Acne vulgaris is as common in Taiwan as in Western countries. Ephelides are not uncommon in our population with the main skin types III-IV. A clustered distribution of the wart infection was noted. The low prevalence of AD in Taiwan seems unaltered over the past decade. AA and psoriasis are rare in our series. Most keloids in our children are caused by BCG vaccination.

Objective To examine rubella seroepidemiology, and estimate rates of catch-up immunisation and persistence of antibody titers in pregnant women in Taiwan after mass immunisation.Design A retrospective study.Setting Two medical centres and four regional hospitals specialising in obstetric care. Main outcome measures Seronegativity, rate of catch-up immunization, and antibody decline.Results The seronegativity was 10.9% in all pregnant women. Immigrant women had higher seronegativity than indigenous women (OR 2.86; 95% CI 2.65, 3.01). Indigenous women born prior to implementation of the vaccination programmes were more susceptible (20.1%) to rubella infection than were women born thereafter (6.7%). Rates of seropositive conversion were low in both Taiwanese-born and foreign-born women (11.5 and 30.7%, respectively). The rubella antibody titers for vaccinated Taiwanese women in the 1971-1976 and after-1976 birth cohorts declined by 0.6 and 2.3% per year, respectively.Conclusions This study demonstrates high seronegativity of older indigenous and immigrant women, a low catch-up immunisation rate, and the persistence of rubella antibodies in Taiwan after mass vaccination. Our study suggests that a single dose of rubella vaccine in teenagers effectively increased rubella seropositivity during their childbearing years. This finding is useful for countries that lack the resources necessary for a two-dose regimen. We recommend free rubella antibody tests to women of childbearing age and free vaccination as required. All postpartum women testing negative for rubella antibodies should be vaccinated before they leave hospital.Keywords Catch-up immunization, congenital rubella syndrome (CRS), rubella.Please cite this paper as: Lin C, Yang C, Shih Y, Hsu H, Yang T, Cheng Y, Chang C, Hsieh L, Chen B, Lee C, Huang Y. Rubella seroepidemiology and estimations of the catch-up immunisation rate and persistence of antibody titers in pregnant women in Taiwan. BJOG 2011;118:706-712.

BackgroundTumor necrosis factor receptor (TNFR)–associated periodic syndrome (TRAPS) is an autosomal-dominant disease caused by gain-of-function mutations in the TNFRSF1A gene, which encodes the 55-kd TNFR type I (TNFRI) protein. Mosaicism has been recently idenitfied in a single patient.1 A 60 year old male presented with a 6 year history of intermittent fever as high as 103.5, lasting 3–4 weeks with associated peritoneal symptoms, arthralgias, myalgias, lymphadenopathy, bilateral episcleritis, erythematous rash in his torso. Prednisone up to 60 mg daily only partially alleviated his symptoms and colchicine was ineffective.ObjectivesTo explore the role of mosaicism in a patient with adult onset TRAPS phenotype.MethodsDNA was extracted from the patient's whole blood, saliva and hair root. The TNFRSF1A gene was analyzed by Sanger sequencing in all tissues, and next-generation sequencing in whole blood. In silico molecular modeling was performed to predict the structural and functional consequences of the tumor necrosis factor receptor (TNFR) type I protein mutation.ResultsSanger sequencing and next-generation sequencing methods revealed differential tissue presence of a misense mutation at c.265 T>C p.Phe89Leu (F89L) Chr12(GRCh37):g.6442960A>G ex3 rs104895245. The mutant allele was present in whole blood and buccal mucosa and absent in hair root, supporting the presence of somatic TNFRSF1A mosaicism. In silico prediction modeling with SIFT and PolyPhen2 suggested that this mutation led to numerous structural rearrangements which resulted in changes in the protein surface profile. The patient had a complete response to treatment with canakinumab an interleukin-1 beta blocker, with resolution of symptoms and normalization of acute-phase protein levels.ConclusionsThis is the second reported case of TNFRSF1A mosaicism in a patient with TRAPS, which was attributable to a de novo mosaic missense mutation in the TNFRSF1A gene. (c.265 T>C) p.Phe89Leu (F89L) The clinical picture in this patient, including the complete response to IL-1 blockade, was typical of that found in TRAPS. This case suggests that adult onset TRAPS phenocopies may be attributed to somatic (or postzygotic) mutations.References Rowczenio et al Association of Tumor Necrosis Factor Receptor–Associated Periodic Syndrome With Gonosomal Mosaicism of a Novel 24-Nucleotide TNFRSF1A Deletion ARTHRITIS & RHEUMATOLOGY, Vol. 68, No. 8, August 2016, pp 2044–2049. Disclosure of InterestNone declared

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