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H J Schneider, B L Herrmann, M Schneider, C Sievers, L Schaaf and G K Stalla

Objective: Patients with traumatic brain injury (TBI) are at moderate risk of GH deficiency (GHD), requiring a diagnostic test with high specificity. The GHRH + arginine (GHRH + ARG) test has been recommended as a reliable alternative to the insulin-tolerance test (ITT) as a standard test with a cutoff level of 9 ng/ml. However, it has recently been questioned for its low specificity in obese subjects, and now BMI-dependent cut-off levels are available. In this study, we compared the ITT and GHRH + ARG test in patients with TBI.

Design: A cross-sectional study

Methods: We performed an ITT and a GHRH + ARG test in 21 patients with TBI (6 women, 15 men; mean age 40.2 ± 12.1 years; BMI 30.7 ± 6.2). The number of patients classified discordantly as GH deficient by the ITT and the GHRH + ARG test with both classical and BMI-dependent cut-off levels was assessed.

Results: Using the GHRH + ARG test with the classical cut-off (≤ 9 ng/ml), we identified 12 patients as GH deficient who had a normal GH response to ITT (> 3 ng/ml), and one patient as GH sufficient who had a blunted GH response to ITT (discordance rate 61.9%). All patients discordantly classified as GH deficient by the GHRH + ARG test had a BMI of ≥ 28. With the BMI-dependent cut-offs (4.2, 8.0, and 11.5 ng/ml in obese, overweight, and lean subjects respectively), only 3 of the 21 patients were discordantly classified (discordance rate 14.3%).

Conclusions: Our results discourage the use of a cut-off level of 9 ng/ml for the GHRH + ARG test in obese subjects. The diagnostic reliability of this test is improved with the BMI-dependent cut-offs.

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M. KNOLL, L. SCHAAF, J. TEUBER, U. SCHWEDES, R. PASCHKE and K. H. USADEL

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L. SCHAAF, W. GEISSLER, E. GROSSMANN, M. EGGSTEIN and F. J. SEIF

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L. SCHAAF, W. F. BLUM, K. KIETZMANN, W. GEISSLER, F. J. SEIF, M. B. RANKE and K. H. USADEL

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I. HARSCH, R. PASCHKE, L. SCHAAF, B. SCHLOTE-SAUTTER, S. KAUMEIER, I. VARDARLI, J. TEUBER, U. SCHWEDES and K. H. USADEL

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I. VARDARLI, IMREN VARDARLI, R. SCHMIDT, J. TEUBER, R. PASCHKE, L. SCHAAF, B. SCHLOTE-SAUTTER, U. SCHWEDES, U. FELDMANN and K.H. USADEL

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JO Thiele, P Lohrer, L Schaaf, M Feirer, W Stummer, M Losa, M Lange, M Tichomirowa, E Arzt, GK Stalla and U Renner

OBJECTIVE: Interleukin-6 (IL-6), a member of the gp130 cytokine family, is considered to be an important modulator of function and growth in endocrine anterior pituitary cells. In pituitary adenomas, where IL-6 is often produced by the tumour cells, it is thought to be involved in pituitary adenoma pathophysiology via autocrine/paracrine mechanisms. METHODS: We have studied in primary cell cultures of human somatotroph adenomas whether IL-6 stimulates growth hormone secretion and whether intratumoral IL-6 is affected by various IL-6-regulating factors. RESULTS: Interleukin-6 stimulated GH secretion in 10 out of 11 somatotroph adenoma cultures (1.4- to 6.5-fold above basal levels). In comparative studies the GH-stimulatory potency of IL-6 was identical, or even stronger, than that of GHRH. In eight out of 11 adenoma cell cultures, IL-6 production was observed. This suggests that GH production might be stimulated by IL-6 in an autocrine/paracrine manner in these tumours. Dexamethasone strongly inhibited basal IL-6 secretion in all IL-6-producing adenoma cell cultures, whereas the IL-6 inhibitory or stimulatory action of other factors (octreotide, transforming growth factor-beta1, insulin-like growth factor-I, pituitary adenylate cyclase-activating peptide and oestradiol) were heterogeneous in the different adenomas. Only transforming growth factor-alpha consistently stimulated IL-6 secretion in all of the adenomas studied. CONCLUSIONS: Intratumoral IL-6, which is differently regulated by various factors, might contribute to excessive GH production in the majority of somatotroph adenomas.

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J Winkelmann, U Pagotto, M Theodoropoulou, K Tatsch, W Saeger, A Muller, T Arzberger, L Schaaf, EM Schumann, C Trenkwalder and GK Stalla

OBJECTIVES: The case presented here describes the clinical evolution of a malignant prolactinoma with occurrence of intra- and extra-cranial metastases. In this case, the presence of dopamine 2 receptor (D2R) was studied at the mRNA and protein level, in order to understand the pathological background of the resistance to treatment with different dopamine agonists. DESIGN: Together with an extensive description of the clinical history of this case, a combination of in vitro and in vivo techniques was performed to provide the basis of the dopamine resistance developed in the course of the disease. METHOD: A comparison of the D2R was performed in specimens obtained at presentation of the disease compared with autoptic specimens derived from local invasion and metastasis using in situ hybridization and immunohistochemical techniques. RESULTS: Intact D2R mRNA was found in the primitive tumor and metastatic tissues, whereas protein for the same receptor was present only in the tissues derived from neurosurgical operations and not in the metastases obtained post-mortem. CONCLUSION: This is the first report of the absence of D2R protein despite the retention of the transcript in an advanced stage of a malignant prolactinoma. The findings of this single case suggest the hypothesis that postranscriptional mechanisms may contribute to the development of dopamine resistance in prolactinomas.