article written by dr. Pop Cristina
medical specialist in rheumatology
As a result of an abnormality in the metabolism of purines (organic molecules present in all the body’s cells that contribute to the formation of adenine and guanine—components of DNA), gout is a condition that manifests biologically through elevated blood uric acid levels exceeding 7 mg/dL and through recurrent clinical episodes of acute arthritis, with the gradual development of gouty tophi around the joints—a process that leads to joint deformities and dysfunction. Extra-articular manifestations include kidney damage due to nephropathy or uric acid urolithiasis.
Although statistics show that only 15% of people with elevated blood uric acid levels will develop gout, hyperuricemia is still considered the most important risk factor for gout—with a significantly higher incidence among people whose uric acid levels exceed 9 mg/dL. The incidence of gout is higher among men; associated risk factors include alcohol consumption, the use of diuretics, and body mass index.
Uric acid is excreted primarily through the kidneys but also via the digestive tract, with the help of bacteria in the large intestine. Normally, in men with a balanced diet, uric acid levels fluctuate around 5 mg/dL, while in women, average levels are slightly lower, at approximately 4.5 mg/dL. Imbalances in serum uric acid levels can result either from overproduction of uric acid or from its inadequate excretion.
The main causes underlying excessive uric acid production are: genetic enzyme abnormalities, excessive consumption of purine-rich foods (particularly high-protein foods of animal origin), alcohol consumption, acute tumor lysis syndrome, and certain systemic diseases such as psoriasis.
Difficult or insufficient elimination of uric acid from the body is involved in 90% of cases of hyperuricemia; causes underlying this phenomenon include kidney disease, low urine output, lactic acidosis or diabetic ketoacidosis, myxedema, hyperparathyroidism, and the use of medications such as diuretics, aspirin (in doses below 2 g/day), antituberculosis drugs (ethambutol and pyrazinamide), cyclosporine, or nicotinic acid.
With regard to alcohol consumption, it should be noted that alcohol contributes to increased uric acid levels through specific mechanisms that trigger both processes simultaneously—both the overproduction of uric acid and its reduced excretion/elimination.
The course of gout is chronic, with four successive stages described: asymptomatic hyperuricemia, acute gouty arthritis, the intercritical period, and chronic tophaceous gout. Kidney involvement (nephropathy or nephrolithiasis) can occur at any stage of the disease.
1. Asymptomatic hyperuricemia – this initial stage is described as the period preceding the first episode of acute gouty arthritis in individuals with elevated uric acid levels, with no other obvious clinical manifestations reported.
2. Acute gouty arthritis, or an acute gout attack, is considered the most dramatic peak of clinical manifestations and can be triggered sooner or later, depending on the duration and severity of hyperuricemia, as well as the overlap of contributing factors such as trauma, overeating, intense physical exertion, surgery, bleeding, infections, or radiation therapy. In 85% of cases, an acute gout attack begins in a single joint, usually the metatarsophalangeal joint of the big toe—a joint characterized by low local temperature and significant mechanical stress during standing and walking—conditions that promote an acidic environment conducive to uric acid crystallization.
The first gout attack can also occur in other joints, such as the ankle, heel, knee, wrist, fingers, and elbows. It is also possible for a first acute gout attack to occur in the shoulder, hip, spine, sacroiliac, or sternoclavicular joints. In extremely rare cases, involvement of the temporomandibular joint has also been reported. Sometimes, before the onset of the first episode of acute gouty arthritis, individuals with elevated uric acid levels report transient sensations of burning, dull pain, or tingling/paresthesia in the joint that will subsequently be affected by the gout attack. The characteristic symptoms of an acute gout attack, in most cases, appear suddenly, usually during the night, waking the patient from sleep due to the intensity of the pain. Within a short time, the joint becomes red, warm, and swollen, sometimes mimicking a localized infection. Over a period ranging from hours to several days, the joint symptoms gradually subside until they disappear.
3. The intercritical period—this is the variable period of time between episodes of acute gouty arthritis during which the patient is completely asymptomatic. Statistically, it is estimated that approximately two-thirds of patients will experience a second gout attack within a maximum of 12 calendar months, while 7% of patients will never experience a second gout attack.
4. Chronic tophaceous gout—this is the most advanced stage of the disease, resulting from the progressive accumulation of uric acid in the body. This stage is characterized by the appearance of tissue deposits of uric acid in the form of tophi, which are described as painless, elastic formations of varying sizes and shapes, with the skin overlying them appearing thin or taut. Sometimes the tophi can ulcerate, allowing a white discharge rich in sodium urate monohydrate crystals to ooze out. The time required for the development of gouty tophi is reported to be, on average, 10–11 years of untreated disease progression from the time of the first gout attack. Given the current state of available treatments, the incidence of this advanced form of the disease has decreased considerably.
Non-pharmacological treatment of gout involves lifestyle changes and following an appropriate diet that excludes the consumption of meat from young animals in particular, but not exclusively (veal, chicken, pork, lamb), game meat (duck, rabbit), organ meats (brain, kidneys, liver), seafood (shrimp, lobster, clams), fatty fish (salmon, tuna), anchovies, herring, mackerel, sardines, certain legumes (dried beans, peas), brewer’s yeast, and alcohol (it is worth noting here that beer, in particular, due to its high guanosine content, can trigger an acute gout attack). It is beneficial to reduce the consumption of refined carbohydrates such as white bread, pastries, and candy—foods that, when consumed, promote weight gain—another factor that contributes to the progression of gout. These dietary restrictions must be strictly followed as part of the treatment for hyperuricemia associated with gout, in conjunction with the prescribed drug therapy and under the regular monitoring of a rheumatologist.
A diet consisting mainly of leafy greens and root vegetables (carrots, parsley, parsnips, celery, beets, etc.) is recommended, along with daily consumption of whole grains, nuts, olives, fruits, and vegetables, and adequate fluid intake (at least 1.5 liters of water per day). cereale integrale
Bibliography
Ruxandra Ionescu, Esențialul în reumatologie ediția a 2-a revizuită, Editura Amaltea, București, 2007
A Kopke; OBW Greeff, Hyperuricaemia and gout: A review, South African Family Practice. 2014
Tuhina Neogi; Clara Chen; Jingbo Niu; Christine Chaisson; David J Hunter; Yuqing Zhang, Alcohol Quantity and Type on Risk of Recurrent Gout Attacks: An Internet-based Case-crossover Study, The American Journal of Medicine, 2014