I. Diagnosis of gout
According to the natural course of gout can be divided into acute phase, intermittent phase and chronic phase, while acute arthritis is the main clinical manifestation of gout, and is often the first symptom.
1.Acute gouty arthritis
Usually under the influence of certain triggers, acute onset of the disease, obvious redness, swelling, burning, severe pain in the joints, often waking up at midnight, early in the morning, the pain reaches its peak in 24 to 48 hours, within a few days or weeks of its own relief, back to normal, and later may recur. About 90% of patients have a first episode involving a single joint, especially the first metatarsophalangeal joint.
Based on the clinical features of recurrent acute monoarthritis and asymptomatic intervals, hyperuricemia, and effectiveness of treatment with colchicine, the diagnosis of typical cases should not be difficult. For a few atypical patients, the clinical diagnosis can be made by using the 12 items (clinical, laboratory, and X-ray manifestations) listed in the 1977 American College of Rheumatology criteria, and meeting 6 or more of them. It should also be differentiated from dengue, cellulitis, septic arthritis, traumatic arthritis, and pseudogout.
It is worth emphasizing that the “gold standard” for the diagnosis of gout is to confirm the presence of uric acid crystals in the synovial fluid or stone tissue. The common method is to use polarized light microscopy to observe the phenomenon of needle-like negative double refraction, or to find needle-like or rod-like crystals under ordinary light microscopy, and can also see the phenomenon of leukocyte phagocytosis crystals, in the acute arthritis period has a 90% positive rate, so this test should be actively carried out.
2. Intermittent gout
This is the remission state between repeated acute attacks, usually without any discomfort or with only mild joint symptoms, therefore, the diagnosis in this period must rely on the past history of acute gouty arthritis attacks and hyperuricemia.
3.Chronic stage of gout
This stage is a consequence of the disease course extending for many years and the persistent high concentration of blood uric acid not being satisfactorily controlled, and the formation of gout stones or persistent non-remission of joint symptoms are the clinical characteristics of this stage. It is not difficult to diagnose in combination with X-ray or nodal biopsy to find uric acid salt, and this stage should be differentiated from rheumatoid arthritis, psoriatic arthritis and bone tumor.
4.Nephritic lesions
Patients with urate nephropathy initially show an increase in nocturia, followed by a decrease in urine specific gravity, hematuria, mild or moderate proteinuria, and even renal insufficiency. At this time, it should be distinguished from secondary gout caused by kidney disease. In the case of uric acid urinary tract stones, renal colic and hematuria are the main clinical manifestations, and most of them do not show up on X-ray plain film, while ultrasound examination may reveal them. Acute uric acid nephropathy should be considered in patients with sudden acute renal failure in patients with widely disseminated tumor or receiving radiotherapy.
Prevention and treatment of hyperuricemia and gout
1.Prevention
Patients with gout should adopt a low-calorie diet and maintain an ideal body weight, while avoiding high-purine foods (animal offal, sardines, clams, oysters and other seafood and thick meat soup, etc.), strictly abstain from drinking various kinds of alcohol, and drink more than 2000ml of water daily to ensure sufficient urine output. At the same time, avoid causative factors, such as overeating and alcoholism, cold and damp, excessive fatigue, mental tension, wearing comfortable shoes, preventing joint damage, and cautious use of drugs that affect uric acid excretion.
However, genetic factors are the root cause of hyperuricemia and gout, and some patients have family tendency to develop the disease clinically. Therefore, patients should not be led to believe that gout can be “cured” by simply controlling their diet. On the contrary, in addition to abstaining from alcohol, reducing purine intake and emphasizing regularity of life, patients’ diets should not be restricted too strictly, and drug intervention is the main means of treating gout.
2.Medication treatment
The drug treatment of gout should be carried out in phases, with the acute phase focusing on the relief and elimination of symptoms. The use of colchicine at the “first moment” of an acute attack can often receive the dramatic effect of rapid, effective and complete termination of the attack (the drug is also used for the prevention of attacks and diagnostic treatment).
It should be noted that the therapeutic dose of colchicine is very close to the toxic dose, and its side effects can cause gastrointestinal reactions such as nausea and vomiting, abdominal pain and diarrhea, as well as leukopenia, aplastic anemia, liver cell damage, hair loss, etc. Use with caution in cases of renal insufficiency. Non-steroidal anti-inflammatory drugs, or even hormones, can also be chosen. During this period, uric acid-lowering drugs should not be added temporarily to avoid prolonging the attack or causing metastatic gout.
