Chronic orchidectomy does not influence the sensitivity of the pituitary somatotropes to varying doses of GHRH administered intravenously to the adult male rhesus monkey.

In the present study, the pituitary growth hormone (GH) response to graded doses of GH-releasing hormone (GHRH) was determined in intact (n = 3) and chronically orchidectomized (n = 3) adult rhesus monkeys (Mucaca mulatta). GHRH in doses of 0, 6.25, 12.5 and 25 microg/kg BW was infused through a teflon cannula implanted in the saphenous vein. Blood samples were collected 60 min before and 90 min after the injection of the neurohormone at 15 min intervals. All bleedings were carried out under ketamine hydrochloride anesthesia. The plasma levels of GH were determined by using AutoDELFIA time-resolved flouroimmunoassay, whereas plasma levels of testosterone and estradiol were determined using specific radioimmunoassay systems. The GH responses to GHRH were not significantly different between intact and chronically orchidectomized monkeys at any of the dose levels tested (p > 0.05). The administration of GHRH resulted in a significant (p < 0.05) stimulation of GH secretion at all the doses tested and in both the groups studied. In both intact and orchidectomized animals, the greatest response was observed at 6.25 microg/kg and no further increase was noted with the higher doses of GHRH. In conclusion, the present study suggests that chronic orchidectomy does not influence the sensitivity of the pituitary somatotropes to GHRH stimulation implying that the responsiveness of the pituitary somatotropes to GHRH is independent of testicular steroid modulation.

Evaluation of the UBC test in the urine of healthy individuals, patients with benign disorders and urinary bladder cancer.

Using the UBC test, the specificity, sensitivity and prognostic information were evaluated in patients with recently diagnosed transitional cell carcinoma (TCC) and in a control group consisting of apparently healthy individuals and individuals with benign disorders. Frozen urine samples from the 485 individuals in the control group and 100 newly diagnosed TCC patients were analyzed with the UBC test, specific for epitopes on cytokeratin fragments released from the urothelial cells. All the samples were analyzed and corrected for creatinine. No significant concentration difference was found between males and females (p=0.65) and there was no age dependent relation. The median concentration for the entire control group was estimated at 3.7 microg/g and the 95th percentile was calculated at 53.0 microg/g. The apparently healthy individuals in the control group had a median value of 3.4 microg/g with a 95th percentile of 24.3 microg/g. An increased frequency of elevated UBC concentrations was found in some benign disorders e.g., anemia, thyroid disorders, diabetes mellitus, hyperlipemia, urosepsis and cystitis. Patients with superficial tumors exhibited a 66% sensitivity (at 95% specificity), and the UBC concentrations did not differ statistically (p=0.16) from those patients with muscle invasive lesions with a 52% sensitivity. When the UBC concentrations were related to histopathological grade, a significant concentration difference (p<0.004) was found between low grade tumors (sensitivity 41%) and high grade tumors (sensitivity 72%). Survival analysis showed that patient with muscle invasive tumors, high-grade tumors and high UBC concentrations have a significantly reduced survival (five-year survival was estimated to 30%, 35% and 30% respectively) compared to patients with superficial tumors, low-grade tumors or low UBC concentrations (five-year survival, 60%, 85% and 75% respectively). The UBC test showed good accuracy and repeatability. Clinically the test could assist in tumor grading and the detection of recurrent disease, which in turn could assist in treatment selection for the individual patient and possibly improve prognosis.

Testosterone modulates growth hormone secretion at the hypothalamic but not at the hypophyseal level in the adult male rhesus monkey.

We investigated a possible modulation of growth hormone (GH) secretion by testosterone by measuring the growth hormone releasing hormone (GHRH)-stimulated and N-methyl-d,l-aspartic acid (NMA)-induced GH secretion in adult rhesus monkeys. Intact, orchidectomized and testosterone-substituted (testosterone enanthate 125 mg/week, i.m. for 5 weeks) orchidectomized monkeys (n=5) were used in the study. GHRH (25 microg/kg body weight) or NMA (15 mg/kg body weight) was infused through a Teflon cannula implanted in the saphenous vein. Sequential blood samples were collected 30-60 min before and 60 min after the injection of the neurohormone or the drug at 10-20-min intervals. All bleedings were carried out under ketamine hydrochloride anaesthesia (initial dose 5 mg/kg body weight i.m., followed by 2.5 mg/kg at 30-min intervals). The plasma concentrations of GH, testosterone and oestradiol (E(2)) were determined by using specific assay systems. Administration of GHRH elicited a significant increase in GH secretion in all three groups of animals. There was no significant difference in the responsiveness of pituitary somatotrophs to exogenous GHRH challenges between intact and orchidectomized monkeys and testosterone replacement in orchidectomized animals did not significantly alter the GHRH-induced GH response. The responsiveness of hypothalamic GHRH neurones apparently did undergo a qualitative change after orchidectomy, as GH response to NMA was less in orchidectomized animals than in intact monkeys. The responsiveness of GHRH neurones to exogenous NMA was restored and even potentiated when orchidectomized monkeys were treated with testosterone. Taken together, these findings suggest that testosterone does not affect the sensitivity of the pituitary somatotrophs to GHRH but stimulates the secretion of GH by modulation of the NMDA drive to GHRH neurones.

