Lupus erythematosus

Introduction to lupus erythematosus Lupus erythematosus (sle) is an autoimmune disease involving multiple organs and multiple organs in the body, complex clinical manifestations, and prolonged course of disease. Lupus erythematosus can be divided into two major categories: systemic lupus erythematosus (SLE) and discoid lupus erythematosus (DLE). Subacute cutaneous lupus erythematosus (SCLE) is a skin lesion between discoid lupus erythematosus and systemic lupus erythematosus. basic knowledge The proportion of illness: 0.003% - 0.008% Susceptible people: no specific population Mode of infection: non-infectious Complications: adult respiratory distress syndrome peritonitis pneumonia

Cause of lupus erythematosus

Genetic (25%):

The prevalence of this disease varies among races. Different strains of mice (NEB/NEWF, MRL1/1pr) spontaneously develop SLE symptoms after several months of birth. Family surveys show that first- and second-degree relatives of SLE patients About 10% to 20% may have the same kind of disease, some have hyperglobulinemia, a variety of autoantibodies and T inhibit cell dysfunction, etc., the coincidence rate of monozygotic twins is 24% to 57%, and double eggs Twins ranged from 3% to 9%. HLA typing showed that SLE patients were associated with HLA-B8, -DR2, and -DR3. Some patients were associated with complement C2, C4 defects, and even TNFa polymorphisms. The lack of zygote C2 gene and the high frequency of -DQ are closely related to DSLE; T cell receptor (TCR) is also associated with the susceptibility of SLE. The low level of TNFa may be the genetic basis of lupus nephritis. Genetic predisposition, according to a survey of 100 SLE family members, is a multi-gene inheritance, and environmental factors also play a role.

Drugs (25%):

It has been reported that in 1193 cases of SLE, the incidence of drug-related patients accounted for 3% to 12%, drug-induced disease can be divided into two categories, the first category is drugs that induce SLE symptoms such as penicillin, sulfonamides, Baotaisong, gold preparations, etc. These drugs enter the body, first cause allergic reactions, and then stimulate the quality of lupus or potential SLE patients with idiopathic SLE, or exacerbate the condition of SLE already suffering, usually stopping the drug can not prevent the disease from developing, the second is to cause lupus Drugs of the syndrome, such as hydrazine hydrochloride (hydralazine), procainamide, chlorpromazine, phenytoin sodium, isoniazid, etc., these drugs are used for a longer period of time and larger doses Afterwards, patients may have clinical signs and laboratory changes in SLE, and their pathogenesis is not clear: for example, chlorpromazine is thought to be slowly combined with double-stranded NDA, and UVA irradiation is rapidly combined with denatured DNA, and clinically exposed to the skin. After daylight, the double-stranded DNA can be denatured and easily combined with chlorpromazine to produce an antigenic substance; and if hydralazine binds to soluble nucleoprotein, it can enhance the immunogenicity of its own tissue components in the body. Syndrome in The symptoms of the drug can be spontaneously subsided or a few symptoms remain. The HLA classification shows that the positive rate of DR4 is significantly increased. It is considered as the genetic quality of drug-induced SLE. The difference between drug-induced wolverine-like syndrome and idiopathic lupus erythematosus is : 1 clinical involvement of the kidney, less skin and nervous system; 2 older age of onset; 3 shorter and lighter course; 4 no reduction in complement in blood; 5 serum single-stranded DNA antibody positive.

Infection (20%):

