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    Gout - Encyclopedia of Natural Medicine PDF

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    nadamau22633

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    © All Rights Reserved
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    Gout ‘Acute onset of intense joint pain, typically involving the first joint of the big toe (about fifty percent of cases) Elevated serum uric acid level Periods without symptoms between acute attacks Kentiication of urate crystals in joint fluid ‘Aggregated deposits of urate crystals in and around the joints of the extremities, but also im subcutaneous tissue, bone, cartilage, and other tissues Uric acid kidney stones out is @ common type of arthritis Ge by an inereased concentration of uric acid (the final breakdown product of purine—one of the units of DNA and RNA—metabolism) in biological fluids. In gout, urie acid crystals (monosodium urate) are deposited in joints, tendons, kidneys, and other tissues, where they cause considerable inflammation and damage.'? Gout may lead to debilitation from the uric acid deposits around the joints and tendons, and kidney in- volvement may result in kidney failure. The first attack of gout is characterized by intense pain, usually involving only one joint The first joint of the big toe is affected in nearly half of the first attacks, and is at some time involved in over ninety percent of indi- Viduals with gout. If the attack progresses, fever and chills will appear. The first attacks usually occur at night and are usually pre- ceded by a specific event, such as dietary ex- cess, alcohol ingestion, trauma, certain drugs (mainly chemotherapy drugs, certain diuret- ies, and high dosages of niacin), or surgery. ‘The classic deseription of gout was written by an English physician, Sydenham, who suf- fered from it in 1683.1 Little has changed in the clinical picture of gout in over three hun- dred years. Sydenham’s classic description: The vietim goes to hed and sleeps in good health About two o'clock in the morning he is awakened bya severe pain in the great toc; more rarely in the hicel, ankle, or instep. The pain is like that ofa dis- location, and yet parts fecl as if cold water were poured over them. Then follows chills and shivers, and a little fever, The pain whieh at first was mod- becomes more intense. With its intensity the Is and fever increase. After a time this comes to «height, accommodating itself to the bones and ligaments of the tarsus and metatarsus. Now itis a violent stretching and tearing of the ligaments, now it isa gnawing pain, and now a pressure and tightening, So exquisite and lively meanwhile is the feeling of the part affected, that it eannot bear the weight of bedclothes nor the jar of a person walk- ing in the room. The night is passed in torture, sleeplessness, turning the part affected, and per- petual change of posture; the tossing about of the body being as incessant as the pain of the tortured Joint, and being worse as the fit comes on. Hence the vain effort by change of posture, both in the [3] cour body and the limb affected, to obtain an abatement of pain Subsequent attacks are common, with the majority of gout patients having another at- tack within one year. However, nearly seven percent never have a second attack. Chronic gout is extremely rare these days, due to the advent of dietary therapy and drugs that lower uric acid levels. Some degree of kidney dysfunction occurs in nearly ninety percent of subjects with gout as a result of uric acid deposits, and there is a higher risk of kidney stones. Causes of Gout Gout is classified into two major categories primary and secondary. Primary gout ac- counts for about ninety percent of all cases, while secondary gont accounts for only ten percent. The cause of primary gout is usually unknown. There are, however, several ge- netic defects in which the exact cause of the elevated uric acid is known, The increased serum uric acid level ob- served in primary gout can be divided into three categories: 1. Increased synthesis of uric acid, found in a majority of gout patients QUICK REVIEW * Gout is caused by uric acid crystals de- posited in joints. * Several dietary factors are known to be causes of go eonsumption of alco- hol, high-purine-content foods, fats, and refined carbohydrates © Elimination of alcohol cor sumption 2. Reduced ability to excrete uric acd, typi- cal ofa smaller group (about thirty per- cent) 3. Overproduction and underexeretion of trie acid, found in a small minority of gout patients Although the exact metabolic defect is not known in the majority of cases, gout is one of the most controllable metabolic diseases. Secondary gout refers to those eases in which the elevated uric acid level is sec- ondary to some other disorder, such as exces sive breakdown of cells or some form of Kidney disease, Diuretic therapy for high blood pressure and low-dose aspirin therapy are also important causes of secondary gout since they cause decreased uric acid exe tion CAUSES OF GouT METABOLIC Incase production of purine (primary causes) loath (uno) lncresed prin inake Speccenyme dle ceased production of purines (secondary oonather focor) Increased umover of purines Cancer reduces urie acid levels and prevents gouty arthritis in many individuals. * Liberal fluid intake dilutes the urine and promotes the excretion of uric acid. * Consuming one-half pound of fresh or canned cherries per day has been found effective in lowering uric acid levels and preventing attacks of gout SESROBEQ EEESgE tiss Chronic hemolytic anemia (Gtooxc drugs Psoriasis Increased sytess Inresed breakdown ofprnes Fructose ingestion or infusion Eerie mney Becrcsed kidney deornce of ric aid (primary) Insc kidney disease ecronsed kidney dearonc of wii (secondary) funcional impairment of kidney funn Drug-induced (e.g, tiaides, says, et) Increased lac oid (9, lactic acidss,acohalsm, toxemia of