GH insensitivity induced by endotoxin injection is associated with decreased liver GH receptors.

Sepsis induces a state of growth hormone (GH) resistance associated with a decrease of circulating insulin-like growth factor (IGF) I, a GH-dependent anabolic hormone mainly produced by the liver. To address the mechanisms that might trigger GH insensitivity in sepsis, we investigated the regulation of liver GH receptor (GHR) and its gene expression by endotoxin. Endotoxin injection in rats decreased serum IGF-I and liver GH-binding sites after 10 h. In contrast to liver GHR, circulating GH-binding protein (GHBP) levels were not significantly reduced after endotoxin injection. The parallel decrease in IGF-I and GHR and in their corresponding liver mRNAs suggests that decreased serum IGF-I and liver GHR were likely to result from decreased liver synthesis. Although GH administration in control animals significantly enhanced serum IGF-I, it did fail to prevent the decline in serum IGF-I and liver GH-binding sites in endotoxemic rats. In this study, we showed that endotoxin injection induces a state of GH insensitivity associated with decreased liver GHR. This decline in GHR, which cannot be prevented by exogenous GH, might contribute to the GH insensitivity observed in sepsis

Dynamic spin-echo imaging with Gd-DTPA: value in the differentiation of hepatic tumors.

Thirty patients with hemangiomas (n = 6), benign liver cell tumors (n = 7), and primary or metastatic malignant tumors of the liver (n = 17) underwent dynamic MR imaging with Gd-DTPA to determine the value of the procedure in the differentiation of hepatic tumors. The diagnoses were proved by histology or follow-up. Hemangiomas had a significantly greater mean T2 value (192.1 +/- 34.8 msec) than did both benign liver cell tumors (71.9 +/- 16.9 msec; p less than .01) and primary or metastatic malignant tumors (79.7 +/- 21.2 msec; p less than .01), but the T2 values of benign liver cell tumors and malignant tumors were not significantly different. Both hemangiomas and benign liver cell tumors had a significantly greater mean signal-intensity ratio (1.86 +/- 0.60 and 1.77 +/- 0.26, respectively) than did malignant tumors (1.04 +/- 0.34; p less than .01) in the early phase after Gd-DTPA administration, and hemangiomas had a significantly greater signal-intensity ratio (1.59 +/- 0.21) than did both benign liver cell tumors (1.21 +/- 0.08; p less than .01) and malignant tumors (1.06 +/- 0.26; p less than .01) in the delayed phase. These results suggest that dynamic MR images obtained after administration of Gd-DTPA are useful in differentiating hepatic hemangiomas, benign liver cell tumors, and malignant liver lesions