Some people think that the pathogenesis of SLE is related to the infection of certain viruses (especially lentivirus). From the patients with glomerular endothelial cytoplasm, vascular endothelial cells, and lesions, substances similar to inclusion bodies can be found, and the serum of patients is increased. Especially for measles virus, parainfluenza virus type III, EB virus, rubella virus and viscovirus. In addition, there are dsRNA, ds-DNA and RNA-DNA antibodies in the serum of the patient. The former is usually only in tissues with viral infection. Can be found, observed under electron microscopy, these inclusion body-like substances in the small tube network structure, diameter 20 ~ 25m, clustered distribution, but can also be seen in dermatomyositis, scleroderma, acute sclerosis encephalitis, has attempted The isolation of viruses from tissues containing inclusion body-like substances has not been successful, so these substances and viral joints have yet to be confirmed. It has recently been suggested that the pathogenesis of SLE is closely related to C-type RNA virus. The authors measured 72.3% of serum interferon results in 47 cases of SLE. Increased, is alpha type, contains acid stability and acid instability. The concentration of interferon is parallel with the disease activity. It is known that alpha interferon is a white blood cell virus, polynucleotide or fine Produced after lipopolysaccharide stimulation, whether this indirect suggesting the possibility of viral infection, some people think that the incidence of tuberculosis LE or streptococcal infection.

Physical factors (10%):

Ultraviolet light can induce skin lesions or aggravate the original lesions. In a few cases, systemic lesions can be induced or aggravated. About 1/3 of SLE patients are allergic to sunlight, and Epstein ultraviolet radiation is used for skin type LE patients. About half of cases are clinically and histologically. Typical skin lesions, positive skin fluorescence test after two months, such as pre-administration of A can prevent skin lesions, normal human skin double-stranded DNA is not immunogenic, after dimerization by UV irradiation, ie DNA solution The polythymidine dimer is converted into a strong immunogenic molecule. LE patients have confirmed the defect of repairing dimerized DNA. Some people think that ultraviolet rays first damage skin cells, and anti-nuclear factors can enter cells. Nuclear effects, skin damage, cold, strong electro-optic irradiation can also induce or aggravate the disease, some localized discoid lupus erythematosus can become a systemic type after exposure, from chronic to acute.

Endocrine factors (12%):

In view of the fact that women with this disease are significantly more than men, and more often in the growth period, it is believed that estrogen is related to the occurrence of this disease. By castration, the condition of female NZB mice is relieved, and the male rats are intensified to support the role of estrogen. Significant reduction in the disease during gonad-free activity, ie under 15 years of age and after 50 years of age, in addition to oral contraceptives can induce lupus-like syndrome, there are authors of 20 male SLE determination of sex hormone levels found in 50% of patients with serum estradiol The level increased (5% in the control group), the testosterone decreased in 65% of patients (10% in the control group), and the estradiol/testosterone ratio was higher than that in the healthy control group. All of the above images support the theory of estrogen, and the condition of SLE during pregnancy. The change is also related to the increase of sex hormone levels. Since the progesterone level is rapidly increased, the progesterone/estradiol ratio is correspondingly increased, so that the condition is relatively stable and the progesterone level is lowered after birth. Therefore, the virus may be aggravated again, and the serum of SLE patients is recently found. A higher prolactin value, leading to secondary changes in sex hormones, is for further study.

Lupus prevention

1. Establish optimism, treat diseases correctly, establish confidence in overcoming diseases, regularize life, pay attention to work and rest, take appropriate rest, and prevent infection.

2, remove all kinds of incentives, including a variety of possible internal drugs, chronic infections, etc., to avoid irritating topical drugs and all external stimuli.

3, to avoid exposure to sunlight and ultraviolet radiation, especially during the active period, if necessary, can add anti-sunlight drugs such as 3% quinine ointment, compound titanium dioxide ointment, 15% ammonia benzoic acid ointment, etc., other such as cold, X-ray, etc. Excessive exposure can also cause the disease to intensify and cannot be ignored.

4. Rational effects on pyridazine, procaine, penicillamine, antibiotics and sulfa drugs.

5, the patient should be birth control, pregnancy should be avoided during the active period, if there is renal damage or multiple system damage, it is necessary to fight for early treatment of abortion.

Lupus complication Complications, adult respiratory distress syndrome, peritonitis, pneumonia

Renal failure and central nervous system complications such as lupus encephalopathy are prone to occur.

1. Acute lupus pneumonia, complicated by pulmonary hemorrhage or development into adult respiratory distress syndrome (ARDS).

2, lupus peritonitis and lupus mesenteric vasculitis, intestinal perforation or intestinal paralysis, hemorrhagic ileitis and intussusception, heavy intestinal necrosis.

