Abstract
Parathormone (PTH) is composed of four glands embedded in the thyroid gland, but its function is mainly to keep calcium in the blood within normal range. It has got sensitive receptors that trigger the PTH to act in correcting serum calcium. As calcium is important for the normal functioning of many organs including vital organs like heart and brain, the PTH has to be prompt in maintaining calcium in the blood within normal. The function of PTH is to increase absorption of calcium in the gut and to reduce its excretion in the kidneys. When vitamin is low it leads to drop of calcium in the blood leading to calcium being mobilized from the high calcium reserves in the bone by the action of PTH. The loss of calcium in the bones leads to decalcification of the bones which makes the clinical features of rickets in the bones. In case of rickets bones become soft leading to bow legs in walking infants. All these features are the result of action of Parathormone as with the rise of PTH it is noticed the gradual increase of calcium together with high alkaline phosphatase as an indication of activity of rickets in infants and osteomalacia in the mothers. This review is to express the mechanism of causation of rickets and osteomalacia by the activity of the hyperparathyroidism which is secondary to hypocalcemia due to vitamin D deficiency in the breast feeding infant and their mothers where the latter is considered in the phase of biochemical osteomalacia.
Highlights
Presentation of rickets in early stages, in the first year of life, is likely to be overlooked except when they develop the most serious presentations namely, convulsions, cardiomyopathy or myelofibrosis or chest infections [1,2,3]
Parathyroid Hormone (PTH) level in the children with active rickets ranged from a mean of 99 pg/ml to 269 pg/ml all levels of PTH above 65 pg were considered to have an early phase of rickets in infants and osteomalacia in the mothers
The Role PTH in rickets associated myelofibrosis: That in every case of rickets or osteomalacia hyperparathyroidism is a constant finding that is why a role of PTH in the development of the associated myelofibrosis seen with vitamin D deficiency is discussed
Summary
Presentation of rickets in early stages, in the first year of life, is likely to be overlooked except when they develop the most serious presentations namely, convulsions, cardiomyopathy or myelofibrosis or chest infections [1,2,3] It is only in a late first year and second year of life that obvious bony deformities are observed by family or medical practitioner especially in breastfed well-nourished growing infants. Hypocalcemia is commonest [7] and earliest feature of rickets, but it is not sustained as it is corrected by the hyperparathyroidism, the main actor in decalcifying the bones leading to the bony features of rickets In this communication, the role of parathyroid in pathogenesis of rickets and its sequel is discussed through data collected from a biochemical and clinical study and by reviewing the literature
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