promise for reducing hyperinflammation associated with OA, which may lead to tissue repair and regeneration. Clinical trials are underway to determine its safety and preliminary efficacy. This may provide a less invasive and cost-effective approach to postpone or reduce the need for joint replacement surgery. Overall, managing OA requires a multidisciplinary approach and further research to develop novel therapies that can effectively treat severe pain and improve the patient’s QOL. Ethical approval Ethics approval was not required for this editorial. Sources of funding Authors declare no extra Mural Funding. Author contributions H.S.R. and H.F.: conceptualisation . H.F., M.S.U., F.R., B.S.R., A.M., and V.Z.: literature and drafting of the manuscript. H.F.: editing and supervision. Conflicts of interest disclosures The authors declare that they have no financial conflict of interest with regard to the content of this report. Research registration unique identifying number (UIN) Not applicable. Guarantor Authors take full guaranty for all work.
Candida auris (C. auris) belongs to the Candida genus and is a fungal yeast resistant to multiple drugs. It is highly virulent and evades current therapeutic remedies. It was first discovered in a Japanese hospital in 2009 from a patient’s external auditory canal1. C. auris infection has a high worldwide mortality, which ranges from 30% to 60%, and is frequently associated with bloodstream infections2. The rapid spread of C. auris infection occurred after 2009. The Centers for Disease Control and Prevention (CDC) has estimated the presence of C. auris isolates in 41 countries, typically in hospital settings, as of March 20203. CDC also reported outbreaks of infections with C. auris in 47 countries globally on February 15, 20214. The United States reported 2377 clinical cases and 5754 screening cases from January 2022 to December 20225. Twenty-six isolates of C. auris from India were different genetically and phenotypically from the ones found in Japan and Korea, which provided evidence for C. auris’s ability to mutate and its resistance to Azoles6. The mechanism of C. auris virulence factors is relatively unknown. According to genomic comparison, C. auris has the ability to adapt to different environments. Two mechanisms of its pathogenesis have been identified, which include hydrolytic enzyme production and attack host cells and tissues. It can also form biofilms that protect it from antifungal drugs and increase its ability in nosocomial transmission4. C. auris can be spread in health care facilities such as hospitals and nursing homes through direct patient-to-patient contact. Contaminated surfaces are a significant culprit in the spread when a person comes in contact with them. As C. auris colonizes the skin and can be transmitted into the environment, both properties make it easily transmissible. Population susceptible are immunocompromised people, recently hospitalized patients in areas where C. auris is endemic; catheter use, extended stay in ICU, previous history of antimicrobial exposure, and resistance to antifungal therapy7. Identifying this pathogen is tricky as the methods used to determine the yeast in laboratories often must be corrected for other fungi. Detection of C. auris requires reliable sampling procedures from the most common sites of colonization, including the axillae and groin. Nares, external auditory canals, urine, rectum, catheter sites, and vagina also serve as colonization sites8. Making use of water and soaps or using a hand sanitizer with a 60% alcohol content is effective in preventing infection. Health care workers should take proper precautions to use gowns and gloves in the hospital setting. Regular disinfection and cleaning of surfaces prevent the survival of C. auris. When referring a patient with C. auris, the health care facility on the receiving end should be informed of the patient’s infection or colonization status to take appropriate measures promptly9. The steadily rising incidence of C. auris outbreaks poses a significant public health threat. C. auris outbreaks are a challenge to control due to poor routine diagnostic detection, prompt transmission, and resistance to disinfection techniques. It is now a leading cause of fungal infections in many medical setups with high mortality rates. Rapid detection methods that provide reliable identification and diagnosis, as well as control measures and necessary precautions, will help contain the spread of C. auris in health care systems. Ethical approval None. Consent for publication None. Sources of funding None. Author contributions The conceptualization was done by H.F. and H.S.R. The literature and drafting of the manuscript were conducted by H.F., A.M.S., F.R., and B.S.R. The editing and supervision were performed by H.S.R. All authors have read and agreed to the final version of the manuscript. Conflict of interest disclosures The authors declare that they have no financial conflict of interest with regard to the content of this report. Research registration unique identifying number (UIN) Not applicable. Guarantor All authors take responsibility for the work, access to data and decision to publish. Provenancer and Peer review Not commissioned, externally peer reviewed.
Hypertension, a leading cause of global mortality and morbidity, affects approximately 1.28 billion adults worldwide, with most cases occurring in low- and middle-income countries. Despite several methods for managing mild to moderate hypertension, effective management of severe or resistant hypertension remains challenging. Renal denervation, a promising non-pharmacological technique, has emerged as a potential solution.Renal denervation works by modifying the renal sympathetic nerve supply through techniques such as ultrasound, radiofrequency energy, or injection of neurolytic agents, reducing blood pressure. Clinical trials, including the RADIANCE series, have shown consistent effectiveness of ultrasound renal denervation in lowering blood pressure, especially in patients who were previously unresponsive to anti-hypertensive medications. After a follow-up of 2 months, mean ambulatory systolic blood pressure during the daytime decreased significantly in the ultrasound renal denervation group compared to the sham group. However, further research is needed to determine renal denervation's long-term safety and efficacy.In conclusion, renal denervation holds great potential in improving the treatment of uncontrolled or resistant hypertension treatment, but more investigations and trials are necessary to establish its effectiveness and safety.
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