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1.
Artigo em Inglês | MEDLINE | ID: mdl-32459867

RESUMO

There has been ongoing interest in the temporal association between the change from whole cell pertussis (wP)-containing to acellular pertussis (aP)-containing vaccines in the routine infant immunization schedule in Australia and increases in childhood food allergies. This is because of the tendency of aP, but not wP, vaccines to promote TH2 immune responses, which are known to predispose children to allergy and allergic disease A recent analysis of ICD coded data for anaphylaxis-related hospitalisations in Australia found that observed increases between the years 1998-1999 and 2004-2005 continued between the years 2005-2006 and 2011-20012, especially in older children.

2.
Int J Mol Sci ; 21(7)2020 Mar 30.
Artigo em Inglês | MEDLINE | ID: mdl-32235485

RESUMO

Aceruloplasminemia is a rare autosomal recessive genetic disease characterized by mild microcytic anemia, diabetes, retinopathy, liver disease, and progressive neurological symptoms due to iron accumulation in pancreas, retina, liver, and brain. The disease is caused by mutations in the Ceruloplasmin (CP) gene that produce a strong reduction or absence of ceruloplasmin ferroxidase activity, leading to an impairment of iron metabolism. Most patients described so far are from Japan. Prompt diagnosis and therapy are crucial to prevent neurological complications since, once established, they are usually irreversible. Here, we describe the largest series of non-Japanese patients with aceruloplasminemia published so far, including 13 individuals from 11 families carrying 13 mutations in the CP gene (7 missense, 3 frameshifts, and 3 splicing mutations), 10 of which are novel. All missense mutations were studied by computational modeling. Clinical manifestations were heterogeneous, but anemia, often but not necessarily microcytic, was frequently the earliest one. This study confirms the clinical and genetic heterogeneity of aceruloplasminemia, a disease expected to be increasingly diagnosed in the Next-Generation Sequencing (NGS) era. Unexplained anemia with low transferrin saturation and high ferritin levels without inflammation should prompt the suspicion of aceruloplasminemia, which can be easily confirmed by low serum ceruloplasmin levels. Collaborative joint efforts are needed to better understand the pathophysiology of this potentially disabling disease.

4.
Seizure ; 78: 49-52, 2020 Mar 16.
Artigo em Inglês | MEDLINE | ID: mdl-32193085

RESUMO

PURPOSE: SCN1A variants cause a spectrum of epilepsy syndromes from Dravet Syndrome, a severe epileptic encephalopathy of early infancy to the milder disorder of genetic epilepsy with febrile seizures plus (GEFS+). These genetic epilepsies are associated with increased risk of poor outcome including complications of status epilepticus and early mortality. Individualised management of young children known to be at increased risk should be considered, such as around vaccination management. METHODS: We describe two siblings with a novel pathogenic SCN1A variant, their management and clinical outcomes following routine childhood vaccinations. RESULTS: The index case who had a family history of epilepsy of unknown genetic aetiology, died from hypoxic ischemic encephalopathy following his 12-month vaccinations, in the context of status epilepticus and enterovirus 71 infection. The sibling of the index case with the same SCN1A variant was subsequently managed with prophylactic regular sodium valproate and additional clobazam post vaccination to reduce the risk of seizure. She has successfully completed the childhood immunisations to 18 months with no seizures and normal neurodevelopmental progress. CONCLUSION: As the aetiology of genetic epilepsies is increasingly known in early childhood, opportunities to personalise care, minimise risks and optimise outcomes are changing. Further research is needed on the risks and benefits of symptomatic and preventative management of seizures around vaccinations in young children with genetic epilepsies.

5.
Pediatr Infect Dis J ; 39(6): e76-e78, 2020 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-32118856

RESUMO

Yellow fever vaccine contains ovalbumin, and guidelines for vaccination of egg allergic patients vary widely. We present our experience of administering yellow fever vaccine to 11 egg-allergic children, including 3 with anaphylaxis to egg, in 2 Australian tertiary pediatric hospitals. There was variation in the vaccination protocols used; however, all patients were successfully vaccinated and no serious adverse events were reported.

