Gout: Causes, Symptoms, and Treatments. View Article Sources Sources. SOURCE: American College of Rheumatology annual meeting, San Diego, Oct. 26-30...
Read More >>>My Gout treatment, Last finding about Gout, Personal experience on Gout
My other site: HTML5Database - A big collection for example to learn HTML, HTML5, CSS, CSS3, JavaScript, jQuery, AJAX
Tuesday, December 3, 2013
Fight Gout with Acupuncture - New Research
References:
Lee, Won Bock, et al. "Acupuncture for gouty arthritis: a concise report of a systematic and meta-analysis approach." Rheumatology (2013).
- See more at: http://www.healthcmi.com/Acupuncture-Continuing-Education-News/708-fightgoutacupuncture#sthash.IZrKYCdf.dpuf Read More >>> HealthCMI
A large, observational study of common gout treatment allopurinol ...
WILMINGTON, Del.--(BUSINESS WIRE)--AstraZeneca and Ardea Biosciences today presented results from a large study of allopurinol, a treatment commonly...
Read More >>> NewsSavient Pharmaceuticals Announces Abstract Related To ...
Wall Street JournalSavient's abstract, #FR-PO417, entitled "Pegloticase, a Recombinant Uricase for the Treatment of Advanced Gout, Maintains Therapeutic Concentrations During...
Read More >>> See all stories on this topic »The right diagnosis is key to effectively treating foot pain after walking
For rheumatoid arthritis, a number of treatments are available to reduce inflammation and modify function of the immune system. For gout, drugs that reduce...
Read More >>> Chicago Tribune (blog)Urate-Lowering Cuts Complications From Gout
SAN DIEGO â" Patients with gout who remain on urate-lowering therapy are less likely to develop kidney damage leading to chronic kidney disease than...
Read More >>> MedscapeMonday, December 2, 2013
Gout increases risk of heart attack and stroke
The findings showed that gout patients are twice as likely to suffer a heart attack or stroke as those without gout. It is thought that the higher levels of uric acid which cause gout are also a strong risk factor for heart attack and stroke.
Conducted by scientists at the University of Oxford, the research used data from NHS England and the Office for National Statistics. Two sets of data for gout patients between 1963 and 2011 were used to track patients’ health and to determine the link between gout and heart attack and stroke in England.
These new findings highlight the need to address co-morbidities and include preventative measures within gout treatment to reduce heart attacks and stroke in gout patients.
Professor Rob Moots, editor of Rheumatology, said:
“This important study tells us that gout is a condition that is more than just a cause of severe pain, it is rather disease that must be taken seriously and treated effectively to prevent unnecessary heart attacks and strokes ”
Dr Chris Deighton, president of the British Society for Rheumatology, said: "This research reminds us that gout needs to be considered in a much broader context than just inflammatory arthritis. The vast majority of care for gout takes place in primary care. GPs need to know that gout is not only a highly curable form of arthritis, but these patients also need vigilance for their increased risk of heart attacks andstrokes. High quality holistic care of people with gout may not only improve their quality of life, but also the quantity of years lived."
Olena Seminog, lead researcher, said:
“By analysing a huge dataset spanning a long period of time for all of England our group found that gout patients have double the risk of myocardial infarction andstroke. This evidence could help to guide ways of improving cardiovascular health for people with gout, while also suggesting that more research is needed to reveal the effects of uric acid on our health.”
Source: http://www.rheumatology.org.uk/
The right diagnosis is key to effectively treating foot pain after walking
For rheumatoid arthritis, a number of treatments are available to reduce inflammation and modify function of the immune system. For gout, drugs that reduce ...
Read MoreMonday, August 5, 2013
Gout's new observations continue to evolve
Gout is frequently encountered in hyperuricemic men and may be accompanied by the development of solid masses of uric acid, known as tophi, which can be seen and palpated over the extensor surfaces of joints and can cause joint erosions, and, by urinary uric acid, calculi.
Colchicine can shorten the duration of an acute attack of gout and can be used to prevent recurrent attacks.
