substantially; and for medical-school staff to apply to teaching methods the same rigorous scrutiny which they so effectively apply to their academic inquiries.
magnesium salts12 might have a beneficial effecton ischaemic heart-disease, perhaps, as well as on retinopathy.
BIOCHEMISTRY OF SURFACTANT HYPOMAGNESÆMIA AND DIABETIC RETINOPATHY THERE is much interest in the possible contribution of suboptimal concentrations of magnesium in ischæmic heart-disease.’-3 Diabetic patients are at increased risk of ischæmic heart disease, and a new study has revealed a significant relation between low concentrations of magnesium in the serum and another vascular complication of diabetes, diabetic retinopathy.’ McNair and his coworkers4 have investigated possible risk factors in patients who had had diabetes for ten to twenty years and 194 normal controls. The diabetic patients were divided by a single observer into two groups: group A (45) had normal fundi or minor changes; group B (26) had more severe changes such as microaneurysms with large haemorrhages and/or exudates and proliferative retinopathy. In the diabetic patients serum-magnesium was significantly lower (0 - 74 + 0 - 012 mmol/1) than in the normal controls (083+_0007). In addition, group B with severe retinopathy had significantly lower serum-magnesiums (0-72±0.018 mmol/1) than group A (0.75 ± 0.014). Groups A and B did not differ significantly from controls with respect to serum concentrations of potassium,
calcium, glucose, lipids, parathyroid hormone, and C-peptide. Group B contained a higher proportion of smokers than group A-reinforcing earlier observations on an association between smoking and retinopathy5,6 - but there was no evidence that serum concentrations of magnesium were related to smoking habits. This work suggests that low concentrations of magnesium may be an additional risk factor in the development of diabetic retinopathy. The reason for the low serum-magnesium in the diabetic patients is obscure. As McNair and others point out, if there was increased urinary excretion of magnesium the metabolism of calcium would also be expected to alter,7-9 and there was no evidence for this in their patients. Serum-magnesium concentrations are not necessarily a good indication of intracellular magnesium, so that the magnesium content of the cells in diabetic patients may well be decreased even more than the serum magnesium. We are by no means sure that strict control of bloodglucose will prevent diabetic retinopathy,1O so other methods of prevention should be explored. Magnesium salts are not very toxic" and cautious administration of Seelig, M. S Adv. cardiac Struct. Metab. 1972, 1, 626. Seelig, M. S., Heggtveit, H. A Am J clin Nutr 1974, 27, 59 3. Chipperfield, B., Chipperfield, J. R. Am. Heart J. 1977, 93, 679. 4. MeNair, I’ , Christiansen, C., Madsbad, S , Lauritzen, E., Faber, O., Binder, C., Transbøl, I. Diabetes, 1978, 27, 1075 5. Paetkau, M. E., Boyd, T. A. S., Winship, B., Grace, M. Diabetes, 1977, 26, 1. 2
46 6. Lancet, 1977, i, 841. 7. I indemann, R. D., Adler, S.,
Yiengst, M. J., Beard, E S. J Lab. clin. Med. 1967, 70, 236. 8 Lemann, J, Lennon, E. J., Piering, W. R , Prien, E. L, Ricanati, E. S. ibid. 1970, 75, 578 9 Lennon, E J, Lemann, J., Piering, W. F., Larson, L. S. J clin. Invest. 1974, 53, 1424 10. Siperstein, M. D., Foster, D. W., Knowles, H. C., Levine, R., Madison, L. L., Roth, J New Engl J. Med. 1977, 296, 1060. 11 Venugopal, B, Luckey, T. D. Metal Toxicity in Mammals, vol. II, New York, 1978.
THE underlying process in hyaline-membrane disease of preterm infants is a deficiency of surfactant.’ This substance, produced by cells of the alveolar lining, enables the full-term infant to emerge safely from its aquatic intrauterine environment, and exist independently in air. It acts at the air/liquid interface throughout the lungs and opposes the effects of surface tension which would otherwise cause alveoli to collapse. Whether or not a preterm infant is able to survive after birth depends largely on the biochemical maturity of the lungs. If surfactant is present in sufficient quantity the lungs remain structurally stable. If not, progressive alveolar collapse occurs, giving rise to the familiar clinical picture of hyaline-membrane disease with cyanosis, grunting, and respiratory distress. Surfactant has proved remarkably amenable to study, even in the maturing fetus in utero: the lining cells of the alveoli actively secrete fluid which passes up the trachea to the pharynx, and some of this finds it way into the amniotic cavity where it is available for sampling by amniocentesis.2 Many units, in making the decision whether or not to deliver an infant thought to be at risk in utero, assess fetal-lung maturity by measuring surfactant in an attempt to predict the onset or severity of hyaline-membrane disease.3 In this case the progress of the disease can be so rapid that the infant provides the answer before a biochemical test result is to hand, but rapid tests which depend on the physical properties of surfactant4 can be carried out and have a useful predictive value. Pulmonary surfactant is biochemically complex, but a major constituent is phospholipid, usually measured as lecithin. Shelley et al. now report that not only the amount but also the precise composition of surface active phospholipid may be important in determining whether or not an infant will get hyaline-membrane disease.
Using a density-gradient centrifuge technique they
have been able to obtain adequate phospholipid for analysis even from heavily contaminated aspirates from infants with clinical surfactant dificiency. They studied 20 preterm infants with hyaline-membrane disease and 12 infants without the disease but of similar gestational age; the fatty-acid composition of phospholipid from the affected group of infants was significantly different from that of the control group, and in those who survived the composition gradually changed over several days to resemble mature surfactant. This study is a valuable contribution to our understanding of the pathophysiology of hyaline membrane disease. But what is its message for the neonatal pxdiatrician ? These tests require elaborate laboratory techniques and presumably could not be done 24 hours a day. It is unlikely then that they would affect the management of the newly born immature infant. But Whacker, W. E. C., Parisi, A. F. New Engl J. Med. 1968, 278, 772. Strang, L. B. Neonatal Respiration; p. 181. Oxford, 1977. Gluck, L., Kulovitch, M. V, Borer, R. C. J., et al. Am. J. of Obstet Gynec 1971, 109, 440. 3 Weller, P. H , Jenkins, P. A., Gupta, J., et al. Lancet, 1976, i, 12. 4. Evans, J. J. New Engl. JMed. 1975, 292, 1113 5. Shelley, S. A., Kovalevic, M., Paciga, J. F., Balis, J. N. ibid 1979, 300, 112
12 1. 2