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Metabolic Bone Disease in Preterm Infants

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Metabolic Bone Disease in Preterm Infants Arch Dis Child: first published as 10.1136/adc.60.7.682 on 1 July 1985. Downloaded from Archives of Disease in Childhood, 1985, 60, 682-685 Current topic Metabolic bone disease in preterm infants 0 G BROOKE AND A LUCAS Department of Child Health, St George's Hospital, London and MRC Dunn Nutrition Unit, Milton Road, Cambridge 'Osteopenia' or 'rickets of prematurity' is a condi- common the problem is and it may well be under tion or group of conditions resulting in reduced bone reported. It is found most often and in its severest mineralisation in preterm infants, and leading, in form in infants of less than 1000 g birthweight, in severe cases, to frank radiological rickets and whom frank radiological rickets has been described spontaneous fractures. A recent one day workshop in up to 57% of cases.4 Reduced bone mineralisa- in Cambridge, sponsored by the British Paediatric tion is almost universal in infants of less than 1500 g, Association's Nutrition Group, was devoted to this since they have poor calcium retention for several disorder. The proceedings are summarised in this weeks after birth.7-9 The problem is deciding when article. what may be regarded as an inevitable event becomes pathological, and there are no clear guide- Nomenclature lines on this. copyright. Metabolic bone disease in extremely preterm infants Diagnosis is now a well recognised problem.l" It has been called 'rickets of prematurity' and 'osteopenia'. Several methods have been used to attempt to Rickets implies radiological disease at the growing quantify demineralisation. Radiological densi- ends of the long bones, while osteopenia implies tometry is imprecise, since minor radiological under mineralisation. Neither term is ideal for a osteopenia represents major loss of bone mineral. http://adc.bmj.com/ condition that encompasses a variety of disturbances, More severe degrees of radiological osteopenia are ranging from mild under mineralisation to severe easy to recognise but still hard to quantify using bone disease with fractures, and for which the routine diagnostic radiographs. The best research aetiology is in dispute. The term rickets has an technique is probably photon absorptiometryl' but additional disadvantage in that it is often associated the equipment is expensive and not generally with vitamin D deficiency, of which there is little available, and the technique gives a measure of bone evidence in most cases of bone disease in preterm mineral density only, not of total bone mineral infants.4 5 Osteopenia, though not an ideal name, mass. Despite its limitations, radiography of the on September 26, 2021 by guest. Protected seems to have been adopted as a general descriptive limbs is reliable for the diagnosis of the marked term for the problem in the published reports. We generalised under mineralisation and bone end feel, however, that the term 'metabolic bone disease changes that are characteristic of the various grades of prematurity' is better-at least until it has become of metabolic bone disease of prematurity. The clear whether or not we are dealing with more than following classification has been suggested," and one pathological entity. The use of the word rickets proves satisfactory in practice: should be reserved for cases in which there are Grade 0-normal bones; definite radiological features of rickets at the ends of Grade I-rarefaction only; the long bones. Grade 1I-bone end changes (fraying and cupping of the metaphysis, subperiosteal new bone forma- Incidence tion); Grade III-the above changes, with fractures. The reported incidence varies widely from centre to Metabolic bone disease of prematurity is associ- centre. -4 6 Since there is no general agreement on ated with raised plasma alkaline phosphatase diagnostic criteria, it is impossible to be certain how activity. 12 The spread of values in subjects with 682 Arch Dis Child: first published as 10.1136/adc.60.7.682 on 1 July 1985. Downloaded from Metabolic bone disease in preterm infants 683 radiological evidence of bone disease, however, even high concentrations of plasma calcium23 24 and overlaps that of infants with radiologically normal raised urinary calcium excretion.16 These findings bones by such a large amount that its diagnostic may be explained if one takes into account the value is limited.'3 Although measurement of alka- overriding need for phosphorus for soft tissue line phosphatase activities has been useful in growth and metabolism in the body. When phos- epidemiological studies, the most one can say in phorus intake is inadequate, plasma reserves fall individual patients is that the majority of infants and phosphorus is withdrawn from the skeleton. with grade II or III changes have activities greater Calcium cannot be used for bone growth in the than 1000 IU/l. Thus, alkaline phosphatase values absence of phosphorus and so is