Popular folk medicine remedy ('The Secret') doesn't prevent ...
Can Medications Help Manage And Treat Gout?
Gout is an inflammatory condition that results in pain in the joints. This pain can worsen when flares occur. Treatment may involve medications that can relieve pain and reduce uric acid production.
Gout is a common form of inflammatory arthritis. Gout develops when high levels of uric acid deposit in the body's tissues. Uric acid forms from the breakdown of purines, a substance found in different foods.
When there is a high level of uric acid in the body, uric acid crystals may accumulate in certain areas of the body. This may result in swelling, heat, pain, and tenderness in the affected areas. Certain medications may help with the short-term and long-term effects of gout.
Read on to learn more about the types of medication available to treat gout, as well as how to prevent gout flares.
The purpose of using short-term medications is to manage acute flare-ups of gout, and they may include:
Some individuals may experience frequent flare-ups of gout. Some medications are available to treat chronic gout long-term, including:
Circumstances that alter the uric acid concentration may trigger a flare-up. According to a 2017 primary care-based cross-sectional study, the most commonly self-reported gout triggers included:
Additionally, risk factors for gout may include:
There are things an individual can do to prevent gout flares. Certain dietary changes that may reduce the likelihood of a gout flare-up occurring include:
Certain lifestyle changes may also reduce the risk of gout flare-ups, including:
Read on to learn more about dietary changes and home remedies for gout.
A person should contact a doctor if they experience redness, heat, swelling, and pain in their joints, especially in the:
Gout flares may be sudden and may last for days or even weeks. If a person is experiencing similar symptoms for a similar time frame, they should contact a doctor.
Gout is a common form of inflammatory arthritis. It occurs due to high levels of uric acid in the body. Uric acid crystals can accumulate in the joints, causing pain, swelling, heat, and redness.
Short-term medications to help treat gout include NSAIDs, colchicine, and corticosteroids. These medications can help manage the pain and inflammation of a gout flare-up. Long-term medications, such as allopurinol, febuxostat, probenecid, lesinurad, and pegloticase, can help lower uric acid levels and prevent future flare-ups.
Certain foods and activities can trigger gout flare-ups, which include alcohol, red meat, and excessively cold or warm weather.
There are things people can do to prevent gout flare-ups, including reducing their intake of purine-rich foods, maintaining a moderate weight, and getting regular exercise.
Arthrosi's Gout Drug Financed With $75 Million Series D
Guangrun Health Industry led the funding round with participation from other investors including Reichstein Biotech (HK) Co. Limited, a subsidiary of Arthrosi's Chinese partner ApicHope Pharmaceuticals. The cash will be used to finance the development of Arthrosi's phase 2b-stage drug AR882 and other programs in its pipeline.
Gout is a common form of arthritis where joints such as in the big toe can become very painful. Lumps called tophi sometimes form where uric acid forms crystals in the joints. The symptoms can appear in brief "flares" and disappear again.
According to Arthrosi's website, the first line of therapy in treating gout is a drug called allopurinol, but not all patients respond to the treatment. Other medications including febuxostat and pegloticase can be used, but can cause unpleasant side effects. It adds that there is no gout medication able to keep urate levels in the blood consistently low enough to reduce flares and tophi in gout.
AR882 is designed to block URAT1, a protein that stops urates from passing into urine. Taking this drug once daily is intended to reduce the amount of uric acid that can build up in the joints and treat flares and tophi.
In January this year, Arthrosi unveiled promising results from a phase 2b trial showing that AR882 has the potential to lower serum urate levels to the point where it could reduce flares and tophi could be treated faster than with current treatments. At the time, the company commented that it looked forward to meeting with regulatory agencies to take the program to phase 3 trials.
"I am not aware of any other molecule that has shown such promising results," said Litain Yeh, CEO of Arthrosi, in a public release. "We continue to be extremely positive about how AR882 can address the significant unmet need in the gout space.
"In the U.S. Alone there are 9 million people who suffer with limited treatment options. The Series D financing and continued partnership with ApicHope will accelerate the development of AR882 and other groundbreaking drugs in Western countries and in Asia."
In 2021, Arthrosi set up a joint venture with ApicHope's subsidiary Ruiao Biopharmaceutical Technology to develop AR882 in the greater China area. The partnership would also let, Arthrosi prepare a second candidate drug called AR035 for the Investigational New Drug (IND) preclinical stage for the treatment of non-small cell lung cancer.
In addition, Arthrosi is developing AR882 for the treatment of chronic kidney disease in phase 1 trials.
Meta-analysis Confirms 17 Key Metabolites As Strong Predictors Of Gout
In the present study published in Nutrients, researchers summarized published scientific literature describing the use of metabolomics to detect metabolites in gout patients, with particular attention to biomarkers that provide an early prediction of gout.
