SLE occurs in women of childbearing age, mostly in the age group of 15 to 45 years, with a female:male ratio of 7 to 9:1.
The epidemiology of SLE in the United States reported a prevalence of 14.6~122/100,000 people in a multi-regional survey, and in a large series of one-time surveys conducted among women textile workers in Shanghai, the prevalence was 70/100,000 people, while among women it was as high as 115/100,000 people. Most of the patients have insidious onset, involving only one to two systems at the beginning, showing mild arthritis, skin rash, occult nephritis, thrombocytopenic purpura, etc. Some patients are stable in subclinical state or light lupus for a long time, some patients can suddenly change from light to severe lupus, and more patients gradually develop multi-system damage from light; some patients involve multiple systems at the onset, and even show lupus crisis. The natural course of SLE is mostly characterized by alternating exacerbation and remission of the disease. 1. Systemic manifestations: Patients with SLE often have fever, which may be a manifestation of SLE activity, but infectious factors should be excluded, especially when fever occurs during immunosuppressive therapy, which requires more vigilance. Fatigue is a common but easily neglected symptom of SLE, and is often a precursor of lupus activity. 2. skin and mucous membranes: erythema distributed in a butterfly shape on the bridge of the nose and cheeks of both cheekbones are characteristic changes of SLE. skin damage in SLE includes photosensitivity, alopecia, palmar and perineural erythema, discoid erythema, nodular erythema, lipofuscinosis, reticular bruising and Raynaud’s phenomenon. no obvious pruritus in SLE rash, obvious pruritus indicates allergy, and pruritic rash after immunosuppressive therapy should be noted for fungal infection. In SLE patients receiving hormonal and immunosuppressive therapy, unexplained localized burning skin pain may be a precursor to herpes zoster. oral ulcers or mucosal erosions are common in SLE. Oral fungal infections should be noted in oral erosions after immunosuppressive and/or antimicrobial therapy. 3. Joints and muscles: Symmetrical multi-joint pain and swelling are often present and usually do not cause bone destruction. Aseptic femoral head necrosis should be noted in patients with SLE on hormone therapy who present with vague discomfort in the hip region. myalgia and muscle weakness may occur in SLE, and a few may have increased muscle enzyme profiles. For patients taking hormones for a long time, hormone-induced myopathy should be excluded. 4. Renal damage: Also known as lupus nephritis (LN,
LN has a significant impact on the prognosis of SLE, and renal failure is one of the major causes of death in SLE. Membrane proliferative, type III focal segmental proliferative, type IV diffuse proliferative, type V membranous, and type VI glomerulosclerotic. The pathological staging has positive implications for estimating prognosis and guiding treatment.
The prognosis is usually better for types I and II and worse for types IV and VI. However, the pathological types of LN are convertible, with the possibility of converting to the worse types for types I and II and to the worse types for types IV and V.
The prognosis is also good with immunosuppressive therapy. Renal pathology also provides indicators of LN activity, such as proliferative glomerular cell changes, fibrinoid necrosis, nuclear fragmentation, cellular crescent, hyaline emboli, metallic rings, inflammatory cell infiltration, and inflammation of the tubular interstitium are indicative of LN activity; while glomerulosclerosis, fibrous crescent, tubular atrophy, and interstitial fibrosis are indicators of chronic LN. High activity indicators, kidney damage progresses faster, but active treatment can be reversed; chronic indicators suggest irreversible degree of kidney damage, drug treatment can only slow down but not reverse the continued rise of chronic index. 5. Neurological damage: also known as neuropsychiatric lupus. In mild cases, only migraine, personality changes, memory loss or mild cognitive impairment are observed; in severe cases, cerebrovascular accidents, coma and persistent status epilepticus may be manifested. Central nervous system manifestations include aseptic meningitis, cerebrovascular disease, demyelination syndrome, headache, movement disorders, myelopathy, seizures, acute psychosis, anxiety, cognitive disorders, mood disorders, and psychotic disorders; peripheral nervous system manifestations include Green-Barre syndrome, plant nervous system dysfunction, mononeuropathy, myasthenia gravis, cranial neuropathy, plexiform neuropathy, multiple neuropathy, totaling 19 types. The presence of one or more of these manifestations, and the exclusion of secondary factors such as infections and drugs, combined with imaging, cerebrospinal fluid, and electroencephalography, can diagnose neuropsychiatric lupus. Neuropsychiatric lupus manifested by diffuse higher cortical dysfunction is mostly associated with anti-neuronal antibodies, anti-ribosomal P protein (Ribsomal
The psychoneurolupus with focal neurolocalization signs can be further divided into two conditions, one with positive antiphospholipid antibodies and the other often with systemic vasculitis manifestations and significant disease activity, which should be focused in the treatment. Transverse myelitis is uncommon in SLE, and once it occurs, it should be treated actively as early as possible. Otherwise, irreversible damage is caused. It manifests as paralysis or weakness of the lower extremities accompanied by positive pathological signs. Magnetic resonance examination of the spinal cord can clarify the diagnosis.