Estimation of monocyte‐chemoattractantprotein‐1 (Mcp‐1) level in patients with lupus nephritis

Aim: To evaluate the use of non‐invasive estimation of CP‐1 in urine as a good indicator for lupus nephritis activity. Methods: The study was conducted on 30 patients with systemic lupus erythematosus (SLE) (group I): 15 of these patients were selected without renal involvement (group I [A]), and the other 15 were selected with evidence of renal involvement (group I [B]). Further 10 age‐ and sex‐matched healthy subjects were taken as a control group (group II). The SLE disease activity index (SLEDAI) was applied. Laboratory investigations done for the studied group of patients included: renal function tests (antinuclear antibody) titer, (anti‐double‐stranded DNA) titer, and monocyte chemotactic protein 1 (MCP‐1) level in serum and urine samples. Results: Serum MCP‐1 was significantly higher in SLE patients with nephritis than in the control group, while no significant difference was found between SLE patients without nephritis and the control group. Urinary MCP‐1 in patients with active lupus nephritis (LN) were significantly higher than both patients with inactive LN and control the group. Urinary MCP‐1 in SLE patients with nephritis was significantly higher than both group I (A) and group II. Urinary MCP‐1 correlated positively with proteinuria, and negatively with creatinine clearance and hemoglobin; thus, urinary MCP‐1 correlates with the severity of nephritis. Conclusion: Urinary and not serum MCP‐1 is a useful invasive technique for the assessment of renal disease activity in patients with LN.     

State‐of‐the‐art treatment of systemic lupus erythematosus

As glucocorticoids and immunosuppressive drugs are non‐specific therapeutic agents that cause many adverse reactions, the development of biologicals aiming to control specific molecular targets is anticipated for the treatment of systemic lupus erythematosus (SLE). The antibody targeting B cell‐activating factor belonging to the tumor necrosis factor family (BAFF) belimumab was the first biological approved for SLE. At present, many biologicals, such as anifrolumab (anti‐type I interferon receptor antibody) and ustekinumab (antibody against interleukin 12/23 [p40]), are in clinical trials. Thus, successful treatments with biologicals targeting “bridging cytokines” produced by dendritic cells, which form a bridge between the innate and acquired immune/autoimmune systems, is of particular interest. Moreover, a phase IIb clinical trial of baricitinib, a low‐molecular‐weight compound targeting Janus kinase 1/2, in patients with SLE revealed that baricitinib was significantly more effective for relieving arthritis and skin manifestations than placebo, and the trial met the primary endpoint. In the future, it is expected that drugs with better efficacy and safety profiles will be used to apply therapeutic strategies, such as precision medicine, in which different molecular target drugs are used for patients classified by their conditions, and to set a therapeutic goal of the discontinuation of glucocorticoids.     

Infliximab‐induced systemic lupus erythematosus

Only six cases of clinical drug‐induced lupus (DIL) following infliximab initiation for rheumatoid arthritis and Crohn's disease are documented dispite studies indicating many patients develop asymptomatic antinuclear ANA (62%) and anti‐dsDNA (15%) antibodies. Our 43‐year‐old female patient with 25 years of RA had active synovitis despite combination sulfasalazine, leflunomide and methotrexate. She received infliximab (3 mg/kg) infusion with rapid resolution of synovitis and then again 2, 6 and 14 weeks later. At 21 weeks she developed acute DIL with typical clinical features and laboratory findings which resolved after 8 weeks of prednisolone treatment. New biologic therapies can not only suppress RA but potentiate clinical DIL.     

An 18‐year follow‐up study of a lupus cohort in Shanghai

Aim: To investigate the long‐term prognosis of systemic lupus erythematosus (SLE) and its risk factors. Methods: An 18‐year (1980–1998) clustering follow‐up study of 50 patients with SLE was performed. Results: The overall survival rate at 1, 5, 10, 15 and 18 years after the onset of illness was 98%, 98%, 84%, 76%, and 70%, respectively. The two major causes of death were infection and renal failure. Cox proportional hazard regression analysis showed that the presence of ≥ 7 of the American College of Rheumatology criteria for SLE at diagnosis and vasculitis were associated with worse survival. Thirteen (26%) patients were in remission with complete discontinuation of drugs, with the mean remission duration being 12 years (range: 2–17 years). Conclusion: It is possible for patients with SLE to get long‐term remission through timely and effective treatment. Prevention of infection and renal failure and reducing dosage of corticosteroids by combined treatment with immunosuppressive drugs may enhance prognosis and survival in SLE.