I. Why does SLE “prefer” women?
It all boils down to sex hormones. Sex hormones can have a significant impact on multiple levels of the immune response, and abnormal levels of sex hormones and their metabolites are one of the factors that disrupt the autoimmune response. Sex hormones are divided into androgenic and estrogenic hormones, and both hormones can be secreted by both men and women, only differing significantly in terms of quantity.
Estrogen has the effect of lowering thymic hormones, while androgenic sex hormones have the effect of enhancing thymic hormones. In addition, estrogen can inhibit a type of action called suppressor T lymphocytes through estrogen receptors, leading to a weakened inhibition of B lymphocytes, resulting in the production of large amounts of abnormal antibodies that cause a variety of rheumatic diseases. Thus, estrogen acts directly or indirectly on the immune system through itself and its receptors, and if estrogen metabolism is abnormal, it can cause an imbalance in immune homeostasis, leading to the development and progression of diseases such as SLE. This is the reason why SLE likes to patronize women.
Diagnosis of SLE
The presence of multisystem involvement (with symptoms of more than two systems mentioned above) and evidence of autoimmunity should alert lupus. The SLE classification criteria recommended by the American College of Rheumatology in 1997 are now commonly used. SLE can be diagnosed when 4 or more of the following 11 criteria are met, excluding infections, tumors and other connective tissue diseases, with immunologic abnormalities and high titers of antinuclear antibodies being of greater diagnostic significance. Specifically, these include.
1. Cheek erythema: fixed erythema, flat or elevated, in the prominent part of both cheekbones.
2.Disciform erythema: flaky, elevated erythema on the skin with adherent keratinous debridement and follicular plugs; atrophic scarring may occur with old lesions.
3.Photosensitivity: marked reaction to sunlight, causing rash, known from medical history or observed by physician.
4, Oral ulcers: ulcers in the mouth or nasopharynx, usually painless, observed by a physician.
5. Arthritis: non-erosive arthritis involving 2 or more peripheral joints with pressure pain, swelling or fluid accumulation.
6. Plasmacytitis: pleurisy or pericarditis.
7. Renal lesions: urine protein >0.5g/24 hours or ++++, or tubular pattern (red blood cells, hemoglobin, granules, or mixed tubular pattern).
8. Neurological lesions: seizures or psychosis, except for drugs or known metabolic disorders.
9, hematologic disorders: hemolytic anemia, or leukopenia, or lymphocytopenia, or thrombocytopenia.
10. Immunologic abnormalities: positive anti-ds-DNA antibody, or positive anti-Sm antibody, or positive antiphospholipid antibody (including one of three positive anti-cardiolipin antibodies, or lupus anticoagulant, or false positive syphilis serologic test lasting for at least 6 months).
Antinuclear antibodies: abnormal titers of antinuclear antibodies at any time and in the absence of drug-induced “pharmacologic lupus”.
What are the manifestations of atypical or early SLE?
1. It includes recurrent fever of unknown origin, and anti-inflammatory and antipyretic treatment is often ineffective.
2. Multiple and recurrent episodes of arthralgia and arthritis, often lasting for years without producing deformities.
3.Persistent or recurrent pleurisy and pericarditis.
4.Pneumonia that cannot be cured by antibiotic or anti-TB treatment.
5.Rash that cannot be explained by other causes, reticular cyanosis, Raynaud’s phenomenon.
6, Renal disease or persistent unexplained proteinuria.
7, Thrombocytopenic purpura or hemolytic anemia.
8, Unexplained hepatitis.
9, Recurrent spontaneous abortion or deep vein thrombosis or stroke attack.
If the above conditions occur, go to a specialized rheumatology department for examination to exclude SLE.