Hyperuricemia And Gout Classification Essay

  • 1.

    Zhu Y, Pandya BJ, Choi HK. Prevalence of gout and hyperuricemia in the US general population: the National Health and Nutrition Examination Survey 2007-2008. Arthritis Rheum. 2011;63(10):3136–41.CrossRefPubMedGoogle Scholar

  • 2.

    Kuo CF, Grainge MJ, Zhang W, Doherty M. Global epidemiology of gout: prevalence, incidence and risk factors. Nat Rev Rheumatol. 2015;11(11):649–62.CrossRefPubMedGoogle Scholar

  • 3.

    Dehlin M, Drivelegka P, Sigurdardottir V, Svard A, Jacobsson LT. Incidence and prevalence of gout in Western Sweden. Arthritis Res Ther. 2016;18:164.CrossRefPubMedPubMedCentralGoogle Scholar

  • 4.

    Lopez AD, Williams TN, Levin A, Tonelli M, Singh JA, Burney PG, et al. Remembering the forgotten non-communicable diseases. BMC Med. 2014;12(1):200.CrossRefPubMedPubMedCentralGoogle Scholar

  • 5.

    Kingsbury SR, Conaghan PG, McDermott MF. The role of the NLRP3 inflammasome in gout. J Inflamm Res. 2011;4:39–49.PubMedPubMedCentralGoogle Scholar

  • 6.

    Martinon F, Petrilli V, Mayor A, Tardivel A, Tschopp J. Gout-associated uric acid crystals activate the NALP3 inflammasome. Nature. 2006;440(7081):237–41.CrossRefPubMedGoogle Scholar

  • 7.

    Pope RM, Tschopp J. The role of interleukin-1 and the inflammasome in gout: implications for therapy. Arthritis Rheum. 2007;56(10):3183–8.CrossRefPubMedGoogle Scholar

  • 8.

    Martin WJ, Walton M, Harper J. Resident macrophages initiating and driving inflammation in a monosodium urate monohydrate crystal-induced murine peritoneal model of acute gout. Arthritis Rheum. 2009;60(1):281–9.CrossRefPubMedGoogle Scholar

  • 9.

    Torres R, Macdonald L, Croll SD, Reinhardt J, Dore A, Stevens S, et al. Hyperalgesia, synovitis and multiple biomarkers of inflammation are suppressed by interleukin 1 inhibition in a novel animal model of gouty arthritis. Ann Rheum Dis. 2009;68(10):1602–8.CrossRefPubMedGoogle Scholar

  • 10.

    McGonagle D, Tan AL, Shankaranarayana S, Madden J, Emery P, McDermott MF. Management of treatment resistant inflammation of acute on chronic tophaceous gout with anakinra. Ann Rheum Dis. 2007;66(12):1683–4.CrossRefPubMedPubMedCentralGoogle Scholar

  • 11.

    Terkeltaub R, Sundy JS, Schumacher HR, Murphy F, Bookbinder S, Biedermann S, et al. The interleukin 1 inhibitor rilonacept in treatment of chronic gouty arthritis: results of a placebo-controlled, monosequence crossover, non-randomised, single-blind pilot study. Ann Rheum Dis. 2009;68(10):1613–7.CrossRefPubMedPubMedCentralGoogle Scholar

  • 12.

    So A, De Smedt T, Revaz S, Tschopp J. A pilot study of IL-1 inhibition by anakinra in acute gout. Arthritis Res Ther. 2007;9(2):R28.CrossRefPubMedPubMedCentralGoogle Scholar

  • 13.

    Neogi T, Jansen TL, Dalbeth N, Fransen J, Schumacher HR, Berendsen D, et al. 2015 Gout Classification Criteria: An American College of Rheumatology/European League Against Rheumatism Collaborative Initiative. Arthritis Rheumatol. 2015;67(10):2557–68.CrossRefPubMedPubMedCentralGoogle Scholar

  • 14.

    Gruber M, Bodner G, Rath E, Supp G, Weber M, Schueller-Weidekamm C. Dual-energy computed tomography compared with ultrasound in the diagnosis of gout. Rheumatology. 2014;53(1):173–9.CrossRefPubMedGoogle Scholar

  • 15.