7.
Artigo em Inglês | MEDLINE | ID: mdl-32178607

RESUMO

This report summarises Australian spontaneous surveillance data for adverse events following immunisation (AEFI) for 2018 reported to the Therapeutic Goods Administration and describes reporting trends over the 19-year period 1 January 2000 to 31 December 2018. There were 4221 AEFI records for vaccines administered in 2018, an annual AEFI reporting rate of 16.9 per 100,000 population. There was a 2.9% increase in the overall AEFI reporting rate in 2018 compared to 2017. This slight increase in reported adverse events in 2018 was likely due to new additions to the National Immunisation Program schedule, namely meningococcal ACWY vaccination for children aged 12 months, enhanced immunogenicity trivalent influenza vaccines for adults aged ≥65 years, and state- and territory-funded seasonal influenza vaccination programs for children aged 6 months to <5 years. AEFI reporting rates for most individual vaccines in 2018 were similar to 2017. The most commonly reported adverse events were injection site reaction (34%), pyrexia (15%), rash (15%), vomiting (8%), headache (6%) and pain (6%). Two deaths were reported to the TGA but no clear causal relationship with vaccination was found.


Assuntos
Sistemas de Notificação de Reações Adversas a Medicamentos , Programas de Imunização , Vacinação/efeitos adversos , Adolescente , Adulto , Idoso , Austrália/epidemiologia , Criança , Pré-Escolar , Exantema/induzido quimicamente , Febre/induzido quimicamente , Humanos , Esquemas de Imunização , Lactente , Vacinas contra Influenza , Reação no Local da Injeção , Masculino , Adulto Jovem
8.
J Paediatr Child Health ; 56(1): 81-89, 2020 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-31136042

RESUMO

AIM: Paediatric vitamin D (25-hydroxyvitamin D (25OHD)) deficiency can lead to nutritional rickets and extra-skeletal complications. Compliance with daily therapy can be difficult, making high-dose, short-term vitamin D (stoss) therapy attractive to correct vitamin D deficiency. We compared the effectiveness and safety of standard versus stoss therapy in treating childhood 25OHD deficiency. METHODS: Children aged 2-16 years with 25OHD <50 nmol/L were randomised to either standard (5000 IU daily for 80 days) or stoss (100 000 IU weekly for 4 weeks) cholecalciferol. Participants underwent an evaluation of effectiveness and safety. The 25OHD level, random spot calcium: creatinine ratio (Ca:Cr) and compliance were measured at 12 weeks. RESULTS: A total of 151 children were enrolled in the study (68 standard and 83 stoss), median age 9 years (inter-quartile range (IQR): 6-12 years). Baseline 25OHD levels were 26 nmol/L (IQR: 19-35 nmol/L) and 32 nmol/L (IQR: 24-39 nmol/L) in the standard and stoss groups, respectively. At 12 weeks, the median 25OHD level was significantly greater in the standard versus stoss group (81 vs. 67 nmol/L; P = 0.005); however, >80% of participants in both groups achieved sufficiency (25OHD > 50 nmol/L) and had normal urinary Ca:Cr, with no significant difference seen between groups. Compliance was similar in the two groups. CONCLUSIONS: Compared to stoss, standard therapy achieved higher 25OHD levels at 12 weeks; however, in both groups, there was a similar proportion of participants who achieved 25OHD sufficiency, with no evidence of toxicity. Unlike other studies, simplifying the treatment regimen did not improve compliance. These results support stoss therapy as an effective and safe alternative therapy for the treatment of paediatric vitamin D deficiency.