Pathogenesis
Hyperuricemia secondary to underexcretion
The majority of patients with gout are hyperuricemic because of a defect in the urinary clearance of uric acid. The tubular mechanisms responsible for this decreased clearance are still not well understood. Many patients, especially postmenopausal women, develop hyperuricemia as a result of prolonged diuretic therapy. Cyclosporin A, which was used primarily in the prevention of allograft rejection and is now being used in the treatment of connective tissue diseases, including rheumatoid arthritis, can cause severe hyperuricemia, with frequent attacks of acute gout and the rapid development of large tophi. The drug appears to inhibit the secretion of uric acid into the proximal renal tubule.
Hyperuricemia secondary to overproduction
Approximately 20% of patients with gout actually have a primary metabolic disorder leading to the overproduction of uric acid. These patients are characterized by an early onset of gout, a high incidence of tophi and urinary calculi. In some of these patients, an enzymatic defect responsible for the increased synthesis of uric acid has been identified.
The enzymatic defects include a deficiency in one of the two enzymes that recycle purines into the nucleotide pool — hypoxanthine guanine phosphoribosyl transferase and hypoxanthine adenine phosphoribosyl transferase. In the absence of these enzymes, most of the purines that are metabolized to hypoxanthine are converted, enzymatically, by xanthine oxidase to uric acid, a metabolic end product in all primates. Another enzymatic defect that appears to be more common involves an alteration in the rate limiting enzyme for de novo purine synthesis — phosphoribosylpyrophosphate glutamine transferase — that makes the enzyme less inhibitable by nucleotides such as guanine.
These genetic mutations account for only a small fraction of the patients who overproduce uric acid. The etiology for the remaining overproducers is still unknown but may represent partial deficiencies of these same enzymes either by different mutations or as heterozygotes.
An Acute Attack
Crystals of uric acid can frequently be seen extracellularly in the synovial fluid of hyperuricemic patients during the intercurrent periods between attacks of gout. It is now believed that the crystals must first be coated with immunoglobulin before they will be phagocytosed (i.e., opsonized). There is some evidence that some of the immunoglobulin coating the crystals is antibody directed against or specifically reactive with uric acid. The intracellular mechanisms responsible for neutrophil degranulation and release of superoxide radicals appear to involve the activation of the enzyme phospholipase D.
The chemotactic factor produced by white cells after phagocytosis of the crystals that augments and perpetuates the inflammatory response appears to be a cytokine — IL8. Almost all attacks of gout resolve while the patients are still hyperuricemic and have normal numbers of circulating polymorphonuclear leukocytes and adequate bone marrow reserves of leukocytes. The mechanisms responsible for the self-limited nature of acute gouty arthritis remain unclear. A serum factor, apolipoprotein B, appears to be capable of coating uric acid crystals and inhibiting their phagocytosis. In addition, local factors in the gouty joint appear to be capable of inhibiting crystal induced inflammation.
Differential Diagnosis
Crystals of calcium pyrphosphate (CPP) can cause an acute arthritis resembling gout — a condition known as pseudogout. In contrast to gout, where the first metatarsal phalangeal joint is most commonly affected, pseudogout more frequently involves the knee or the wrist and the patients are normouricemic. The differential diagnosis is best made by the identification of the positively birefringent CPP crystals in polymorphonuclear neutrophils in the synovial fluid of the inflamed joint as opposed to the uric acid crystals which are negatively birefringent. The CPP often deposits in the articular cartilages and menisci, resulting in the radiological finding of chondrocalcinosis which may lead the physician to suspect CPP arthritis rather than gout.
Basic calcium phosphate (BCP), hydroxyapatite, may also elicit intra-articular inflammation as well as periarticular inflammation that tends to be less intense and more chronic than that seen in gout and CPP arthritis. The BCP crystals are amorphous in shape, are not birefringent and, therefore, cannot be seen in the polarizing microscope. The condition can be suspected by the soft tissue calcification seen on routine x-rays.
Unusual Clinical Presentations
In addition to the typical acute attack, both gout and pseudogout can be associated with pyogenic infections of the joint. For all febrile patients or patients with atypical features, the synovial fluid should be Gram stained and cultured.
Both gout and pseudogout can occasionally present with hemarthrosis, so crystal arthritis should be on the differential of a bloody synovial fluid. Erosive tophaceous arthritis of the interphalangeal of the hands has been recognized in elderly patients and is often mistaken for erosive osteoarthritis. The majority of these patients has been women on diuretic therapy and many have mild renal insufficiency. Most of these women do not have a history of podagra so that the diagnosis of gout may not be suspected.
