A patient Shweta with raised serum alkaline phosphatase and raised parathormone level along with low calcium and low phosphate level is likely to have-
clinical syndrome of vitamin D deficiency can be a result of deficient production of vitamin D in the skin, lack of dietary intake, accelerated losses of vitamin D, impaired vitamin D activation, or resistance to the biologic effects of 1,25(OH) 2 D The elderly and nursing home residents are paicularly at risk for vitamin D deficiency, since both the efficiency of vitamin D synthe- sis in the skin and the absorption of vitamin D from the intestine decline with age. Similarly, intestinal malabsorption of dietary fats leads to vitamin D deficiency.The most specific screening test for vitamin D deficiency in oth- erwise healthy individuals is a serum 25(OH)D level. Although the normal ranges vary, levels of 25(OH)D <37 nmol/L (<15 ng/ mL) are associated with increasing PTH levels and lower bone density; optimal vitamin D levels are >80 nmol/L (>32 ng/mL). Vitamin D deficiency leads to impaired intestinal absorption of calcium, resulting in decreased serum total and ionized calcium val- ues. This hypocalcemia results in secondary hyperparathyroidism, a homeostatic response that initially maintains serum calcium levels at the expense of the skeleton. Due to the PTH-induced increase in bone turnover, alkaline phosphatase levels are often increased. In addition to increasing bone resorption, PTH decreases urinary calcium excretion while promoting phosphaturia. This results in hypophosphatemia, which exacerbates the mineralization defect in the skeleton. With prolonged vitamin D deficiency resulting in osteomalacia, calcium stores in the skeleton become relatively inaccessible, since osteoclasts cannot resorb unmineralized osteoid, and frank hypocalcemia ensues( Harrison 17 pg 2376)
Primary hyperparathyroidism
Paget's disease
Osteoporosis
Vitamin D deficiency
Endocrinology