Furthermore, ZNF831 (zinc finger protein 831) and its loci on chromosome 20q13 were identified as another significant factor in pre-eclampsia. The risk allele rs259983 is also associated with both pre-eclampsia and hypertension, further evidence that the two traits are possibly linked. While the current understanding suggests that maternal alleles are the main hereditary cause of pre-eclampsia, paternal loci have also been implicated. In one study, paternal DLX5 (Distal-Less Homeobox 5) was identified as an imprinted gene. Located on chromosome 7 in the q21 region, DLX5 serves as a transcription factor often linked with the developmental growth of organs. When paternally inherited, DLX5 and its SNP rs73708843 are shown to play a role in trophoblast proliferation, affecting vascular growth and nutrient delivery.Besides specific loci, several important genetic regulatory factors contribute to the development of pre-eclampsia. Micro RNAs, or miRNAs, are noncoding mRNAs that down-regulate posttranscriptional gene expression through RNA-induced silencing complexes. In the placenta, miRNAs are crucial for regulating cell growth, angiogenesis, cell proliferation, and metabolism. These placental-specific miRNAs are clustered in large groups, mainly on chromosomes 14 and 19, and irregular expression of either is associated with an increased risk of an affected pregnancy. For instance, miR-16 and miR-29 are vascular endothelial growth factors (VEGFs) and play a role in upregulating sFLT-1. In particular, the overexpression of miRNA miR-210 has been shown to induce hypoxia, which affects spiral artery remodeling, an important part of the pathogenesis of pre-eclampsia.
It has been previously suggested that children with JIA are at an increased risk of malignancies when being treated with anti-TNF therapy. More recent data has not confirmed this association: it is thought that the disease itself is linked with a slightly higher background risk of malignancy. Ongoing data analysis on large patient populations continues in this area. Epidemiology
Juvenile Idiopathic Arthritis is the most common, chronic rheumatic disease of childhood. In high-income countries, yearly incidence has been estimated at 2–20 cases per 100,000 population; prevalence in these areas is estimated at 16–150 cases per 100,000 population. However, there is also a suggestion that these numbers underestimate disease prevalence: one community-based survey of school children in Western Australia reported a prevalence of 400 per 100,000. Overall prevalence is often summarised as one per thousand children.Incidence and prevalence data vary across different population and ethnic groups, with lower overall prevalence in Afro-Caribbean and Asian populations. There are also ethnic differences in the frequency of JIA subtypes: for example, oligoarthritis is the most common subtype in European populations, whilst polyarticular disease predominates in many other countries including Costa Rica, India, New Zealand, and South Africa.There are differences in age of onset, gender and disease outcomes based on JIA subtype: these are outlined in the table above. Terminology
The terminology used to describe JIA is evolving, and each term has some limitations. Previous terminology included Juvenile Rheumatoid Arthritis and Juvenile Chronic Arthritis.