The doctor on duty came by and said that a difficult patient was admitted to the ward yesterday from out of town. A 13-year-old girl, suffering from irregular fever and joint pain for more than 1 year, had been seen in a local tertiary care hospital, with hemoglobin of 100g/L, red blood cells of 3.4×1012/L, white blood cells of 4.14×109/L, neutrophils of 36%, lymphocytes of 64%, platelets of 152×106/L, ASO>500u, rheumatoid factor (+), hematocrit of 50 mm/h, diagnosed as “juvenile rheumatoid arthritis”. He was diagnosed as “juvenile rheumatoid arthritis” and was treated intermittently with prednisone, naproxen, and rhodopsin, but his symptoms were sometimes mild and his schooling was intermittent, and his parents and child were under great pressure. Half a month ago, the child started to feel headache and sometimes irritable. Just one day ago, the child suddenly developed convulsions, and the family called out to him, and he became incontinent. On physical examination, the child was found to be clear, poorly nourished, moderately anemic, with a body temperature of 37.6°C. Lymph nodes the size of soybeans to peanuts could be felt in the neck, axillae and groin, the liver and spleen were just palpable under the ribs, and the knee, ankle and wrist joints were painful to touch, but the redness and swelling were not obvious. The muscle strength of the right limb was grade IV, and the muscle tone of all four limbs was slightly high. There was hyperalgesia on the right side, active tendon reflexes bilaterally, positive baroreflexes bilaterally, and no cranial nerve abnormalities. After admission, we performed the necessary and relevant laboratory tests: hemoglobin 75 g/L, erythrocytes 2.5×1012/L, leukocytes 3.7×109/L, sorted neutrophils 60%, lymphocytes 40%, platelets 110×106/L. Routine urinalysis was negative. Renal function tests showed normal urea nitrogen and creatinine. Rheumatoid factor (+). Glutathione transaminase 155 U, glutathione transaminase AST 50 U. Blood IgA 3.25 g/L, IgG 15.37 g/L, IgM 0.45 g/L, C3 430 mg/L (600-1400 mg/L). Bone marrow showed hyperplastic bone marrow picture. pPD test (-). Cerebrospinal fluid pressure was 150 mmH2O, cell count was 10×106/L, protein was 2.34 g/L, sugar was 2.8 g/L, and chloride was 119 mmol/L. EEG showed diffuse irregular high amplitude slow waves in all leads, especially on the left side. CT reported left parietal, occipital, and basal ganglia infarction and cerebral atrophy. Skeletal radiographs showed normal joint surfaces of knee, ankle, wrist and hand, and no osteoarthritic damage was observed. Chest radiographs showed blunted rib diaphragm angle on both sides and the presence of a small amount of pleural effusion. Based on the above characteristics of the child and the laboratory tests, we carefully considered and differentiated the following diagnoses in order to find the real source of the child’s pain that had been haunting him for more than a year. The child presented clinically with irregular fever, joint pain, positive rheumatoid factor, and a long medical history. According to the conventional clinical diagnosis, “juvenile rheumatoid arthritis” should be considered first. However, there are several points of suspicion that caught our attention: the case had been irregularly treated for more than a year, but the skeletal radiographs did not show joint destruction; also, rheumatoid arthritis usually does not show brain damage. So is there something else going on in this child with fever, arthralgia and convulsions. The child is a 13-year-old girl with fever, joint pain and swelling that is wandering, and an increased ASO titer at the beginning of the disease. However, rheumatic fever patients have more frequent heart inflammation, subcutaneous nodules and annular erythema, and central nervous damage mainly manifested as rheumatic chorea, without convulsions and cerebral infarction foci. Therefore, the diagnosis of rheumatic fever is not supported in this case. In contrast, “tuberculous meningitis combined with allergic arthritis” may have prolonged fever, personality changes, convulsions, and low-density foci in CT of the brain with joint symptoms. However, the medical history, PPD test and cerebrospinal fluid test results do not conform to the developmental pattern of tuberculous meningitis. Among the hematologic diseases in children, acute leukemia is more common. The term “acute leukemia” is undoubtedly like a sword that cuts through the sea of tranquility of doctors and patients in the course of routine consultation and treatment. Acute leukemia mostly has fever, anemia, bleeding, enlarged liver and spleen lymph nodes, central nervous system infiltration symptoms, and bone and joint infiltration symptoms. About 25% of children with the disease have the first symptoms in the long bones of the limbs, shoulders, knees, wrists, ankles and other