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Systemic lupus erythematosus (SLE) is an autoimmune systemic disease characterised by a broad spectrum of clinical manifestations that may also affect the central nervous system. Among the neurological symptoms, seizures were included in the criteria for the classification of SLE published by EULAR/ACR in 2019. Several studies have been undertaken to explore the role of SLE antibodies in the onset of seizures, however, their complex relation is still a matter of debate. The most common seizure type reported is generalised tonic-clonic. EEG and MRI findings are usually non-specific; background slowing, brain atrophy and hyper-intense lesions on the white matter are the most common finding. Prognosis is overall favourable, with a good response to antiepileptic drugs and immunosuppressive therapy. The purpose of this review is to summarise the most relevant literature contributions published over the years on the epidemiology, aetiopathogenesis, clinical aspects, diagnosis and treatment of seizures in the context of SLE.

In most childhood rheumatic diseases, specific diagnostic markers are not yet available. Therefore, a major emphasis in medical research today is directed to the discovery of new inflammation molecules, like calprotectin. Calprotectin (MRP8/MRP14) is a complex of calcium- and zinc-binding proteins that belong to the S100 protein family. This protein is directly released by leukocytes during the interaction with inflammatory activated endothelium at the site of inflammation. Increased plasma calprotectin levels have been found in inflammatory chronic diseases such as rheumatoid arthritis (RA), juvenile idiopathic arthritis (JIA), inflammatory bowel diseases (IBD), multiple sclerosis, cystic fibrosis and systemic lupus erythematosus (SLE). In these diseases, serum calprotectin has been shown to correlate with disease activity and laboratory variables of inflammation such as C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR). This review outlines the validity and the possible applications of calprotectin as a new inflammation marker in paediatric rheumatic diseases.

Pericarditis has several different causes, however, in about 70% of paediatric patients, a specific aetiology cannot be detected and the pericarditis is considered idiopathic. Recurrences may occur in up to 15-30% of cases. The pathogenesis of recurrent disease is controversial. Infectious, autoimmune and autoinflammatory pathways have been proposed as mechanisms involved in recurrences. Therapeutic strategies are not standardised, non-steroidal anti-inflammatory drugs at high dosages being the mainstay of therapy with the possible addition of low dose colchicine to prevent recurrences. Biological agents are considered a possible new therapeutic frontiers in the care of idiopathic recurrent pericarditis.

Growth disorders are common among patients with juvenile idiopathic arthritis (JIA). These disorders range from general growth retardation to local acceleration of growth in the affected limb, and are associated with an increased production of pro-inflammatory cytokines, such as interleukin-1β (IL-1β), tumour necrosis factor-α (TNF-α) and interleukin-6 (IL-6). Pro-inflammatory cytokines may act individually or in combination to impair child growth through systemic mechanisms and/or a local action. Whereas IL-6 affects growth mainly via systemic mechanisms altering growth hormone secretion, IL-1β and TNF-α can directly affect growth plate chondrocyte dynamics as well as longitudinal bone growth. There are emerging data suggesting that interleukin-15 and interleukin-5 may be new cytokines implicated in inflammatory diseases, but further well-designed longitudinal studies in larger groups of children are required to establish a causal relationship. Other factors, which might contribute to growth suppression associated with childhood arthritis, include the degree, extent, and duration of disease activity, age at onset, immobility, sub-optimal nutrition and corticosteroid therapy.