Saturday, September 28, 2013
DISEASES
Hyperuricemia
| Asymptomatic hyperuricemia | |
|---|---|
| Classification and external resources | |
| ICD-10 | E79.0 |
| ICD-9 | 790.6 |
| DiseasesDB | 5375 |
| eMedicine | med/1112 |
| MeSH | D033461 |
Hyperuricemia is a level of uric acid in the blood that is abnormally high. In humans, the upper end of the normal range is 360 µmol/L (6 mg/dL) for women and 400 µmol/L (6.8 mg/dL) for men.
Causes
Many factors contribute to hyperuricemia, including: genetics, insulin resistance, hypertension, renal insufficiency, obesity, diet, use of diuretics, and consumption of alcoholic beverages. Of these, alcohol consumption is the most important.
Causes of hyperuricemia can be classified into three functional types: increased production of uric acid, decreased excretion of uric acid, and mixed type. Causes of increased production include high levels of purine in the diet and increased purine metabolism. Causes of decreased excretion include kidney disease, certain drugs, and competition for excretion between uric acid and other molecules. Mixed causes include high levels of alcohol and/or fructose in the diet, and starvation
Increased production[edit source]
A purine-rich diet is a common but minor cause of hyperuricemia. Diet alone generally is not sufficient to cause hyperuricemia. Purine content of foods varies (see Gout). Foods high in the purinesadenine and hypoxanthine may be more potent in exacerbating hyperuricemia.
Hyperuricemia of this type is a common complication of solid organ transplant. Apart from normal variation (with a genetic component), tumor lysis syndrome produces extreme levels of uric acid, mainly leading to renal failure. The Lesch-Nyhan syndrome is also associated with extremely high levels of uric acid.
Decreased excretion
The principal drugs that contribute to hyperuricemia by decreased excretion are the primary antiuricosurics. Other drugs and agents include diuretics, salicylates, pyrazinamide, ethambutol,nicotinic acid, ciclosporin, 2-ethylamino-1,3,4-thiadiazole, and cytotoxic agents.
The gene SLC2A9 encodes a protein that helps to transport uric acid in the kidney. Several single nucleotide polymorphisms of this gene are known to have a significant correlation with blood uric acid.
A ketogenic diet impairs the ability of the kidney to excrete uric acid, due to competition for transport between uric acid and ketones.
Elevated blood lead is significantly correlated with both impaired kidney function and hyperuricemia (although the causal relationship among these correlations is not known). In a study of over 2500 people resident in Taiwan, a blood lead level exceeding 7.5 microg/dL (a small elevation) had odds ratios of 1.92 (95% CI: 1.18-3.10) for renal dysfunction and 2.72 (95% CI: 1.64-4.52) for hyperuricemia.
Mixed[edit source]
Causes of hyperuricemia that are of mixed type have a dual action, both increasing production and decreasing excretion of uric acid.
High intake of alcohol (ethanol), a significant cause of hyperuricemia, has a dual action that is compounded by multiple mechanisms. Ethanol increases production of uric acid by increasing production of lactic acid, hence lactic acidosis. Ethanol also increases the plasma concentrations of hypoxanthine and xanthine via the acceleration of adenine nucleotide degradation, and is a possible weak inhibitor of xanthine dehydrogenase. As a byproduct of its fermentation process, beer additionally contributes purines. Ethanol decreases excretion of uric acid by promotingdehydration and (rarely) clinical ketoacidosis.[3]
High dietary intake of fructose contributes significantly to hyperuricemia. In a large study in the United States, consumption of four or more sugar-sweetened soft drinks per day gave anodds ratio of 1.82 for hyperuricemia. Increased production of uric acid is the result of interference, by a product of fructose metabolism, in purine metabolism. This interference has a dual action, both increasing the conversion of ATP to inosine and hence uric acid and increasing the synthesis of purine.[16] Fructose also inhibits the excretion of uric acid, apparently by competing with uric acid for access to the transport protein SLC2A9. The effect of fructose in reducing excretion of uric acid is increased in people with a hereditary (genetic) predisposition toward hyperuricemia and/or gout.