    Ruiz Santiago F, Guzman Alvarez L, Del Mar Castellano Garcia M. Ultrasound pathology of the elbow: a pictorial essay. Ultraschall Med. 2012;33(7):E344–9.CrossRefPubMedGoogle Scholar

  • 16.

    Glazebrook KN, Guimaraes LS, Murthy NS, Black DF, Bongartz T, Manek NJ, et al. Identification of intraarticular and periarticular uric acid crystals with dual-energy CT: initial evaluation. Radiology. 2011;261(2):516–24.CrossRefPubMedGoogle Scholar

  • 17.

    Loffler C, Sattler H, Peters L, Loffler U, Uppenkamp M, Bergner R. Distinguishing gouty arthritis from calcium pyrophosphate disease and other arthritides. J Rheumatol. 2015;42(3):513–20.CrossRefPubMedGoogle Scholar

  • 18.

    Singh JA, Dalbeth N. Is the double contour sign specific for gout? Or only for crystal arthritis? J Rheumatol. 2015;42(3):353–4.CrossRefPubMedGoogle Scholar

  • 19.

    Khanna D, Fitzgerald JD, Khanna PP, Bae S, Singh MK, Neogi T, et al. 2012 American College of Rheumatology guidelines for management of gout. Part 1: systematic nonpharmacologic and pharmacologic therapeutic approaches to hyperuricemia. Arthritis Care Res. 2012;64(10):1431–46.CrossRefGoogle Scholar

  • 20.

    Khanna D, Khanna PP, Fitzgerald JD, Singh MK, Bae S, Neogi T, et al. 2012 American College of Rheumatology guidelines for management of gout. Part 2: Therapy and antiinflammatory prophylaxis of acute gouty arthritis. Arthritis Care Res. 2012;64(10):1447–61.CrossRefGoogle Scholar

  • 21.

    Richette P, Doherty M, Pascual E, Barskova V, Becce F, Castaneda-Sanabria J, et al. 2016 updated EULAR evidence-based recommendations for the management of gout. Ann Rheum Dis. 2016. Ahead of print.Google Scholar

  • 22.

    Singh JA. Quality of life and quality of care for patients with gout. Curr Rheumatol Rep. 2009;11(2):154–60.CrossRefPubMedPubMedCentralGoogle Scholar

  • 23.

    Neogi T, Dalbeth N, Stamp L, Castelar G, Fitzgerald J, Gaffo A, et al. Renal dosing of allopurinol results in suboptimal gout care. Ann Rheum Dis. 2016. Ahead of print.Google Scholar

  • 24.

    Stamp LK, Taylor WJ, Jones PB, Dockerty JL, Drake J, Frampton C, et al. Starting dose is a risk factor for allopurinol hypersensitivity syndrome: a proposed safe starting dose of allopurinol. Arthritis Rheum. 2012;64(8):2529–36.CrossRefPubMedGoogle Scholar

  • 25.

    Kiltz U, Smolen J, Bardin T, Cohen Solal A, Dalbeth N, Doherty M, et al. Treat-to-target (T2T) recommendations for gout. Ann Rheum Dis. 2016. Ahead of print.Google Scholar

  • 26.

    Becker MA, Schumacher HR, MacDonald PA, Lloyd E, Lademacher C. Clinical efficacy and safety of successful longterm urate lowering with febuxostat or allopurinol in subjects with gout. J Rheumatol. 2009;36(6):1273–82.CrossRefPubMedGoogle Scholar

  • 27.

    Halpern R, Fuldeore MJ, Mody RR, Patel PA, Mikuls TR. The effect of serum urate on gout flares and their associated costs: an administrative claims analysis. J Clin Rheumatol. 2009;15(1):3–7.CrossRefPubMedGoogle Scholar

  • 28.

    Shoji A, Yamanaka H, Kamatani N. A retrospective study of the relationship between serum urate level and recurrent attacks of gouty arthritis: evidence for reduction of recurrent gouty arthritis with antihyperuricemic therapy. Arthritis Rheum. 2004;51(3):321–5.CrossRefPubMedGoogle Scholar

  • 29.

