Kimura N, Miura W, Noshiro T, Mizunashi K, Hanew K, Shimizu K, Watanabe T, Shibukawa S, Sohn H E, Abe K, Miura Y, Nagura H
Department of Pathology, Tohoku University School of Medicine, Sendai, Japan.
Endocr J. 1997 Apr;44(2):319-27. doi: 10.1507/endocrj.44.319.
Plasma levels of chromogranin A (CgA) were measured by ELISA in 22 patients with pheochromocytoma (18 non-metastatic, 3 metastatic, and 1 mixed neuroendocrine-neural tumor), 9 patients with primary hyperparathyroidism, and 9 patients with pituitary adenoma. The plasma levels of CgA were compared with norepinephrine, epinephrine, parathyroid hormone and pituitary hormones, i.e., growth hormone and prolactin. In pheochromocytoma, CgA in preoperative plasma of the patients without metastasis was 228 +/- 38 U/L (mean +/- SEM) and significantly higher than healthy controls (30 +/- 11 U/L, n = 40). Plasma CgA was decreased after removal of the tumors (28 +/- 6.0 U/L), except in three patients with metastatic pheochromocytoma and a mixed neuroendocrine neural tumor. The concentration of CgA in the patients with non-metastatic pheochromocytoma was significantly correlated with that of plasma norepinephrine (P < 0.005, r = 0.68) and urinary norepinephrine (P < 0.05, r = 0.65), but not with that of epinephrine. There was an exceptional case in which CgA was extremely high, but the CA level was normal. This tumor was a highly malignant pheochromocytoma with extensive metastases composed of small tumor cells which were occasionally positive for tyrosine hydroxylase immunohistochemically. These cells were considered to be poorly differentiated tumor cells and synthesized a very small amount of norepinephrine. Plasma levels of the patients with primary hyperparathyroidism and the patients with pituitary adenoma were 44 +/- 4 U/L and 48 +/- 8 U/L, respectively. Only one patient with a growth hormone-producing pituitary adenoma had a high level of CgA. Plasma CgA is a useful tumor marker for pheochromocytoma, even for malignant pheochromocytoma without elevated CA level, but not for hyperparathyroidism, or pituitary adenoma.
采用酶联免疫吸附测定法(ELISA)检测了22例嗜铬细胞瘤患者(18例非转移性、3例转移性和1例混合性神经内分泌-神经肿瘤)、9例原发性甲状旁腺功能亢进患者和9例垂体腺瘤患者的血浆嗜铬粒蛋白A(CgA)水平。将CgA的血浆水平与去甲肾上腺素、肾上腺素、甲状旁腺激素以及垂体激素(即生长激素和催乳素)进行了比较。在嗜铬细胞瘤患者中,无转移患者术前血浆CgA为228±38 U/L(平均值±标准误),显著高于健康对照(30±11 U/L,n = 40)。肿瘤切除后血浆CgA降低(28±6.0 U/L),但3例转移性嗜铬细胞瘤患者和1例混合性神经内分泌神经肿瘤患者除外。非转移性嗜铬细胞瘤患者的CgA浓度与血浆去甲肾上腺素浓度显著相关(P < 0.005,r = 0.68)以及尿去甲肾上腺素浓度显著相关(P < 0.05,r = 0.65),但与肾上腺素浓度无关。有1例特殊病例,CgA极高,但儿茶酚胺(CA)水平正常。该肿瘤是1例具有广泛转移的高恶性嗜铬细胞瘤,由小肿瘤细胞组成,酪氨酸羟化酶免疫组化偶尔呈阳性。这些细胞被认为是低分化肿瘤细胞,合成的去甲肾上腺素非常少。原发性甲状旁腺功能亢进患者和垂体腺瘤患者的血浆水平分别为44±4 U/L和48±8 U/L。仅1例分泌生长激素的垂体腺瘤患者CgA水平较高。血浆CgA是嗜铬细胞瘤的一种有用的肿瘤标志物,即使对于CA水平未升高的恶性嗜铬细胞瘤也是如此,但对甲状旁腺功能亢进或垂体腺瘤则无用。