Starvation causes the body to metabolize its own (purine-rich) tissues for energy. Thus, like a high purine diet, starvation increases the amount of purine converted to uric acid. A very low calorie diet without carbohydrate can induce extreme hyperuricemia; including some carbohydrate (and reducing the protein) reduces the level of hyperuricemia.[18] Starvation also impairs the ability of the kidney to excrete uric acid, due to competition for transport between uric acid and ketones
Non-medication treatments for hyperuricemia include a low purine diet (see Gout) and a variety of dietary supplements. Treatment with lithium salts has been used as lithium improves uric acid solubility.
Dietary supplements that can be used to make the urine more alkaline include sodium bicarbonate, potassium citrate,magnesium citrate, and Shohl's Solution (now replaced by Bicitra). Medications that have a similar effect include acetazolamide
Temperature
Low temperature is a commonly reported trigger of acute gout: an example would be a day spent standing in cold water, followed by an attack of gout the next morning. This is believed to be due to temperature-dependent precipitation of uric acid crystals in tissues at below normal temperature. Thus, one aim of prevention is to keep the hands and feet warm, and soaking in hot water may be therapeutic.
Asymptomatic hyperuricemia
Most patients with asymptomatic hyperuricemia never develop gout or stones. Treatment for asymptomatic hyperuricemia carries some risk. It is not considered beneficial or cost-effective and, generally, is not recommended. The exception to this is in an oncologic setting in which patients receiving cytolytic treatment may be treated prophylactically to prevent acute uric acid nephropathy.
Symptomatic hyperuricemia
The clinical scenarios under which hyperuricemia can be symptomatic are gout, uric acid stones, or uric acid nephropathy.
Acute gouty arthritis
- The initial goal in acute gouty arthritis is to provide symptomatic relief from pain.
- Indomethacin and other nonsteroidal anti-inflammatory drugs (NSAIDs) are the drugs of choice for acute gouty arthritis. NSAIDs are prescribed for approximately a 7- to 10-day course or until 3-4 days after all signs of inflammation have resolved. Use NSAIDs with caution or avoid them in patients in edematous states, such as heart failure, and in patients with peptic ulcer disease or renal insufficiency.
- Colchicine, which inhibits neutrophil activation, is effective but is currently used less frequently because of its adverse effects. Traditionally, colchicine is administered as a 0.6-mg dose every hour until improvement occurs, adverse gastrointestinal effects occur, or a total of 10 doses is reached and no relief is noted. The adverse gastrointestinal effects include abdominal pain, diarrhea, and nausea, which occur in most patients started on colchicine. Although colchicine can be administered intravenously, this is usually avoided because of its potential for serious toxicity.
- Use intra-articular glucocorticoids in patients with contraindications to NSAID or colchicine use. Occasionally, intra-articular glucocorticoids may be used in patients with gouty arthritis refractory to NSAIDs or colchicine.
Chronic gout therapy
- After the symptoms of acute gout subside, patients enter the intercritical period during which a decision must be made regarding the need for treating the patient with a urate-lowering medication. One important point to consider during treatment is that abrupt lowering of urate levels can precipitate an attack of acute gout during the intercritical period. Thus, these patients receive prophylactic colchicine coverage irrespective of which urate-lowering medication is used.
- The choice of urate-lowering medications is uricosuric drugs (which promote uric acid excretion) or xanthine oxidase inhibitors (which inhibit uric acid production).
- Probenecid, which is a uricosuric drug, inhibits the tubular reabsorption of filtered and secreted urate, thereby increasing urate excretion. The ideal candidates for probenecid therapy are those with a 24-hour urine uric acid excretion of less than 800 mg in 24 hours, no history of nephrolithiasis, and good renal function (creatinine clearance >80 mL/min). The starting dose for probenecid is 250 mg twice a day, which can be increased gradually to a maximum daily dose of 3 g/d. Some degree of gastrointestinal irritation is experienced by approximately 2% of patients.
- Allopurinol is the most widely used antihyperuricemic agent. The major metabolite of allopurinol is oxypurinol, and both allopurinol and oxypurinol are competitive inhibitors of the enzyme xanthine oxidase.