9.
Ann Neurol ; 87(2): 281-288, 2020 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-31755124

RESUMO

OBJECTIVE: Febrile seizures may follow vaccination. Common variants in the sodium channel gene, SCN1A, are associated with febrile seizures, and rare pathogenic variants in SCN1A cause the severe developmental and epileptic encephalopathy Dravet syndrome. Following vaccination, febrile seizures may raise the specter of poor outcome and inappropriately implicate vaccination as the cause. We aimed to determine the prevalence of SCN1A variants in children having their first febrile seizure either proximal to vaccination or unrelated to vaccination compared to controls. METHODS: We performed SCN1A sequencing, blind to clinical category, in a prospective cohort of children presenting with their first febrile seizure as vaccine proximate (n = 69) or as non-vaccine proximate (n = 75), and children with no history of seizures (n = 90) recruited in Australian pediatric hospitals. RESULTS: We detected 2 pathogenic variants in vaccine-proximate cases (p.R568X and p.W932R), both of whom developed Dravet syndrome, and 1 in a non-vaccine-proximate case (p.V947L) who had febrile seizures plus from 9 months. All had generalized tonic-clonic seizures lasting >15 minutes. We also found enrichment of a reported risk allele, rs6432860-T, in children with febrile seizures compared to controls (odds ratio = 1.91, 95% confidence interval = 1.31-2.81). INTERPRETATION: Pathogenic SCN1A variants may be identified in infants with vaccine-proximate febrile seizures. As early diagnosis of Dravet syndrome is essential for optimal management and outcome, SCN1A sequencing in infants with prolonged febrile seizures, proximate to vaccination, should become routine. ANN NEUROL 2020;87:281-288.

10.
Zoonoses Public Health ; 67(1): 79-88, 2020 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-31677254

RESUMO

Q fever (caused by Coxiella burnetii) is a serious zoonotic disease that occurs almost worldwide. Occupational contact with animals increases the risk of exposure, and Q fever vaccination is recommended for veterinary workers in Australia. This study aimed to investigate C. burnetii seroprevalence among unvaccinated veterinary workers in Australia and determine factors associated with a positive serological result. During 2014 and 2015, convenience sampling at veterinary conferences and workplace vaccination clinics was undertaken. Participants completed a questionnaire and provided a blood sample for C. burnetii serology. Participants were predominantly veterinarians (77%), but veterinary support staff, animal scientists, and administration workers also participated. Blood samples (n = 192) were analysed by an immunofluorescence assay and considered positive where the phase I or phase II IgG titre was ≥1/50. Seroprevalence was 19% (36/192; 95% CI 14%-25%). A positive serological result was significantly associated with (a) working in outer regional/remote areas (odds ratio [OR] 6.2; 95% CI 1.9-20.8; reference = major cities; p = .009) and (b) having spent more than 50% of total career working with ruminants (OR 4.8; 95% CI 1.7-13.5; reference = <15% of career; p = .025). These findings confirm an increased risk of exposure to C. burnetii compared to the general population, providing new evidence to support Q fever vaccination of veterinary workers in Australia.

12.
Lancet Neurol ; 18(12): 1091-1102, 2019 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-31701892

RESUMO

BACKGROUND: Genome-wide association studies (GWAS) in Parkinson's disease have increased the scope of biological knowledge about the disease over the past decade. We aimed to use the largest aggregate of GWAS data to identify novel risk loci and gain further insight into the causes of Parkinson's disease. METHODS: We did a meta-analysis of 17 datasets from Parkinson's disease GWAS available from European ancestry samples to nominate novel loci for disease risk. These datasets incorporated all available data. We then used these data to estimate heritable risk and develop predictive models of this heritability. We also used large gene expression and methylation resources to examine possible functional consequences as well as tissue, cell type, and biological pathway enrichments for the identified risk factors. Additionally, we examined shared genetic risk between Parkinson's disease and other phenotypes of interest via genetic correlations followed by Mendelian randomisation. FINDINGS: Between Oct 1, 2017, and Aug 9, 2018, we analysed 7·8 million single nucleotide polymorphisms in 37 688 cases, 18 618 UK Biobank proxy-cases (ie, individuals who do not have Parkinson's disease but have a first degree relative that does), and 1·4 million controls. We identified 90 independent genome-wide significant risk signals across 78 genomic regions, including 38 novel independent risk signals in 37 loci. These 90 variants explained 16-36% of the heritable risk of Parkinson's disease depending on prevalence. Integrating methylation and expression data within a Mendelian randomisation framework identified putatively associated genes at 70 risk signals underlying GWAS loci for follow-up functional studies. Tissue-specific expression enrichment analyses suggested Parkinson's disease loci were heavily brain-enriched, with specific neuronal cell types being implicated from single cell data. We found significant genetic correlations with brain volumes (false discovery rate-adjusted p=0·0035 for intracranial volume, p=0·024 for putamen volume), smoking status (p=0·024), and educational attainment (p=0·038). Mendelian randomisation between cognitive performance and Parkinson's disease risk showed a robust association (p=8·00 × 10-7). INTERPRETATION: These data provide the most comprehensive survey of genetic risk within Parkinson's disease to date, to the best of our knowledge, by revealing many additional Parkinson's disease risk loci, providing a biological context for these risk factors, and showing that a considerable genetic component of this disease remains unidentified. These associations derived from European ancestry datasets will need to be followed-up with more diverse data. FUNDING: The National Institute on Aging at the National Institutes of Health (USA), The Michael J Fox Foundation, and The Parkinson's Foundation (see appendix for full list of funding sources).

