Systemic lupus erythematosus with chronic persistent intracranial hypertension: A case report.

OBJECTIVE: The aim is to investigate the clinical characteristics of systemic lupus erythematosus with intracranial hypertension. METHODS: The clinical characteristics of one case of systemic lupus erythematosus with chronic persistent intracranial hypertension were analyzed, and related literature was reviewed by searching Medline and Wanfang databases. RESULTS: Intracranial hypertension in SLE patients may occur at the onset or during the course of the disease. Our patient was diagnosed with IH 3 years after the onset of SLE. Headache and papilledema were the most common symptoms of intracranial hypertension, followed by nausea or vomiting, vision changes, and cerebral palsy. Our patient had a headache and cranial hypertension that lasted for years, but no papilledema was found. Corticosteroid is currently the mainstay of the treatment of IIH in patients with SLE, and immunosuppressive agents, acetazolamide, intravenous mannitol and furosemide are also used. However, our patient did not respond to these treatments and presents the characteristics of chronic persistent intracranial hypertension. CONCLUSION: Systemic lupus erythematosus with intracranial hypertension is a rare manifestation of SLE, which is not completely parallel to SLE activity. Headache and papilledema were the most common presenting symptoms. Different from previous reported cases, our patient had poor response to treatments, showing chronic and persistent characteristics.

Leptin accelerates B cell dysfunctions via activating JAK/STAT3/5 and ERK1/2 pathways in patients with systemic lupus erythematosus.

OBJECTIVES: Our previous studies found that serum leptin was increased significantly in SLE, characterised by dysregulated autoreactive B cells producing excessive inflammatory cytokines and autoantibodies. The aim of this study was to explore the effects of leptin on B cell functions in SLE and clarify the key pathways in leptin dysregulated B cells. METHODS: Peripheral blood samples were obtained from 86 SLE patients and 28 normal controls. Purified B cells were stimulated with leptin or SLE serum and with or without anti-leptin antibody. The frequencies of CD19-CD138+ plasma cells and the expression of leptin receptor (LEPR) on B cells were determined with flow cytometry. The levels of antibodies and cytokines were assayed by ELISA. Classic signalling pathways were detected with western blotting method. RESULTS: Increased plasma cells and the levels of IgG and anti-dsDNA antibodies were positively correlated with serum leptin in SLE patients. LEPR+CD19+B cells were increased in SLE patients. Leptin up-regulated LEPR on B cells and activated B cells to produce higher levels of IL-6, IL-10 and TNF-α, and induced B cells to differentiated into plasma cells secreting more IgG and IgM. More importantly, anti-leptin neutralising antibody could partially restore increased cytokines, antibodies and plasma cells induced by SLE serum. Mechanistically, both leptin and SLE serum activated JAK/STAT3/5 and ERK1/2 signalling pathways in B cells, and the secretion-enhancing effects were restored by their inhibitors. CONCLUSIONS: Leptin may be a key factor leading to B cell dysfunction by activating JAK/STAT3/5 and ERK1/2 signalling pathways in SLE.