- The ideal candidates for allopurinol treatment are uric acid overproducers (24-h urinary uric acid excretion >800 mg on general diet or >600 mg on a purine-restricted diet); patients with renal insufficiency, nephrolithiasis, or tophaceous gout; or patients at risk for developing uric acid nephropathy. Although allopurinol can be used in almost any hyperuricemic state, the above-mentioned conditions are more specific indications for allopurinol use. The usual maintenance dose for adults is 200-300 mg/d. The long half-life of oxypurinol makes once-daily dosing possible. Very importantly, adjust the dose in persons with chronic renal insufficiency because a higher incidence of adverse effects is observed if the dose is not adjusted.
- Allopurinol is well tolerated by most patients, but hypersensitivity reactions may develop, which can be severe or fatal. Because a skin rash may progress to a severe hypersensitivity reaction, patients who develop a skin rash should discontinue allopurinol. Hepatotoxicity, bone marrow depression, and interstitial nephritis are rare but serious adverse effects of allopurinol.
Uric acid nephrolithiasis
- Allopurinol is the mainstay of drug therapy in patients with hyperuricemia who develop uric acid stones. Patients with calcium stones who are hyperuricosuric may also benefit from allopurinol because urate crystals in the urine may act as a nidus for other stones to form.
- Potassium citrate and occasionally sodium bicarbonate or acetazolamide may be required to alkalinize the urine and to decrease the solubility of uric acid.
- Adequate hydration is recommended to maintain a high urine output of at least 2 L unless otherwise contraindicated for other medical conditions where volume overload may be a concern.
Uric acid nephropathy
- Over the years, efforts to prevent uric acid nephropathy, especially in the oncological setting, have resulted in a decrease in mortality from uric acid nephropathy.
- Intravenous hydration with saline and the administration of furosemide or mannitol (to dilute the urine) are necessary to prevent further precipitation of uric acid. Alkalinizing the urine with sodium bicarbonate or acetazolamide may be necessary to further enhance uric acid elimination.
- Rasburicase, a recombinant urate oxidase, is now approved for use in preventing complications of hyperuricemia during the tumor lysis syndrome. It facilitates the conversion of urate to a more soluble product, allantoin.
- Higher doses than usual of rasburicase (600-900 mg/d) are administered to decrease uric acid production prior to chemotherapy in patients with leukemias and lymphomas; allopurinol and hydration are continued for several days.
- If acute renal failure develops despite these measures, then early hemodialysis is indicated to reduce the total body burden of uric acid, thereby facilitating recovery of renal function.
- Pegloticase is another uric acid oxidizer that has been recently approved for gout.
Diet
The use of a low-purine diet may significantly lower serum uric acid levels.
- This diet principally consists of sugars, starches, and fats, with protein supplied by eggs and cheese.
- Meats, poultry, fish, seafood, organ meats, alcohol, beans, and peas should be avoided.
Medication Summary
The goals of pharmacotherapy are to reduce morbidity and to prevent complications.
Pharmacotherapy for hyperuricemia is based on whether patients are overproducers or undersecretors. Allopurinol continues to be the mainstay for the treatment of patients who are overproducers, although the drug febuxostat is being investigated as a possible replacement for allopurinol. Febuxostat is a nonpurine selective xanthine oxidase inhibitor for the treatment of gout.[9, 10]
A 52-week randomized study published in 2005 evaluated over 700 patients with gout and serum uric acid levels of at least 8 mg/dL. More than 50% of patients taking 80 mg/d of febuxostat achieved a serum uric acid level of less than 6 mg/dL at the last 3 monthly measurements, according to the study. This was in comparison to 62% of patients who reached this primary endpoint with 120 mg/d of febuxostat and 21% of patients who achieved this target with 300 mg/d of allopurinol.
However, follow-up comments by the author acknowledged that discontinuation of the drug occurred 2 times as often in the low-dose febuxostat group and 3 times as often in the high-dose febuxostat group, as it did in the allopurinol group. Moreover, the occurrence of 4 deaths in the febuxostat groups, as compared with none in the allopurinol group, is a concern, and therefore, febuxostat needs further study.[9, 11, 12] Febuxostat was approved by the US Food and Drug Administration (FDA) in February 2009 for long-term treatment of hyperuricemia in gout.
Rasburicase is another medication that was introduced to control hyperuricemia. It is a recombinant urate oxidase that is indicated for preventing complications of hyperuricemia during the tumor lysis syndrome. Since losartan has been found to have an uricosuric property, it may be worthwhile to use it in hypertensive patients with hyperuricemia that lack any contraindication to angiotensin receptor blockers. Other uricosuric drugs used in underexcretors are mentioned below.