    Becker MA, Schumacher Jr HR, Wortmann RL, MacDonald PA, Eustace D, Palo WA, et al. Febuxostat compared with allopurinol in patients with hyperuricemia and gout. N Engl J Med. 2005;353(23):2450–61.CrossRefPubMedGoogle Scholar

  • 30.

    Sundy JS, Baraf HS, Yood RA, Edwards NL, Gutierrez-Urena SR, Treadwell EL, et al. Efficacy and tolerability of pegloticase for the treatment of chronic gout in patients refractory to conventional treatment: two randomized controlled trials. JAMA. 2011;306(7):711–20.CrossRefPubMedGoogle Scholar

  • 31.

    Effective Health Care Program. Management of Gout. Executive Summary. Rockville: Agency for Healthcare Research and Quality; 2016. https://effectivehealthcare.ahrq.gov/ehc/products/564/2196/gout-management-executive-160314.pdf.Google Scholar

  • 32.

    Shahid H, Singh JA. Investigational drugs for hyperuricemia. Expert Opin Investig Drugs. 2015;24(8):1013–30.CrossRefPubMedGoogle Scholar

  • 33.

    FDA news release. FDA approves Zurampic to treat high blood uric acid levels associated with gout. 2015. http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm478791.htm. Accessed 10 Jan 2016.Google Scholar

  • 34.

    European Medicines Agency. Zurampic. Lesinurad. 2016. http://www.ema.europa.eu/ema/index.jsp?curl=pages/medicines/human/medicines/003932/human_med_001963.jsp&mid=WC0b01ac058001d124. Accessed 10 Jan 2016.

  • 35.

    So A, Thorens B. Uric acid transport and disease. J Clin Invest. 2010;120(6):1791–9.CrossRefPubMedPubMedCentralGoogle Scholar

  • 36.

    Saag KG, Fitz-Patrick D, Kopicko J, Fung M, Bhakta N, Adler S, et al. Lesinurad combined with allopurinol: randomized, double-blind, placebo-controlled study in gout subjects with inadequate response to standard of care allopurinol (A US-based Study). Arthritis Rheumatol. 2016. doi:10.1002/art.39840.Aheadofprint.Google Scholar

  • 37.

    Poiley J, Steinberg AS, Choi YJ, Davis CS, Martin RL, McWherter CA, et al. A randomized, double-blind, active- and placebo-controlled efficacy and safety study of arhalofenate for reducing flare in patients with gout. Arthritis Rheumatol. 2016;68(8):2027–34.CrossRefPubMedPubMedCentralGoogle Scholar

  • 38.

    Annemans L, Spaepen E, Gaskin M, Bonnemaire M, Malier V, Gilbert T, et al. Gout in the UK and Germany: prevalence, comorbidities and management in general practice 2000-2005. Ann Rheum Dis. 2008;67(7):960–6.CrossRefPubMedGoogle Scholar

  • 39.

    Primatesta P, Plana E, Rothenbacher D. Gout treatment and comorbidities: a retrospective cohort study in a large US managed care population. BMC Musculoskelet Disord. 2011;12:103.CrossRefPubMedPubMedCentralGoogle Scholar

  • 40.

    Zhu Y, Pandya BJ, Choi HK. Comorbidities of gout and hyperuricemia in the US general population: NHANES 2007-2008. Am J Med. 2012;125(7):679–87. e671.CrossRefPubMedGoogle Scholar

  • 41.

    de Abajo FJ, Gil MJ, Rodriguez A, Garcia-Poza P, Alvarez A, Bryant V, et al. Allopurinol use and risk of non-fatal acute myocardial infarction. Heart. 2015;101(9):679–85.CrossRefPubMedGoogle Scholar

  • 42.

    Kanji T, Gandhi M, Clase CM, Yang R. Urate lowering therapy to improve renal outcomes in patients with chronic kidney disease: systematic review and meta-analysis. BMC Nephrol. 2015;16:58.CrossRefPubMedPubMedCentralGoogle Scholar

  • 43.