Study: Analysis of Metabolites in Gout: A Systematic Review and Meta-Analysis. Image Credit: jittawit21/Shutterstock.Com
In the past, metabolomics, a platform making robust use of spectroscopy and separation techniques, facilitated metabolite determination and the search for predictive biomarkers for many serious diseases, e.G., liver cancer and osteoarthritis. It identifies metabolites comprehensively and with exceptional accuracy.
Gout, a metabolic-immune disease caused by the super-saturation of uric acid (UA), gradually progresses to joint damage, deformity, and reduced productivity, leading to high healthcare costs.
Doctors treat acute gout with high doses of drugs, such as glucocorticoids and colchicine. However, there is increasing evidence that medication adherence to these therapies is poor worldwide. Thus, prevention of acute and chronic gout and its early diagnosis appears to be the most cost-effective path for reducing healthcare costs.
After concerted efforts over many years, scholars have found some specific metabolites with promising prospects for gout prediction, examples of which are hypoxanthine, xanthine, and creatinine. Yet, a consistent and comprehensive concluding approach in this research direction is lacking.
About the studyIn the present study, researchers used three keywords and their synonyms, gout, metabolites, and metabolomics, to compile all relevant studies published up to July 2022 in databases, such as the Cochrane Library, PubMed, EMBASE, VIP Date, Web of Science, CNKI, and Wanfang Data.
They screened studies based on meeting these four criteria:
i) encompassed gout patients;
ii) used some metabolomic techniques to analyze patient and control samples;
iii) documented the profile of the identified metabolites; and
iv) were human subjects based cohort or case-control studies or randomized controlled trials (RCTs).
Next, two independent researchers used the Newcastle–Ottawa Scale (NOS) to assess the risk of bias in all studies included in this systematic review and meta-analysis. Finally, the team performed a qualitative analysis to change the direction of metabolites.
They used the standardized mean difference (SMD) of 46 metabolites and 95% confidence intervals of 95% (95% CI) for the meta-analysis across studies, where they considered heterogeneity as substantial only when above 60%.
ResultsThe current study highlighted and helped better understand the intricacies of metabolism and immune systems in humans, which developed hand-in-hand from an evolutionary and survival perspective in the long history of human existence.
As resisting starvation and mounting an immune response to pathogens was paramount, nutrients use the pathogen-sensing system(s) to trigger inflammatory responses. This suggests that functional units controlling these functions originated from the same ancestral structure during evolution.
In today's world, most humans do not have to face food scarcity. Thus, once beneficial, UA metabolism triggers the accumulation of fats and inflammation even without infection, a biological process driving renal impairment.
The current analysis found a characteristic metabolite profile for gout, in which 10 of 46 metabolites showed marked differences, and nearly all were related to metabolic inflammation.
The authors noted that DL-2-aminoadipic acid, an intermediate lysine metabolism metabolite, and creatinine levels varied between gout patients and healthy controls.
The former plays a key role in glucose and lipid metabolism; thus, its elevated concentrations promote fat consumption. However, that damages renal function in gout patients by enhancing their metabolism. These findings confirmed the hypothesis that metabolic and immune systems use the same or overlapping signaling systems in humans to maximize energy efficiency.
The authors also noted that hypoxanthine could cause inflammation in the kidneys. Likewise, adenosine, a purine metabolite, bound different purinergic receptors to regulate interleukin-1beta (IL-1β) secretion and played an anti-inflammatory role in gout development and remission.
Similarly, kynurenic acid (KYNA), a byproduct of the tryptophan metabolism, regulates immune system cells and several immune-mediated diseases. Recent research suggests chronic stress or mild inflammation could promote KYNA production and immunomodulatory actions.
Furthermore, the researchers investigated the meta-inflammatory basis of gout attacks. As is known, sodium urate crystals precipitate in joints during the vicious cycle of nutrient surplus and inflammation, eventually causing gout arthritis.
The precipitation of sodium urate crystals also promotes pro-inflammatory cytokine secretion, further hampering kidney function. Similarly, monosodium urate crystals precipitate in the other types of joints to trigger a pro-inflammatory immune response.
Finally, they confirmed the significance of metabolic inflammation in gout pathogenesis. The authors found that the signaling pathways used by metabolic and traditional inflammation were relatively consistent and originated from the energy metabolism pathways finding related biomarkers in the evolutionary journey, which could help detect or prevent gout attacks.
ConclusionsOverall, the current study results pointed to how changes in the levels of metabolites, such as UA, hypoxanthine, adenosine, creatinine, and DL-2-aminoadipic acid, form the basis of gout development.
As prospective studies with larger cohorts validate these findings, all or at least some of these specific metabolites could serve as predictive biomarkers of gout.
Comments
Post a Comment