Predictors of lipid abnormalities in children with new-onset systemic lupus erythematosus.

Objective: Lipid abnormalities in patients with systemic lupus erythematosus (SLE) are common and likely are one of the causes of premature atherosclerosis in these patients. Our aims were to determine the frequency and pattern of dyslipoproteinemia at presentation of pediatric SLE; and to determine the association between dyslipoproteinemia and markers of disease activity and inflammatory markers at presentation of pediatric SLE.

Methods: Serum lipid measurements were obtained at diagnosis before corticosteroid treatment for an inception cohort of 54 patients.

Longitudinal examination of lipid profiles in pediatric systemic lupus erythematosus.

Objective: Lipid abnormalities in patients with systemic lupus erythematosus (SLE) are common and are likely to be one of the causes of premature atherosclerosis in these patients. This study was undertaken to serially examine the lipid profile in pediatric patients with SLE to determine the roles of active disease and therapy in altering lipid levels.

Methods: Serial lipid measurements were obtained in an inception cohort of 139 pediatric patients with SLE at the time of treatment with either a constant dose or differing doses of prednisone, and annually.

The complex nature of the interaction between disease activity and therapy on the lipid profile in patients with pediatric systemic lupus erythematosus.

Objective: To determine the prevalence of lipid abnormalities at different times and to determine the influence of both the disease and corticosteroid therapy on lipid abnormalities in pediatric patients with systemic lupus erythematosus (SLE).

Methods: Lipid measurements were obtained in an inception cohort of 139 pediatric patients with SLE (114 females). Fasting levels of total cholesterol, triglycerides, low-density lipoprotein (LDL) cholesterol, and high-density lipoprotein (HDL) cholesterol in the SLE patients were compared with those in age- and sex-matched control subjects.

Chk2 is a tumor suppressor that regulates apoptosis in both an ataxia telangiectasia mutated (ATM)-dependent and an ATM-independent manner.

In response to ionizing radiation (IR), the tumor suppressor p53 is stabilized and promotes either cell cycle arrest or apoptosis. Chk2 activated by IR contributes to this stabilization, possibly by direct phosphorylation. Like p53, Chk2 is mutated in patients with Li-Fraumeni syndrome.