Hyperuricemia is a group of diseases caused by disorders of purine metabolism, characterized by increased synthesis or decreased excretion of uric acid (oxidized metabolite of purine) and deposition of uric acid in the soft tissues of joints, resulting in recurrent episodes of metabolic arthritis, gout stone deposition, joint deformities, etc. The lesions often involve the kidneys and cause chronic interstitial nephritis and uric acid kidney stone formation. The lesions often involve the kidneys and cause chronic interstitial nephritis and uric acid kidney stone formation.
I. Causes of gout
The long-term increase of uric acid in the blood is the key cause of gout. Uric acid in human body mainly comes from two sources: (1) endogenous uric acid: nucleic acid and other purine compounds produced by protein metabolism in human cells through the action of some enzymes; (2) exogenous uric acid: nucleic acid and nucleoprotein components of purine compounds contained in food are produced through the action of some enzymes after digestion and absorption.
The production of uric acid is a complex process that requires the participation of some enzymes, which can be broadly classified into two categories: enzymes that promote uric acid synthesis and enzymes that inhibit uric acid synthesis. Gout is caused by various factors that lead to abnormal activity of these enzymes (such as enhanced activity of enzymes that promote uric acid synthesis and reduced activity of enzymes that inhibit uric acid synthesis), resulting in excessive production of uric acid, or various factors that lead to kidney excretion of uric acid, resulting in the accumulation of uric acid in the blood and hyperuricemia.
If hyperuricemia persists for a long time, uric acid will be deposited in the form of urate in joints, subcutaneous tissues and kidneys, causing a series of clinical manifestations such as arthritis, subcutaneous gout stones, kidney stones or gouty nephropathy.
The disease develops as acute or chronic arthritis of peripheral joints, and is caused by the deposition of monosodium urate crystals in and around joints and tendons due to oversaturation hyperuricemia.
Symptoms and signs of gout
Gout can be clinically divided into four stages.
The first stage: the period of hyperuricemia, in which the patient does not have clinical symptoms of gout except for elevated blood uric acid.
The second stage: the early stage of gout, the blood uric acid continues to increase, resulting in a sudden attack of acute gouty arthritis, most people are woken up in their sleep like a knife cut pain, the first site is often the big toe, the joint is red, swollen, burning and swollen, can not cover the quilt, feet stretched out, if the slightest wind blowing or slightly touched, move the toe, immediately pain like a heart, but in a few days or This phenomenon of “coming and going like the wind” is called “self-limiting”. After one painful episode, it seems that the inflammation in the joint has been eliminated and the person is as normal as usual, but in fact, the uric acid crystals do not disappear and continue to act as a monster, and gradually the joint becomes swollen and stiff, and the flexion and extension are unfavorable.
The third stage: the middle stage of gout, from the initial onset of a toe joint, gouty arthritis repeated acute attacks, after several acute attacks, gradually spread to the fingers, toes, wrists, ankles, knees and other joints throughout the body, and then the surrounding soft tissues and bones are also damaged to varying degrees and dysfunction, uric acid crystals continue to deposit, slowly forming a stone like ” gout stones”, at which time, the kidney function is normal or shows a mild decrease.
Stage 4: In the late stage of gout, joint deformity and dysfunction become more and more serious, and gout stones increase in size and easily break out white urate crystals, which affects daily study, work and life due to permanent joint deformity and brings great physical and mental pain to patients. Uric acid salt is deposited into the kidney, forming kidney stones, etc. Clinical swelling, oliguria, proteinuria, increased nocturia, hypertension, anemia, etc. indicate that kidney function is damaged and kidney function is significantly reduced. If the disease develops further, kidney failure will occur which is not easily reversible and life-threatening.
Diagnosis of gout
There is no uniform standard for the diagnosis of gout in China, but the classification criteria of the American Rheumatism Association for acute gouty arthritis are generally adopted.
1.Specific urate crystals are detected in the bursal fluid.
2, gout stones confirmed to contain sodium urate crystals by chemical methods or polarized light microscopy.
3, with 6 of the following 12 clinical, laboratory and x-ray signs
(1) More than 1 episode of acute arthritis.
(2) Inflammatory manifestations peaking within 1 day.
(3) Episodes of monoarthritis.
(4) Dark red color of the skin of the affected joint.
(5) Pain or swelling of the first metatarsal joint.
(6) Unilateral attacks involving the first metatarsophalangeal joint.
(7) Unilateral attacks involving the tarsal joints.
(8) Suspected gout stones.
(9) hyperuricemia.
(10) X-rays showing asymmetric swelling of the joint.
(11) X-ray showing subcortical cysts without mass erosion.
(12) Negative microbiological culture of joint fluid during the inflammatory phase of the joint.
If there is difficulty in confirming the diagnosis during acute arthritis, colchicine can be used as a diagnostic treatment. Acute gout is not difficult to diagnose based on typical clinical manifestations, laboratory tests and treatment response, but the diagnosis of chronic gouty arthritis requires careful differentiation and should be based on urate crystals as much as possible.
Acute gout should be distinguished from acute rheumatoid arthritis, pseudogout, septic arthritis, traumatic arthritis, and gonorrheal arthritis; chronic gout should be distinguished from chronic rheumatoid arthritis, psoriatic arthritis, and tuberculous metaplastic arthritis.
Prognosis of gout
Gout is a lifelong disease, without renal impairment or joint deformity, with effective treatment can generally maintain normal life and work, and will not affect life expectancy, but if improperly treated, recurrent attacks of acute arthritis can cause greater pain, and those with joint deformity and nephrolithiasis will have a certain impact on quality of life, and those with serious renal impairment will have a poorer prognosis.
The life expectancy of gout patients is statistically 5 years shorter than that of the general population, but this is entirely related to the individual situation and the effectiveness of treatment. The life expectancy of patients is often related to the presence or absence of complications, and these factors are summarized as follows.
1. the younger the age of onset, the more severe the disease.
2. the more severe the disease in those with a positive family history
3, the longer the course of the disease the more severe the progressive damage
4, those with high frequency of recurrence and rapid disease progression.
5, the prognosis is poor for those with rapid gout nodules.
6, gout is more severe in those with hypertension, coronary heart disease and kidney disease.
7. dietary control or not, especially in the interval.
8.Therapeutic measures and how to control the disease, whether the acute control is rapid, and whether to adhere to treatment during the interval are closely related to the prognosis.