13.
Mov Disord ; 34(12): 1864-1872, 2019 12.
Artigo em Inglês | MEDLINE | ID: mdl-31659794

RESUMO

BACKGROUND: Mendelian randomization is a method for exploring observational associations to find evidence of causality. OBJECTIVE: To apply Mendelian randomization between risk factors/phenotypic traits (exposures) and PD in a large, unbiased manner, and to create a public resource for research. METHODS: We used two-sample Mendelian randomization in which the summary statistics relating to single-nucleotide polymorphisms from 5,839 genome-wide association studies of exposures were used to assess causal relationships with PD. We selected the highest-quality exposure genome-wide association studies for this report (n = 401). For the disease outcome, summary statistics from the largest published PD genome-wide association studies were used. For each exposure, the causal effect on PD was assessed using the inverse variance weighted method, followed by a range of sensitivity analyses. We used a false discovery rate of 5% from the inverse variance weighted analysis to prioritize exposures of interest. RESULTS: We observed evidence for causal associations between 12 exposures and risk of PD. Of these, nine were effects related to increasing adiposity and decreasing risk of PD. The remaining top three exposures that affected PD risk were tea drinking, time spent watching television, and forced vital capacity, but these may have been biased and were less convincing. Other exposures at nominal statistical significance included inverse effects of smoking and alcohol. CONCLUSIONS: We present a new platform which offers Mendelian randomization analyses for a total of 5,839 genome-wide association studies versus the largest PD genome-wide association studies available (https://pdgenetics.shinyapps.io/MRportal/). Alongside, we report further evidence to support a causal role for adiposity on lowering the risk of PD. © 2019 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society.

14.
Aust Prescr ; 42(4): 131-135, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-31427844
15.
Artigo em Inglês | MEDLINE | ID: mdl-31315166

RESUMO

This report summarises Australian passive surveillance data for adverse events following immunisation (AEFI) for 2017 reported to the Therapeutic Goods Administration and describes reporting trends over the 18-year period 1 January 2000 to 31 December 2017. There were 3,878 AEFI records for vaccines administered in 2017; an annual AEFI reporting rate of 15.8 per 100,000 population. There was a 12% increase in the overall AEFI reporting rate in 2017 compared with 2016. This increase in reported adverse events in 2017 compared to the previous year was likely due to the introduction of the zoster vaccine (Zostavax®) provided free for people aged 70­79 years under the National Immunisation Program (NIP) and also the state- and territory-based meningococcal ACWY conjugate vaccination programs. AEFI reporting rates for most other individual vaccines in 2017 were similar to 2016. The most commonly reported reactions were injection site reaction (34%), pyrexia (17%), rash (15%), vomiting (8%) and pain (7%). The majority of AEFI reports (88%) described non-serious events. Two deaths were reported that were determined to have a causal relationship with vaccination; they occurred in immunocompromised people contraindicated to receive the vaccines.