    Maahs DM, Caramori L, Cherney DZ, Galecki AT, Gao C, Jalal D, et al. Uric acid lowering to prevent kidney function loss in diabetes: the preventing early renal function loss (PERL) allopurinol study. Curr Diab Rep. 2013;13(4):550–9.CrossRefPubMedPubMedCentralGoogle Scholar

  • 44.

    Kim HA, Seo YI, Song YW. Four-week effects of allopurinol and febuxostat treatments on blood pressure and serum creatinine level in gouty men. J Korean Med Sci. 2014;29(8):1077–81.CrossRefPubMedPubMedCentralGoogle Scholar

  • Nutritional therapy for Arthritis and Osteoarthritis.

    Dietary therapy options for the patient with Arthritis urica (Gout), Rheumatism, Arthritis and Osteoarthritis by Sven-David Müller, M.Sc.

    Musculoskeletal disorders can be of inflammatory as well as degenerative nature. 10 to 15 percent of all patients presenting at medical surgeries suffer from diseases and conditions affecting the musculoskeletal system. It is estimated that about 2.5 to 3 percent of the German population suffer from inflammatory rheumatic diseases, such as rheumatoid arthritis. These figures emphasise both, the need for providing those affected and interested in the prevention, diagnosis and treatment of inflammatory and degenerative diseases of the musculoskeletal system with up-to-date information, and the socio-economic impact and burden on the health-care system of this group of diseases. Rheumatoid diseases involve conditions associated with pain and functional limitations of the musculoskeletal system and as such, diseases of the peripheral joints have to be differentiated from diseases affecting the root skeleton and the ones affecting connective tissues. People adversely affected by rheumatoid arthritis, are known to benefit from an anti-inflammatory nutritional therapy, as it is described in this book. This diet is low in inflammation-promoting arachidonic acid and rich in omega-3 fatty acids, which are known to reduce inflammatory reactions. At least 800.000 people in Germany suffer from rheumatoid arthritis. Osteoarthritis, also known as degenerative joint disease is characterised by the progressive degradation of cartilage. As part of the nutritional therapy, sufferers of osteoarthritis benefit from a healthy, balanced diet that helps to reduce weight and to prevent weight gain. Patients suffering from osteoarthritis often develop secondary inflammatory complications (activated osteoarthritis) and, hence, benefit from a similar diet recommended in patients suffering from rheumatoid arthritis.

    Gout (Arthritis urica)

    In the past, gout (hyperuricemia) predominantly affected wealthy people. Gout used to be called 'Zipperlein' and was considered to be a typical rich man's disease. Gout, today and in the past, is and used to be associated with general overeating and reduced physical activity. Nowadays, about 3 percent of men who reach the age of 65 suffer from an acute gout attack.


    Gout is a rheumatic disease that is characterised by recurrent attacks. It results from an elevated concentration of uric acid in the blood, which leads to the deposition of monosodium urate crystals mainly in the joint capsules and cartilage, in the pinna of the ear and in the renal tubules. The accretions of urate crystals in the gout nodules are called tophi. Gout most often affects the big toe joint, and in those cases is referred to as podagra. The condition can be classified into primary (familial) and secondary hyperuricemia. Primary hyperuricemia is due to a congenital disorder of the purine metabolism, which in 75 to 80 % of all cases affects the excretion via the kidneys and in 20 to 25 % leads to an increase in uric acid formation. In contrast, secondary hyperuricemia is not based on a dysfunctional metabolism, but is the result of urate hypoexcretion or an elevated synthesis of uric acid. Despite many similarities with rheumatic diseases (joint pain, -inflammation, -destruction, involvement of bone, cartilage, tendons and bursae), gout classifies as a metabolic disease.


    Gout is the result of a dysfunctional purine metabolism. Purines such as adenine, hypoxanthine and guanine are components of nucleic acids and thus, of the DNA or RNA, and are present in all animal and human cell nuclei. Uric acid is the end product of the human purine metabolism. The size of the body uric acid pool depends directly on both intrinsic purine synthesis (350 mg daily) and extrinsic intake of purines via the diet with more than 300 mg daily. In healthy subjects, the supply/production and the excretion of uric acid is well-balanced. This balance is disturbed in patients suffering from gout, which may result in a significantly higher total body uric acid pool than in nonhyperuricemics. Healthy individuals maintain a relatively stable serum uric acid concentration between 2 and 7 mg/dl. Is the uric acid concentration greater than 6.5 mg/l, it may promote uric acid precipitation.