In addition to the usual sites of tophaceous deposits (helix of the ear, over the extensor surfaces of joints and in the olecranon bursae), tophi have also been noted frequently in the finger pads of patients with tophaceous gout.
Treatment
Acute attack
The use of oral colchicine for the treatment of an acute attack of gout has been largely abandoned. Antiinflammatory doses of a nonsteroidal antiinflammatory agent (NSAID), often with an initial extra dose on the first day of treatment, is now the treatment of choice.
Many patients, however, have contraindications to NSAID administration — such as a history of gastric bleeding or renal insufficiency. These patients may be treated with short courses of corticosteroids or intravenous colchicine. When using colchicine, it should be remembered not to exceed 4 mg in any 72-hour period.
Prophylaxis
Daily doses of colchicine, 0.6 mg bid, can significantly decrease the frequency of acute attacks and is indicated in most patients who have had more than one attack of gout per year. New evidence suggests that colchicine acts, at these low doses, by altering the display of adhesion molecules (E-selectin) on the surface of activated endothelial cells. These molecules normally react with ligands on the surface of circulating neutrophils and, thereby, control egress of inflammatory cells in response to chemotactic stimuli. Allopurinol, an inhibitor of xanthine oxidase, can effectively reduce the synthesis of uric acid. The use of allopurinol should be limited to patients who are overproducers, have a history of urinary calculi, tophi or recurrent gouty attacks despite colchicine prophylaxis and have persistent hyperuricemia with levels of > 9mg/dL.
Summary
Gout is one of oldest and best understood of all the human metabolic disorders but new observations continue to evolve. These observations include: the presence of serum factors such as apolipoprotein B which inhibits the initial phase of gout — the phagocytosis of uric acid crystals; serum factors such as immunoglobulins specific for uric acid which promote phagocytosis; synovial factors such as IL 8 which amplify the immune response and other synovial factors which dampen the inflamatory response. All of these factors represent potential targets for treatment and prophylaxis of gout.
Wednesday, July 17, 2013
A sample menu for Gout: Breakfast, Lunch, Dinner + Snack
- Whole-grain, unsweetened cereal with skim or low-fat milk, topped with fresh fruit
- Whole-wheat toast with trans-free margarine
- 100 percent fruit juice
- Coffee
- Lean meat, poultry or fish (2 to 3 ounces) sandwich on whole-wheat bread, with lettuce, tomato and low-fat spread
- Carrot and celery sticks, side salad or vegetable soup
- Fresh fruit, such as apple, orange or pear
- Skim or low-fat milk
- Baked or roasted chicken (2 to 3 ounces)
- Steamed vegetables
- Baked potato with low-fat sour cream
- Green salad with tomatoes and low-fat dressing
- Fresh fruit, such as berries or melon
- Nonalcoholic beverage, such as water or tea
Saturday, July 13, 2013
2012 American College of Rheumatology Guidelines for managing gout
Monday, July 1, 2013
New Bawell report said, Using Alkaline Ionized Water As a Natural Gout Treatment
"Using Alkaline Ionized Water As a Natural Gout Treatment" Report Is Released by Bawell Water Ionizers
Medical and scientific experts that have studied alkaline ionized water as a healthy alternative Gout treatment are interviewed in the new Bawell report.
Dr. Hidemitsu Hayashi, M.D. Director, Water Institute of Japan gives advice on how to pick the best water ionizer machines. He also explains how a water ionizer works, "The Ionized Water unit, is an electrical appliance connected to your kitchen water supply to perform electrolysis on tap water before you drink it. A special attachment re-directs tap water out of the faucet through a plastic hose into the Ionized Water unit. The reduced water comes out of the faucet, and the oxidized water comes out of a separate hose leading into the sink" (Water Institute of Japan).
The doctor continues by mentioning some water ionizer health benefits, "One way to protect healthy tissue from the ravages of oxidation caused by active oxygen is to provide free electrons to active oxygen radicals, thus neutralizing their high oxidation potential and preventing them from reacting with healthy tissue. Water treated by electrolysis to increase its reduction potential is the best solution to the problem of providing a safe source of free electrons to block the oxidation of normal tissue by free oxygen radicals."
As a final piece of advice in the new Bawell report, "But first and foremost, one must change his lifestyle and eating habits for the better. As much as possible, eat less of acidic foods and switch into a more healthier diet such as green leafy vegetables, salads, and the likes. All the medications will be of no use if one doesn't comply with this."
