Povidone-iodine ointment and gauze covered by transparent dressings were compared with transparent dressings alone in historical controls (both changed twice weekly) in neurosurgical patients needing catheter placement for prolonged periods. Colonization and bloodstream infection were both reduced with the new method (P < .01 and P = .062, respectively).
We analyzed the expression of Pit-1 and growth hormone-releasing hormone receptor (GHRH-R) mRNA in various types of functioning and nonfunctioning adenomas using a quantitative reverse transcriptase polymerase chain reaction (RT-PCR) method. Among clinically nonfunctioning adenomas, tumors considered as silent adenomas were reclassified on a pathologic basis. Competitive RT-PCR showed that the levels of Pit-1 and GHRH-R mRNA expression in silent somatotroph adenomas and silent prolactinomas were similar to those in the corresponding functioning adenomas. In silent thyrotroph adenomas, both mRNAs showed high levels of expression that were similar to those in functioning and silent somatotroph adenomas. The results suggest that the cause of the silence in these tumors seems to be in the downstream to transcription of Pit-1 gene in the signaling pathway leading to hormone secretion. Competitive RT-PCR assay could distinguish silent adenomas of the Pit-1 group from the other nonfunctioning adenomas in the expression levels of Pit-1 and GHRH-R mRNAs. In the future, precise diagnosis of various adenomas may become possible by assaying transcription factors such as steroidogenic factor-1 and thyrotroph embryonic factor, which are thought to be related to adenohypophyseal cytodifferentiation.
A 38-year-old male presented with a cystic lesion at the foramen magnum due to intracranial dis semination from a pituitary adenoma. The primary tumor had required reoperation for regrowth twice . The tumor at the foramen magnum was removed surgically. Two smaller solid tumors were located in the left parietal convexity and the right temporal lobe. The former tumor was also removed surgically and the latter was observed. Histological examination showed the typical characteristics of pituitary adenoma in both surgical specimens. Immunohistochemical staining with MIB-1 and p53 antibodies showed low (< 1%) and negative reaction. Patients with pituitary adenoma , even benign tumors, must be carefully followed up for signs of metastasis.
GH-producing adenomas clinically are endocrine-active tumors accompanied with acromegaly in most instances. However, GH-producing adenomas apparently unassociated with acromegaly, or so-called silent somatotroph adenomas (SSA), have recently been reported but rarely. The reported cases are characterized by normal or slightly elevated serum levels of GH but without acromegaly. Tumor cells contain moderate, trace or no GH immunoreactivity. We experienced 7 cases of SSA which were not always similar in morphology and pathogenetic mechanism. They could be further divided into the following 3 subtypes. Subtype 1 (N = 2): a moderate number of cells were immunopositive for GH, and GH mRNA was also expressed in moderate or numerous cells. Densely granulated cells were noted. It is assumed that inhibition of hormone release into circulation. Subtype 2 (N = 3): a small number of cells were immunopositive for GH, while GH mRNA was expressed in numerous tumor cells. They were sparsely granulated cells containing fibrous bodies. These findings suggest that posttranslational processing of the gene product may be defective. Subtype 3 (N = 2): Only a scattered number of cells were immunopositive for GH and GH mRNA was co-localized in immunopositive cells. They were sparsely granulated cells containing poorly developed organelles that did not resemble those of typical sparsely granulated GH cells. The findings indicate that adenoma cells are largely immature with minimal GH lineage differentiation.
Abstract. A 38-yr-old female with a TSH-and GH-secreting pituitary adenoma is described, who had both overt symptoms, hyperthyroidism and acromegaly. Her serum TSH was not suppressed despite high concentrations of free T3 and free T4, and her a-subunit/TSH molar ratio was high. Her serum GH was consistently high, and was not suppressed by an oral glucose tolerance test. Preoperative testing revealed that, although the TSH response was impaired, TSH, a-subunit and GH were increased by TRH injection, and that these hormones were reduced by bromocriptine or somatostatin analog. Although she did not have hyperprolactinemia, the in vitro culture and immunohistochemical studies revealed that the adenoma cells produced and released PRL, in addition to TSH, a-subunit and GH. Immunohistochemical studies showed the presence of GH in the cytoplasm of many adenoma cells. TSHI3-positive adenoma cells were less frequently seen than GH-positive adenoma cells. No cells showed the coexistence of GH and TSHI3, and a few cells were positive for PRL. By electron microscopy, the adenoma was found to be composed of a single cell type resembling thyrotrophs, and did not have any characteristics of somatotrophs. This case was considered to be of interest, because the adenoma was ultrastructurally monomorphous, but immunohistochemically polymorphous.
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