Assuntos
Doenças do Sistema Imunitário/epidemiologia , Vacinação/efeitos adversos , Vacinas/efeitos adversos , Adolescente , Adulto , Sistemas de Notificação de Reações Adversas a Medicamentos , Idoso , Austrália/epidemiologia , Criança , Pré-Escolar , Exantema/induzido quimicamente , Exantema/epidemiologia , Feminino , Febre/induzido quimicamente , Febre/epidemiologia , Vacina contra Herpes Zoster , Humanos , Programas de Imunização , Lactente , Reação no Local da Injeção/epidemiologia , Masculino , Pessoa de Meia-Idade , Dor/induzido quimicamente , Dor/epidemiologia , Vigilância da População , Vacinação/normas , Vacinação/estatística & dados numéricos , Vacinas/administração & dosagem , Vômito/induzido quimicamente , Vômito/epidemiologia , Adulto Jovem
16.
Brain ; 142(9): 2828-2844, 2019 Sep 01.
Artigo em Inglês | MEDLINE | ID: mdl-31324919

RESUMO

Our objective was to define the prevalence and clinical features of genetic Parkinson's disease in a large UK population-based cohort, the largest multicentre prospective clinico-genetic incident study in the world. We collected demographic data, Movement Disorder Society Unified Parkinson's Disease Rating Scale scores, and Montreal Cognitive Assessment scores. We analysed mutations in PRKN (parkin), PINK1, LRRK2 and SNCA in relation to age at symptom onset, family history and clinical features. Of the 2262 participants recruited to the Tracking Parkinson's study, 424 had young-onset Parkinson's disease (age at onset ≤ 50) and 1799 had late onset Parkinson's disease. A range of methods were used to genotype 2005 patients: 302 young-onset patients were fully genotyped with multiplex ligation-dependent probe amplification and either Sanger and/or exome sequencing; and 1701 late-onset patients were genotyped with the LRRK2 'Kompetitive' allele-specific polymerase chain reaction assay and/or exome sequencing (two patients had missing age at onset). We identified 29 (1.4%) patients carrying pathogenic mutations. Eighteen patients carried the G2019S or R1441C mutations in LRRK2, and one patient carried a heterozygous duplication in SNCA. In PRKN, we identified patients carrying deletions of exons 1, 4 and 5, and P113Xfs, R275W, G430D and R33X. In PINK1, two patients carried deletions in exon 1 and 5, and the W90Xfs point mutation. Eighteen per cent of patients with age at onset ≤30 and 7.4% of patients from large dominant families carried pathogenic Mendelian gene mutations. Of all young-onset patients, 10 (3.3%) carried biallelic mutations in PRKN or PINK1. Across the whole cohort, 18 patients (0.9%) carried pathogenic LRRK2 mutations and one (0.05%) carried an SNCA duplication. There is a significant burden of LRRK2 G2019S in patients with both apparently sporadic and familial disease. In young-onset patients, dominant and recessive mutations were equally common. There were no differences in clinical features between LRRK2 carriers and non-carriers. However, we did find that PRKN and PINK1 mutation carriers have distinctive clinical features compared to young-onset non-carriers, with more postural symptoms at diagnosis and less cognitive impairment, after adjusting for age and disease duration. This supports the idea that there is a distinct clinical profile of PRKN and PINK1-related Parkinson's disease. We estimate that there are approaching 1000 patients with a known genetic aetiology in the UK Parkinson's disease population. A small but significant number of patients carry causal variants in LRRK2, SNCA, PRKN and PINK1 that could potentially be targeted by new therapies, such as LRRK2 inhibitors.