Visit the Bawell website at http://www.bawellwaterionizers.com/faq.html for information on the health benefits of alkaline ionized water, and to see the different models of Bawell brand water ionizers.
High consumption of sugar-filled beverages cause gout
Based on 40,000 data entries on gout patients he has accumulated since 1981, Chen said gout occurred mainly among men in their 50s and 60s in the 1980s but grew increasingly prevalent among men in their 30s in the 1990s and among men in their 20s in recent years.
Today, Chen said, 20-somethings account for 20 percent of Taiwan's gout population, an unheard of percentage two decades ago.
He attributed the growing number of young people with gout to their frequent consumption of sugary drinks, which contain high levels of purine that result in excess uric acid in the blood — the main cause of the disease.
Friday, June 28, 2013
Mayo Clinic: Big Toe Isn't Biggest Culprit in Gout Flare-Ups; Other Joints Tied to Higher Risk, Gout as a warning light that is alerting us to other problems
Mayo Clinic: Big Toe Isn't Biggest Culprit in Gout Flare-Ups; Other Joints Tied to Higher Risk
A new Mayo Clinic study shows that patients whose gout starts in joints other than the big toe – such as the elbows or knees – are more likely to have recurrent flares than patients whose gout starts in the traditional site. The findings, recently presented in Madrid at the 2013 Annual Congress of the European League Against Rheumatism (EULAR), may help doctors determine which patients should be put on drug therapy to reduce their risk of a subsequent flare, as opposed to being treated with lifestyle changes alone.
...
Dr. Bongartz adds that the implications of the study may extend beyond painful joints. “Gout is often associated with other diseases such as obesity, hypertension and hyperlipidemia [high cholesterol and triglycerides],” he says. “I like to refer to gout as a warning light that is alerting us to other problems.”
Saturday, June 22, 2013
8 Gout-Causing Foods
Monday, June 17, 2013
Chicken is fine for gout BUT not KFC Chicken
Today, my pain level goes...up. The only suspect is I had KFC Chicken for lunch...
As you all know, the doctor advise is to control your diet....there is a food table for gout(Purine table)...
http://www.acumedico.com/purine.htm or table everywhere.
In fact, inside your body, many organisms have metabolic pathways to synthesize and break down purines. http://www.purineresearchsociety.org/
I agreed "WHY WE AREN'T WHAT WE EAT","THE BODY'S ANSWER --- METABOLISM"
But not to accept the simple but mysterious reason...Genetic
Anyway, you cannot really avoid Purine by just not taking food with purine...
The real problem, I believe should be what cause your body METABOLISM malfunction.
We were surrounded by "unknown" "SAFE" food enhancers, especially in your fast food, package food...KFC, McDonald...
MY ADVICE to gout patient:
Have healthy fresh meat. No more KFC, McDonald, ..., FAST FOOD
Wednesday, June 5, 2013
My reading: New therapeutic options for gout here and on the horizon
My prescription medicine
Very very typical advise for Gout patient,
"control your diet, eat less meat, drink more water, weight control, don't try to catch bus, ..."
Piroxicam 10mg, 1 tablet daily, after meal, Anti-inflammation, Pain
Etodolac 200mg, 1 tablet, 2 times daily, day and night, after meal, Anti-inflammation, Pain
Diclofenac sodium 25mg, 2 tablet, 4 times daily, every 4 hours, after meal, Anti-inflammation, Pain
Acetaminophen 500mg, 1 tablet, 4 times daily, every 4 hours, after meal, Pain
At least, these tablets works. My pain decrease 80% after 1 day of medication.
Starting the very very simple diet...bread, rice, non - red meal, chicken, egg, milk...
Gout Fight continue!!!!!!
Saturday, June 1, 2013
Why this blog of gout and "Avoid Curry food"
My last servious attack was about 4 months ago. I was in the middle of recovery. This time, I should say this lunch, I used my body to find our what food are likely to cause the gout attack on me.
I always keep an eye on my food, my weight and my activities and investigate on the gout attack pattern on me. I read book, search a lot on Internet, of course listen to doctors and diet advises. But nothing more important than monitoring my body .
I have a strong feeling that I will recovery from Gout. I have some my personal experience to share here.
SO, What I had on lunch that cause "GOUT ATTACK"?"Curry chicken rice"