Nonsteroidal Anti-Inflammatory Drugs
Class Summary
Management of pain and inflammation in gout. Have analgesic, anti-inflammatory, and antipyretic properties. Inhibit the enzyme cyclooxygenase, thus inhibiting biosynthesis of prostaglandins and thromboxanes from arachidonic acid.
Indomethacin (Indochron E-R, Indocin)
Rapidly absorbed. Metabolism occurs in liver by demethylation, deacetylation, and glucuronide conjugation. Inhibits prostaglandin synthesis.
Discontinue 3-4 d following symptom resolution.
Class Summary
Prevent gouty arthritis attacks and nephropathy. Used to treat hyperuricemia secondary to diuretics or antineoplastics. Prevent recurrent uric acid nephrolithiasis.
Allopurinol (Zyloprim)
Inhibits xanthine oxidase, the enzyme that synthesizes uric acid from hypoxanthine. Reduces synthesis of uric acid without disrupting biosynthesis of vital purines.
Febuxostat (Uloric)
Xanthine oxidase inhibitor. Prevents uric acid production and lowers elevated serum uric acid levels. Indicated for long-term management of hyperuricemia associated with gout.
Class Summary
Treatment of gouty arthritis attacks and prevention of their recurrence. Used in management of familial Mediterranean fever.
Reduces formation of uric acid crystals in affected joint, thereby reducing amount of acute inflammation and pain; also decreases uric acid levels in blood. Can be used in combination with probenecid on long-term to prevent gout or can be used alone to treat pain and inflammation of acute gout attacks. Discontinue when pain of gout attack begins to subside, when maximum dose is reached, or when GI symptoms (eg, nausea, vomiting, diarrhea) indicate cellular poisoning. Decreases leukocyte motility and phagocytosis in inflammatory responsesColchicine
Uricosuric Agents
Class Summary
Competitively inhibit reabsorption of uric acid in proximal renal tubule. This promotes excretion of uric acid and lowers serum uric acid levels.
Probenecid (Benemid)
Used to treat and prevent hyperuricemia associated with gout and gouty arthritis
Class Summary
Decrease solubility of uric acid. Adequate hydration recommended to maintain high urine output.
Acetazolamide (Diamox, Diamox sequels)
Used to further enhance uric acid elimination.
Summary Lifestyle and dietary recommendations for gout patients should consider overall health benefits and risk, since gout is often associated with the metabolic syndrome and an increased future risk of cardiovascular disease (CVD) and mortality. Weight reduction with daily exercise and limiting intake of red meat and sugary beverages would help reduce uric acid levels, the risk of gout, insulin resistance, and comorbidities. Heavy drinking should be avoided, whereas moderate drinking, sweet fruits, and seafood intake, particularly oily fish, should be tailored to the individual, considering their anticipated health benefits against CVD. Dairy products, vegetables, nuts, legumes, fruits (less sugary ones), and whole grains are healthy choices for the comorbidities of gout and may also help prevent gout by reducing insulin resistance. Coffee and vitamin C supplementation could be considered as preventive measures as these can lower urate levels, as well as the risk of gout and some of its comorbidities.
Does coffee lower uric acid levels in the blood?
When you suffer from gout or hyperuricemia (high levels of uric acid) it’s very likely that you’ve been told to be cautious with your diet. Choosing between foods, that would have once taken you a moment, now seems to take an eternity, as you agonize over the risks and benefits of each ingredient. Skip the pork chops and beef rolls and choose low uric acid foods like tossed salads with cabbage, parsley and green leafy vegetables. Gulp down large glasses of orange and sweet lime juice or a fresh banana milkshake. Sauté soy chunks…they serve as a good substitute for meat.
Following a uric acid reduction diet will help you make your way to a healthier, more energetic life!
With conflicting information from various sources - some saying that coffee’s good for hyperuricemia and others saying it’s bad; you’re at the end of your tether and are probably ready to toss out your diet plans. Before you give up or decide to make any drastic changes to your diet, it may be a good idea to make sure if the food or ingredient in question, like coffee, is actually bad for you.
