ESPE Abstracts

In accordance with the present data on children with nutritional rickets, there are three stages for biochemical findings. We aim to update the stages of nutritional rickets. Biochemical manifestations of nutritional rickets were first described in 2005 as three stages of vitamin D deficiency. Table 1 shows the biochemical findings according to the rickets stage. Accordingly, the first stage is characterized by osteopenia and subclinical hypocalcemia. The second stage begins with an increase in serum PTH, which causes the mobilization of calcium from bone in an attempt to compensate for the hypocalcemia. In stage 3, hypocalcemia develops again, and bone changes become evident. The presence of both very low dietary calcium intake and vitamin D deficiency leads to biochemical features of PTH resistance, with laboratory findings of hypocalcemia, hyperphosphatemia or normophosphatemia, and elevated serum alkaline phosphatase and PTH. As urinary phosphate excretion is low in these patients, their biochemical findings may resemble those of pseudohypoparathyroidism type I or II. Some physicians also faced the dilemma of pseudohypoparathyroidism or severe vitamin D deficiency in two patients with severe vitamin D deficiency secondary to restrictive eating disorders. Despite a high PTH level, the patient exhibited increased tubular phosphate reabsorption, mimicking pseudohypoparathyroidism type II. After serum calcium and phosphate normalization with calcium and vitamin D treatment, the phosphaturic response of the luminal membrane of proximal tubules was corrected. Therefore, Stage 4 of vitamin D deficiency should be considered in cases with very low hypocalcemia and hyperphosphatemia or normophosphatemia, especially those mimicking pseudohypoparathyroidism (Table 1). As calcium can modify renal phosphate transport on the luminal membrane of proximal tubules and calcium-sensing receptor activation can regulate PTH-induced phosphate excretion, we hypothesize that nutritional rickets accompanied by very low dietary calcium intake lead to an impaired effect of PTH on the luminal membrane of proximal tubules for phosphate excretion, resulting in a clinical presentation similar to that of pseudohypoparathyroidism type I or II. In conclusion, this new classification of ricket stages according to biochemical findings will be very useful for evaluating patients with nutritional rickets. Since stage 4 cases were not included in the current classification for biochemical findings of nutritional rickets classification, a new classification including stage 4 might be needed.