17.
Ann Neurol ; 86(2): 225-240, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-31187503

RESUMO

OBJECTIVE: To identify disease-causing variants in autosomal recessive axonal polyneuropathy with optic atrophy and provide targeted replacement therapy. METHODS: We performed genome-wide sequencing, homozygosity mapping, and segregation analysis for novel disease-causing gene discovery. We used circular dichroism to show secondary structure changes and isothermal titration calorimetry to investigate the impact of variants on adenosine triphosphate (ATP) binding. Pathogenicity was further supported by enzymatic assays and mass spectroscopy on recombinant protein, patient-derived fibroblasts, plasma, and erythrocytes. Response to supplementation was measured with clinical validated rating scales, electrophysiology, and biochemical quantification. RESULTS: We identified biallelic mutations in PDXK in 5 individuals from 2 unrelated families with primary axonal polyneuropathy and optic atrophy. The natural history of this disorder suggests that untreated, affected individuals become wheelchair-bound and blind. We identified conformational rearrangement in the mutant enzyme around the ATP-binding pocket. Low PDXK ATP binding resulted in decreased erythrocyte PDXK activity and low pyridoxal 5'-phosphate (PLP) concentrations. We rescued the clinical and biochemical profile with PLP supplementation in 1 family, improvement in power, pain, and fatigue contributing to patients regaining their ability to walk independently during the first year of PLP normalization. INTERPRETATION: We show that mutations in PDXK cause autosomal recessive axonal peripheral polyneuropathy leading to disease via reduced PDXK enzymatic activity and low PLP. We show that the biochemical profile can be rescued with PLP supplementation associated with clinical improvement. As B6 is a cofactor in diverse essential biological pathways, our findings may have direct implications for neuropathies of unknown etiology characterized by reduced PLP levels. ANN NEUROL 2019;86:225-240.

18.
Parkinsonism Relat Disord ; 65: 55-61, 2019 08.
Artigo em Inglês | MEDLINE | ID: mdl-31105012

RESUMO

BACKGROUND: L-dopa responsiveness in Parkinson's disease (PD) varies, but the clinical correlates and significance of this are ill-defined. METHODS: Patients were assessed before and after their usual morning L-dopa dose, using the MDS Unified PD Rating Scale Part 3 (MDS UPDRS 3), and rated as definite responders (≥24.5% improvement) or limited responders (<24.5%). RESULTS: 1007 cases, mean age 66.1 years (SD 9.1) at diagnosis, were assessed 3.4 (SD 0.9) years after diagnosis. The L-dopa response was definite in 614 cases (61.0%), median reduction in MDS UPDRS 3 scores was 42.0%, (IQR 33.3, 53.1), and was limited in 393 cases (39.0%), median reduction in MDS UPDRS 3 scores 11.5% (IQR 4.3, 18.2). Definite responders were younger (66.3 years at study entry, SD 9.3) than limited responders (69.2 years, SD 8.4, p < 0.001). The MDS UPDRS 3 score at study entry in definite responders (21.0, SD 10.5) was significantly lower than in limited responders (24.7, SD 13.4, p < 0.001). The MDS UPDRS 3 increase over 18 months was less in definite responders at 3.0 (SD 10.4), compared to limited responders (6.4, SD 11.0, p < 0.001). The levodopa equivalent daily dose (LEDD) was not significantly different at study entry (definite responders 317 mg, SD 199, vs limited responders 305 mg, SD 191, p = 0.53). However, LEDD was significantly higher at the time of the L-dopa challenge test in definite responders (541 mg, SD 293) compared to limited responders (485 mg, SD 215, p = 0.01). Responsiveness to L-dopa was unaffected by the challenge test dose (p = 0.54). CONCLUSIONS: The main determinants of variation in the L-dopa response in early PD are age and motor severity. A limited L-dopa response is associated with faster motor progression.