pregnancy, etc) Inceesed keoaid levels, dabei ketoacidosis) Crone ed intoxication ante About 200 to 600 mg of uric acid is ex- cereted daily in the urine of an adult male, andl another 100 to 300 mg is excreted in the bile and other gastrointestinal tract secretions The dietary contribution to the level of uric acid in the blood is usually only ten percent to twenty percent of the total, but purines and uric acid through the diet can increase ‘crystal formation in tissues nonetheless, Urie acid is a highly insoluble molec ‘ule, and at pH 7.4 and body temperature, the serum (blood minus the blood cells) is satu- rated at 64 to 7.0 mg/100 mil. Although higher concentrations do not necessarily re- sult in uric acid crystals being deposited in tissues (some unknown factor in serum ap- Pears to inhibit crystal precipitation), the chance of an acute attack of gout is greater than ninety percent when the level is above 9 mg/100 ml. Lower body temperatures decrease the saturation point of uric acid, which may ex. plain why urie acid deposits tend to form in areas such as the top of the ear, where the temperature is lower than the average body cour TABLET Prevalence of Gouty Arthritis by ‘Maximum Uric Add Level SERUM URIC 0D LeveL Men Women <6 19/100 ml 0.6% 0.08% 60-69 19 33 70-79 167 74 20-89 25.0 ° 9 90.0 ° ee eeeeeeteeel temperature, Uric acid is insoluble below pH 6.0 and can lead to kidney stones, as the urine is concentrated in the collecting ducts of the kidneys and passed to the bladder Thempeut ic Considerations The current standard medical treatment for acute gout is administration of colchicine, the anti-inflammatory drug originally. isolated from the plant Colchicum autumnale (autumn crocus, meadow saffron). Colchicine has no effect on uric acid levels; rather, it stops the inflainmnatory process by inhibiting neutrophil migration into areas of inflammation, Over seventy-five percent of patients with gout show major improvement in symptoms within the first twelve hours alter receiving colchicine, However, as many as eighty per- cent of patients are unable to tolerate an opti mal dose because of gastrointestinal side effects, which may precede or coincide with clinical improvement Colchicine may also cause bone marrow depression, hair loss, liver damage, depres sion, seizures, respiratory depression, and even death. Other anti-inflammatory agents our are also used in acute gout, including: indomethacin, phenylbutazone, naproxen, and fenoprofen. Once the acute episode has resolved, a number of measures are taken to reduce the likelihood of recurrence: + Drugs to keep uric acid levels within a nor- mal range + Controlled weight loss in obese individuals + Avoidance of known triggering factors, such as heavy alcohol consumption or a diet rich in purines + Low doses of colchicine to prevent further acute attacks Several di causes of gout, including consumption of rary factors are known to be Alcohol * High-purine-content foods (organ meats meat, yeast, poultry, etc.) + Fats * Refined carbohydrates + Excessive calories! Individuals with gout are typically obese prone to hypertension and diabetes, and at a greater risk for cardiovascular disease. Obe- sity is probably the most important diet-r lated factor? In concept, the naturopathic approach for treating chronic gout does not differ substan- tially from the standard medical approach: * Dietary ployed, instead of drugs, to keep uric acid levels within the normal range * Obese individuals are put on a careful weight-loss program + Known precipitating factors, such as heavy and herbal measures are em- alcohol consumption and numerous di- etary factors, are controlled ‘+ Nutritional substances are used to prevent further acute attacks Dietory Considerations The dietary treatment of gout involves the following guidelines: ‘* Elimination of alcohol intake © Low-purine diet Achievement of ideal body weight * Liberal consumption of complex carbohy- drates © Low fat intake * Low protein intake * Liberal fluid intake Alcohol Alcohol increases uric acid production by ac colerating purine breakdown, It also reduces uric acid excretion by increasing lactate pro- duction, which impairs kidney fimetion. The net effect is a significant increase in serum urie acid levels. This explains why aleohal consumption is often a trigger in acute at- tacks of gout. Elimination of alcohol is all that is needed to reduce uric acid levels and pre- vent gouty arthritis in many individuals 2-4 Low-Purine Diet A low-purine diet has long been the mainstay of dietary therapy for gout. However, with the advent of potent drugs that lower uric acid levels, many physicians choose to simply ‘write out a prescription rather than edueate the patient how to control the gout by dietary measures. Foods with high purine levels should be entirely omitted. These inchi organ meats, meats, shellfish, yeast (brews and baker's), herring, sardines, mackerel, and anchovies. Foods with moderate levels of protein should be curtailed as well. T dried legumes, spinach, asparagus, fish, poultry, and mushrooms. clude Weight Reduction Fxcess weight is associated with an increased rate of gout.® Weight reduction in obese indi- ‘weds antly reduces serum uric acid fimebs, W222: reduction should involve the umes ber. low-fat diet, a this type of diet will =+!> manage the elevated choles- (teonl anc == Zyceride levels that are also com- om = onbelegcrates. Fats, and Protein v= of refined carbohydrates, fruc- — ted fats should be kept to 2 miner mple sugars (refined sugar, mrs. c.2D'e syrup, com syrup, fructose, ate J incr=ase urie acid production, while sat- aumied fix: decrease uric acid excretion.+6 ‘Whe dee <:ould focus on complex carbohy- dimes 5:2 as legumes, whole grains, and vmegetabies rather than on simple sugars. Frote:=. intake should not be excessive fie erea:+s than 0.8 g/kg of body weight), as itt has Seer, shown that uric acid synthesis ‘max be ::

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