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Falsely Elevated Serum Parathyroid Hormone Levels due to Immunoglobulin G in a Patient with Idiopathic Hypoparathyroidism^*

Institute of Clinical Endocrinology (K.K., K.Sa., E.O., T.T., H.D.) and the Radioassay Center (T.S., R.D.), Tokyo Women's Medical College Kawada-cho 8-1, Shinjuku-ku, Tokyo, Japan
The Research Institute of the Foundation for Growth Science (K.Sh.) Shinjuku-ku, Tokyo, Japan

Address requests for reprints to: Kanji Sato, Department of Medicine, Tokyo Women's Medical College, Kawada-cho 8-1, Shinjuku-ku, Tokyo 162, Japan.

A 73-yr-old patient with idiopathic hypoparathyroidism was admitted to our hospital in May 1981. The immunoreactive PTH (iPTH) level determined by RIA using antiserum specific for the C-terminal region of PTH-(65-69) was in the upper normal range (0.6 ng/mL) and over the next 7 yr increased gradually to 6 ng/mL. Since iPTH levels determined using other commercial RIA kits remained constantly decreased or in the undetectable range, we studied the mechanism of false elevation of iPTH in this patient.

The patient's serum contained no binding protein to the tracer ([¹²⁵I][Tyr⁴⁵]human PTH-(46/84)), nor was any heterophilic antibody to the first [guinea pig immunoglobulin G (IgG)] or the second antibody (goat IgG) detected. Consistent with these findings, the dilution curve of the serum was parallel with that of standard bovine PTH-(l–84).

Gel filtration analysis revealed that the iPTH-like substance was eluted in the void volume (apparent mol wt, >70,000). Almost all of the iPTH-like substance was adsorbod by a protein-A-Sepharose column. When the IgG fraction purified by protein-A-Sepharose affinity chromatography was applied to an antihuman IgG-Sepharose column, 72% of the iPTH-like substance was detected in the IgG.

These results suggest that the falsely elevated iPTH in the patient's serum was due to IgGs (mainly IgG), which were cross-reactive with the antiserum highly specific for the Cterminal region of human PTH-(65–69).

^* Part of this work was presented at the Eighth International Congress of Endocrinology, Kyoto, Japan, July 1988 (Abstract 18–22–049). This work was supported by a grant from the Foundation of Growth Science in Japan and a Grant-in-Aid for Scientific Research from the Ministry of Education, Science, and Culture of Japan (62570521 and 02671109).

Received April 2, 1990.

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