Background: Hypophosphatemia is observed in both genetic diseases and acquired disorders, although it has never been described in systemic lupus erythematosus (SLE). The present study reports hypophosphatemia observed in patients with SLE, and investigates whether serum phosphorus (P) concentration is associated with disease activity and some cytokines. Methods: Six girls with SLE (age 10 to 16 years) and seven age-matched controls were studied. Relationships between serum P and parameters that represented disease activity were evaluated. Interleukin (IL) 6 and tumor necrosis factor α (TNF-α) levels were measured by enzyme-linked immunosorbent assay (ELISA). Results: Two of the patients with SLE developed marked hypophosphatemia during active disease. Their serum P significantly correlated positively with serum complements, red blood cell (RBC) and platelet counts, and negatively with anti-double-stranded DNA antibody (dsDNAab). Three of the remaining four patients showed the same trend, in which their serum P significantly correlated with RBC, platelets, dsDNAab and/or serum complement concentrations. Serum and urinary IL-6 and serum TNF-α were higher in active SLE patients than those with inactive disease or in the control group. In addition, the concentrations of these cytokines significantly correlated inversely with serum P. Renal tubular reabsorption of P was significantly lower in patients with active disease both with and without lupus nephritis. Conclusions: Hypophosphatemia may be another sign of juvenile SLE, and serum P may represent disease activity. Both TNF-α and IL-6 may be related to hypophosphatemia in patients with SLE. Waste of P from renal tubules may be a possible mechanism of hypophosphatemia in SLE.
- Systemic lupus erythematosus
- Tubular reabsorption
ASJC Scopus subject areas
- Pediatrics, Perinatology, and Child Health