Lupus symptoms common symptoms fatigue discoid erythema loss of appetite limb weakness, dizziness, pale muscles, soreness, bloating, low fever, morning stiffness

1, fever

The immune function of lupus erythematosus is abnormal, and many kinds of substances can be produced in the body, and the body is heated as a heat source. About 80% of patients have fever, most of them are high fever, and about 12% of patients show low fever. The first symptom of some patients is fever of unknown origin. It should be noted that a young woman has a long-term unexplained fever, joint pain and swelling, and a rash. It is highly suspected of the possibility of suffering from lupus erythematosus. Please consult a specialist for further examination. Look at the presence of various autoantibodies to confirm the diagnosis.

Fever often indicates that the condition of lupus erythematosus is active, and measures should be taken to treat it in time to prevent the disease from developing. Another characteristic of fever caused by lupus erythematosus is that after using glucocorticoids, the body temperature can quickly subside and return to normal. If the hormone is stopped, the body temperature can rise again. However, in patients with lupus erythematosus, especially after long-term use of hormones, fever may occur. At this time, it is necessary to be alert to the presence of infection. Because the hormones use, it inhibits human immunity and reduces the body's ability to resist disease and resist bacterial infection. At this time, bacteria can invade the body by taking advantage of it. The most common is lung infection, especially the infection of Mycobacterium tuberculosis. It is necessary to use appropriate antibiotics in a timely manner so as not to endanger the life of the disease.

2, increased erythrocyte sedimentation rate

Because of the convenient detection method of erythrocyte sedimentation rate, it is one of the most commonly used methods for detecting patients with lupus erythematosus. So is it possible that the increase in erythrocyte sedimentation rate can represent the disease activity? This depends on the specific circumstances. In the case of exclusion of infection, normal menstrual changes, and some physical and chemical factors, the increase in erythrocyte sedimentation rate in patients with lupus erythematosus can be said to be in the activity. Such as arthritis, rash, visceral lesions, etc., can cause increased erythrocyte sedimentation rate. After the condition is controlled, the erythrocyte sedimentation rate can gradually return to normal. If a patient's erythrocyte sedimentation rate is stable within a normal range for a long time, the amount of hormone is small, and it can be said that her condition has been controlled. However, normal erythrocyte sedimentation does not necessarily mean that the condition is stable, but also depends on clinical symptoms and hormone dosage.

3, erythema rash

More than 80% of patients have skin lesions, and erythema and rash are diverse. Facial butterfly-like erythema and nail circumference, apical erythema erythema showed characteristic features of lupus erythematosus. Butterfly erythema does not exceed the nasolabial fold, and the nose, forehead, and auricle may also have irregular erythema. There may also be different shapes of erythema on the elbow back, palm back, knuckle, back of the toe, palm, foot and the like. The shape has discoid erythema, ring erythema, edematous erythema, polymorphous erythema and the like.

The shape of the punctate erythema is flaky, the boundary is clear, the middle bulge is flat, and the horny stalk adheres to it. It can not be wiped off, and is connected with the hair follicle below. It is a follicular horn plug, which can be left with atrophic scar. There are depressions.

The rash has red papules and maculopapular rash. It is generally not itchy or itchy. It can occur in all parts of the body. It is more common in the face, neck and limbs. A few people have blisters and blood bubbles. After erythema and blisters subsided, epidermal atrophy, hyperpigmentation and keratinization may occur.

Light sensitive, about one-third of the patients appear to be red when the sun shines. Mainly sensitive to ultraviolet light, in the shade of the house in summer, due to radiation, the face will also be red, some patients have sun allergic rash after ultraviolet radiation.

4, mucosal ulcers and hair loss

About 1/5 of the patients have mucosal damage, involving the lips, tongue, cheeks, nose, cavities, etc., and painless mucosal ulcers appear. If there is a secondary infection, there may be pain. Patients with lupus erythematosus are prone to hair loss. In addition to hair loss due to inflammation of the rash area, other parts will also lose hair, not only hair but also eyelashes. Eyebrows and body hair will also fall off.

