A A  Prevalence of gout 1-2% of population ,middle and old age ,A  male to female ratio is 5:1 . Gout manifests as acute intermittent attacks of joint and tenosynovial inflammation {redness, swelling, intense pain (worstA  pain ever) ,fever, chills }.
A Attacks often begin during the night , reaching maximum severity in 6-12 hours often waking the patient in the early morning . Early attacks of gout are typically monoarticular and involve joints in the lower extremities {50%A  in 1st metatarsophalangial joint ( podagra) } , typically last 5-14 days then resolve completely spontaneously , over time these acute attacks became more frequent and increasingly polyarticular and begin to involve upper extremities . Tophi takes about 10 years to develop after first acute attack , but < 1 year in patient with chronic renal failure .
A An elevated serum uric acid level is not diagnostic of gout, and a normal or low serum uric acid level does not exclude gout. Radiographs of patients with chronic advanced gout typically reveal asymmetric erosions with overhanging edges. During an attack a marked acute phase response (elevated CRP, neutrophilia) is usual; the ESR is often modestly raised in tophaceous gout.
A Dietary purine restriction, weight loss, and discontinuation of alcohol may help to decrease uric acid levels in patients with mild hyperuricemia and symptomatic gout. Medications that raise serum uric acid levels, such as thiazide diuretics and low-dose salicylates, should be discontinued if alternative therapy is appropriate.
Rapid control of serum uric acid levels generally is not necessary during an acute attack, and acute increases and decreases in the uric acid level alter the steady state and may prolong the current attack or precipitate new attacks. A A  pegylated uricase are under investigation and show promise for the treatment of refractory gout. Uricosuric drugs such as probenecid or sulfinpyrazone , Uricosurics are contraindicated in: over-producers (they already have gross uricosuria), those with renal impairment (ineffective) and in patients with urolithiasis (increased stone formation). Approximately 90% of gout is caused by the inability of the kidneys remove uric acid from the body completely through urine.
Eating calcium-rich foods such as vegetables and fruits such as bananas, potatoes, avocados, milk and yogurt.

Alcohol can lead to increased production of uric acid, while soft drink consumption may inhibit the absorption of calcium and calcium even throw in vain. The following pathways account for the degradation of endogenous purine nucleotides, as well as of the free bases that result from the phosphorolysis of dietary ones. The AMP deaminase reaction is shown in the next slide; the adenosine deaminase reaction is analogous.
Partial proteolysis, or the introduction of a strategic disulfide bond, prevent the interaction of the enzyme with NAD+, and the molecule then switches to O2 reduction, as shown in this slide. Nucleosides and free bases that arise during the degradation of nucleic acids and nucleotides can be salvaged and reused. Uric acid is the end product of purine metabolism and is present in the serum and tissues in the form of MSU .
Discontinuing chronic therapy also alters serum uric acid levels and may precipitate attacks. The uricosuric benzbromarone is effective in patients with mild to moderate renal impairment but can cause hepatotoxicity and has limited availability in most countries. Several hundred years ago gout was thought to be caused by drops of viscous humors that seeped from blood into the joints.
These tips include changes in lifestyle and diet should be regularly and strictly adhered to, if not affected by gout or uric acid disease relapse.
Foods that can cause gout such as beans, mushrooms, cooked spinach, and mustard greens, goat meat, offal and lard (fat), shellfish, duck and turkey, salmon, mackerel, sardines, crab, shrimp , anchovy and some other fish, cream and ice cream, and sweet bread. Water consumption is believed to improve the disposal of substances that are not useful as excessive uric acid from the body.
Sexual activity, such as a kiss can make the body become more relaxed, so easy to boost the immune system. You should also take the time to learn about the food you eat, and take note of foods that seem to trigger your gout. Even though there are a lot of resources online to help you, consulting with your doctor is still the best way to fine tune your diet and reduce uric acid levels.

The latter enzyme also occurs in a second variation, which arises through protein modification. The oxidase activity is found in extracellular enzyme molecules, which lack a supply of NAD+ anyway.
Xanthine dehydrogenase or oxidase both can convert hypoxanthine to xanthine and the latter to uric acid. Typically, when present in the lumen of the tubule, such compounds will compete with urate for reuptake; this is the mode of action of uricosuric drugs like benzbromarone or probenecid. The reason for their delayed discovery is that urate oxidase alone is sufficient for the conversion of urate to allantoin, since the subsequent reactions also occur spontaneously. This scheme shows the reactions involved in purine salvage, which produce AMP, GMP and IMP. Rancid fats which can quickly destroy vitamin E and causes an increase in uric acid in the blood.
In addition, sexual intercourse can facilitate the production of urine so it can reduce the concentration of uric acid in the blood. There is no set uric acid level that triggers gout attacks, each person has a different threshold so you should pay attention to how your body reacts. Intracellularly, most enzyme molecules function as a dehydrogenase and reduce NAD+, as shown in the previous slide. The major difference is that the spontaneous decay produces allantoin as a racemic mixture, whereas enzymatic formation gives rise to one enantiomer only.
When a patient experiences the symptoms of a gout attack uric acid has been accumulating in his blood, and uric acid deposits have been forming in the joints. It should be remembered that the sensitivity of a person to be exposed to uric acid after eating these foods will vary.

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