The survival rate of VLBW or ULBW infants considerably increased as the degree of therapy for premature infants continued to advance. MBD has thus become more common in premature infants[6, 7]. Previous research has shown that a number of risk factors, such as premature delivery, low birth weight, medications that influence the metabolism of calcium and phosphorus, long-term parenteral nutrition, and a delayed start to total enteral feeding, are associated with the development of MBD[6]. Additionally, the placenta provides the majority of the needed nutrients for the developing fetus, and the mother's nutritional health throughout pregnancy has a direct impact on the growth of the fetus[8]. Celestial bodies of the MBD group have insufficient calcium and phosphorus reserves.When combined with prolonged fasting following delivery, intravenous nourishment alone is unable to provide nutritional needs, resulting in insufficient calcium and phosphorus intake.
The bone mineral content of premature infants with gestational age < 32 weeks is 25–70% lower than that of term infants due to complications that affect the metabolism of calcium, phosphorus, and vitamin D. These complications include premature birth, sudden interruption of mineral transport, sudden changes in hormone levels, insufficient supplementation of calcium, phosphorus, and vitamin D in early enteral and parenteral nutrition after birth, or an improper proportion of calcium and phosphorus[9].Our research demonstrates that the GA and BW were significantly lower in the MBD group as compared to the control group. GA (OR = 0.457) and BW (OR = 0.634) were independently protective factors for MBD in VLBW babies, according to multivariate analyses. MBD has been linked to fast bone growth in the weeks following birth, insufficient prenatal calcium and phosphorus storage, and insufficient postnatal intake [10]. Because approximately 80% of the calcium and phosphorus reserves form between 24 and 40 weeks of gestation [11], the smaller the GA, the less calcium and phosphorus the fetus receives from the mother, causing a lack of significant inorganic substances in synthetic bones and increasing the likelihood of MBD.
Chin et al[12] found that IUGR is an independent risk factor for MBD.The prevalence of MBD in VLBW babies with IUGR was found to be considerably higher in this study. IUGR was identified as an independent risk factor for MBD in VLBW babies by multivariate analysis. And the majority of IUGR cases were linked to maternal illnesses that occurred during pregnancy. According to our study, the MBD group had higher levels of gynecological inflammation and gestational diabetes mellitus than the control group. Numerous factors have an impact on how bones develop and mineralize. Protein and energy are necessary for the creation of the collagen matrix, whereas calcium and phosphorus are necessary for the mineralization of bones[13].Reduced intrauterine transport of calcium, phosphorus, and other minerals is caused by maternal pregnancy problems like gestational diabetes mellitus and complex infections, which also raises the risk of MBD.
Caffeine, diuretics, and steroid use can result in calcium and phosphorus metabolism problems as well as bone mineral loss[11]. According to earlier research[1, 14], these medicines may influence bone production and resorption, increasing the risk of MBD. In this study, univariate analysis revealed that the MBD group had greater consumption rates for caffeine, diuretics, steroids, phenobarbital sodium, and aminophylline. Inhibiting osteoblast growth, reducing calcium absorption in the gastrointestinal tract, and promoting calcium excretion in the renal tubules are all effects of glucocorticoids and loop diuretics, respectively.
The risk of MBD can increase as a result of phenobarbital's ability to accelerate the breakdown of 25 (OH) D[15]. According to previous research [16], there is a direct link between long-term caffeine usage and the development of MBD. While the use of diuretics had no statistically significant relationship with osteopenia of preterm, steroids did. Further large sample studies are required. These variances may be attributed to the inclusion criteria for patients and various drug dosing times. In the MBD group, BPD was more common and MV lasted an average of longer than it did in the control group. In addition to taking into account the link between gestational age and organ immaturity, infants with BPD frequently require hormones, diuretics, and caffeine, which causes a lack of bone mineralization. Besides, mechanical factors are crucial in fetal mineral growth[17]. Because of respiratory conditions, low resistance, and infections, premature infants frequently require invasive ventilator-assisted ventilation after birth. These conditions make it difficult to distinguish between non-invasive and invasive ventilation for an extended period of time. Reducing the stimulation of mechanical forces to reduce the load on the bones and promote the production of new bone[18].
Gestational age and birth weight were independent protective variables for MBD, according to a multivariate analysis. The peak of osteogenesis occurs at 35 weeks of gestation, and premature infants, especially very premature infants, miss the best stage of mineral deposition such as calcium and phosphorus[19]. Three months after conception, when 80 percent of the fetal mineral reserve is present, the absorption rate is the fastest. Metabolic bone disease is also independently at risk due to low birth weight. Low birth weight babies must complete the catch-up growing of their bones after delivery. Babies with birth weights under 1000g have undeveloped digestive systems. It is challenging to provide adequate mineral intake since they are readily confounded by digestive tract illnesses such necrotizing colitis (NEC) and small bowel syndrome, which cause decreased intestinal intake, delayed PN, and impaired mineral absorption. According to earlier research[20], the EN start time and PN time are the two most important risk factors in this study. The 2015 Canadian feeding recommendations[21] advise beginning enteral feeding within 24 hours of birth, finishing it within one week for newborns with very low birth weights, and finishing it within two weeks for newborns with ultra-low birth weights. Both the entire enteral feeding and the average milk opening time in this study fell short of the recommendations.In addition to the early gestational age and low birth weight, the critical group also has many early problems, compromised gastrointestinal function, and other concerns.
Due to the shorter gestational age and more immature intestinal development in the study group, the incidence of NEC in the MBD group was greater than that in the control group. This group began enteral feeding later and maintained entire enteral feeding for a considerable amount of time, which raised the risk of NEC. Infants with NEC also experience prolonged fasting, intestinal obstructions that prevent calcium and phosphorus absorption, and a need for parenteral feeding for all nutritional supplements. Parenteral nutrition's lack of sufficient calcium and phosphorus for VLBW infants' growth and development increases their chance of developing MBD[22].