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Key Clinical Message: This case report describes the clinical course of a juvenile female with FGF23-related hypophosphatemic rickets preceding the onset of SLE. Our study demonstrates the possibility of hypophosphatemic rickets as an early symptom of SLE. Abstract: Fibroblast growth factor 23 (FGF23)-related hypophosphatemic rickets is observed in both genetic and acquired disorders. Various reports describe FGF23-related hypophosphatemia with systemic lupus erythematosus (SLE), although FGF23-related hypophosphatemia preceding the onset of SLE has never been described. Here, we report the case of a 9-year-old female with FGF23-related hypophosphatemic rickets preceding the onset of SLE. The patient presented to us with arthralgia in the lower extremities and abnormality of gait lasting for 8 months. She was diagnosed with FGF23 hypophosphatemic rickets due to the presence of hypophosphatemic rickets symptoms and high serum levels of FGF23. Additional examination excluded hereditary diseases and tumor-induced osteomalacia. Three months after diagnosis of FGF23-related hypophosphatemic rickets, she developed nephritis and was diagnosed with SLE. She was treated with prednisolone, hemodialysis, and disease-modifying drugs, as well as oral sodium phosphate to improve hypophosphatemia. Serum anti-double-stranded DNA antibody (dsDNAab) and plasma tumor necrosis factor-α (TNF-α) were elevated at FGF23-related hypophosphatemic rickets diagnosis. During the clinical course, serum FGF23 correlated with dsDNAab and TNF-α serum levels, which are involved in SLE disease activity. In this case, FGF23-related hypophosphatemic rickets without hereditary diseases or tumor-induced osteomalacia occurred before the appearance of juvenile SLE symptoms, and serum FGF23 represented disease activity in SLE.
RESUMEN
Background: Liposomes have been a useful tool to analyze membrane behavior. Various studies have attempted to induce biological activities, for example, buddings, divisions, and endocytosis, on liposomes, focusing on lipid rafts that move along electric fields. Materials and Methods: Liposomes consisting of soybean lecithin, phosphatidylcholine, and cholesterol were prepared, with inner and outer liquid conductivities of 0.595 and 1.564 S/m, respectively. Results: We tried to induce buddings by pulsed electric fields (PEFs) on liposomes. Results demonstrated that 1.248 kV/cm, 400 µs PEF promoted postpulse liposome buddings, which were preceded by a membrane relaxation. Although a transient thick area (a lipid raft-like area) on the membrane just after PEF application preceded buddings, it was not the sufficient factor for buddings. Conclusion: We established a brief model as follows: 1.248 kV/cm, 400 µs PEF induced the lipid membrane relaxation without electroporation to trigger buddings. The current results could be a new frontier in bioelectrics.
