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• Comments of Faerk et al.
  Samudra Mukherjee
  Published on: 22 March 2016

• Published on: 22 March 2016

  Comments of Faerk et al.

  • Samudra Mukherjee, Specialist registrar
  • Other Contributors:
    • Surangama Mukherjee

  Dear Editor

  We read the article by Faerk et al.[1] on the relation of bone mineral content (BMC), ALP and serum phosphate; two commonly used markers for monitoring of metabolic bone diseases of prematurity (MBDP). In-fact, the author has tried to break the long-standing myth of regular monitoring of these two parameters for early detection and possibly prevention of this condition. However, we were disappoin...

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  Dear Editor

  We read the article by Faerk et al.[1] on the relation of bone mineral content (BMC), ALP and serum phosphate; two commonly used markers for monitoring of metabolic bone diseases of prematurity (MBDP). In-fact, the author has tried to break the long-standing myth of regular monitoring of these two parameters for early detection and possibly prevention of this condition. However, we were disappointed to see that the authors failed to explain their finding in the context of current research evidence.

  There are two theories of MBDP. According to the traditional biochemical theory, crystallization of Ca and phosphate in the previously formed osteoid matrix heralds mineralization and appropriate concentration of calcium and phosphate is the most crucial factor. However, it has long been felt that even with a maximum oral intake of 200ml/kg/day and supplementation/fortification with calcium and phosphate, it is almost impossible to match the rate of intrauterine accretion of these 2 in the 3rd trimester (for Ca it is about3.5 mmol/Kg/day and for P it is about 2.7 mmol/Kg/day). It is therefore often presumed that reduced bone formation is the primary cause of MBDP. However some evidence suggest that increased bone resorption is the main factor.[2,3] Two separate groups have already demonstrated that urinary excretion of bone resorption markers like hydroxyproline, type 1 collagen telopeptide, calcium and phosphorus concentration is 3 to 4 times higher in preterm in comparison to term babies.

  There is however a growing evidence that increased bone resorption is a result of lesser degree of mechanical load on preterm bone following birth. In comparison, term infant gets the effect of intrauterine kicking, bouncing etc as mechanical stimulus for bone formation over last few crucial weeks. Therefore, apart from fortification,it may be important to introduce some form of physical exercise in order to prevent MBDP. This can be good topic for future trial .

  We believe that, the serum phosphate as measured in the laboratory, is a combination of phosphate coming out of bone due to bone resorption and the dietary phosphate. Therefore, a high serum phosphate may indicate increased bone resorption leading to reduced BMC. On the other hand, a low phosphate may be a marker of less bone resorption and thereby a normal BMC. Therfore it is premature to conclude( according to Author’s other article) [4] that supplementation of phosphate has no effect on BMC. Previous studies have shown that preterm infants have a rapid phase of mineral accretion between 40 and 60 weeks’ postconceptional age.[5]

  We still do not know the actual chemical assimilation pathway of dietary phosphorus. In fact We suggest that one of the ways to solve the problem is to do a tracer study where a specific isotope of phosphate molecule can be used as dietary source and subsequently chasing its course by radioisotope study. (I am bit skeptical about getting an ethics committee permission).

  We also beg to differ with the author’s statement "Alkaline phosphates in the vesicle membrane transports phosphate into the vesicle. Calcium diffuses passively through the membrane". ALP act upon inorganic and organic phosphates from different sources and break it down to inorganic phosphorus (Pi). Pi is then transported inside the matrix vesicle by Na-Pi symport system. Calcium enters through the specific calcium channels (annexins).[6]

  Reference

  (1) J Faerk, B Peitersen, S Petersen, and K F Michaelsen. Bone mineralisation in premature infants cannot be predicted from serum alkaline phosphatase or serum phosphate. Arch Dis Child Fetal Neonatal Ed. 2002; 87: F133-F136.

  (2) Beyers N, Alheit B , Taljaard JF et al. High turnover osteopinea in preterm infants.Bone 1994;15:5-13.

  (3) Mora S, Weber G et al. Bone modeling alteration in preterm infants. Arch Ped Adolesc Medicine 1994;148: 1215-1217.

  (4) Faerk J, Petersen S, Peitersen B, et al. Phosphorus intake is of major importance for growth velocity in premature infants. Pediatr Res 1999;45:915.

  (5) Horseman A, Ryan SW, Congdon PJ et al. Bone mineral content and body size 56 to 100 weeks postconception in preterm and full term infants. Arch Dis Child 1989; 64 : 1579-1586.

  (6) Montesuit C,Caverzasio J,Banjour JP. Characterization of Pi transport system in cartilage matrix vesicle. Potential role in calcification process. Journal boil chemistry 1991, 266 : 17791-17797.

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  Conflict of Interest:
  None declared.

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