**3.2 Urinary markers**

*Mineral Deficiencies - Electrolyte Disturbances, Genes, Diet and Disease Interface*

Some drugs that are frequently used in premature births also support the incidence of MBD. Some of the prominent classes of such drugs are loop diuretics such as furosemides, corticosteroids, methylxanthines, antifungals, and certain antiepileptics. The most probable reason may be activation of osteoclasts and reduction of osteoblast proliferation and decreased absorption, thereby the ultimate elimination

The concentration of minerals such as calcium and phosphorus in premature breast milk is inadequate in regard to the estimated requirement, presuming that they ingest approximately one third that is essential in fetal life [9]. In addition, milk products are high in concentration of the stated minerals but have a lower bioavailability; hence, consumption of mineral fortified milk is essential for

Biomechanical factors that impact the alteration of bone structure is accountable

for the reduction of bone mass caused by reduced activity level. The majority of bone-loading process occurs during the third trimester. Nevertheless, in the absence of bone loading, bone formation stops and further osteoclasts are activated leading to a reduction in bone strength [10]. Neonatal demineralization of the skeleton may result from immobilization due to the prevalence of other disease conditions or

Thyroid hormones are prerequisite for the development of the skeleton and are prime regulators of bone maintenance. Hypothyroidism induces delayed development of the skeleton and growth retardation with delayed bone development owing to inadequate endochondral ossification. Hyperparathyroidism also impacts bone metabolism, which causes significant conditions such as hypercalcemia, demineralization of the bone, and delay in growth and development. Due to these abovementioned-stated issues, a decline in the normal function of kidneys eventually leads to mineral and bone metabolism disturbances culminating in

Since there are no ultimate diagnosis and therapy indications for MBD, and the related sign and symptoms also appear very late, it is, therefore, appropriate to

Levels of alkaline phosphatase (ALP) rise physiologically at about 6–12 weeks of age over the first 3 weeks of life. Regardless of the lack of signs and symptoms, ALP levels > 500 IU/L suggest impaired bone homeostasis and values >700 IU/L is

monitor the subjects at risk for the development of the related disorder.

**2.3 Drug-related factors**

of calcium by the kidneys [9].

**2.4 Parent related nutrition**

preventing and treating MBD.

**2.5 Biomechanical factors**

neurological implications.

**2.6 Endocrinology-related factors**

serious skeletal deformities [11].

associated with bone demineralisation [12].

**3. Diagnosis**

**3.1 Serum markers**

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Hypophosphatemia is the most prevalent physiological modification coupled with premature MBD, which causes a reduced release of PTH and thereby increases the reabsorption of phosphate from the renal tubular. Infants born <28 weeks of gestation have a reduced baseline value for phosphate, resulting in increased excretion of phosphate in urine, even in the mere existence of lower levels of phosphate that appear as a significant marker for MBD incidence [14].
