Biomedical subjects

Terence Stephenson

Publications and source records attributed to Terence Stephenson.

21 records · Page 2Linked to original sources

PubMed2002

Long-term ophthalmic outcome of low birth weight children with and without retinopathy of prematurity.

OBJECTIVE: A prospective study of retinopathy of prematurity (ROP) of 505 infants who weighed <1701 g at birth was undertaken in the mid-1980s. This cohort was traced at 10 to 12 years of age to determine how low birth weight alone and ROP might influence their ophthalmic outcome. METHODS: Outcome measures were 1) visual functions (visual acuity, contrast sensitivity, stereoacuity, perimetry, and color vision), 2) presence of strabismus, and 3), measurements of eye size and the dimensions of its components including refractive state. A total of 169 11-year-olds who were born at term were recruited as control subjects and examined under the same conditions. RESULTS: A total of 448 of the original cohort were traced, and 254 consented to a further examination. Compared with the control group, the follow-up cohort differed significantly with reduced visual functions and increased incidence of both myopia and strabismus. Compared with published data, eye size was smaller in the low birth weight cohort. To summarize the ophthalmic data, we defined ophthalmic morbidity as visual acuity below 0.0 log units or the presence of strabismus, myopia, color vision defect, or visual field defect. The rate of ophthalmic morbidity was 50.8% (n = 129/254) in the study cohort compared with 19.5% (n = 33/169) in the control group. The highest rate of ophthalmic morbidity was associated with severe ROP (stages 3/4), although those with no ROP had a less favorable outcome than the control group. CONCLUSION: This study shows that low birth weight children are at increased risk of visual impairments compared with children who are born at full term. Visual impairments are associated with low birth weight per se and severe ROP. Regressed mild ROP is only a risk factor for strabismus. The functional significance of these deficits is largely unknown.

Case-Control Studies↗

PubMed2002

Double-blind, randomized trial of long-chain polyunsaturated fatty acid supplementation in formula fed to preterm infants.

OBJECTIVE: We tested the hypothesis that balanced addition of long-chain polyunsaturated fatty acid (LCPUFA) to preterm formula during the first weeks of life would confer long-term neurodevelopmental advantage in a double-blind, randomized, controlled trial of preterm formula with and without preformed LCPUFA. METHODS: The participants were 195 formula-fed preterm infants (birth weight <1750 g, gestation <37 weeks) from 2 UK neonatal units and 88 breast milk-fed infants. Main outcome measures were Bayley Mental Developmental Index (MDI) and Psychomotor Developmental Index (PDI) at 18 months and Knobloch, Passamanick and Sherrard's Developmental Screening Inventory at 9 months' corrected age. Safety outcome measures were anthropometry at 9 and 18 months, tolerance, infection, necrotizing enterocolitis, and death. RESULTS: There were no significant differences in developmental scores between randomized groups, although infants who were fed LCPUFA-supplemented formula showed a nonsignificant 2.6-point (0.25 standard deviation) advantage in MDI and PDI at 18 months, with a greater (nonsignificant) advantage (MDI: 4.5 points; PDI: 5.8 points) in infants below 30 weeks' gestation. LCPUFA-supplemented infants were shorter than control infants at 18 months (difference in length standard deviation score: 0.44; 95% confidence interval: 0.08-0.8). No other significant short- or long-term differences in safety outcomes were observed. Breastfed infants had significantly higher developmental scores at 9 and 18 months than both formula groups and were significantly heavier and longer at 18 months than LCPUFA-supplemented but not control infants. CONCLUSIONS: With the dose, duration, and preparation of LCPUFA used, efficacy was not demonstrated, although an advantage in later neurodevelopment cannot be excluded by global tests of development up to 18 months, particularly in infants below 30 weeks' gestation. The surprising effect of LCPUFA-supplemented formula on growth 18 months beyond the intervention period needs to be confirmed in other studies using similar supplementation strategies. Additional follow-up of this cohort is critical at an age when more specific tests of cognitive function are possible.

Age Factors↗

PubMedDate not supplied

Leptin, fetal nutrition, and long-term outcomes for adult hypertension.

One factor contributing to later hypertension, particularly in response to nutritional challenges is excess fat deposition around the kidney. In this review we discuss the hypothesis that these adverse conditions can be entrained by exposure of the conceptus to maternal nutrient restriction in early pregnancy. To this end we have shown in sheep that maternal nutrient restriction coincident with the time of embryogenesis and placental growth results in an early increase in fetal fat mass around the kidney that persists into later life. This is accompanied by an increase in leptin mRNA abundance and growth factor sensitivity. These adaptations occur in conjunction with reduced maternal plasma cortisol, thyroid hormones and leptin concentrations over the period of nutrient restriction. Some, but not all of these effects on fat development are accompanied by long term cardiovascular adaptations. As young adults, offspring from mothers nutrient restricted between early to mid gestation exhibit a leftward resetting, and blunting, of the cardiovascular baroreflex that appears to be mediated centrally through altered regional angiotensinogen II activity. At the same time, fat mass remains raised in nutrient restricted offspring. These animals demonstrate a marked increase in plasma leptin following sympathetic stimulation which is not observed in controls that indicates resetting of adipocyte sensitivity to stress. In conclusion, global nutrient restriction confined to the periods of embryonic and placental development therefore, programmes adult physiology, which may enhance predisposition to later disease given the appropriate environmental stimuli.

Adipose Tissue↗