Morrison T.: Preventing Metabolic Bone Disease in Children on Home Parenteral Nutrition
Good morning, evening, afternoon — whenever and wherever you may be — ESPGHAN is bringing you another podcast, this one, as we say in Hungary, egy unikum, a one-off and a first for this series. We’ve done gastroenterologists and hepatologists to death, really; it’s long been time for a new start, a new star. And we’ve found him in Dr Timothy Morris of the University of Manchester, a clinical pathologist.
A glance at Dr Morris’ curriculum vitae is shaming — unlike me, for one, who am very much a Feld-, Wald-, und Wiesenpathologe; it’s the parable of the talents, really, and I’m the servant who has kept them buried — he has done so much, in so many different areas, and done it so well! First carrying away all the prizes with a degree in genetics; throwing over post-graduate studies in plant genetics for three years as a financial analyst; a second degree in medicine; and, after two years on the wards as a junior doctor, entry into his present field — chemical pathology — but who can predict if he will stay there? Something tells me that he has a restless eye, and that he already is considering which field next to conquer.
Today he’s asked us to work through a problem in calcium metabolism, namely metabolic bone disease, or MBD, in children with intestinal failure who are on home parenteral nutrition. His team’s findings, from Tridimas A et al., as published in JPGN Rep, require a bit of background for best appreciation. Let’s start by addressing MBD.
Rickets and osteomalacia are two types of MBD. Osteoid mineralisation is deficient in both conditions. To be rickety, you must have active growth plates. Osteomalacia is a broader church, with not only children but also adults among her communicants. Contributors to osteomalacia in persons receiving parenteral nutrition (PN) are many; aluminium toxicity aside, they converge in hypocalcaemia, with secondary hyperparathyroidism in consequence. This aggravates deficiency of mineralisation and leads to frank osteopenia and osteoporosis, with broken bones. Osteopenia occurs in approximately 45% of children with intestinal failure, with 16%–25% having osteoporosis. MBD can be assessed by bone biopsy or by X-ray densitometry, but “blood work” is generally deployed instead.
Dr Morris’ team began by determining how frequently MBD was found in a cohort of 37 children with intestinal failure who were receiving PN at home. Laboratory data over a span of 4½ years found elevated parathyroid hormone (PTH) values in 22 (59%). Of these, 5 had elevated PTH values in >50% of measurements. A flow-chart protocol was followed for 4 months, cascading from an initial PTH determination — high, normal, or low? — via determinations of calcium and magnesium, adjustments in calcium and phosphate concentrations in administered PN, and PTH determinations that began the cascade again. During protocol use, PTH values were elevated in 6 children (18%), and persistent elevation of PTH was found in none.
Are the before-and-after comparisons fair? Would longer follow-up during protocol use have found more instances of secondary hyperparathyroidism? An open question, perhaps. But to monitor PTH values closely, using the flow-chart protocol to guide intervention, appears promising in respect of slowing or halting the development of MBD in children who receive PN at home.
LiteratureTridimas A et al. Reducing metabolic bone disease burden in intestinal failure children on home parenteral nutrition.JPGN Rep. 2023 Nov 6;4(4):e368. doi: 10.1097/PG9.0000000000000368. eCollection 2023 Nov. PMID: 38034429. PMCID: PMC10684215.
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