    Figure: Synthesis, supply and excretion of uric acid Gout symptoms

    An acute attack of gout is characterised by the swelling and redness of the joints.

    In 2/3 of all cases, the big toe joint is affected. However, this can extend to adjacent areas. Further accompanying symptoms are the general feeling of being unwell, fever, increased pulse rate, headache and vomiting. Four different types of gout can be distinguished:

    Asymptomatic hyperuricemia: elevated uric acid levels, usually discovered by accident. The patient is usually completely asymptomatic.

    Acute gout attack: is caused by sodium urate in the synovial space and results in significant swelling, inflammation and effusion. An acute attack commonly occurs at night or early in the morning and is extremely painful. Opulent meals together with the consumption of alcohol can trigger an attack. Characteristic is the infection of the big toe joint, but also of finger -and wrist joints and also the ankle joint may be affected.

    Intercritical gout: the time between two attacks of gout. These periods are asymptomatic. It may take months or years until a new attack occurs.

    Chronic (tophaceous) gout: is characterised by uric acid crystal deposits in multiple joints mediating an acute inflammatory response, as well as cartilage and bone damage with characteristic arthritic joint changes.

    Diagnosis of gout

    A diagnosis of hyperuricemia is based on the measurement of the uric acid level and the detection of monosodium urate crystals in the tissues and joints.

    The treatment of gout

    The aim of long-term treatment of gout is to permanently reduce the serum urate levels in the body. A nutrition therapy can help with achieving this goal. The overall supply of purines, which are present in animal and in plant foods as the building blocks of RNA, DNA and nucleotides, has to be reduced. Medical therapy involves the employment of pharmaceutical drugs that (a) inhibit the synthesis of uric acid (uricostatic drugs) and (b) increase the excretion of uric acid (uricosuric drugs).

    Nutrition therapy of patients with hyperuricemia and gout

    A consistent change of diet helps to reduce the number of prescribed pharmaceutical drugs or indeed renders them unnecessary. The frequent over- and malnutrition in western industrialised countries is considered to be one of the ultimate causes for the development of hyperuricemia and gout. The objectives of a change in diet in case of hyperuricemia are as follows:

    Restricted intake of dietary purine Reduction of body weight in overweight patients Milk and dairy products are recommended as sources of protein Restricted alcohol consumption A diet low in purines should not contain more than 300 to 500 mg of uric acid per day or up to 3500 mg per week.

    Meat, meat products and fish consumption should be limited to 100 g per day. The purine-rich skin of poultry should be removed.

    Animal foods with more than 200 mg of purines per 100 g, such as offal, pork rinds, meat extract, certain fish species and all herbal products containing more than 50 mg of purines per 100 g, such as legumes, green peas, broccoli, and wheat germ should be avoided.

    Preference for low-fat dairy products and eggs are recommended as sources for animal protein.

    Offal, such as liver, kidney, thymus, heart, some types of fish and crustaceans, such as salt herring and lobster should be avoided.

    Legumes and purine-rich plant-based foods should be avoided (cabbage, Brussels sprouts, peas, beans and lentils).

    Limit alcohol consumption to one glass of wine or beer daily. 100 ml beer contains 15 mg uric acid. Non-alcoholic beer contains about the same amount of purines.

    Tea, cocoa and coffee are allowed.

    The daily fluid intake should exceed 2.5 litres. The induced diuresis results in an increase of uric acid excretion via the kidneys. Alkalising carbonated sparkling mineral waters (mediating an increase of the urinary pH) are recommended.

    It is best to cook the food, because part of the purines break down and dissolve into the cooking water.

    A strict diet contains no more than 300 mg of uric acid per day or 2000 mg per week. The rules of a low-purine diet apply. In addition, meat, -sausage or fish intake should be limited to a maximum of 100 g once or twice a week.