joints, some of which show wandering arthralgia, and local redness and swelling are not obvious. The main cause of bone and joint pain is due to the proliferation of leukemic cells in the bone marrow cavity, which compress and destroy the adjacent bone and periosteal infiltration. Acute leukemia has a rapid onset and progresses rapidly, and enters a state of failure soon after unreasonable treatment, with a very poor prognosis. It was clear that the child’s condition was not consistent with the development of acute leukemia, and the bone marrow picture excluded the diagnosis of acute leukemia. When we informed the child’s parents of this conclusion, a rare moment of relief passed over the family’s face. So who was the culprit? In our previous clinical practice, we had admitted many cases that were poorly treated locally with “nephritis” or “nephropathy” and found that the patients were commonly found to have persistent hypocomplementemic C3. After a follow-up history, physical examination and related tests, the patient was finally diagnosed with “lupus nephritis”. At present, this patient had decreased blood C3, non-erosive arthritis, pleurisy, neurological lesions and hematological abnormalities, and the possibility of “SLE combined with lupus encephalopathy” should be highly suspected. In this regard, we further examined the child for anti-nuclear antibody, anti-dsDNA and anti-Sm antibody, and found that all of these indicators were positive. The diagnosis of SLE in this case was undoubted. The truth was revealed that it was all caused by “SLE combined with lupus encephalopathy”. As an autoimmune disease of the connective tissue of the whole body invading multiple systems and organs, SLE is relatively rare in pediatrics, and according to foreign data, the prevalence of this disease before the age of 15 is 0.53-0.6/100,000 population, and lupus encephalitis is even rarer. With the development of laboratory testing techniques and increased awareness of the disease, its diagnosis has increased significantly. It is second only to juvenile rheumatoid arthritis in terms of incidence among connective tissue diseases. The clinical manifestations of the disease are diverse and variable. In the early stages, the disease may invade one or two organs, and thus the presentation is atypical and easily misdiagnosed. Later, it can invade multiple organs and has a complex clinical presentation. Most patients have alternating remission and exacerbation. The current diagnosis of the disease is mainly based on the 1982 diagnostic criteria of the American Rheumatism Association. Specifically, these include (1) zygomatic erythema: flat or fixed erythema above the skin; (2) discoid erythema: raised erythema on the face covered with scales; (3) photosensitivity: allergy after sun exposure; (4) oral ulcers; (5) arthritis: non-erosive arthritis; (6) plagiocele: pleurisy or pericarditis; (7) renal lesions; (8) neurological lesions: seizures or psychiatric symptoms; (9) Hematologic abnormalities: hemolytic anemia or blood leukopenia or absolute lymphocytopenia or thrombocytopenia; (10) immunologic abnormalities: positive lupus cells or positive anti-dsDNA antibody or anti-Sm antibody or false positive syphilis serologic test; (11) positive antinuclear antibody. If ≥4 of the above are positive, the diagnosis of SLE can be confirmed with a specificity of 98% and a sensitivity of 97%. The disease is not diagnosed because of the following factors: (1) the presentation is extremely atypical. Only fever and joint symptoms appear in the early stages, and there is never any manifestation of skin damage, indicating that skin damage can appear before, after or without manifestation of other symptoms. The possibility of SLE should be considered for the disease with unexplained multisystem damage, and relevant laboratory tests should be done early to clarify the diagnosis; (2) Only fever and joint symptoms are noted in the early stage, and the decrease in blood complement C3 level is not given enough attention. Patients with fever and multi-system damage accompanied by reduced blood complement C3 level should be highly alert to SLE, and the positive rate of low C3 in such patients is about 80% with high specificity; (3) During the treatment of this disease, drugs such as “prednisone and rhodopsin” are applied, which have a certain effect on disease remission and conceal the disease. (3) During the treatment of this disease, we applied drugs such as “prednisone” and “leptoside”, which had a certain effect on the remission of the disease and concealed the disease and interfered with the analysis of the etiology. After the diagnosis, we gave the patient reasonable and regular medication, and the symptoms were controlled. The child is already enjoying the long-awaited happiness of school, teachers and classmates like other normal children.