There are two forms of hair loss: one is diffuse hair loss, the remaining hair is sparse, the tinge is loose or yellow, the hair is thin and easy to break, forming thin hair or alopecia areata; the other hair loss is concentrated in the forehead, which is usually said At the "bangs", the hair is sparse, yellow and easy to break, and the hair is uneven in length and length, forming a "lupus hair".

The hair loss caused by lupus erythematosus and the "seborrheic alopecia" mentioned in peacetime are completely different things, and the pathological basis is different. Lupus alopecia is mainly caused by small vasculitis under the skin, which leads to a nutritional supply disorder to the hair follicle, which causes the growth of hair to be affected. It is a clinical manifestation of lupus erythematosus. The first episode of a patient with lupus erythematosus is hair loss, so it is necessary to pay attention to the hair loss of lupus erythematosus.

Hair can be regenerated after the condition is controlled. It is particularly noteworthy that re-hair loss in patients with lupus erythematosus may be the first symptom of recurrence of the disease, which should be brought to the attention of doctors and patients.

5, joint pain

More than 90% of patients have joint pain, which can occur in all stages. Some joint pains have appeared in the years before the onset of the disease, and some soft tissue around the joints are swollen, tender and effusion, showing acute arthritis. Most of the affected parts are proximal knuckles, metacarpophalangeal joints, wrists, elbows, knees, toe joints, etc., often with symmetry. Some patients have morning stiffness. Some patients have a longer joint disease, and some patients have only a short-term appearance, even a transient joint pain.

X-rays mostly do not see bone changes and concerns about deformity. Long-term use of glucocorticoids for more than 5 years, about 5% of patients may have aseptic osteonecrosis.

6, blood cell reduction

Due to the presence of autoantibodies, red blood cells, white blood cells, and platelets are all destroyed by themselves. Most of the anemia is positive cell anemia, anti-erythrocyte antibodies are mostly lgG type, and hemoglobin is also decreased. Leukocytes are generally reduced in granulocytes or lymphocytes. Thrombocytopenia, short survival time, and platelets cause self-destruction due to their surface lgG type anti-platelet.

7, heart damage

About one-fourth of patients have pericarditis, mild symptoms can be asymptomatic, and obvious pain in the anterior region, chest tightness, and sometimes a pericardial rubbing sound, clinically not necessarily found. Cardiac ultrasound images or B-ultrasound and X-ray chest radiographs should be routinely examined to show pericardial effusion. The patients with pericardial effusion found in SLE treated in our hospital accounted for 34.15%.

8, lung damage

Many patients with SLE showed two punctate nodules and stenosis or reticular shadows in the X-ray chest radiograph, which were interstitial changes, mostly without symptoms.

Pleurisy can be asymptomatic and found only in the following examinations: small to moderate pleural effusions in B-mode and chest X-rays, sometimes with pericardial effusion. LE cells can be found in the pleural effusion.

9, lupus nephritis

Clinically, about 75% of SLE patients have kidney damage. There are proteins, red blood cells, and white blood cells in the urine test. A few patients have casts. Lupus nephritis occurs early on. The lesion persists for many years and may be extensively damaged and evolve into renal dysfunction resulting in uremia.

10, brain damage

SLE neurological damage has a variety of manifestations. Psychopathic manifestations are schizophrenia reactions, various mental disorders such as irritability, insomnia, hallucinations, suspicion, delusions, obsessive attitudes, etc.

Brain damage is common in severe cases of chronic SLE end stage or acute exacerbation of SLE. There are a few cases of chronic mild brain damage, frequent headache and dizziness, abnormal EEG changes, and the first symptoms in the acute phase in rare cases. Under normal circumstances, brain damage is reversible after timely treatment, and abnormal changes in EEG and brain CT scans are also reversible. Severe intracranial hemorrhage, cerebral palsy can lead to death.

Lupus check

1. Blood routine: leukopenia (<4000/mm3) or lymphopenia (<1500/mm3) or thrombocytopenia (<100000/mm3).

2, ESR: increase.

