ObjectiveTo describe infants aged <12 months reported with microcephaly to the Australian Paediatric Surveillance Unit (APSU) following emergence of Zika virus infection internationally.Design, setting and patientsNational, active, monthly surveillance for microcephaly using the APSU. Microcephaly was defined as occipitofrontal circumference (OFC) of more than 2 SDs below the mean for age, gender and gestation.Main outcome measuresClinical spectrum, aetiology and birth prevalence of microcephaly reported by paediatricians.ResultsBetween June 2016 and July 2018, 106 notifications were received, with clinical details provided for 96 (91%). After excluding ineligible notifications, 70 cases were confirmed, giving an annual birth prevalence of 1.12 (95% CI 0.88 to 1.42) per 10 000 live births. Of the total number of cases, 47 (67%) had primary microcephaly (at birth); and 25 (36%) had severe microcephaly (OFC >3 SDs). Birth defects were reported in 42 (60%). Of 49 infants with developmental assessment details available, 25 (51%) had failed to reach all milestones. Vision impairment was reported in 14 (26%). The cause of microcephaly was unknown in 60%: 13 (19%) had been diagnosed with genetic disorders; 22 (39%) had anomalies on neuroimaging. No congenital or probable Zika infection was identified. Severe microcephaly was more often associated with hearing impairment than microcephaly of >2 SDs but ≤3 SDs below the mean (p<0.007). Indigenous children and children with socioeconomic advantage were over-represented among children with microcephaly.ConclusionNovel national data on microcephaly highlight the high proportion of idiopathic cases. This has implications for prevention and management and suggests the need for a standardised diagnostic approach and ongoing surveillance mechanism in Australia.
Prostate cancer (PC) is the most common non-cutaneous cancer in men worldwide. The relationships between PC and possible risk factors for PC cases (n = 1,181) and male controls (n = 875) from the New South Wales (NSW) Cancer, Lifestyle and Evaluation of Risk Study (CLEAR) were examined in this study. The associations between PC risk and paternal history of PC, body mass index (BMI), medical conditions, sexual behaviour, balding pattern and puberty, after adjusting for age, income, region of birth, place of residence, and PSA testing, were examined. Adjusted risk of PC was higher for men with a paternal history of PC (OR = 2.31; 95%CI: 1.70-3.14), personal history of prostatitis (OR = 2.30; 95%CI: 1.44-3.70), benign prostatic hyperplasia (OR = 2.29; 95%CI: 1.79-2.93), being overweight (vs. normal; OR = 1.24; 95%CI: 0.99-1.55) or obese (vs. normal; OR = 1.44; 95%CI: 1.09-1.89), having reported more than seven sexual partners in a lifetime (vs. < 3 partners; OR = 2.00; 95%CI: 1.49-2.68), and having reported more than 5 orgasms a month prior to PC diagnosis (vs. ≤3 orgasms; OR = 1.59; 95%CI: 1.18-2.15). PC risk was lower for men whose timing of puberty was later than their peers (vs. same as peers; OR = 0.75; 95%CI: 0.59-0.97), and a smaller risk reduction of was observed in men whose timing of puberty was earlier than their peers (vs. same as peers; OR = 0.85; 95%CI: 0.61-1.17). No associations were found between PC risk and vertex balding, erectile function, acne, circumcision, vasectomy, asthma or diabetes. These results support a role for adult body size, sexual activity, and adolescent sexual development in PC development.
BackgroundObesity and physical activity (PA) are predictors of colon (CC) and rectal (RC) cancers. Prolonged sitting is also emerging as a potential predictor for these cancers. Little knowledge exists about the interactive effects of obesity, PA and prolonged sitting on cancer risk. This analysis assessed independent and interactive effects of PA, body mass index (BMI) and sitting time on CC and RC risks.MethodsThis analysis used data from a prospective study of 226,584 participants aged 45 years and over in New South Wales (NSW), Australia, who joined the 45 and Up study between 2006 and 2009. Baseline data were linked with data relating to mortality, cancer registration, hospital admission and Department of Human Services to December 2010. Multivariable Cox regression was used to estimate adjusted hazard ratios (referred to as relative risks, RRs) and 95% confidence intervals (Cis). Statistical significance was defined as p < 0.05.ResultsThere were 846 and 369 ascertained cases of CC and RC. BMI was positively associated with CC risk (p = 0.003, P-trend = 0.0006) but not with RC. CC risk was increased in participants in the highest BMI quartile (≥29.4-≤50 kg/m2) compared to the lowest (15- < 23.6 kg/m2), (RR = 1.32, 95% CI:1.08–1.63). PA was associated with CC risk (p = 0.02) but not with RC. Specifically, CC risk was lower in individuals partaking in any amount of vigorous activity (time/week) compared to participants with no engagement (RR = 0.78, 95% CI:0.65–0.93). Sitting time was not associated with CC or RC. We found no evidence of interactive effects of PA, BMI and prolonged sitting on cancer risk.ConclusionThis evidence suggests that a healthy weight and vigorous activity are essential to reduce CC risk since these factors may be independent of each other.
Little knowledge exists about the role of cardiorespiratory fitness (CRF) or its interaction with excess adiposity determined by body mass index (BMI) in cancer prevention. A total of 5,128 middle-aged men, without a history of cancer at baseline in 1970–71, were examined for subsequent incidence and mortality of several cancer types. Participants’ data were linked with cancer registration and mortality data to March 2017. During 47 years of follow-up, a total of 1,920 incident cases and 1,638 cancer-related deaths were ascertained. BMI, particularly obesity, was associated with (i) incidence and (ii) mortality from respiratory/thoracic cancers; and (iii) all cancer-cause mortality. The respective adjusted hazard ratios (HRs) were: (i) 0.51 (95%CI:0.32–0.79), (ii) 0.48 (95%CI:0.30–0.75) and (iii) 0.73 (95%CI:0.59–0.89) when compared obese men (BMI ≥30 kg/m2) to men with healthy-BMI (<25 kg/m2). Increasing CRF was inversely associated with incidence and mortality of respiratory/thoracic cancers, HRs 0.78 (95%CI:0.67–0.90) and 0.73 (95%CI:0.63–0.84) respectively; and all cancer-cause incidence 0.92 (95%CI:0.86–0.98) and mortality 0.85 (95%CI:0.79–0.91). Physical activity (PA) was not associated with most outcomes. We found no evidence of interactions between CRF or PA and BMI on cancer risk. This evidence suggests that midlife CRF is associated with lowered risk of cancer incidence and mortality with no evidence of cancer risk modification by BMI.
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