The signs of gout may include pain, swollen and red joints, or fever and a raised creatinine level. The signs usually last a few days and tend to lessen over several days. It is very rare to have signs all at one time.
The number of people with gout increased from about 10 million in 1980 to 18 million in 2001. More than 100,000, or 0.1%, of the gout population are estimated in the US to be hospitalized for gout in a given year. Findings from a recent study may help inform the policy development needed to treat and prevent primary and secondary prevention of gout and the associated comorbidities.
Gout is not a treatable disease. In the past, a long, painful and painful disease of limited duration, it has largely been left to self-palliative measures until now, but since the advent of methotrexate and other successful drugs, the aim of treatment has been to prolong life and reduce the cumulative dose of NSAIDs (by reducing cumulative dose of paracetamol), and to maintain remission in chronic disease. Since, this aims at reducing disease progression and avoiding disability, rather than just preventing the disease. The goal now is to avoid development of erosive joints.
The typical pharmacotherapy is generally supportive to the clinical and functional outcomes associated with the disease. Aspirin is probably the most common medication used for the treatment of gout. Other drugs like colchicine (a drug used in treating gouty arthritis) have shown favourable effects as well.
The current data demonstrate that a variety of environmental and social factors appear to be associated with an increased risk of gout. Gout occurs when the body's normal way of metabolizing cholesterol and other fat molecules becomes out of balance and produces acidic uric acid. This can occur if the body's metabolism does not adjust quickly enough. Gout occurs most often when there is an underlying medical problem or disease that can cause the body to not be able to metabolize fats correctly.
Gout is largely familial, with the parents often showing gouty symptoms. Findings from a recent study suggests that the primary cause of the clustering of gout in families is the increased prevalence of genetic predisposition to developing gout.
Results from a recent clinical trial of this study do not show any significant difference in side effects between the 2 treatment cohorts at the doses investigated.
Gout, due to its chronic nature and the frequent recurrence of flares, presents a considerable investment of money and time for both the patient and health-care system. Clinicians are sometimes not aware of the long-term costs of recurrent disease. Given the small number of people benefiting from a new treatment, we must consider when and who it is best to evaluate the short- and long-term value of a new medication. These questions depend on many parameters, including how we define "gout", what the time frame is to assess long-term outcomes, the cost of alternative therapies for treating gout, and how much value we place on quality of life.
The latest research in this area has been quite limited. However, the most recent one is that hyperuricemia increases the risk of gout. Most importantly, there has been a study showing that allopuridine (a purine analogue) is an effective treatment for gout, especially in gout patients with hyperuricemia. Another treatment strategy is that the combination of allopurazine and colchicine is very effective in gout patients with hyperuricemia.
At low doses, sel-212b is able to reduce inflammation without causing neurotoxicity, as predicted by its known antioxidant action. Sel-212b, with its known effects as an antimutagenic agent, is promising in the treatment of diseases involving oxidative stress, including atherosclerosis, cancer, and other autoimmune diseases.
Results from a recent clinical trial show that sel-212b can safely be used as a monotherapy to treat patients with severe gout. More studies are needed to identify the specific pharmacological mechanism that is responsible for the clinical benefits observed in this study.