Systemic lupus erythematosus is one of several diseases of a number of “great imitators.” Such a sonorous name defines a pathology that shows nonspecific symptoms that greatly complicate an accurate diagnosis. Such a phenomenon is associated, first of all, with a very large set of clinical signs that manifest in various organs and systems, which in the overwhelming majority of cases provokes an incorrect diagnosis.
Symptoms of systemic lupus erythematosus vary widely, appearing and disappearing unpredictably. Many patients live with SLE for many years before they are diagnosed with the disease.
What do patients complain more about in the early stages of the disease?
- Manifestation of a fever.
- General malaise.
- Pain in joints and muscles.
- Indomitable fatigue.
Since similar symptoms are very common among many other diseases, these signs are not part of the diagnostic criteria for SLE.
The disease, although with a different frequency, but still occurs, regardless of gender, the clinical signs of each sex differ.
For the female type of disease, one thing is characteristic.
- More relapses.
- Relatively low white blood cell count.
- More vivid manifestation of arthritis.
- Psychological disorders against the general background of the course of the disease.
And in men, more often note another.
- Convulsive phenomena.
- Pathology of the kidneys.
- Serositis of internal organs, more often – lungs and heart.
- Disorders of the skin epithelium.
- Peripheral neuropathy.
Violations of the body systems characteristic of systemic lupus erythematosus
About 70% of patients diagnosed with SLE exhibit dermatological symptoms. There are three main categories of skin lesions.
The most common symptom is pain in the joints, mainly in the area of the hand and wrist. 90% of all patients complain of this disorder, which manifests itself with varying intensity for no apparent reason.
Unlike rheumatoid arthritis, SLE usually does not cause serious disturbances in the anatomy of the joints. Only 10% of patients report any significant deformation of the articular elements. True, these people fall into the red danger zone for the development of bone-articular tuberculosis in them. In addition, SLE increases the fragility of bones in women, which is fraught with frequent fractures, even with a slight compression effect.
About 50% of patients with SLE suffer from anemia amid low platelet and white blood cell counts, which is often attributed to side effects of drug treatment.
In addition, in almost all cases, the presence of autoantibodies to platelet phospholipids is noted, which reduces the functionality of the latter.
The heart is one of the most common targets for SLE. Patients note:
- fibrous endocarditis. Endocarditis with lupus erythematosus is characterized by a non-infectious form of the flow – Liebman-Sachs endocarditis, affecting the inner membrane lining the mitral and tricuspid valve.
In all patients with lupus erythematosus, atherosclerotic changes in the large and medium coronary arteries, as well as veins, are noted.
Patients often have pleurisy, fluid accumulation in the pleural cavity, dystrophic changes in the epithelial cells of the bronchi and bronchioles, chronic interstitial pathologies in the lung parenchyma, pulmonary hypertension, embolism, pulmonary hemorrhage and pulmonary tissue collapse syndrome.
Laboratory tests of urine determine the presence of blood and protein in it, which indicates the initial pathological changes in the kidneys. Acute or chronic renal failure develops with the localization of pathological processes in the glomerular-tubular system, which usually ends in the terminal stage in 5% of patients.
Histological studies confirm membrane glomerulonephritis with a wire loop abnormality resulting from the deposition of immune complexes along the glomerular basement membrane.
Neuropsychiatric syndromes can occur in a number of cases of SLE incidence and include central and peripheral disorders. Modern medicine defines 19 neuropsychiatric syndromes associated with systemic lupus erythematosus. It is worth noting that the diagnosis of such symptoms in the presence of SLE is one of the most complex processes, since it includes a very large number of different models of clinical signs that may be mistaken for a concomitant clinic for infectious diseases or strokes.
The most common symptom of this complex in SLE is a headache. In addition, there are other common neuropsychiatric manifestations.
- Cognitive dysfunction
- Cerebrovascular disease.
- Epileptic seizures.
- Anxiety disorder.
- Psychoses of various genesis.
Syndrome of intracranial hypertension is much less common due to increased intracranial pressure, swelling of the optic nerve head and headache against the general background of the absence of lesions in the cerebral ventricles and the normal chemical-hematological picture of the composition of the cerebrospinal fluid.
In isolated cases, patients can experience the appearance of delirium, Guillain-Barré syndrome, aseptic meningitis, autonomic neuropathy, demyelinating syndromes, mononeuropathy, motor disorders, myasthenia gravis, myelopathy, cranial neuropathy and plexopathy.
SLE causes an increased risk of fetal death in the womb and miscarriage. The overall live birth rate was estimated at more than 72% in women with lupus, and the vivid symptoms of SLE begin to manifest itself during pregnancy.
Neonatal lupus in a child born to a mother with SLE is most often represented by a rash that resembles a chronic, discoid type of disease with possible systemic disorders, such as heart block, enlarged liver and spleen.
The true reasons for the development of SLE have not yet been established. There are several theories of the development of systemic lupus erythematosus, which are controversial and have both confirming and refuting factors:
- Genetic theory. According to this theory, the disease is genetically determined. However, a specific gene that provokes the development of SLE has not yet been discovered.
- Viral theory. It was found that in patients suffering from SLE, the Epstein-Barr virus is often detected.
- Bacterial theory. It has been proven that the DNA of a number of bacteria can stimulate the synthesis of antinuclear autoantibodies.
- Hormonal theory. Women with SLE often have elevated levels of the hormones prolactin and estrogen. There is also a frequent primary manifestation of SLE during pregnancy or after childbirth, when the female body undergoes huge hormonal changes.
- The action of physical factors. It is known that ultraviolet radiation can start the synthesis of autoantibodies by skin cells (in people predisposed to SLE).
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