19.
Med J Aust ; 210(10): 447-453, 2019 06.
Artigo em Inglês | MEDLINE | ID: mdl-31066061

RESUMO

OBJECTIVE: To estimate rates of respiratory syncytial virus (RSV)-associated hospitalisation across the age spectrum, and to identify groups at particular risk of serious RSV-associated disease. DESIGN, SETTING AND PARTICIPANTS: Retrospective review of National Hospital Morbidity Database data for all RSV-associated hospitalisations in Australia, 2006-2015. MAIN OUTCOMES AND MEASURES: RSV-coded hospitalisation rates by age, sex, Indigenous status, jurisdiction, and seasonality (month and year); hospital length of stay; in-hospital deaths. RESULTS: During 2006-2015, there were 63 814 hospitalisations with an RSV-specific principal diagnostic code; 60 551 (94.9%) were of children under 5 years of age. The hospitalisation rate for children under 5 years was 418 per 100 000 population; for children under 6 months of age it was 2224 per 100 000 population; the highest rate was for infants aged 0-2 months (2778 per 100 000 population). RSV-coded hospitalisation rates were higher for adults aged 65 or more than for people aged 5-64 years (incidence rate ratio [IRR], 6.6; 95% CI, 6.2-7.1), and were also higher for Indigenous Australians than other Australians (IRR, 3.3; 95% CI, 3.2-3.5). A total of 138 in-hospital deaths were recorded, including 82 of adults aged 65 years or more (59%). CONCLUSIONS: Prevention strategies targeting infants, such as maternal or early infant vaccination, would probably have the greatest impact in reducing RSV disease rates. Further characterisation of RSV disease epidemiology, particularly in older adults and Indigenous Australians, is needed to inform health care strategies.


Assuntos
Hospitalização/estatística & dados numéricos , Infecções por Vírus Respiratório Sincicial/epidemiologia , Vírus Sincicial Respiratório Humano/isolamento & purificação , Adolescente , Adulto , Fatores Etários , Idoso , Austrália/epidemiologia , Criança , Pré-Escolar , Bases de Dados Factuais , Feminino , Humanos , Lactente , Masculino , Pessoa de Meia-Idade , Estudos Retrospectivos , Fatores de Risco , Estações do Ano , Adulto Jovem
20.
Pediatrics ; 143(5)2019 05.
Artigo em Inglês | MEDLINE | ID: mdl-31004046

RESUMO

BACKGROUND: Febrile seizures (FSs) are a common pediatric condition caused by a sudden rise in temperature, affecting 3% to 5% of children aged ≤6 years. Although vaccination can cause FSs, little is known on whether FSs occurring in the time soon after vaccination (vaccine-proximate febrile seizures [VP-FSs] differ clinically from non-vaccine-proximate febrile seizures [NVP-FSs]). We compared the clinical profile and outcomes of VP-FS to NVP-FS. METHODS: Prospective cohort study of children aged ≤6 years presenting with their first FS at 1 of 5 Australian pediatric hospitals between May 2013 and June 2014. Clinical features, management, and outcomes were compared between VP-FS and NVP-FS. RESULTS: Of 1022 first FS cases (median age 19.8 months; interquartile range 13.6-27.6), 67 (6%) were VP-FSs. When comparing VP-FS to NVP-FS, there was no increased risk of prolonged (>1 day) hospitalization (odds ratio [OR] 1.61; 95% confidence interval [95% CI] 0.84-3.10), ICU admission (OR 0.72; 95% CI 0.10-5.48), seizure duration >15 minutes (OR 1.47; 95% CI 0.73-2.98), repeat FS within 24 hours (OR 0.80; 95% CI 0.34-1.89), or requirement for antiepileptic treatment on discharge (OR 1.81; 95% CI 0.41-8.02). VP-FS patients with a laboratory-confirmed infection (12%) were more likely to have a prolonged admission compared with those without. CONCLUSIONS: VP-FS accounted for a small proportion of all FS hospital presentations. There was no difference in outcomes of VP-FS compared with NVP-FS. This is reassuring data for clinicians and parents of children who experience FS after vaccination and can help guide decisions on revaccination.


Assuntos
Convulsões Febris/diagnóstico , Convulsões Febris/epidemiologia , Índice de Gravidade de Doença , Vacinação/efeitos adversos , Austrália/epidemiologia , Criança , Pré-Escolar , Estudos de Coortes , Feminino , Humanos , Lactente , Recém-Nascido , Masculino , Estudos Prospectivos , Resultado do Tratamento , Vacinação/tendências
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