3, serum protein: albumin decreased, 2 and gamma globulin increased, fibrinogen increased, cold globulin and condensed agglutinin can be increased.

4, immunoglobulin: active blood IgG, IgA and IgM are increased, especially IgG, inactive period is not obvious or not increased, a large number of proteinuria and long patients, blood Ig can be reduced, urine Can be positive.

5, rheumatoid factor: about 20% to 40% of cases are positive.

6, syphilis biological false positive reaction : 2% ~ 15% positive.

7, anti-cardiolipin antibodies: IgG type positive rate of 64%, IgM type of 56%, and patients with thrombosis, cutaneous vasculitis, thrombocytopenia, myocardial infarction, central neuropathy and habitual abortion or intrauterine stillbirth .

8, LE cells : Hargraves (1948) first found in the bone marrow, Haserick (1949) found LE cells from the peripheral blood, miecher (1954) proved that lupus cytokines is an anti-nuclear factor, is a gamma globulin, It is now clear that the formation of LE cells requires four factors:

1LE cytokine, an anti-nuclear protein antibody present in peripheral blood, bone marrow, pericardium, thoracic and peritoneal effusion, blister fluid and cerebrospinal fluid, the corresponding antigen is a set of protein complexes of deoxyribonucleic acid, this antigen is present in Inside the nucleus.

2 damaged or dead nuclei, no species and + organ specificity, that is, the nucleus of various organs of human or animal can act with LE cytokines.

3 active phagocytic cells, usually neutrophils.

4 Complement: In the process of phagocytosis, the involvement of complement is required. The process of LE cell formation firstly acts on the cytokine of LE cells and the damaged or dead nuclei, causing the nucleus to swell, losing its chromatin structure, and dissolving the nuclear membrane to become uniform. The structural substance, the so-called "homogeneous body" cell membrane ruptures, the rounded body breaks into the blood, and many phagocytic cells aggregate to phagocytose the denatured nucleus, form a petal-shaped cluster of cells, and then the denatured nucleus is swallowed by a phagocytic cell, forming a so-called In LE cells, complement is involved in promoting phagocytosis.

About 90% to 70% of active SLE patients, LE cells are positive, and other diseases such as scleroderma, rheumatoid arthritis, etc. can be found in about 10% of cases, in addition, chronic active hepatitis, drug eruption Rucainamide and pyridazine (hydralazine) can also be positive.

9. Antinuclear antibody test (ANA): This test has high sensitivity and poor specificity. As a screening test, the indirect immunofluorescence method is generally used to detect serum ANA, and the rat liver print is used as a substrate. -2 cells, Hep-2 cells, etc. as substrates, about 80% to 95% of cases are positive for ANA test, especially for active period, repeated positive cumulative rate, serum ANA titer 1:80, significance Larger, the change in potency is basically consistent with the clinical disease activity. The fluorescent karyotype can be seen in peripheral type, homogeneous type and spot type, occasionally nucleoli type, and 5% to 10% cases, the clinical symptoms are consistent with SLE. However, ANA continues to be negative and has other immunological characteristics, which may be a subtype.

Antinuclear antibodies are a general term for their own antibodies to various nuclear components. What you see in SLE are:

1, anti-deoxyribonucleic acid (DNA) antibodies: can be divided into anti-natural or double-stranded deoxyribonucleic acid (n-DNA or ds-DNA) antibodies and anti-denatured or single-stranded deoxyribonucleic acid (d-DNA or ss-DNA) antibody.

Detection of anti-ds-DNA antibodies by indirect immunofluorescence using Crithidia: luciliae or Trypanosoma: equiperdum or Trypanossma (evansi) as substrates The positive rate can be as high as 93%-100%, but the positive rate of radioimmunoassay is 60%-70%. The anti-ds-DNA antibody karyotype shows that the peripheral type is the most specific, suggesting that patients often have kidney damage. The prognosis is poor. In the remission period, the positive rate decreases and even turns negative. The terminal patients can also be negative, and the anti-ss-DNA antibody specificity is poor. It can also be seen in other diffuse connective tissue diseases except SLE.

