After adjustment for potential confounders, prone and side sleeping positions, maternal smoking, and the joint exposure to bed sharing and maternal smoking were associated with statistically significant increased risk of SIDS. A change from the side to the supine sleeping position could result in a substantial reduction in SIDS. Maternal smoking is common in New Zealand and with the reduction in the prevalence of prone sleeping position is now the major risk factor in this country. However, smoking behavior has been difficult to change. Bed sharing is also a major factor but appears only to be a risk to infants of mothers who smoke. Addressing bed sharing among mothers who smoke could reduce SIDS by at least one third. Breastfeeding did not appear to offer a statistically significant reduction in SIDS risk after adjustment of potential confounders, but as breastfeeding rates are comparatively good in New Zealand, this result should be interpreted with caution as the power of this study to detect a benefit is small.

Recent research has implicated infant sleeping body position and bed sharing as risk factors in the sudden infant death syndrome. The sociodemographic associations of infant sleeping body position and location were examined in this study. This showed that the majority (86.40/o) of New Zealand parents now place their infants to sleep on their sides. The remainder place their infants supine (1-3%), prone (4.8%), or no particular way (7. 5%). In the waking position, 57-9% were usually found on their sides, 18.2% supine, and 6l1% prone. Infant sleeping position showed marked sociodemographic variability. These findings are a marked contrast to previous New Zealand studies which showed a reversed pattern, with most infants put to sleep prone.There were also highly significant sociodemographic differences in the place of sleeping. Overall 12.2% of infants shared a bed, with infants of younger less well educated mothers who were of nonEuropean origin, with a parity of five or more, or unmarried significantly more likely to do so. Infants of unemployed and lower socioeconomic group (Elley-Irving groups 5 and 6) fathers were also more likely to share a parental bed.

The study reaffirms the high prevalence of overweight and obesity in pre-school children in New Zealand, and demonstrates the variations in prevalence when using different reference standards.

Objectives Concern has been expressed about possible neonatal side effects after the use of maternal anti‐platelet agents in pregnancy, particularly low dose aspirin treatment. We have studied neonatal platelet behaviour using whole blood techniques, and assessed the neonatal effect of the maternal ingestion of 60 mg aspirin daily. Design Cross sectional and randomised, double‐blind, placebo‐controlled. Setting University hospital. Subject 1. Eight normal women, studied before conception, and their infants. 2. Twenty‐four infants whose mothers had been randomised to receive either 60 mg aspirin daily, or placebo, in double‐blind fashion. Methods The Clay Adams Ultra Flo 100 whole blood single platelet counter was employed to measure platelet aggregation in response to various agonists. The platelet release reaction was also measured in whole blood, and serum thromboxane B2 (TxB2) production was measured by radio‐immunoassay. Umbilical cord blood samples were obtained at delivery. Results 1. Neonatal platelet aggregation induced by adrenaline, ADP and platelet activating factor was reduced in comparison with their mothers (P < 0.01), whereas the neonatal platelet release reaction was reduced when stimulated by collagen and U46619 (a thromboxane mimetic) (P < 0.01). Serum TxB2 production was similar in mothers and babies. 2. Neonatal platelet aggregation, release reaction and serum TxB2 production were not significantly reduced in infants exposed to maternal aspirin in comparison with those neonates exposed to maternal placebo. This is in contrast to the effect on maternal platelets. Conclusions Although only a small number of patients were studied, we interpret this as a relative sparing of neonatal platelet reactivity due to the presystemic action of low dose aspirin.

A 10-year-old boy with precocious puberty of 2 1/2 years' duration presented with a malignant thoracic teratoma with elevated levels of beta human chorionic gonadotropin (beta-HCG) and alpha fetoprotein (alpha FP). The mediastinal tumor was completely excised and adjuvant chemotherapy commenced. Within 3 weeks of commencing chemotherapy he developed hematologic abnormalities that, with the subsequent clinical illness, led to a diagnosis of malignant histiocytosis. Death occurred a few days after start of therapy for malignant histiocytosis. Cytogenic studies showed the somatic karyotype to be that of Klinefelter's syndrome, while the malignant cells in marrow and lymph node carried an additional marker chromosome. This case, with others reported, suggest that the XXY karyotype may influence the development of mediastinal germ cell tumors, which in themselves appear to be associated with the early onset of a malignancy of the hemopoietic system.

Objective To investigate the effect of 60 mg aspirin daily on platelet reactivity and prostaglandin production in various groups of patients. Similar regimens, which are thought to act through inhibition of platelet thromboxane production, are currently undergoing clinical assessment for the prevention of pre‐eclampsia and intrauterine growth retardation. Design A prospective randomized placebo controlled study. Setting University Hospital, Nottingham. Subjects 12 non‐pregnant female volunteers, 18 normal primigravidae before 16 weeks gestation and 16 pregnant women admitted with gestational hypertension (GH) at a mean gestation of 38 weeks. Interventions In the non‐pregnant women blood samples were taken before and after a 10‐day course of 60 mg aspirin daily. The primigravidae had blood samples taken at 16 weeks and then they were randomized to receive either 60 mg aspirin daily or a matched placebo. Further blood samples were obtained at 28, 32 and 36 weeks. Main outcome measures Changes in platelet reactivity and release reaction, and serum thromboxane production, were estimated in whole blood. Results 60 mg aspirin daily significantly inhibited cyclo‐oxygenase dependent platelet aggregation, release reaction and serum thromboxane production in non‐pregnant and pregnant women, and in women with GH (P<0.01). When adrenaline was used as the aggregating agent, the cyclo‐oxygenase pathway was recruited in the increased reactivity seen in the third trimester of normal pregnancy, and was sensitive to inhibition by low dose aspirin. Conclusion Low dose aspirin would appear to be an appropriate agent for the inhibition of platelet reactivity associated with hypertensive pregnancy.

Community-based screening may be useful for identifying VPT children with school readiness difficulties, but low referral rates may limit the effectiveness of such programmes.

No abstract