    Treatment of an acute gout attack

    In case of an acute gout attack, a liquid-enriched, strictly low-purine diet should be implemented. Tea, juices and alkalising mineral waters are suitable to cover the recommended fluid intake. The diet should be light and easily digestible. For the duration of the acute phase, a rice-fruit or fruit diet is recommended.

    Rheumatoid arthritis

    Already the Greek physician Hippocrates (460-377 BC) and the great German physician Paracelsus (1493-1541) were familiar with rheumatism and its treatment. Rheumatic diseases comprise a wide spectrum of different conditions. Rheumatic disorders are all musculoskeletal and connective tissue disorders. The term rheumatism is derived from Greek and means flowing, streaming. It is an outdated, inaccurate traditional term, not sufficient to describe the wide variety of rheumatic diseases, associated with flowing, raging and pulling musculoskeletal pains. Only inflammatory rheumatic diseases such as rheumatoid arthritis can be modified by nutritional therapy.

    Only recently, scientific studies have established that only animal foods contain substances that promote inflammation of the joints. The inflammation is closely associated with an elevated level of arachidonic acid. It is contained only in fatty animal foods. About one in 10 adults in Germany suffers from the symptoms of rheumatic disorders. Rheumatism is a term describing painful diseases affecting the musculoskeletal system (joints, spine or muscles). In fact, rheumatism is a collective term for more than a 100 different diseases. They are all characterised by pains affecting the musculoskeletal system and by limited joint mobility. Further complications are swelling and partial or even complete loss of function of the affected body regions.

    The underlying immunological mechanisms in the pathogenesis of rheumatic diseases are poorly understood and addressed in medical scientific research. In addition to hereditary factors, which play a major role in both the inflammatory as well as the degenerative rheumatic diseases, bacterial infections, stress, and chemical and physical agents may also be relevant triggers. The inflammatory reactions characteristic for inflammatory rheumatic diseases are mediated by eicosanoids and cytokines (inflammatory mediators). The most common forms of rheumatism are arthritis, osteoarthritis, soft tissue rheumatism, deterioration of the spine and chronic polyarthritis. Also diseases like gout, osteoporosis and Morbus Bechterew (Spondylitis ankylosans) belong to this group of rheumatic diseases.

    Treatment of rheumatic disease

    Medical treatment is primarily aimed at the alleviation of clinical symptoms. The most commonly used anti-rheumatic drugs are non-steroidal anti-inflammatory drugs, like cortisone and disease-modifying anti-rheumatic drugs which predominantly target inflammation. Different types of non-steroidal anti-inflammatory drugs have different degrees of efficacy in treating rheumatic pain. Disadvantages of these pharmaceutical drugs are the relatively frequent adverse events (side effects) of partly serious nature, as well as contraindications that prohibit the use in patients.

    Principles of nutrition therapy in rheumatic diseases

    Nutrition therapy instead of medical treatment – a dream for many rheumatic patients struggling with side effects or suffering from severe pain, despite the use of medication. A proper diet and regular physiotherapy cannot replace the medical treatment of rheumatism, but it provides side-effect free, cheap, and delicious tasting support in the fight against chronic disease. Rheumatic diseases are not diet-related, such as obesity, gout or diabetes mellitus type 2. However, already Hippocrates described the correlation between diet and the pathogenesis of rheumatic diseases.

    Rheumatoid arthritis is an autoimmune disease caused by chronic inflammation of the joints, the symptoms of which can be alleviated by nutrition therapy. Basically, it has been discovered, that patients suffering from primary chronic polyarthritis, experience alleviation of their discomforts and can potentially reduce their medication, if they eat mainly plant-based foods, low-fat animal foods, plenty of fish (at least 3-4 times a week) and use supplements like antioxidant vitamins, minerals, and omega-3-fatty acids. In a survey, 61 of 140 of rheumatic patients stated, that eating meat and sausage products lead to a worsening of rheumatic pains and 27 indicated that this was caused by eating animal fats and dairy products. 40 of 140 rheumatic patients observed an improvement of their symptoms after consuming vegetable food, 36 after fasting, 57 after a diet with a high ratio of raw food and 17 after eating vegetable fats.