2, anti-nuclear protein (DNP) and histone antibodies: insoluble anti-DNP antibody is also an anti-nuclear factor of LE cells - anti-DNA and histone complex antibodies, fluorescent karyotype is homogeneous, often in SLE During the active phase, more than 90% of cases of lupus-like syndrome caused by procainamide, isoniazid, etc.: anti-histone antibodies can be found.

3, anti-saline extractable nuclear antigen (ENA) antibody: antigen from the calf thymus or rabbit thymus in the sputum, using agar diffusion method or convective immunoelectrophoresis detection, in recent years also useful for immunoblotting detection, anti-NNA antibodies mainly include anti-NNA antibodies Seven antibodies, such as Sm and nRNP, mRNP or U1RNP antigen are complexes of seven proteins of different molecular weight (12-68KD) and U1RNA (U is uracil nucleotide). Sm is a complex of the same seven proteins with U2, U1, U4, U5, U6 RNA. The positive rate of anti-Sm antibody in SLE is 20% to 25%, which is a labeled antibody of SLE, which is often accompanied by anti-ds-DNA antibody, and has nothing to do with disease activity, and can be used as a reference for retrospective diagnosis. Anti-U1RNP antibodies can occur in a variety of connective tissue diseases, and their high titer, in addition to SLE, is often an important serological basis for the diagnosis of mixed connective tissue disease.

4. Anti-Ro/SS-A and anti-La/SS-B antibodies: usually detected by convection immunoelectrophoresis, and can also be determined by immunoblotting. The positive rate of anti-Ro/SS-A antibody detected by the former method is 30%~ 39%, anti-La/SS-B is 13%. The two antibodies have high positive rate and important reference value for primary Sjogren's syndrome and SLE with Sjogren's syndrome and subacute cutaneous lupus erythematosus. Anti-Ro/SS-A antibody is an important serological marker for neonatal lupus erythematosus: , related to light sensitivity.

5, anti-ribosomal protein antibody: by immunoblotting Han detection, the positive rate is about 10%, is a labeled antibody of SLE.

6. Others: Anti-Ku antibody, anti-endothelial cell antibody, anti-neutrophil cytoplasmic antibody, anti-neuronal antibody, anti-layer and anti-fibronectin antibody, anti-VII type can be detected in SLE patients reported in the literature. Collagen antibodies and anti-ganglioside antibodies, etc., the correlation between the positive rate and specificity of these antibodies and clinical symptoms need further study.

10, lupus belt test (LBT): the application of direct immunofluorescence antibody technology to detect skin immunofluorescence band or lupus belt, that is, a limited immunoglobulin deposition zone can be seen at the dermal epithelial junction, the positive rate of skin lesions SLE is 92% , DLE is 90%, normal skin exposure SLE is 70%, non-exposure is 50%, but not in DLE normal skin, in the chronic atrophic or hyperkeratotic skin lesions fluorescent banding, new The rash is deposited like a granule or a thin line, and is stained in the normal skin of SLE. The immunofluorescence band is caused by the deposition of Ig (mainly IgG, also IgM, IgA) and complement at the dermal epithelial junction.

Zeng Fanyin and other human skin DIF methods using 1M.Nacl to study lupus in SLE patients, found that the positive rate of this method is 90.9%, the most common deposition of Ig on the dermis side, followed by deposition on both sides of the real epidermis. However, in the case of the epidermis side alone, the fluorescence pattern is more linear, and a few are granules. Recently, Zhang Xuejun and others used the thermal separation epidermal dermis method to treat 3 cases of bullous SLE in 5 cases of bullous SLE. Two cases and the dermis side showed antibody heterogeneity.

11, cellular immune function assay: lymphocyte transformation test (PHA-LTT), old tuberculin (OT), streptococcal deoxyribonuclease and streptokinase (SD-SK) skin test is often negative.

Detection of T cell subsets: Monoclonal antibody fluorescence technique showed a significant decrease in total T cells (CD3) and inhibitory T lymphocytes (CD8) in active cases, and helper T cells (CD4)/inhibitory T cells (CD4) (CD8) The ratio increased, and as the treatment progressed, the T-suppressed cells returned to normal, and the T-helper cells decreased, and the ratio of the two recovered or was lower than normal.

