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In hereditary arthritis-dermatitis-uveitis syndrome (HADU) and hyper-IgM syndrome, there is evidence of an autoinflammatory disease. In some patients, this may be the result of a recessive autosomal disorder, and in others it may be the result of a dominant polygenic disorder. It has previously been proposed that these diseases may be caused by mutations in members of the Nalp family of inflammasome components; however, such mutations have not been found in HADU patients. In this study, we investigated three patients with HADU syndrome, on the basis of positive family histories and clinical features suggestive of an autoinflammatory disease, with the aim of identifying the genetic cause of their disease. We identified mutations in the NACHT, LRR and pyrin domains (NLRP3) of NLRP3 in all three patients, including one patient who had been previously considered to be genetically uncharacterized. Patients with HADU syndrome have a distinct phenotype characterized by arthralgia, dermatitis, and recurrent lower respiratory tract infections. Severe systemic amyloidosis may develop as a complication of the disease. In some cases, arthritis may be the most striking feature of the syndrome, and diagnosis may be delayed because of previous misdiagnosis as juvenile rheumatoid arthritis. In this study, we identified mutations in NALP3 in three patients who had been previously considered to have genetically uncharacterized HADU syndrome, providing a genetic basis for this syndrome. AA amyloidosis is a life-threatening complication of the hereditary periodic fever syndromes (HPFS), which are otherwise often compatible with normal life expectancy. This study was undertaken to determine the characteristics, presentation, natural history, and response to treatment in 46 patients who had been referred for evaluation at the UK National Amyloidosis Centre. Disease activity was monitored by serial measurement of serum amyloid A. Renal function was assessed by measurement of serum creatinine and albumin levels, the estimated glomerular filtration rate, and proteinuria from 24-hour urine collections. The amyloid load was measured by serum amyloid P scintigraphy.

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