    Obesity: The enemy of the rheumatic patient

    Many rheumatic patients are overweight. Every kilo too much counts and puts strain on the musculoskeletal system. Weight reduction for the obese rheumatic patient is the first and most important step to reduce pain.

    How to best lose weight when suffering from rheumatic disease

    After years of discussion about the appropriate way to lose weight, it has become evident that a low-fat diet will result in weight loss. Weight loss of 500 g per week is completely sufficient. During a weight-reducing diet the energy supply should ideally be 1200-1800 kilocalories. It is not the potatoes, rice, pasta, bread, bananas or grapes that are fattening the nation, but the huge meat and sausage portions, which increase the uric acid pool in the body. Unlike fats, carbohydrates are not fattening and do not contain arachidonic acid.


    The body’s energy supply is directly derived from carbohydrate-containing foods, such as grain products (whole grain bread, whole grain rolls, whole grain rice, and whole grain pasta), vegetables, salads, potatoes, fruit and sugar. Apart from sugar and white flour products, carbohydrate-rich foods are relatively low in calories but rich in valuable fibre.


    Albumen is scientifically referred to as protein, one of the building blocks necessary for life. Protein is required for the building and repair of body tissues, including muscles. Other substances, for instance hormones and enzymes are usually protein-based. Rheumatic patients meet their protein needs by eating plant-based foods, low fat dairy products and in particular fish. Contrary to general belief, the consumption of pork has no negative effect on joint diseases or rheumatic disorders.


    Fat is the most energy-rich nutrient, which is why physicians and dieticians suggest that fat makes you fat. Rheumatic patients should use only high quality vitamin E-rich vegetable oils and low fat- or low-salt margarine. Rheumatic patients, especially those suffering from obesity, benefit from an economical use of the ‘good fats’.

    The recommended fluid-intake when suffering from rheumatism

    Everyone should drink at least 2 litres a day. Most drinks have absolutely no effect on the course of rheumatic disease. Only alcoholic beverages may enhance the inflammatory process and hence, should be largely avoided. Especially recommended are black-, herbal- and fruit teas, coffee (up to 4 cups per day), nutrient-rich fruit and vegetable juice and mineral water (rich in calcium> 250 mg/l).

    Inflammatory mediators

    Primary chronic polyarthritis is considered to be the ‘true/original arthritis’. The causes of the inflammatory processes are well-known in this type of arthritis. They are mediated by cell-derived substances (inflammatory mediators such as leukotriene B4). Nutrition therapy aims to reduce the synthesis of eicosanoid-derived inflammatory mediators. Eicosanoids are hormone-like substances, derived from 20-carbon polyunsaturated fatty acids. Therefore, scientists refer to these mediators as eicosanoids (eikos means 20 in Greek).

    The body’s inflammatory responses play a pivotal role in the pathogenesis of rheumatic disease. Inflammatory mediators, on the other hand, are affected by our diet, such as antioxidant vitamins and minerals, and in particular the fatty acids. Particularly, eicosanoids derived from the polyunsaturated fatty acid arachidonic acid, have profound physiological effects by mediating the inflammatory response of the joints.

    The Culprit: Arachidonic acid

    Arachidonic acid is a polyunsaturated fatty acid which is synthesised in all mammals, including humans, and is converted from a vegetable fatty acid called linolenic acid. In addition to the endogenous biosynthesis of arachidonic acid, humans consume arachidonic acid-rich animal-derived foods. It is easier for the human body to metabolise arachidonic acid supplied via various animal food sources, rather than synthesising it from a precursor via the endogenous metabolism. Arachidonic acid is supplied exclusively and in abundance with a normal diet of animal-derived foods. All plant-based foods are free of arachidonic acid. The more arachidonic acid is available, the more pro-inflammatory eicosanoids are synthesised. Leukotriene B4 is an eicosanoid inflammatory mediator and is produced by oxidation of arachidonic acid.


    0 Thoughts to “Hyperuricemia And Gout Classification Essay

    Leave a comment

    L'indirizzo email non verrà pubblicato. I campi obbligatori sono contrassegnati *