Hypoglycemia in Primary Carcinoma of the Liver.wer

McFadzean, A. J. S.; Tse, Yeung Tse

doi:10.1001/archinte.1956.00250300038006

Cited by 88 publications

(20 citation statements)

References 15 publications

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“…Polycythemia has been reported in B6C3F, mice with spontaneously occurring hepatocellular carcinomas : increases in erythrocyte count, hematocrit, hemoglobin concentration, and absolute reticulocyte count, and decreases in mean corpuscular volume and mean corpuscular hemoglobin, and is considered to be developed as a consequence of increased circulating erythropoietin levels (11). Secondary erythropoiesis with inappropriate erythropoietin synthesis has been reported in humans, and the elevated circulating erythropoietin levels appeared to be derived from an ectopic source such as renal or liver tumors (4,13,18,21,25). In addition, some hepatoma cell lines are known to produce erythropoietin under hypoxic conditions (7,15,24 Liver tissues fixed in neutral phosphate-buffered 10% formalin were cut into 1-mm cubes, refixed in 2.5% glu- (Table II and Fig.…”

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confidence: 99%

Secondary Polycythemia in Male B6C3F1 Mice with Spontaneously Occurring Hepatocellular Carcinomas

et al. 1997

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The purpose of this study was to investigate the cause of polycythemia occurring in control male B6C3F, mice with hepatocellular carcinomas from 2-yr carcinogenicity studies. Erythrocyte counts and plasma erythropoietin levels in these mice were significantly increased compared to those in nontumor-bearing mice. Hepatocellular carcinomas in the mice were well differentiated, and the neoplastic hepatocytes contained either or both of 2 types of intracytoplasmic inclusion bodies; one was relatively large and weakly eosinophilic (pale inclusion body), while the other was relatively small and strongly eosinophilic (globular inclusion body). The pale eosinophilic inclusions but not the globular ones were immunohistochemically positive for erythropoietin. Ultrastructurally, the erythropoietin-positive inclusions were characterized by granular materials in dilated cisternae of rough endoplasmic reticulum, suggesting increased protein synthesis. Erythropoietin-negative inclusions were dense bodies that were not surrounded by a delimiting membrane. These findings indicate that polycythemia in hepatocellular carcinoma-bearing mice occurs secondary to excess synthesis and secretion of erythropoietin by neoplastic hepatocytes.

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Secondary Polycythemia in Male B6C3F1 Mice with Spontaneously Occurring Hepatocellular Carcinomas

et al. 1997

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“…HCC often presents as a paraneoplastic syndrome (7-lo), and erythrocytosis is the most common paraneoplastic syndrome after hypoglycemia. Several studies have reported that 3% to 12% of HCC was associated with erythrocytosis (7,11). This HCC-associated erythrocytosis is considered to result from Epo production by the HCC cells, and many HCC patients have, in fact, had high plasma Epo levels (12).…”

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confidence: 99%

Erythropoietin production in hepatocellular carcinoma cells associated with polycythemia: Immunohistochemical evidence

et al. 1993

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Patients with hepatocellular carcinoma sometimes have erythrocytosis and high plasma erythropoietin levels. However, previous studies have not revealed direct evidence that the carcinoma cells produce the erythropoietin. To address this question, we carried out light and electron microscopic immunohistochemical studies, using a human erythropoietin antibody to the liver in three male patients with hepatocellular carcinoma and erythrocytosis. alpha-Feto-protein localization was also examined in serial liver sections by light microscopic immunohistochemistry with an antibody to alpha-fetoprotein. All three patients demonstrated high hemoglobin levels (16.7, 17.6 and 18.1 gm/dl) and high plasma erythropoietin levels (227, 266 and 280 mU/ml). In one patient the plasma erythropoietin level in the hepatic vein was significantly higher than that in the hepatic artery. The levels of plasma erythropoietin, as well as such tumor markers for hepatocellular carcinoma as serum alpha-fetoprotein and plasma des-gamma-carboxyprothrombin, were significantly reduced after treatment with an anticancer drug, cisplatin. Light microscopic immunohistochemistry showed that erythropoietin was definitely present in the cytoplasm of the hepatocellular carcinoma cells, but not in normal hepatocytes around the carcinoma lesion or in other nonparenchymal cells such as vascular endothelial cells and Kupffer cells. In electron microscopic immunohistochemistry, reaction products for erythropoietin were revealed in the cisternae of the endoplasmic reticulum in the carcinoma cells, suggesting the production of erythropoietin by these cells. Light microscopic immunohistochemistry showed that alpha-fetoprotein was localized in the hepatocellular carcinoma cells that were erythropoietin positive in the serial sections. These findings indicated that hepatocellular carcinoma cells produced erythropoietin as well as alpha-fetoprotein in these cases, leading to the complication of erythrocytosis.

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“…Erythrocytosis is one of the more common of the paraneoplastic syndromes in HCC, with an incidence ranging from 2.2-12% [7][8][9]. The mechanism of erythrocytosis is not completely understood.…”

Section: Discussionmentioning

confidence: 99%

Erythrocytosis caused by an erythropoietin-producing hepatocellular carcinoma

et al. 2000

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A case of erythrocytosis caused by a hepatocellular carcinoma (HCC) that produced erythropoietin (Epo) is described. A 64-year-old man, with a huge HCC tumor in the right lobe of the liver, showed a high concentration of hemoglobin and increased levels of serum Epo, alpha-fetoprotein (AFP), and protein induced by vitamin K absence II (PIVKA-II). Right lobectomy of the liver was performed. Histological findings of the specimen showed a moderately differentiated HCC. The existence of Epo was confirmed immunohistochemically only in the tumor tissue and not in the normal liver tissue. Erythrocytosis disappeared and the serum levels of Epo, AFP, and PIVKA-II returned to the normal range after the operation. Within 2 months after the operation, recurrent tumors appeared in the remnant liver, and the patient died 13 months after the operation.

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Hypoglycemia in Primary Carcinoma of the Liver.wer

Cited by 88 publications

References 15 publications

Secondary Polycythemia in Male B6C3F1 Mice with Spontaneously Occurring Hepatocellular Carcinomas

Secondary Polycythemia in Male B6C3F1 Mice with Spontaneously Occurring Hepatocellular Carcinomas

Erythropoietin production in hepatocellular carcinoma cells associated with polycythemia: Immunohistochemical evidence

Erythrocytosis caused by an erythropoietin-producing hepatocellular carcinoma

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