Case report and discussion of hearing preservation after translabyrinthine excision of small acoustic tumors.

OBJECTIVE: Since 1991, three separate reports have shown how hearing may be salvaged after translabyrinthine excision of small acoustic tumors. The authors submit yet another report of a complete translabyrinthine excision of a 1.4-cm intracanalicular acoustic tumor with modest hearing preservation. An attempt is made to retrace the steps of the operation and recognize and discuss what particular events may have safeguarded the viability of the cochlea. With the availability of cochlear implantation, there should be added incentive to preserve the cochlear neurones if hair cells cannot be saved. STUDY DESIGN: The study design was a retrospective case review. SETTING: The study was conducted at a primary care hospital. INTERVENTION: Therapeutic and rehabilitative measures were performed. MAIN OUTCOME MEASURES: Hearing preservation was measured. CASE REPORT: A 55-year-old woman presented with a left-sided hearing loss and a 1.4-cm left acoustic tumor completely filling the internal auditory canal (speech reception threshold [SRT] 30 dB, discrimination [Pb] 28%). A successful translabyrinthine excision of the tumor was performed in November 1995. A 1-year postoperative audiogram showed a mixed hearing loss in the left ear with SRT 85 dB and Pb 0%. Average pure-tone threshold for 500 Hz, 1 kHz, and 3 kHz was 50 dB and aided SRT 40 dB with Pb 64%. Postoperative magnetic resonance imaging confirmed complete excision of the tumor. CONCLUSION: An exceptional case of hearing preservation after translabyrinthine excision of a small acoustic tumor illustrates how it may be possible to preserve cochlear hair cells and neurones simultaneously in certain selected cases. A review of the surgical events shows the value of sealing the cochlear duct with bone wax, selectively removing the vestibular nerves with the tumor by sharp dissection, and safeguarding the meatal segment of the anterior inferior cerebellar artery by a limited dural incision.

Hearing preservation in microvascular decompression for trigeminal neuralgia.

OBJECTIVE/HYPOTHESIS: Sensorineural hearing loss is a disturbing complication of microvascular decompression (MVD) for trigeminal neuralgia with an incidence of 1% to 23.8%. Cerebellar retraction with increasing I-V interpeak latency (IPL) during intraoperative brainstem auditory evoked potentials (BAEP) has been identified as the chief cause of acoustic injury. This study was designed to eliminate cerebellar retraction by a modification of the standard suboccipital craniectomy. STUDY DESIGN: Nine consecutive patients undergoing surgery for trigeminal neuralgia were prospectively selected for this study between 1994 and 1995. METHODS: Preoperative and postoperative audiograms were obtained. Preoperative and intraoperative BAEPs were performed. The surgical modification describes initiating a partial mastoidectomy to enhance early recognition and delineation of the sigmoid and transverse sinuses crucial to maximizing the lateral extent of the craniectomy. The additional exposure gained by this technique allows for improved visualization of the brainstem without cerebellar retraction. RESULTS: All patients were relieved of neuralgic pain. Postoperative IPL values were not significantly different from preoperative values (4.9+/-0.6 vs. 4.7+/-0.3 ms). Maintaining IPL of less than 1.5 ms is considered critical for preventing injury to the auditory nerve. In this study the average increase in postoperative IPL was 0.25 ms for the ipsilateral ear and 0.1 ms for the contralateral ear. CONCLUSIONS: The authors offer a surgical modification of the standard suboccipital craniectomy and furnish intraoperative neurophysiologic data to demonstrate how cerebellar compression can be eliminated and hearing preserved in MVD for trigeminal neuralgia.