So here it is! There is no conclusive research or study to prove coffee’s beneficial effect on uric acid levels. However, the June 2007 issue of Arthritis Care & Research published an article about a large scale study examining the relationship between levels of uric acid and the amount of coffee consumed. The study concluded that high consumption of coffee did result in lowered levels of uric acid, but this change was not brought about by caffeine. Something other than caffeine was found to have caused it. Another study conducted by the University of British Columbia in Vancouver, Canada based on the U.S. Third National Health and Nutrition Examination Survey, reported similar results. While the increased consumption of coffee may lower uric acid levels, it could aggravate or even cause other unrelated health problems. This is why coffee does not appear on most lists of uric acid foods.
Does green tea help lower uric acid levels in the blood?
Green tea is often recommended for a wide variety of ailments including weight loss, better bowel function, prevention of heart diseases, and even as protection from certain cancers. Researchers at the University of Tokyo have concluded that green tea can even increase bone mineral density. In addition to all these health benefits, there is also a definite link between green tea and uric acid levels. Consume green tea on a regular basis to control hyperuricemia (high uric acid levels) and lower your risk of developing gout. A diet chart for uric acid patients is a must as it helps the individual choose recipes and meals that will not cause a flare-up.
There are certain enzymes in our body that support the creation of uric acid in the blood and this causes an increase in blood uric acid levels. So how can green tea reduce uric acid levels? Green tea contains a group of natural chemicals called catechins that have antioxidant properties. When you have a glass of fresh Green tea, the catechins in your tea slow down the effects of just those enzymes and so the production of uric acid is reduced. If you suffer from hyperuricemia, make sure you sip on green tea and stay hydrated throughout the day as dehydration can cause an increase in the concentration of uric acid in the blood.
It is possible to control hyperuricemia through the consumption of green tea. While it may be easy to find a readymade diet chart for uric acid patients, it would be best to consult your doctor before you make any changes to your daily diet. Do not ignore high uric acid levels in the blood as this can lead to severe kidney problems, high blood pressure, heart diseases, and gout. Go slow on red meats and protein rich foods, and instead feast on green leafy vegetables and fresh fruits. Adding papaya cubes to a glass of cool green tea could increase the benefits of your health drink… and make it yummier!
Which fruits and vegetables lower uric acid?
Now that you’ve learnt about your hyperuricemia you’ve become fastidious about the food you consume. No shepherd’s pie over the weekends, and no steaks to gorge on at the dinner table with your pals. Red meats feature high on the list of foods to avoid for uric acid. The breakdown of purines in the body impacts the level of uric acid in the blood, and the resultant hyperuricemia causes kidney problems and gout. If you are overweight, try your best to shed the excess pounds and get in shape. This will enable the kidneys to eliminate uric acid and also reduce the production of uric acid in the body.
Some of the foods high in uric acid which you need to avoid include:
- Fish like anchovies, mackerel, shellfish, sardines, herring
- Meats like beef, mutton, pork
- Avoid eating products including brewer’s yeast and baker’s yeast
- Avoid alcohol; it restricts the elimination of uric acid from the body
- Skip vegetables like spinach and asparagus that have high purine levels
Once you know what foods and vegetables are high in uric acid, you will need to find low uric acid foods that you should include as part of your uric acid diet plan.
- Cherries, strawberries, and blueberries have anti-inflammatory properties so include them in your uric acid diet.
- Raspberries, corn and bran are high fiber foods that can help improve bowel movement, and promote the elimination of uric acid through stools.
- Lemonade with no sugar mixed in, is beneficial for those suffering from hyperuricemia. Lemons contain vitamin C, which disintegrates uric acid and forces it out of the body through urine.
- Low fat dairy products promote kidney health.
- Tomatoes, broccoli, and cucumbers are some of the veggies that you need to start including in your meals.
Are tomatoes, beans and peanuts high in uric acid?
When your doctor first informed you that you have increased uric acid levels, you probably realized the need for changes to your dietary habits. As you begin to ponder over the foods you can and cannot eat, despair begins to set in as you realize that you may just have to give up on a lot of those foods that you love to eat. You start to go through a quick checklist “is there uric acid in tomatoes, bean sprouts, peanuts…?” Well, let’s see if all these foods are bad for uric acid problems!
- Tomatoes: Tomatoes are one of the best vegetables that you could have for lowering uric acid. Tomato by nature is alkaline and when it is exposed to the blood stream it increases the alkalinity of the blood. Eat fresh tomatoes and not processed ones and avoid over eating.
