-transparent.png){kind=logo}
The effects of calcium injection (3 mg/Kg/10 min) or oral calcium administration (calcium lactate 7.7 g) on plasma iPTH and Nephrogenous cyclic AMP (NcAMP) were studied in 6 normal controls and 13 patients with primary hyperparathyroidism. In the control subjects, plasma iPTH determined by a predominantly carboxyl-terminal antiserum was less than 0.3 ng/ml before and after both calcium loads, whereas 41 approximately 98% (mean 67%) of NcAMP was rapidly and uniformly suppressed to a level lower than the normal value. In 2 patients with primary hyperparathyroidism, iPTH was clearly reduced from 8.0 to 4.6 ng/ml and 1.6 to 0.96 ng/ml, respectively, by the calcium load. However, in the other 7 patients with primary hyperparathyroidism who showed only a slight elevation of iPTH: less than 0.3 approximately 0.9 ng/ml, the reductions in iPTH were not detected after the calcium load: less than 0.3 approximately 0.7 ng/ml. In contrast, 30 approximately 54% (1.02 approximately 3.85 nmol/dl GF) of NcAMP, which was greater than the diurnal variation, was suppressed after calcium injection in 5 patients with primary hyperparathyroidism (2 of 4 patients with urological, and 3 of 5 patients with chemical hyperparathyroidism). But NcAMP was not suppressed in all 4 patients with skeletal hyperparathyroidism including one with proximal renal tubular dysfunction whose basal iPTH was elevated markedly but reduced clearly by the calcium load. In general, suppression of NcAMP was followed by a decrease of phosphate excretion. On the other hand, even in a patient with primary hyperparathyroidism whose NcAMP was not suppressed at all after the calcium injection, calcium infusion (15 mg/Kg/3h) resulted in some (23%) decrease in NcAMP. Oral calcium administration resulted in responses which were almost the same as those produced by calcium injection. These results suggest that NcAMP provides a useful index in the parathyroid suppression test in patients with primary hyperparathyroidism, especially those who display a rather mild elevation of iPTH. This is not the case, however, in a few patients who show a marked elevation of iPTH and/or proximal renal tubular dysfunction.
H E Sohn, and
S Yumita, and
H Unakami, and
R Miura, and
Y Furukawa
January 1979,
Nephron,
H E Sohn, and
S Yumita, and
H Unakami, and
R Miura, and
Y Furukawa
October 1976,
Archives of internal medicine,
H E Sohn, and
S Yumita, and
H Unakami, and
R Miura, and
Y Furukawa
June 1980,
Nihon Naibunpi Gakkai zasshi,
H E Sohn, and
S Yumita, and
H Unakami, and
R Miura, and
Y Furukawa
June 1980,
Nihon Hinyokika Gakkai zasshi. The japanese journal of urology,
H E Sohn, and
S Yumita, and
H Unakami, and
R Miura, and
Y Furukawa
January 1980,
Archivos de investigacion medica,
H E Sohn, and
S Yumita, and
H Unakami, and
R Miura, and
Y Furukawa
January 2007,
Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists,
H E Sohn, and
S Yumita, and
H Unakami, and
R Miura, and
Y Furukawa
April 1990,
Clinical endocrinology,
H E Sohn, and
S Yumita, and
H Unakami, and
R Miura, and
Y Furukawa
January 1986,
Endocrine research,
H E Sohn, and
S Yumita, and
H Unakami, and
R Miura, and
Y Furukawa
October 1977,
The Journal of clinical investigation,
H E Sohn, and
S Yumita, and
H Unakami, and
R Miura, and
Y Furukawa
March 1983,
Schweizerische medizinische Wochenschrift,