lost in the urine. provide confirmatory evidence in severe cases, but When sufficient phosphorus is given to meet soft metabolic bone disease of prematurity remains a tissue needs, hydroxyapatite can again be formed in radiological diagnosis in clinical practice. bone and calcium absorbed from the diet is avidly retained, with consequent noticeable reduction in its Pathogenesis excretion in the urine.24 Other evidence for a central role of phosphorus deficiency is provided by the findings that in infants (1) Role of vitamin D deficiency. Severe bone disease with grade II and III bone changes, phosphorus is not prevented by vitamin D intakes as high as 2000 intake was significantly lower than in infants without IU/day,4 and occurs in the presence of normal or serious bone disease,25 and that the incidence and raised Dlasma concentrations of 25-OH vitamin severity of osteopenia in infants of birthweight less D.14 5 Although vitamin D intakes of 800 to 1000 than 1000 g fed expressed breast milk declined when IU/day may be required to ensure adequate hepatic the milk was supplemented with phosphate alone. In 25-hydroxylation and optimum calcium absorption,16 a multicentre study, the plasma phosphate concen- indicating some immaturity of hepatic vitamin D tration was found to be lower and alkaline phospha- metabolism, there is little evidence that vitamin D tase activity higher in infants fed breast milk than in deficiency is the primary problem. It is possible that those fed formula. It is not possible at present to there may be the occasional very immature infant define an independent role of calcium deficiency in copyright. who has deficient renal la hydroxylase and hence bone disease of prematurity, though some studies inadequate conversion of 24-OH vitamin D to suggest that breast fed, preterm infants may benefit 1,24(OH)2 vitamin D.17 There is a problem of from both calcium and phosphorus supple- specificity in the assays that have been used for mentation. 1,25(OH)2 vitamin D, but the few studies in which The incidence of bone disease in formula fed this metabolite has been measured have shown it to infants of extremely low birthweight (less than http://adc.bmj.com/ be within the normal adult range or high, rather 1000 g) requires further investigation. In the mul- 15 18-20 than low. ticentre study cited above, however, infants with birthweights under 1200 g, fed solely on a preterm (2) Substrate deficiency. Probably the main cause of formula with twice the phosphorus and calcium metabolic bone disease of prematurity is substrate concentration of human milk, and receiving a high deficiency. The increasing recognition of the disease intake of vitamin D (more than 1500 IU/day), still in the last few years coincides with rapidly improv- developed alkaline phosphatase activities greater ing survival figures for infants weighing less than than 1000 IU/I in 30% of cases compared with 66% on September 26, 2021 by guest. Protected 1000 g whose requirements for calcium and phos- in infants fed banked breast milk. It seems unlikely phorus are large, and with the common tendency to therefore that bone disease in preterm infants will feed such very small infants on breast milk. It is be eradicated by these formulas, though its fre- evident that unsupplemented breast milk can supply quency and severity is likely to be reduced substan- only a fraction of the quantity of calcium and tially. phosphorus retained by the fetus during the last trimester of pregnancy,2' and there are well Other factors documented reports of rickets in preterm infants on calcium or phosphorus deficient diets. 18 22 Although net calcium absorption by preterm infants is usually Information is lacking on the influence of prenatal poor, while phosphate is well absorbed, evidence is nutrition on the risk of developing bone disease, but accumulating that phosphorus deficiency is an im- it is possible that poor placental transfer of calcium portant factor in bone disease of prematurity. and phosphorus is a contributing factor, since Infants fed breast milk may have extremely low osteopenia has been found to occur more commonly concentrations of plasma phosphate, but normal or after deliveries complicated by pre-eclampsia.26 Arch Dis Child: first published as 10.1136/adc.60.7.682 on 1 July 1985. Downloaded from 684 Brooke and Lucas Prophylaxis and treatment a lack of information on the clinical outcome of infants with asymptomatic osteopenia. Severe metabolic bone disease of prematurity with frank rickets and fractures may well be a prevent- We thank Professor J Senterre, Dr D R Fraser, and Dr J C L Shaw able disease. Infants of less than 1000 g birthweight for their helpful criticism during the preparation of the manuscript. are most at risk, and these babies should receive phosphorus supplements if fed on breast milk alone. It may be sensible to give phosphorus supplements References to larger infants as well, perhaps up to 1200 g 'Kulkarni PB, Hall RT, Rodes PG, et al.
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