1967 年 17 巻 1 号 p. 43-48
Our present cases are 1, 3, 4, 7 and 38 years old female whose main complaints are retardation of growth and bow leg.
The characteristic laboratoric finding of the cases are increased alkaline phosphatase activity, decreased inorganic phosphorus in serum and lowered tubular reabsorption of phosphorus less than sixty per cent.
The curable dosis of vitamin D which varies with each cases is decided by try and error, using serum calcium level within 11.5mg/dl, serum inorganic phosphorus above 3mg/dl, urinary calcium excretion below 400mg/day and toxic signs as indicators.
The troublesome case to control the effective dosis of vitamin D has a narrow range between toxic dosis and therapeutic one, but it is not clear if the range is constant with individuals through life or is changeable according to the age of patient.
In such case the toxic signs tend to appear easily. When the serum calcium increased, corticosteroid was given intramuscularly which acts antagonistically to hypercalcemia. However, its lowering effect for serum calcium was not remarkable in our series.
It is rather difficult to normalize serum inorganic phosphorus without hypercalcemia even under vitamin D administration. Otherwise, renal tubular reabsorption of phosphorus could not be kept up between the normal range. In one case, the TRP as well as the serum phosphorus remains at remarkably low level even under hypercalcemia.
Even if serum inorganic phosphorus does not increase, the rachitic change on X ray film can recover, following slowly lowered activity of serum alkaline phosphatase.