Breast feeding and hypertrophic pyloric stenosis: population based case-control study

Abstract

Fig 1-Mean changes in blood flow, diastolic diameter, and distensibility ofbrachial artery in 12 diabetic subjects and 12 controls during reactive hyperaemia, 1Oug glyceryl trinitrate, and 400 ,ug glyceryl trinitrate. Bars show 95% confidence intervals (9) mm Hg; blood flow 45 (28) v 49 (41) m/min; diastolic diameter 482 (0 60) v 4-47 (1P05) mm; distensibility 4-8 (1-4) v 5 9 (1-6) per kPa). During reactive hyperaemia, heart rate, blood pressure, and the increase in brachial artery blood flow (5548% (99 5%) v 590% (106&6%)) were similar in diabetic and normal subjects (figure 1) but the increases in brachial artery diastolic diameter (1 2% (2-7%) v 9-1% (4-4%); difference 6-9% (95% confidence interval 4.9% to 11%)) and distensibility (-15-3% (10-4%) v 31% (31-7%); difference 46-3% (25-5% to 67<1%)) were significantly less in diabetic subjects (both P < 0-00 1). After 10 ,ug glyceryl trinitrate or 400 ,ug glyceryl trinitrate the increase in flow, diameter, and distensibility was similar in diabetic and normal subjects (figure 1). 700-Comment Endothelium dependent, flow related dilatation and increase in distensibility of the brachial artery are greatly impaired in patients with non-insulin dependent diabetes, but endothelium independent responses induced by glyceryl trinitrate are similar to those in normal subjects. Loss of flow related increase in arterial distensibility will augment systolic pressure, myocardial wall stress, and heart work relative to stroke output, potentially promoting left ventricular hypertrophy and lowering ischaemic threshold. Late systolic pressure will be further augmented by early wave reflection from the periphery3 because pulse wave velocity is increased when distensibility is reduced. Loss of flow mediated vasodilatation reflects endothelial dysfunction and may thus also provide a marker of atherogenetic susceptibility. Our data provide evidence ofvascular dysfunction in non-insulin dependent diabetes before the appearance of microalbuminuria, previously regarded as its earliest marker.4We thank Dr J R Peters for allowing us to study patients under his care and Wendy Simons and Julie-Ann Davies for their secretarial assistance.Funding: British Heart Foundation. Conflict of interest: None.

Bottle-feeding and the Risk of Pyloric Stenosis

“…A recent 30-year retrospective study of infants diagnosed with PS in Nigeria revealed that all 57 infants developing PS in the survey area were infants who used artificial feeds. 25 Pisacane et al 20 observed that infants developing PS were less likely to have been exclusively breastfed during the first week after birth compared with control infants. Consistent with our findings, they estimated a similar risk of PS for the exclusively formula-fed infants and the both breast and formula-fed infants.…”

“…13,18 However, a few recent analytical studies have revealed a distinct risk association between early bottle-feeding and PS. 19,20,25 In a 1:1 case-control study, Habbick et al 19 examined feeding practice at the time of postdelivery discharge and found that bottle-feeding was 2.9 times more common among infants who developed PS than among the control subjects. A recent 30-year retrospective study of infants diagnosed with PS in Nigeria revealed that all 57 infants developing PS in the survey area were infants who used artificial feeds.…”

“…20 Breast milk also has lower osmolarity, which could provide better gastric emptying. 26 It is also theoretically possible that breastfeeding protects against an infectious trigger by unknown agents because previous studies have revealed that breastfeeding confers protection against gastrointestinal infections.…”

“…[13][14][15][16][17][18] Two casecontrol studies revealed a two-to threefold higher risk for infants being bottle-fed. 19,20 The authors of these studies examined the association between feeding practice at the time of postdelivery discharge or the first week after birth and the subsequent risk of PS. However, PS onset is typically between 3 and 8 weeks of age, 7 several weeks after this feeding information was obtained.…”

Congenital anomalies associated with autism spectrum disorders

“…In the current study, there was a significantly increased risk for ASD associated with gastrointestinal anomalies after controlling for these factors. The etiology of pyloric stenosis is unknown although, like ASD, it is considered to have strong genetic and environmental determinants (Pisacane et al 1996, Schechter et al 1997, James 2004. Additionally, many parents report that their children with ASD experience gastrointestinal dysfunction (Horvath et al 1999).…”