The detection of NK activity by natural killer cells (NK) using the enzyme (LDH) release method showed a significant decrease in activity, which was more pronounced during the active phase.

12, serum complement determination: about 75% to 90% of patients with SLE serum complement reduction, especially in the active phase, with C3, C4, but in other connective tissue diseases such as dermatomyositis, scleroderma, rheumatoid arthritis No reduction in the middle.

13, circulating immune complex (CIC) : serum CIC increased during the active period.

14. Skin test : skin test with self or the same kind of white blood cells, 75% SLE case positive, using calf bone nucleoprotein for skin test, 84% (21/25) positive, using deoxyribonucleic acid in calf thymus Skin test, 48% (12/25) positive, using histamine in the thymus of the calf for skin test, 92% (23/25) positive.

15, capillary angioscopy: in the SLE patients with fingernail wrinkles and tip microcirculation can be seen in a variety of obstacles, as follows:

1 microvascular vasospasm increased, microvascular tension is poor, microvascular dilatation, especially venous tube expansion is more prominent, and even giant blood vessels appear.

2 micro-blood flow disorders, such as dark red blood, microvascular sputum blood stasis, blood cells in the sputum, flow rate slowed or stagnant.

3 There are exudation and bleeding around the microvessels.

These microcirculatory disorders lead to blood stasis and blood cell aggregation, abnormal microvessels, giant microvessels and dilated microvessels, which can form exudation and hemorrhage around the microvessels, and at the same time can further develop the formation of blood flow, even microthrombus Produced, causing a vicious circle.

16. Hemorheological measurement: Significant abnormalities, such as whole blood specific viscosity, whole blood reduced viscosity, and increased plasma viscosity, suggesting an increase in blood viscosity and a decrease in blood fluidity. The red blood cell electrophoresis time is prolonged, the blood sedimentation is fast, and the K value is increased, which consistently indicates an increase in erythrocyte aggregation, but the hematocrit is generally slightly lower (anemia). Increased fibrinogen in the blood, increased blood cohesiveness, resulting in slow blood flow, providing a theoretical basis for the treatment of blood stasis and phlegm.

Diagnosis and diagnosis of lupus erythematosus

Diabetic diagnostic criteria:

1, butterfly erythema or discoid erythema: flat or higher than the skin fixed erythema, often does not involve the nasolabial area, discoid erythema, bulging erythema covered with horny scales and hair follicle damage, return to the lesion There is skin shrinkage.

2, light sensitivity: sun exposure causes skin allergies.

3, oral mucosal ulcers: painless ulcers in the mouth or nasopharynx.

4, non-arthritis or polyarticular pain: non-erosive arthritis, involving 2 or more peripheral joints, characterized by joint swelling, pain or exudate.

5, pleurisy or pericarditis: chest pain, pleural friction or pleural effusion; pericarditis, abnormal ECG, pericardial friction or pericardial exudate.

6, epilepsy or mental symptoms: non-drug or metabolic disorders, such as uremia, ketoacidosis or electrolyte imbalance; psychosis: non-drug or metabolic disorders, such as uremia, ketoacidosis or electrolyte imbalance.

7, proteinuria, tubular urine or hematuria: proteinuria > 0.5g / dl or 3 +; cell tube type, can be red blood cells, hemoglobin, granular tube type or mixed tube type.

8. Leukocytes are less than 4x10'/L or platelets are less than 100 x 10'/L or hemolytic anemia.

9. Fluorescent antinuclear antibody is positive.

10. Positive for anti-double-stranded DNA antibodies or positive for lupus cells.

11, anti-Sm antibody positive.

12, O decreases.

13, skin lupus belt test (non-lesional site) positive or positive renal biopsy.

Any of the above 13 items can be diagnosed as lupus erythematosus.

The material in this site is intended to be of general informational use and is not intended to constitute medical advice, probable diagnosis, or recommended treatments.