The aim of intermittent treatment is to maintain blood uric acid in the normal range. If dietary control is not effective for the first time, patients should receive uric acid-lowering treatment to reduce acute attacks and delay or avoid the occurrence of chronic gout and renal lesions. In the chronic phase, the main objective is to reduce the blood uric acid level, and at the same time, to treat chronic arthritis and possible complications of renal lesions, and to treat gout stones if necessary, in order to improve the quality of life of patients.
Uric acid-lowering drugs are divided into pro-uric acid excreting drugs and anti-uric acid producing drugs, which can be selected with reference to the 24-hour urinary uric acid excretion of patients. A uric acid excretion of more than 600 mg 3.6 mmol on a low purine diet or more than 800 mg 4.8 mmol on a regular diet indicates excessive uric acid production; the opposite is considered to be a decrease in uric acid excretion.
If the kidney function is normal or mildly impaired, and there is no uric acid nephropathy or urinary stones, the use of uric acid excretory drugs such as benzbromarone, benzosulfanilone and propoxur can be used. Alkaline drugs such as sodium bicarbonate or alkaline combination should be taken to keep urine pH around 6.5 to prevent uric acid from forming stones in kidney tissues (but alkaline combination should not be overdosed to prevent calcium stone formation), and plenty of water should be taken to maintain urine output.
Allopurinol is used for hyperuricemia with excessive production of uric acid or for those who are not suitable for uric acid excretory drugs, and also for secondary gout (reduce the dosage for renal insufficiency). The possible side effects are rash, drug fever, gastrointestinal reactions, bone marrow suppression, liver function impairment, etc. and should be monitored regularly. In fact, it is not uncommon to have a mixed type of decreased uric acid excretion and excessive uric acid production at the same time, such as significantly elevated blood uric acid, gout stone formation or when one class of drugs alone is not effective, a combination of two classes of drugs can be used.
All uric acid-lowering drugs should be started in small doses and gradually increased to the therapeutic amount to prevent acute arthritis induced by fluctuations in blood uric acid after medication, and colchicine or non-steroidal anti-inflammatory drugs can be taken prophylactically while starting to use uric acid-lowering drugs. After the effectiveness of uric acid-lowering drugs, the patients should be switched to maintenance doses for long-term use to keep the blood uric acid level below 5.5 mg/dl (327 μmol/L). Therefore, patients should be educated for long-term follow-up and regular testing of blood uric acid and related biochemical indicators in order to adjust medication in time and control the progress of the disease. Do not stop the medication once the blood uric acid test is normal.
In addition, Acetate is a particulate activated carbon, which adsorbs uric acid and creatinine in the intestine after oral administration, increasing uric acid excretion from the intestine and thus reducing blood uric acid level. It is suitable for patients with hyperuricemia and gout with renal insufficiency.
The principles of management of hyperuricemia
The current tendency is to classify primary hyperuricemia as a metabolic syndrome. Metabolic syndrome is a group of diseases with insulin resistance, including abnormal glucose tolerance (diabetes, hypoglycemia), central obesity, hypertension, disorders of lipid metabolism, microalbuminuria and other metabolic abnormalities, all of which are related to the occurrence of cardiovascular and cerebrovascular diseases.
More than half of the patients with primary gout are clinically associated with one or more of these diseases, and several studies have demonstrated after long-term follow-up that elevated blood uric acid levels are closely associated with cardiovascular mortality, suggesting that hyperuricemia is an independent risk factor for poor prognosis in patients with coronary heart disease; it has also been suggested that hyperuricemia may cause renal damage prior to a gout attack.
However, to date there is no direct evidence that dissolved uric acid is harmful, nor is there a good reason to treat asymptomatic hyperuricemia. Clinical pharmacological intervention is only indicated for asymptomatic hyperuricemia with a family history of gout or blood uric acid >9.0 mg/dl 535 μmol/L and 24-hour uric acid >1000 mg 5.9 mmol; conversely, no uric acid-lowering drugs are required, but diet should be controlled, triggers avoided, and closely followed.
In case of concomitant hypertension, diabetes mellitus, hyperlipidemia, cardiovascular and cerebrovascular diseases, appropriate reduction of blood uric acid should be performed along with the treatment of concomitant diseases. For secondary hyperuricemia and gout, treatment of the primary disease should be the main focus, along with uric acid-lowering treatment.