- Beans sprouts: Consuming bean sprouts when you are suffering with high uric acid levels is a bad idea! Beans are rich in proteins which increase the purine levels, leading to high uric acid levels.
- Peanuts: Peanuts have a low purine content and so you can consume peanuts in moderation.
It is also necessary to keep a check on the amount of food that you consume rather than just the food types.
B12 Deficiency:
Fatigue
Weight Loss
Constipation/Diarrhea
Nausea, Vomiting
Abdominal Bloating, Gas
Numbness, Tingling in the Hands, Feet
Sore, Red Tongue.
BLOOD PRESSURE
Potassium
Fruits
Vegetables
Dairy Foods
Fish
Calcium
Low Fat Milk
Yogurt
Cheese
Ragi
Magnesium
Whole Grains
Green Leafy Vegetables
Nuts, Seeds, Dry Peas, Beans
Fish oils
. A type of fat called "omega-3 fatty acids" is found in fatty fish like mackerel and salmon. Large amounts of fish oils may help reduce high blood pressure, but their role in prevention is unclear. Taking fish oil pills is not recommended, because high doses can cause unpleasant side effects. Most fish, if not fried or made with added fat, is low in saturated fat and calories and can be eaten often.
Garlic
. There has been some evidence to suggest garlic’s effect in lowering blood pressure, in addition to improving cholesterol and reducing some cancers. Further research is being conducted to fully assess garlic’s potential health benefits.
INSOMNIA:
Magnesium rich foods:
Green leafy vegetables,
Wheat germ,
Pumpkin seeds
Almonds.
Whole Grains
Oatmeal, whole-grain cereals and breads, and other complex carbohydrates increase production of serotonin, a kind of chemical lullaby, if you will. Serotonin slows nerve activity, calming the brain and spreading a "feel-good" message throughout your body. When darkness enters the picture, the brain converts serotonin to yet another hormone, melatonin, which regulates sleep.
Red Meat and Other Iron-Rich Foods
If restless legs keep you awake, it's possible that you have a form of anemia caused by iron deficiency. Consult a physician to find out if you do. The doctor may prescribe supplements or a diet rich in iron to help correct the problem. Choose lean red meat for the least saturated fat, and eat it for lunch rather than dinner because its protein can counteract sleep-inducing
Turkey
You've probably heard the jokes about the Thanksgiving turkey putting people to sleep, but this folk wisdom has a leg—make that two legs—to stand on. Turkey is rich in tryptophan, an amino acid that the body uses to produce serotonin.
You can also try honey with warm milk. A fast-digesting carbohydrate like honey or mashed potatoes stimulates the release of insulin, which in turn allows more tryptophan to enter the brain.
You can also try honey with warm milk. A fast-digesting carbohydrate like honey or mashed potatoes stimulates the release of insulin, which in turn allows more tryptophan to enter the brain.
Chamomile Tea
Sometimes all it takes to fall asleep is going to bed with the confidence that you will fall asleep. The scientific evidence on chamomile tea for insomnia is thin, but many people find it relaxing. If you think a nice warm cup of this tea before bed will help you drift off, it probably will.
DIABETIS:
General Rule: Even good things need to be taken in moderate for diabetics.
NO:
Coffee with Caffeine
GOOD:
- Green Tea (excess will have bad effects on glaucoma, uric acid etc.)
- Brewer's yeast
- Buckwheat
- Broccoli and other related greens
- Cinnamon
- Cloves
- Coffee
- Okra
- Peas
- Fenugreek seeds
- Sage
BAD:
- Pastries, Bacon, Candy, Raisins, Whole Milk, White Bread
General Information:
Fruits:
Good: papaya, apple, orange, pear and guava
Bad: Mangoes, bananas, and grapes
TIPS:
Do the following if you do not have uric acid complaints :
. 1 teaspoon menthi seeds - soak over night in 100ml of water and have it next morning.
. Tomato juice with salt and pepper. (no salt if BP)
. Soak 6 badam overnight.
CANCER
Herbs
Turmeric
Turmeric
Ginger
Cinnamon
Cayenne Pepper
Garlic
Vegetable
Rosemary
Parsley
Thyme
Mint
Dill
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