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Ectopic Production of Parathyroid Hormone by Small Cell Lung Cancer in a Patient with Hypercalcemia^*

First Department of Internal Medicine, School of Medicine, University of Tokushima (K.Y., R.Y., S.S.) Tokushima 770, Japan
the Department of Internal Medicine (H.S., U.T.) and Laboratory Department (M.T.), Tokushima Prefectural Central Hospital Tokushima, Japan
the Oncogene Division, National Cancer Center Research Institute (M.I., T.S.) Tokyo 104, Japan

Address all correspondence and requests for reprints to: Katsuhiko Yoshimoto, M.D., First Department of Internal Medicine, School of Medicine, University of Tokushima, Kuramoto-cho 3-18-15, Tokushima 770, Japan.

Severe hypercalcemia (serum calcium, 4.37–4.84 nmol/L) was found in a 70-yr-old man who had a small cell carcinoma of the lung with multiple metastases. The plasma immunoreactive PTH concentration was markedly elevated, as measured in three different PTH assays [N-terminal PTH, 4,650 ng/L (normal, 230–630); midregion PTH, 13,850 ng/L (normal, 180-560); C-terminal PTH, 9,900 ng/L (normal, < 1,300)], but at autopsy the parathyroid glands were histologically normal. The PTH concentration of a liver metastasis was 503.5 ng/g wet wt (normal liver, <4.2–5.9), and the PTH in the tumor extract eluted at nearly the same position as synthetic human PTH-(1–84) on gel filtration chromatography. Northern blot analysis revealed PTH mRNA in the tumor as a single band of 0.9 kilobase. These results indicate that the ectopic PTH production by the lung cancer was the cause of hypercalcemia in this patient.

^* This work was supported in part by a Grant-in-Aid from the Ministry of Health and Welfare for a Comprehensive 10-Year Strategy for Cancer Control, Japan.

Received September 7, 1988.

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